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EFFECTS OF CHANGES IN PLASMA VOLUME, OSMOLALITY AND

SODIUM LEVELS ON CORE TEMPERATURE DURING PROLONGEDEXERCISE IN HEAT

byWilliam S: Lackland

Thesis submitted to the faculty of theVirginia Polytechnic Institute and State University

in partial fulfillment of the requirements for the degree ofMASTER OF SCIENCE

****"""""“"“‘”‘“““_’———_——’———————————“"""___————————————_—————””%H%0EIII

I

"‘ .EFFECTS OF CHANGES IN PLASMA VOLUME,

_ OSMOLALITY AND SODIUM LEVELS ON CORE

é TEMPERATURE DURING PROLONGED EXERCISE IN HEAT

bv

William S. Lackland

(ABSTRACT)

Six adult males of similar body composition and aerobiccapacity were tested to study the effects of changes inplasma volume (PV), osmolality (OSM) and sodium (Na+) oncore temperature (Tc) under three exercise-thermoregulatory

stress conditions. The protocol consisted of 120 min ofupright stationary cycling at 50% V02max under neutral (24°C, 50% RH) - euhydrated (NE), hot (35°C, 50% RH) -euhydrated (HE), and hot-hypohydrated (HH) environmental

conditions. Venous blood samples were obtained at -30 min,

0 min and at 15 min intervals through a 30 min recovery andwere analyzed for blood hematocrit and hemoglobin, and forplasma osmolality and sodium. Hematocrit and hemoglobinwere used to calculate relative changes in plasma volume.Tc showed qualitatively similar linear increases in thefirst 45 min of each trial. At 60 min, Tc in the NE trial

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plateaued at 37.9°C. In the HE trial, Tc continued to showa slight further increase after 45 min while in NE it becamesignificantly (p<0.05) lower at 45 min as compared to HE andHH; at 60 min of exercise, the core temperature of all threetrials differed significantly (p<0.05), with HH being thehighest (38.3°C). Percent change in plasma volume was notdifferent between trials, but did show the greatest decreasein all trials from O to 15 min of the exercise phase with atleast -4.3%. Osmolality was significantly different(p<0.05) between the NE (X = 283.3 m0smol/kg) and the HH (X= 292.5 m0smo1/kg). Plasma sodium was significantly(p<0.05) higher for all intervals of HH (X = 137.9 meq/L) ascompared to the NE (X = 135.1 meq/L) and HE (X = 134.8meq/L). These data suggest that core temperature (Tc)

increase in moderate intensity endurance exercise is lessrelated to a decreased circulating plasma volume, but ismore strongly associated with rising osmolality,

specifically the increase in the Na+ electrolyte, whichoccur with progressive hypohydration.

Index terms: core temperature; plasma volume; osmolality;sodium; prolonged exercise thermoregulation; euhydration;

hypohydration.

»

ACKNOWLEDGEMENTSA

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Finally, I would like to thank all my friends for theirconstant support, encouragement, and understanding duringthe writing of this thesis.

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TABLE OF CONTENTS

Page

ABSTRACT............................................. iiACKNOWLEDGEMENTS..................................... ivLIST OF TABLES....................................... ixLIST OF FIGURES...................................... x

I: INTRODUCTION................................... lStatement of the Problem....................... 4Research Hypotheses............................ 4Delimitations.................................. 5„ Limitations.................................... 5Definitions of Terms........................... 6

II: LITERATURE REVIEW.............................. 7Heat Injuries and Prevention in ProlongedExercise...................................... 7Heat Cramps and Treatment.................... 7Heat Exhaustion and Treatment................ 8Heat Stroke, Complications and Treatment..... 9Advice to Race Officials..................... 14

Theoretical Considerations of TemperatureRegulation during Prolonged Exercise in theHeat.......................................... 17Central Mechanism Control Factor Theories.... 19Peripheral Factors........................... 27

Baroreceptors.............................. 28Chemoreceptors............................. 29Sweat Gland Function....................... 30Skin Temperature........................... 32

Constitutional·Factors Modifying TemperatureRegulation.................................... 33Age.......................................... 34Sex.......................................... 36Exercise Capacity............................ 36Acclimatization and Training................. 38Anthropometry (mass/body surface arearatio)...............................„...... 39

Environmental Factors Modifying TemperatureControl....................................... 4lAmbient Temperature.......................... 41Relative Humidity............................ 42Wind Velocity................................ 43

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u

Heat Loss Modes.............................. 44Individual Factors Modifying TemperatureControl....................................... 45Intensity and Duration....................... 46Mode of Exercise............................. 47Hydration State.............................. 48Intracellular Fluid Compartment andExtracellular Fluid Compartment............. 50

Electrolytes................................. 52Osmolality................................... 53Protein...................................... 54

Summary........................................ 55III: JOURNAL MANUSCRIPT............................. 56

Abstract....................................... 57Introduction................................... 59Methods........................................ 60Results........................................ 63Discussion..................................... 66References..................................... 70

IV: SUMMARY AND RECOMMENDATIONS FOR FUTURERESEARCH....................................... 84Summary........................................ 84Recommendations for Future Research............ 87Recommendations for Race Sponsors and Runners.. 89

REFERENCES........................................... 92APPENDIXES........................................... 103

A: Detailed Methodology........................... 103B: Detailed Blood Procedures...................... 115C: Mean Data Tables.........,..................... 132D: Data Tables..................,................. 137E: Raw Data....................................... 142F: Informed Consent............................... 149G: Correlation Matrices........................... 155VITA................................................. 157

•

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LIST OF TABLES

TablePage1:

Summary of Analysis of Variance................. 762: Subject Characteristics (means f SD)............ 773: Mean Core Temperature Response (°C) During

120 min of Stationary Cycling in DifferentEnvironments and States of Hydration............ 79

4: Mean Plasma Volume Responses (Z) During 120min of Stationary Cycling in Different -Environments and States of Hydration............ 80

5: Mean Osmolality Responses (mosmol/kg) During120 min of Stationary Cycling in DifferentEnvironments and States of Hydration............ 82

6: Mean Sodium Responses (mEq/L) During 120min of Stationary Cycling in DifferentEnvironments and States of Hydration............ 83

7: Mean Core Temperature Response (°C) During120 min of Stationary Cycling in DifferentEnvironments and States of Hydration............ 133

8: Mean Plasma Volume Responses (Z) During 120”min of Stationary Cycling in DifferentEnvironments and States of Hydration............ 134

9: Mean Osmolality Responses (mosmol/kg) During120 min of Stationary Cycling in DifferentEnvironments and States of Hydration............ 135

10: Mean Sodium Responses (mEq/L) During 120min of Stationary Cycling in DifferentEnvironments and States of Hydration............ 136

ll: Individual Weight Loss (Z) During 120 minof Stationary Cycling in DifferentEnvironments and States of Hydration............ 138

12: Environmental Conditions of NeutralEuhydration Trials.............................. 139

13: Environmental Conditions of HotEuhydration Trials.............................. 140

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I14: Envitonmental Conditions of Hot

Hypohydration Trials............................ 14115: Raw Data for Subject #1 (DG).................... 143

16: Raw Data for Subject #2 (ED).................... 144

17: Raw Data for Subject #3 (TK).................... 145

18: Raw Data for Subject #4 (JW).................... 14619: Raw Data for Subject #5 (GJ).................... 14720: Raw Data for Subject #6 (BL).................... 148

21: Correlation Matrices............................ 155

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E- LIST OF FIGURES

Figure Page

l: Schematic Representation of the Thermo-regulatory System and Factors thatInfluence its Control. C=cold, W=warm,A=sensor activity, T=temperature, HP=heat production, and HL=heat loss............... 26

ll: Graphic Representation of Mean Values ofSix Subjects for Core Temperature andPlasma Volume During Cycle Ergometry............ 78

2: Graphic Representation of the Mean Valuesof Six Subjects for Plasma Osmolality andPlasma Sodium During Cycle Ergometry............ 8l

x

éChapter I

INTRODUCTION

Exertional heat stroke is a clinical problem thatresults from prolonged physical exercise under variousenvironmental conditions. It is a most prevalent problemwhen ambient temperature and relative humidity are high.The human body must dissipate heat even while resting in ahot environment, but the additional heat production ofexercise compounds the situation. During intensiveexercise, such as marathon running, heat is produced in thecontracting muscles at rates in excess of 1100 W, a ratewhich is 15 to 18 times greater than the basal metabolicrate (Nadel, Wenger, Roberts, Stolwijk, & Cafarelli, 1977).Therefore, running a marathon in a hot environment with a

high relative humidity will compromise both performance andhealth, even for the elite athlete, if adjustments in pacing

and fluid intake are not made. An increase in environmentalhumidity reduces the vapor pressure gradient between theskin and air, and thus, diminishes the evaporative process.Even when the external heat load is moderate, strenuousphysical effort can contribute to the pathophysiology ofexertional heat stroke (Hubbard, 1979).

In 1980 more than 1,000 deaths in the United Statesalone were attributed to the heat (Abromowicz, 1980).

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Everyone is a potential victim of a heat related injury.This includes well trained athletes to novices, young andold, and physically fit to the seriously ill. However, theindividuals that are most susceptible to heat injuries arethe young and old and the seriously ill or least fit.Relatively high proportions of heat stroke cases are beingreported during sporting events, particularly those whichlast an hour or more, in warm and humid weather. Trainedathletes are not exempt; examples include a Tour de Francecyclist (Bernheim & Cox, 1960), 3 Danish cyclists at thesummer Olympics in Rome 1960 (Shibolet, Coll, Gilat, &Soher, 1967), and marathon runners (Pugh, Corbett, &Johnson, 1967; Wyndham, 1977). The most vulnerable

I

participants in a long distance run are the novices

(Hughson, Green, Houston, Thomson, MacLean, & Sutton, 1980).( Among those who compete in road races of 10K or longer

distances, a small number of novices will generally be foundicollapsed at the finish line on warm days due to heat

stress. Novice runners have a tendency to push themselvesbeyond their capacities to attain personal records. Novicesoverestimate their abilities when the day is warm, the sunis bright (high radiant heat) and they feel great. They canpush for that personal record, ignoring their exerciselimitations and water replacement. Novice runners will

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compromise their training and begin the race at a much

faster pace than they can maintain without experiencing heat

storage. Then they try to hold a pace seconds, even aminute, faster than they are accustomed to running. Trying

to hold this pace, they will not stop to gain waterreplacement and will not foresee the early warning signs ofheat strain.

Other related literature on heat injuries includescases involving football players (Graber, Reinhold, &Breman, 1971), industrial workers (Wyndham, 1965), andrecruits in the armed forces (O'Donnell, 1975). There hasbeen increasing evidence that in healthy young males, anexcessive exercise intensity is the essential factor in the

development of exertional heat stroke; the individuals areforced to complete a task in a hot environment for aprolonged period of time and usually without proper fluidreplacement.

In summary, there are four main factors that can affectthe possibility of a heat stroke. They include theenvironmental aspects such as ambient temperature, humidity,wind velocity, insulation and clothing; water intake; the

intensity and duration of the exercise; and the recent

acclimatization to heat. It becomes evident, when examiningthese factors, that even a slight variation in the stress

conditions could result in an unexpected response, leadingto widespread functional and tissue damage or even death tothe individual.

Statement gf th; Problem

When man is subjected to moderate-vigorous prolongedphysical exercise in a warm environment his core temperature(Tc) rises progressively over time; this rise can possibly

lead to exertional heat exhaustion and/or heat stroke. Theprecise mechanism for this rise in core temperature is stillunclear. Thus, the primary problem seems to relate tounderstanding the stimuli which lead to ineffective controlof the temperature regulatory centers. Could this center

(hypothalamus) be impaired by declining circulating bloodvolume, rising body fluid osmolarity or hypernatremia (highNa+)? Therefore, the objective of this study was to

investigate the role of selected hematologic factors in therise of the core temperature.Research Hypothesesl. Ho: There will be no time related changes in core

temperature, or in plasma volume, osmolality, and sodiumduring a prolonged cycling exercise of moderateintensity in three different thermogenic conditions.

2. Ho: Core temperature, plasma volume, osmolality andsodium patterns in prolonged exercise do not

5 2significantly differ between the aforementioned Etreatment conditions. E

3. Ho: If there are any changes in plasma volume,‘

osmolality, or sodium under these different thermalconditions, these do not influence the rate of rise incore temperature.

DelimitationsThe following delimitations were imposed:

l. only male subjects with less than 20% body fat, who weremoderately active and possessed maximal oxygen uptakesbetween 40-60 ml•kg‘*•min°*, were studied;

2. a 2 h cycling bout at 50% Ü02max served as the criterionexercise;

3. only two environmental conditions were imposed, i.e., 24°C, 50% RH vs 35°C, 50% RH.

LimitationsDue to the foregoing delimitations, the following major

limitations apply to this study:

l. these results may be applicable only to males possessingthe same physiological characteristics as the subjectsin the study;

2. these results may only be applicable to individualsinvolved in stationary leg cycling at of moderateintensity (50% Ü02max);

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3. these results may not be applicable to environmentalchamber conditions used beyond the temperature andhumidity ranges imposed in this study;

4. the sample size was limited to six volunteers.Definitions

l. ggg; Temgerature (Tc): Deep body temperature obtained

by esophageal, rectal or tympanium measurements.2. Euhydration: The process of replacing body water losses

and maintaining a water balance within the body.3. Hyoerhydration: A state of excessive water content in

the body due to ingestion of "extra" water.4. Hygohydratiog: A state of decreased water content of

the body. A greater loss of water than salt.5. Maximal Oxygen Ugtake (VO2max): The maximal amount of

oxygen that can be consumed in dynamic, large-muscleactivity, usually expressed in liters•min 1 or

ml•kg’1•min“1.16. Osmolalitv: osmotic concentration, defined as the

number of osmols of solute per liter of solution.7. Plasma Volume (PV): The total non-cellular fluid volume

of the circulating blood found in the intravascularspace.

10. Rectal Temgerature (Tr): The temperature measured15-17 cm into the rectum. An acceptable means ofestimating core temperature.

Chapter II

REVIEW OF LITERATURE

ggg; Injuries ggg Prevention gg Prolonged Exercise

When the body is unable to adapt to a heat stresscondition, three major clinical disorders might presentthemselves: heat cramps, heat exhaustion, and heat stroke.Although these conditions are all mediated by a loss of bodywater and/or electrolytes, coupled with an inability todissipate heat, the etiologies and clinical significance aresomewhat different with each disorder.

ggg; Cramgs. Heat cramps are the least severe of theheat disorders and are common, even in well—acclimatizedathletes who are in good physical condition. The main signis an acute, intermittent, painful cramping in skeletalmuscles, generally in the calf or abdominal area. The exactcause is unknown, but it is speculated to be prolonged,excessive sweating, which results in a loss of body fluidsJand/or local electrolyte imbalances, mainly sodium chloride,potassium, and magnesium (Cain, 1985). In a case of heatcramps no abnormal signs or symptoms will appear and thecramps will disappear within a few minutes, spontaneously.The treatment for this disorder would be to rest in a coolplace and replace lost fluids. To prevent heat cramps, itis important to insure adequate hydration and increase the

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8 II

consumption of foods rich in these electrolyes, but withoutthe salt tablets due to the electrolyte imbalance produced(Dasler, 1973).

Hga; Exhaustion. Heat exhaustion, or heat prostration,

is the most common heat disorder. It results from prolongedexposure in high environmental temperature and humidity,which causes an excessive water loss in the body. Thisdisorder occurs mainly in unacclimatized individuals.Fatalities are rare, but when such do occur, a predisposingconstitutional disorder has generally been involved.Depending on the severity of the water loss, a wide range ofsymptoms may be presented including fatigue, excessive

thirst, anxiety, weakness, and impaired judgment. These

symptoms may lead to central nervous system impairmentsmanifested by hyperventilation, muscle incoordination,agitation and hysteria (Feinstein, 1985). The clinicalsigns are a rectal temperature of approximately 40°C,Jdehydration, and a reduced ability to sweat in some cases.The treatment for heat exhaustion is to move the individualto a cooler and less humid surrounding, give fluids if thevictim is able to swallow; if voluntary water consumption is

not possible, intravenous fluids of isotonic saline shouldbe started, and a blood chemistry and urinalysis performed.If recovery is slow, it is important to evaluate the victim

9

and treat for any underlying factors or secondarycomplications (Cain, 1985).

Egg; Stroke. Heat stroke is the least common but themost serious of the heat disorders. Heat strokes alone inthe last 10 years have killed 50 football players, and inorder of prevalence, heat stroke ranks second after spinalinjuries among reported cases of death in high school

athletes (Knochel, 1975). Heat strokes are preventable andto allow their continuous occurrence in sports events isinexcusable. Obviously, a preventive approach is betterthan emergency treatment, but for prevention to beeffective, there must be a clear understanding of both thecircumstances that lead to the disorder and its

pathophysiology.

Healthy, highly acclimatized, and physically fitathletes can suffer a fatal heat stroke when the body's heatload exceeds its ability to dissipate heat. This failure isa result of a breakdown of the normal sweating andthermoregulatory mechanisms and leads to mental confusion,

anhidrosis, and a rectal temperature in excess of 41°C(l08.8°F). The rectal temperature is the most importantpart of a triage. It helps distinguish between heat strokeand heat exhaustion and indicates the severity of thesituation. Heat stroke is invariably fatal unless

10recognizedearly and treated accurately. A11 untreatedvictims of heat stroke will die (Cain, 1985).

Even with rapid treatment, the mortality rate can be as

high as 50%, especially in the elderly with predisposingfactors such as heart disease, obesity, heavy-alcoholingestion, diabetes mellitus, previous heat injuries, andthose taking certain medications (diuretics, tricyclic

antidepressants, anticholinergics, phenothiazines,amphetamines, and lithium). The normal circulatoryadjustments for the elderly person or individuals with theaforementioned predisposing factors or secondarycomplications is to compensate for heat stress by decreasinglthe cardiac output (0) and increasing their peripheral

resistance. However, when the environmental conditions

cause an excess of heat in the body, a tachycardia anddecreased peripheral resistance will cause peripheralpooling and a hypovolemic condition will then exist whicheventually will lead to circulatory failure (Khogali, 1983).

"Exertiona1" heat stroke occurs in athletes, military

recruits, and industrial workers who perform manual labor inhot, humid environments. The circulatory adjustments that

are required to dissipate heat loads in healthy individualsare an increase in heart rate, an increased cardiac output

(0), and a decrease in peripheral resistance (O'Donnell &

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Clowes, 1972). With an exertional heat stroke, there willbe, in most cases, profuse sweating, but as the temperature

of the body increases rapidly above 4l°C sweating willeventually cease due to probable heat damage to the sweatglands causing anhidrosis (Shibolet, Lancaster, & Danon,1976). Early warning signs of both environmental and"exertional" heat stroke are headache or throbbingsensations in the temples, nausea, vomiting, dizziness,piloerection (gooseflesh) of the upper chest and arms,unsteady gait, and disorientation with gradual impairment ofconsciousness (Hubbard, 1979). „

With the excessive heat load that occurs in heatstroke, eventual widespread cellular damage may begin to '

occur in the vital organs and skeletal muscles. Centralnervous system complications can include a coma, convulsionsor even a cerebrovascular accident. Heart failure due tosinus tachycardia, and an accompanying hypotension ormyocardial infarction may also occur in the heart (Kew,

Tucker, & Bersohn, 1969).

During "exertional" heat stroke, serum

glutamicoxaloacetic transaminase (SGOT) and lactate

dehydrogenase (LDH) are grossly elevated, andhyperbilirubinemia may occur arising from liver damage (Kew,Bersohn, & Kent, 1970). Impaired coagulation may occur in

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severe cases with complications of thrombocytopenia,prolonged bleeding and clotting, lowered plasma fibrinogenand prothrombin levels and increased fibrinolytic enzymeactivity (Hart, Egier, Shimizu, Tandon, & Sutton, 1980).

Kidney problems may arise secondary to heat stroke,including conditions ranging from acute renal failure toNchronic nephritis (Kew, Abrahams, & Levine, 1967).Myoglobinuria may also be present, suggesting muscle celldamage (rhabdomyolysis) and renal insufficiency. Ifphysical activity continues under conditions of impending orevolving heat stroke, so will the release of certain timeenzymes SGOT, LDH, and creatine phosphate kinase (CPK) occur

into the circulatory system from vital organs, indicating

thermal injury (Hart et al., 1980; Hubbard, 1979).Myoglobinuria, excessively high serum CPK and uric acidlevels from the skeletal muscle will complicate renalfunction leading to possible renal failure, following theacute period (Hart et al., 1980).

The treatment of heat stroke requires trained personnelto immediately recognize imminent warning signs, and ifthese are present, procedures must be started promptly to

effect cooling, rehydrate and correct circulatory collapse.When the rectal temperature is measured at 4l°C or

above, cooling strategies must begin immediately. The old

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method of cooling was to remove all the clothing of thevictim and place him in an ice bath. This method proved tobe difficult if the victim was disoriented and combative.It was also dangerous since it was very difficult to controlthe extent of fall in the rectal temperature. If the bodyis cooled below 38.9°C (102°F), it is hard to control bodytemperature and the victim become hypothermic. Thus,circulatory shock and death might subsequently occur duringthe rewarming phase. Ice baths can also cause peripheralvasoconstriction which interferes with proper heat loss(Abromowicz, 1980).

The most effective method of cooling the body is viaice water sponge baths and application of ice packs to theabdomen, axilla, neck and groin regions. An alternative isto place the victim in a shaded area or an air conditionedroom and sprinkle cold water on him while fanning the body.Rectal temperatures should be taken every 5 minutes. Duringcooling it will take about one hour to reduce the victim'srectal temperature below 30°C. During this time medicalattendants should guard against possible circulatory shockand metabolic acidosis. Intravenous fluids should bestarted to guard against this circulatory shock and sodiumbicarbonate should be infused to guard against metabolicacidosis (Feinstein, 1985).

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The victim should be moved to a shaded, cool placewhere cooling and rehydration can begin. No fluidpreparation is better than water in replacing sweat and

preventing heat injuries. A person with heat stroke shouldbe moved as soon as possible to a hospital to be stabilizedand observed at least for 24 to 36 hours (Hart, et al.,1980). Thereafter, an accurate record of intake/output ofbody fluids must be made and serum electrolytes and enzymesmonitored closely during the hospitalization (O'Donnell,1975).

The medical director, the race director, and theirstaffs, and all competitors in an event need to be educatedabout the awareness prevention of heat injuries. Themedical director should be knowledgeable in exercisephysiology and sports medicine and should coordinate allpreventive and therapeutic aspects of the running event(ACSM, 1984). A hospital in close proximity to the runshould be notified and available ambulance service should beplanned far in advance. These arrangements should beverified periodically before the actual date to insureadequate support for the event. The medical staff should bewell trained and equipped to handle any emergency at acentralized location at the race site, and they should havea step by step procedure for triage and treatment of all

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emergencies. Medical personnel with transportation shouldbe positioned along the route to give immediate aid whenneeded.

The race director and his staff should be aware of thelikelihood of heat injuries when planning a race. If theysponsor an event in the hot summer months, they shouldschedule the event before 8 a.m. or after 6 p.m. (ACSM,1984). The event should be delayed or rescheduled if thereis a 5°C increase in air temperature above that for thepreceding day and the relative humidity is above 50%(Hughson et al., 1980). The race route should be designedas an "out—and—back" course to make supervision easier andshould be located predominantly in shaded areas (Moore,1982). 0n the entry form, all precautions for hotconditions should be listed because information at thestarting line is usually not heard or heeded. Warning flagsfor thermal stress should be clearly visible at the startingline, if heat stress conditions prevail. During the race,accurate and frequent split times should be given.Additionally, well-staffed watering stations must be spacedevery 2-3 km along the course (ACSM, 1984).

Hyperthermia is still the most common serious problemencountered in North American fun runs and races, andcompetitors should be made fully aware of this fact (ACSM,

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E1984). Competitors need to be educated about water intake,the early warning signs of heat stress, proper clothing,prior training and acclimatization. Inadequate fluid intake

is a major factor in the occurrence of man's heat injuries.

Asking runners to drink "to satiation" is not adequate.

Thirst mechanisms are satisfied well before body fluid

losses are replenished. Man, when subjected to heat stress,

will not drink sufficient fluids to replace evaporativewater loss, but will suffer from voluntary dehydration(Shibolet et al., 1976). Therefore, everyone participatingin prolonged exercise in heat should be encouraged to drinkat least 500 ml of cool water 15 to 20 minutes prior to theevent, and to drink 250 ml at every water station. _Competitors should avoid solution with high sugarconcentration since they retard gastric emptying and water

assumption in the intestines (Ribisl & Herbert, 1980).Competitors should be constantly aware of the early

warning signs. Runners can and should assume a major role

in the prevention of serious heat injuries; these are

dizziness, weakness, confusion, unsteady gait, irritability,or disorientation. The ACSM position stand of 1984 suggests

"partner running," with each partner being responsible forthe other's well-being and watching for the warning signs.A given competitor should refrain from participation if he

17

or she has had a recent fever or has one at the time of the

g event. Clothing should be light·weight and consist of onlyone layer of absorbant (cotton) material; such attire willaid in the evaporative process. Up to 70% of the coolingeffect of evaporation can be lost when clothing inhibits airconvection, radiation and evaporation (Robertshaw, 1983).Furthermore, a light colored hat is vital to protect the

ßhead because it reflects solar radiation and allows properdissipation of heat.

Prior training and acclimatization are preferred foroptimal performance in heat. A competitor should know hisexercise capacities and stay well within these whileperforming in a hot environment. But competitors should

also avoid any sudden increases in pace at the end of arace, as this has been shown to cause problems in heat(Hanson & Zimmerman, 1979). Finally, by graduallyincreasing the amount of exercise per day, acclimatizationcan occur with 10 to 14 days after exposure to a warmenvironment and this adaptation will markedly improve thecapacity for dissipating heat loads during the race.

Theoretical Considerations gf Temgerature Regulation

During Prolonged Exercise ig ;Eg Egg;

A basic overview of the neurogenic pathways, on whichthermoregulatory signals travel, is necessary to understand

118

before discussing the theories of the thermoregulatorysystem. The operation of the thermoregulatory system willbe divided into two main sections: 1) central mechanismcontrol factor theories, and 2) peripheral factors.

The basic network is centered around a central nervousinterface, which lies between the temperature sensors andthe thermoregulatory correction effectors. The centralnervous interface receives and interprets information

transmitted to it from the sensors and issues appropriate

signals to the effectors to correct the disturbance. Theprincipal central nervous interface is located in thepreoptic anterior hypothalamus, a region of the midbrain.Secondary central nervous interfaces are located in themedulla oblongata and the thoracic spinal cord (Bligh,1979).

The pathway from warm sensors leads through thehypothalamus directly to heat loss effectors and from cold-sensors to heat production effectors. These sensors arefree-nerve endings located superficially, in the body coreand in the hypothalamus itself. Cold-sensors are closer tothe surface of the skin and much more abundant than warm-sensors, but warm sensors are more abundant around thehypothalamus (McArdle, Katch, & Katch, 1986).

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19 F

These sensors are stimulated externallyby)

environmental temperature changes, and internally byincreased heat production due to exercise or increasedenergy demands. The venous blood from the tissues active inheat production or heat loss drains back to the heart andlungs, and becomes thermally well mixed. The temperature ofthe arterial blood pumped out of the left side of the heartacts as a thermal feedback to the sensors (thermoreceptors),thus reducing or negating the disturbance signals (Bligh,1979). Through a set-point determinant and the hypothalamicthermoreceptors, a comparison is made, and according to thedirection and amount of offset, the appropriate effectorsystem is activated to help maintain a constant deep body

temperature.

Central Mechanisms

Many theoretical views have been proposed to describe

thermoregulatory control. The major differences in theseviews entail: 1) whether or not there is a set-pointdeterminant, 2) whether or not there is a central control

and its location(s), and 3) the mechanism(s) by whichthermoregulation operates.

Vendrik (1959) was one of the first to describe a set-point hypothesis of thermoregulation. According to him, thesystem was a genetically fixed activity/temperature

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characteristic of the warm- and cold—sensors. The opposingactivity/temperature of these sensors would function as a

set—point determinant by adjusting the intensities of

thermoregulatory heat production and heat loss effectors inopposing ways. A point of equilibrium would then be reachedbetween heat production and heat loss. Therefore, thespecialties of temperature regulation lie in the propertiesof the sensors and the thermoregulatory effector, ratherthan in the central nervous interface.

Benzinger, Kitzinger and Pratt (1963) described the

thermoregulatory mechanism as a reflex response to loss orgain of heat from the stimuli of temperature at the sensorylevel. His hypothesis was that the behavioral defense

l

against overheating originates from central hypothermia.The core temperature, not the skin temperature, is thesource of the heat complaint. Therefore, the autonomic andbehavioral thermoregulation originated from the core, notskin temperature. Central warm-sensors in the pre—optic

anterior hypothalamus elicit sweat secretion and cutaneousvasodilation for increased heat loss, and cold—sensors underthe surface of the skin elicit metabolic overproduction inresponse to cold. Skin cold-sensors inhibit sweating andcentral warm-sensors inhibit overproduction of heat.

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They also demonstrated that the core temperaturethresholds for heat production and evaporative heat lossVary with Variation in the ambient temperature or skin

temperature. The power of the responses compared to thesmall amount of stimulation is unbelievablec A O.1°C changeof central temperature may double the normal rate of heatloss or heat production.

One of the first theoretical Views using thehypothalamus as the control center with a set—pointdeterminant, was presented by Feldberg and Myers (1963).They stated that the mechanism was a biochemical gatinginfluence on thermosensors to the thermoregulatory pathways.Their concept was that adrenaline and nor-adrenaline are

Acontinuously released in sufficient amounts in the anteriorhypothalamus to keep the temperature at a constant level.When pyrogens or 5-hydroxytryptamine (5-HT) were introduced

into the body, the temperature would increase, and whenadrenaline and nor-adrenaline were injected into thecerebral Ventricles, the temperature was brought down tonormal or nearly normal depending on the amounts injected.Through biochemical gating, 5-HT and nor—adrenaline releasedfrom the anterior hypothalamus are in functional oppositionto one another in order to control body temperature around aset—point. A rise in temperature could also be obtained byinhibiting the release of non—adrenaline or adrenaline.

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Hammel (1965) described a theoretical neuronal model hecalled temperature sensitive neurons "high Q10 units" andtemperature insensitive neurons "low Q10 units". Theinteraction between the two populations of neurons

determined the set—point. The set point was reached whenthe activities between the two populations were equal. Whenthe temperature was above the set-point, the activity of the

n

high Q10 neuerons was greater than that of the low Q10neurons. The thermoregulatory responses when the coretemperature was above the set-point increased heat losseffectors and reduced heat production effectors. When thecore temperature was below the set-point, the opposite wastrue. These populations of neurons were interneurons uponwhich the pathways from peripheral temperature sensorsimpinged (Hammel, 1965). _

The set—point was affected by many physiologicalfactors including changes in skin temperature. Thisadjustment in the set—point temperature due to changes in

skin temperature was attributed by Hammel (1965) to a shift

in the activity/temperature characteristics of both the highQ10 and the low Q10 neurons, and to the hypothalamictemperature at which the activities of the neurons wererated in response to a fall in skin temperature. Theseshifts in set-point temperature could account for an

‘ 23 {

increase in heat production in response to a fall in skintemperature and an increase in heat loss in response to arise in skin temperature in the absence of any prior changein hypothalamic temperature.

A possible ionic mechanism used to regulate bodytemperature was given by Myers and Veale (1970). Theseresearchers proposed that the set—point for body temperaturewas controlled by osmoreceptors within the posteriorhypothalamus, and that the set-point was maintained anddetermined by the ratio in the concentrations of twoessential cations, Na+ and Ca++. If a normal physiologicalconcentration of both Na+ and Ca++ was perfused at sites inthe posterior hypothalamus, the temperature was unchanged.If the Na+ ratio to the concentration was increased, itproduced shivering and immediately, the temperatureincreased sharply. When Na+ was omitted and Ca++ was normalor in excess, the temperature fell sharply. Myers and Veale(1970) hypothesized that the constancy in the concentrationof extracellular ionic constituents maintains the firingrate of the neurons of the posterior hypothalamus.

At a procedural symposium in Paris on temperature

regulation and drug action, Myers (1974) integrated themonoamine mechanism and the ionic mechanism of control by

the hypothalamus of body temperature. He hypothesized that

24

the monoamine-containing neurons controlled the anteriorhypothalamic set—point mechanism (Feldberg & Myers, 1963),and the ratio of cations determined the posterior

hypothalamic set—point mechanism (Myers & Veale, 1970) andadded that acetylcholine (ACh) transmitted the impulsesignaling thermostasis. The net effect of 5-HT,

acetylcoline, Na+ ions, and pyrogens was the same:hyperthermia, conversely, nor-adrenaline, adrenaline, andCa++ ions bring hyperthermia back to a set—pointdeterminant.

Houdas, Lecroart, Ledru, Carette and Guieu (1978)doubted whether a set—point existed at all. They suggesteda model in which the controlled variable was the heatcontent of the body, and the load error signal thatactivates the control actions is a change in heat control.These changes in heat content are measured as changes oftemperature at various sites by means of signals originatingin all the thermoreceptors of the body. Therefore, what ismeasured in an average body temperature, as long as the heatcapacity of the body does not change, the average bodytemperature remains parallel with heat content. But thiscorrelation will not work with changing heat capacity, whichoccurs during growth and during gain or loss of weight inadults.

25Bligh(1984) combined his work from 1979 with themodels (Figure 1) presented by Hammel (1965), Wyndham andAtkins (1968), and the principles of central neurology(Sherrington, 1906). The resulting model allowed for the"resetting" of the set—point with changes in skintemperature and within other non—thermal environmental andphysiological disturbances. The variability of theeffective set—point in temperature regulation is a

consequence of the synaptic convergence of other influenceswithin the central nervous system. It allowed for speciesand seasonal variations in the level at which bodytemperature is held. These variations could depend on:genetically—fixed differences in the activity/temperatureprofiles of the warm- and cold-sensors (Vendrik, 1959); theconcentrations of warm and cold sensors located in variousparts of the body; and upon seasonal variations in theintensities of excitatory and inhibitory influences actingon the central neuronal pathways.

The cutaneous tissues, spinal cord, and hypothalamicthermoreceptors send disturbance spinals along afferentpathways to the central nervous interface. Applying theSherrington principle of the summation of stimuli in thecentral nervous interface would demand a dominant influenceby the core temperature sensors when the core temperature is

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fairly stable, as in man. From the central nervousinterface, the stimulus for heat production or heat losstravels to the effectors in the behavioral and autonomicsystems. But a behavioral response can modify the relationsbetween man and his environment, and the need for autonomicthermoregulatory response. This implies no need for centralnervous system coordination between behavioral and autonomicthermoregulation. The arterial blood, which has beenthermally mixed is fed back to the thermoreceptors once thecorrection is made to stabilize temperature regulation.

In this section the central mechanisms, theoreticalviews, and neuronal models have been stated chronologicallyto show the necessity for a central nervous interface(hypothalamus) to control a "set-point." Only (Houdas etal., 1978) disaffirmed this idea, but their theory was notaccepted due to other biological factors. Bligh (1984) hasgiven the most complete explanation, considering all thevariability involved with thermoregulation, and his modelwould be controlled primarily by central nervous systemfactors.

Peripheral factors which play a major role inthermoregulation are the baroreceptors and chemoreceptors,within the circulatory system, sweat glands and theirfunctions, and the skin temperature. All of these factorsare discussed in detail in this section.

28

Baroreceptors

Two types of baroreceptors identified in the humancirculatory system function as high pressure and lowpressure sensors. Baroreceptive reflexes are activated bychanges in cardiac filling pressure and stroke volume. Bothof these sensors are compensated by changes in heat rate(HR) and vasoconstriction in the peripheral vascular beds

(Nielsen, 1984)._

High pressure baroreceptors are located at thebifurcation of the common carotid arteries, the carotidsinus, and throughout the wall of the aortic arch (theaortic bodies). High pressure baroreceptors are stretchreceptors that send information to the central nervous

system reporting the level of arterial blood pressure. Anyfall in arterial blood pressure is detected by high pressurebaroreceptors resulting in neural feedback which leads toincreased heart rate and a parallel rise in aortic pulsepressure (Rowell, 1977). This decrease in arterial bloodpressure activates the sympathetic nerves to increasecontractility of the heart and to increase peripheralresistance by vasoconstriction, thus increasing arterialblood pressure (Thew, Mutschler & Vaupel, 1985).

The low pressure (atrial) baroreceptors are located inboth atria and the wall of the vena cava. These

29

baroreceptors respond to a decreased cardiac fillingÜ

pressure and decreased blood volume. Hypovolemia, i.e.,lowered blood volume, stimulates low pressure baroreceptorsto modify neural information to the hypothalamus which thencauses an upward shift in the threshold for cutaneousvasodilation and controlling sweat rate (Nadel, Fortney, &Wenger, 1980). Thus, a reduced circulating blood volumestimulates a baroreflex to maintain blood pressure byvasoconstricting cutaneous vascular beds and decreasing

maximum cutaneous blood flow (Nadel, 1983). Moreover,

hypovolemia decreases the cardiac filling pressure, whichreduces neural input to the hypothalamus. The response isan increased secretion of the antidiuretic hormone (ADH)that reduces water excretion by the kidney (Best & Taylor,1985).

Chemoreceptors

Chemoreceptors are located in specialized cells nearthe carotid sinus and aortic bodies. They are sensitive tochanges in blood gases and pH. When chemoreceptors becomehypoxic and/or acidic due to decreased ventricular function,they will reflexly stimulate vasoconstriction in theperipheral circulation (Biscoe, 1971).

30 é

Qwgag Qlang Function

Sweat is hypotonic compared to blood and Na+ and Cl-are the principal ions lost from the extracellularcompartment. Sweat rate is the major factor regulating theconcentrations of these ions in perspiration (Costill,1977). If the sweat rate is slow, the Na+ content of sweatwill be low because the sweat duct is able to reabsorb mostof the Na+, but as the sweat rate increases the loss of Na+also increases (Houdas et al., 1978). Exercise sweatingresults in a total body hypohydration and an increasedhemoconcentration (Kozlowski & Saltin, 1964). The loss ofplasma with exercise exerts an increased osmolality, and theincreased serum_osmolality then further leads to a decrease _

in sweating (Greenleaf, 1972).Sweat glands are innervated by a sympathetic

cholinergic fibers which are controlled by thethermoregulatory center in the hypothalamus (Fortney, Nadel,Wenger, & Bove, 1981), and acetylcholine is the chemicalactivator. Sweating transfers metabolic heat to the

environment by evaporation and compensates for changes inthe ambient temperature. Evaporation cools the skin to helpmaintain a proper core-to—skin thermal gradient for heatloss. The main factor limiting the evaporative process isthe difference in water Vapor pressure between the skin and

3 1 ;

the air. If the water Vapor pressure of the air is higher,evaporation at the skin surface cannot occur (Nadel et al.,1977). With a low ambient water Vapor pressure, evaporation

tends to increase as the Sweat rate increases until heat

loss equals heat production. Once this occurs, the body isno longer Storing heat and the Ts stabilizes.

Ts and Tc act together to control the rate of Sweat

secretion. If the TS is above 33°C, it has no effect on thecontrol of Sweat rate, but if Ts is below 33°C, itsystematically Suppresses sweating (Brengelman, Johnson,

Hermansen, & Rowell, 1977). During exercise, the metabolicheat load is high, and this drives the Tc up to stimulate aSweat response. The sweating mechanism is primarily

responsive to the deep body temperatures (Nadel, 1985).° The final factor which limits Sweat gland function is

hypovolemia, i.e., a reduced blood volume. Total Sweat lossat anytime during exercise is lower when hypovolemia exists(Fortney et al., 1981). This is at least partly due to animpaired ability to maintain optimal cutaneous circulation

and that to metabolically active muscle. AS a consequence,heat transportation from muscle to body Surface is reducedand Tc will increase, even if sweating and evaporation aremaintained.

32 J

gkig Temperature

Major thermoregulatory effects via the circulatorysystem are mediated by the skin. When exercising in a hotenvironment, the circulatory system is under stress to

maintain adequate cardiac output (0) for the metabolism ofactive muscles, "resting" muscles and tissues, and heattransport to the skin (Benzinger et al., 1963). The heatproduction that occurs within the active muscles duringexercise can increase the basal metabolic rate as much as 15to 20 times and is sufficient to raise the core temperatureby l°C every 5 min. if no thermoregulatory mechanism wereactivated (Nadel et al., 1977). Heat is transported to theskin by the circulating blood, and the temperature of theskin maintains an equilibrium between heat production andheat loss.

The human body must maintain a proper thermal gradientwhere the core temperature (Tc) is greater than the skintemperature (Ts) to make heat transport possible (Houdas et

al., 1978). As the Tc increases with exercise, thesympathetic vasomotor tone decreases allowing vasodilationof cutaneous vessels and skin blood flow increases(Mitchell, 1977).

The most important factor determining heat transfer isTs. The temperature of the skin is constantly changing to

l

133

adjust to both external and internal factors. The major1

external factors are the ambient temperature (Ta), and to a

lesser extent, air velocity and relative humidity. When theTa increases to 35°C the range of the Ts is minimal, but asTa decreases, the range will increase. The temperature ofthe skin will rarely exceed 3796. Cutaneous vesselsregulate cardiovascular mechanisms and are triggered bychanges in the environmental temperature.

The internal factors are initiated by increases in thecore temperature (Tc). The Tc can effect Ts directlythrough tissue conductivity from underlying organs andtissues, especially subcutaneous tissues, or indirectly, byblood convection. Blood convection is dependent on the lossof sympathetic vasomotor control to the skin allowing forincreased skin blood flow (Houdas et al., 1978).Constitutional Factors Modifying Temperature Regulation

Numerous factors effect the body itself, and how thebody adapts to these natural occurring phenomena, is themajor concern in this section. The constitutional factors

which are discussed in this section are age, sex,anthropometry, exercise capacity, physical training and heat

acclimatization. All of these have internal and externaleffects on the body's thermal adaptations to exercise in ahot environment.

34Thermalinjuries are of major concern throughout one'slife, but the most susceptible groups in the population arechildren and the elderly. In newborns, due to the thinnessof their skin, involuntary heat loss is much greater than anadult’s at the same water vapor pressure level (Houdas etal., 1978). The sweat gland functioning of newborns' formaximal secretion is only one—third to one—half that of anadult, but by the postnatal phase of growth the childreaches maximal secretion levels (Houdas et al., 1978). Butchildren still perspire less than adults and have a lowerheat—exercise tolerance (Bar-Or, 1980). When childrenbecome dehydrated, they will have a greater increase in coretemperature (Tc) than an adult at the same level of

dehydration.

The susceptibility to thermal injuries in the elderlywas confirmed by Austin and Barry (1956) and Levine (1969).A reduced basal metabolic rate due to loss of lean body massand lack of physical activity are two reasons why theelderly prefer a higher ambient temperature than youngerpeople (Langkilde, 1979). But in a hot environment, theelderly have a reduced ability to discriminate (perceive)between temperatures.

l

35

Under thermal stress conditions, preexisting medicalconditions can add to the susceptibility of the elderly.During prolonged exposures in hot environments, the elderlyare reported to have a decrease in sweat production and thisfactor places a strain on the cardiovascular system(Schwartz & Itoh, 1956). Foster, Ellis, Dore, Exton-Smith,and Weiner (1976) reported this reduction was manifested inthe quantity of sweat secreted by each gland rather than thenumber of active glands, as age increased. Furthermore,older subjects have a significantly lower body conductance

and are much less able to dissipate heat by radiation andconvention. Therefore, there is a relatively greaterdependence on peripheral blood flow for heat dissipation,and this puts an increased strain on the agingcardiovascular system (Irion, Wailgum, Stevens, Kendrick, &Padlone, 1984). Exacerbating this problem is the fact thatthe elderly have a reduced capacity for increasing thecardiac output to allow for the necessary increase inperipheral blood flow to dissipate heat from the core of thebody (Hellon & Lind, 1958). It has been reported that thelower skin temperatures observed in the elderly are at leastpartly due to a lower skin blood flow than in youngersubjects (Wenger, 1984).

36Fleisch(1980) found evidence of a decreasedsensitivity to vasoactive substances in the smooth musclesof blood vessels in older animals. A decrease in vasculardistensibility is characterized by aging, and the stretchreceptors in the blood vessels are less effective (Wenger,1984).

äääThe most common thermoregulatory difference observed

between males and females is in the sweating response. TheTc during steady—state exercise in males is initiallyhigher, and males are more sensitive to increases in Ts(Hardy, 1981). However, females start sweating at lower Tsand Tc (Leithead & Lind, 1964). Females produce less sweatfor the same exercise heat load (Dill, Soholt, Drost, &Loughran, 1977). Even with this lower sweat output, femalesare able to maintain a similar heat—exercise tolerance ascompared to males at the same percentage of the exercisecapacity (Bar—0r, Lundegren, & Buskirk, 1969).

Drinkwater, Denton, Kupprat, Talag, and Horvath (1976)explained the sweating differences between males and femalesin that females rely more on peripheral blood flow(specifically vasomotor control) whereas males depend moreon their ability to cool the body through evaporative means.Exercise Capacity

l0

37

The core temperature rises to a level which isproportional to the oxygen intake (Ü02) and is independentof a wide range of ambient temperatures. The coretemperature and the temperature of the working muscle isproportional to the relative work load and not to theabsolute work load of the individual (Nielsen & Nielsen,1962). Astrand (1970), Davies, Brotherhood and Zeidifard

l(1976), and Saltin and Hermansen (1966) all found that whatfirst appears to be large intra—subject variability of coretemperature is reduced if it is related, not to the absolutebut to the relative metabolic rate. Therefore, at any fixedlevel of work, individuals with low ÜQ2max develop higherbody temperature while exercising in a hot environment thanindividuals with higher Ü02max (Wyndham, Strydom, VanRensburg, Benade, & Heyns, 1970). A fit individual at thesame %Ü02max produces more energy in exercise and still hasthe same core temperature as the unfit individual (Herbert,1979). A fit individual at the same workload as an unfitindividual will exercise at a lower core temperature andwill be at an advantage at any given absolute exerciseintensity (Senay, 1979).

Saltin and Hermansen (1966) found the core temperatureto %V0 max relationship to be linear, but their study islimited to relative workloads at or below 75% of Ü02max. A

lF

38l

follow-up study by Davies et al. (1976) at higher relativeworkloads shows that the core temperature becomes a

curvilinear function of ZVO2max.Acclimatization ang Training

The major time course adaptations which take placeduring acclimatization and training are related to thecardiovascular system. When man is initially exposed toheat, an acute decrease in blood volume (BV) occurs duringan exercise bout due to a decrease in plasma volume (PV)(Houdas, 1978). Another initial problem is peripheralpooling of blood, due to the dilation of peripheral bloodvessels, and causing a decreased venous return to the heart(Roberts & Wenger, 1979). Therefore, stroke volume (SV)decreases and cardiac output (Ö) can only be maintained byan increase in heart rate (HR) to near maximal levels; this

circulatory inadequacy may contribute to heat syndromes

(Rowell, Kraning, Kennedy, & Evans, 1967).The instability of the cardiovascular system is

affected by volume receptors that stimulate the secretion ofthe antidiuretic hormone (ADH) and aldosterone (Wyndham,Benade, Williams, Strydom, Goldin, & Heyns, 1968). Thesehormones function to help the body retain sodium chlorideand water retention which helps maintain BV, regulateosmolarity of extracellular fluids and protect againstdehydration (Sawka, Toner, Francesconi, & Pandolf, 1983).

} .

V

‘ 39

During the first few days of acclimatization andtraining, PV expands to account for an increase in BV

(Greenleaf, Sciaraffa, Shvartz, Keil & Brock, 1981). Venousreturn to the heart increases and augments an increase inSV. Stabilization of the cardiovascular system occurs withthis increase in SV, and can be maintained at a lower HRfor a given intensity, thus providing a wider safety margin

in emergency situations, i.e., peripheral pooling.The improvement of central circulation increases the

capacity for heat conductance to the skin and facilitatesthe onset of sweating at a lower Tc; this provides for alower steady—state Ts and Tc, respectively. Throughtraining and acclimatization, the sweating mechanism becomesmore responsive and heat dissipation occurs more rapidly

(Nadel et al., 1977). The number of active sweat glandsincreases and according to Sato and Sato (1985), the sweatglands actually hypertrophy with training. The amount ofsweat secreted increases and becomes more dilute, thus

minimizing loss of electrolytes (Nadel, Pandolf, Roberts, &Stolwijk, 1974).

Anthropometry (Mass[Body Surface ggg; Rgggg)

Individuals with excess adipose tissue have anincreased heat insulative capacity. Subcutaneous body fathas a fixed resistance that insulates the core from the

11

40 L

skin. The thermal conductance of fat is less than 50Z thatof muscle tissue and about 35Z that of blood. Therefore,those with endomorphic body types are at a definitedisadvantage in the heat due to the increase in insulationof fat tissue (Nadel, 1977).

Smaller individuals weighing 50 kg or less, are shownto be at a disadvantage when performing strenuous physicaltasks (i.e., external loads, Z watts) in the heat. Themaximal oxygen intake of a heavier individual is higher thanthat of a lighter person. Therefore when performing at thesame workload, the heavier individual will be working at alower Z 90 max than the lighter individual. Secondly, thesmall individual has a smaller surface area through which toevaporate sweat and to dissipate heat fast enough to offsetheat production (Strydom, Benade, Heyns, & Hons, 1971).

According to Robinson (1942), if a large individua1'stotal increase in heat production is the same as the smallindividual for a given workload, the larger man candistribute this extra heat through the tissues moreeffectively. But when both men walked at the same rate andheat production was proportional to weight, the larger manproduced, in relation to surface area, about 20Z more heatthan the smaller man. However, in a hot—humid environment alarge man's heat dissipation is restricted because

V

41

evaporative cooling is impeded, and he is forced to storeheat.

Environmental Factors Modifying Temperature Control

Environmental factors, which modify temperature controlin the human body are ambient temperature, relativehumidity, wind velocity, and the heat loss modes ofradiation, conduction, convection and evaporation. A11 ofthese factors can increase the heat load upon thethermoregulatory system.

Ambient Temperature

The ambient temperature has the greatest effect onwhich heat loss mode will be used to dissipate the body'sheat load (Mitchell, 1977). At low ambient temperatures,

convection is the major mode of heat loss, and radiation,

evaporation, and conduction play minor roles. As long asthe temperature of the skin is considerably higher than theambient temperature, the heat loss by convection and

radiation are high (Saltin et al., 1966). However, when theambient temperature is greater than the internal bodytemperature, the thermal gradient is reversed. Instead oflosing heat by radiation, convection and conduction, thebody will gain heat by these modes. Hence, leavingevaporation as the only potential mode for effective heatdissipation (Costill, 1977).

42 l

The core temperature of the body is independent ofambient temperatures when the latter is between -59 to 30°Cand is determined mainly by metabolic rate (Snellen, 1969).

Wyndham (1973) stated that the higher the metabolic rate,

the lower the critical air temperature had to be foracclimitization to occur with hard work. Ambient

temperature has the greatest effect on skin temperature, but

skin temperature is independent of the workload placed onthe body (Saltin et al., 1966). The rate of sweatproduction increases directly with increasing ambient

temperature and, at 35°C, 85% of the heat loss must beachieved by evaporative sweating (Mitchell, 1977).Relative Humiditv

The heat loss mode affected the most by relativehumidity is the evaporative process. In a hot dryenvironment sweat evaporates freely and cools the skin.Therefore, the level of evaporative heat loss loss requiredto dissipate the metabolic heat load is reached at a lowerinternal body temperature (Roberts & Wenger, 1979). As therelative humidity increases, the evaporative processdecreases, and the sweat rate is suppressed. This causesthe body temperature to rise and a thermal equilibrium

cannot occur until a higher core temperature is attained(Nadel, 1977).

43

The sweat rate is suppressed by a hidromeiotic effect(skin wettedness) (Fox, Lofstedt, woodward, Eriksson, &Werkstrom, 1969). Different ambient humidities requiredifferent amounts of skin wettedness to achieve the sameevaporative heat loss, but with a high relative humidity,the evaporative process is ineffectiveg this causes

hypohydration and leads to a steady—state body temperaturethat is much higher than would occur under conditions oflower humidity (Mitchell, 1977). The amount of heatreleased by the evaporative process is dependent on thewater Vapor pressure differential between the skin and air.If the water Vapor pressure of the skin is lower than thatof the air, the evaporative process is reduced. But even ata relative humidity of 100%, the evaporative process canoccur as long as the temperature of the skin is greater than

the ambient temperature (Thew et al., 1985).

Higd Yelocity

When cool air blows across the surface of the skin,heat produced by the body can be lost through convection.The Velocity and temperature of the air are the majorfactors determining the amount of heat loss (Fox & Matthews,1981). Increasing the air Velocity on an exercising subjectallows a lower steady—state core temperature to be reachedwith less evaporative sweating (Nadel, 1977). Accordingly,

44

an increase in convective heat loss reduces the need forevaporation, but even large changes in air Velocity produceonly small changes in the amount of heat loss (Mitchell,1977). Clothing or any barrier between the skin and theenvironment reduce the wind Velocity at the surface of theskin and, in addition, decrease the evaporative capacity(Nadel, 1977).

äätgäßdäThe major mode of heat loss under "normal" conditions

is radiation. According to research by Fox and Matthews(1981), who collected data from a nude person restingquietly in a room temperature of 2l°C, sixty percent of theheat loss was due to radiation. However, when the ambienttemperature exceeds the temperature of the skin at 35°C orabove, other evidence suggests that radiant heat is gainedfrom the environment (McArdle, et al., 1986).

In order for conduction to occur two solid objects ofdifferent temperatures must be in contact. As long as theskin temperature is greater than that of an external solidin contact with the skin, body heat loss occurs, but whenthe external object's temperature exceeds the skintemperature, heat will be gained. Two barriers, whichresist conductive heat transfer from the body, are adiposetissue and clothing (Houdas, 1982).

III

asSo

long as the ambient temperature does not exceed skintemperature, convection is a major mode of heat loss.

Internally, blood convection is the ability of the blood topick up excess metabolic heat from active tissue andtransfer this "waste" heat to the skin, where it is thantransferred to the ambient environment. Externally, warmedair molecules are removed from the skin by air movement, andcooler molecules replace them. The temperature of bloodarriving at different tissues dictates the thermal state ofthat tissue (Houdas, 1982). Thus, heat gained by bloodleaving thermogenic active muscle, is transferred to thecooler tissues of the skin.

Evaporation is constantly occurring at the bodysurface. Evaporation serves a minor mechanism for heatdissipation compared with other modes when the ambienttemperature and relative humidity are low, i.e.,

"insensible" perspiration. However, when the ambienttemperature increases above that of the skin, evaporation

becomes the only mode of heat loss. All other modes at thispoint reverse their gradients and cause heat to be gained.Individual Factors Modifying Temperature Control

The exercise conditions, such as the intensity andduration of the activity, can be major factors which affectthe body's ability to regulate heat. The mode of exercise

IIIrii.

46 ¥

(running vs biking) also must be considered. Furthermore,

the internal individual physiologic conditions that affectthermoregulation must be addressed, e.g., fluid balance andelectrolye, osmolality and plasma protein status in bodyfluids. Fluctuations in these factors can be detrimental totemperature regulation in exercise.

Exercise Conditions

Intensity and Duration

The steady-state core temperature is proportional to

the relative intensity of the exercise, i.e., % ÜO2max.

When a subject increases the intensity of exercise, the heatproduction with the active muscles increases, and the risein core temperature is proportional (Nadel, et al., 1977).

Water losses from the blood plasma are alsoproportional to the relative intensity of exercise (Nadel etal., 1980). At the onset of exercise the decrease in plasma

volume is attributed to a rise in the mean arterial pressure(Myhre, Hartung, Nunneley, & Tucker, 1985). According toMiles, Sawka, Glaser and Petrofsky (1983), blood plasmawater losses in progressive arm and leg exercises areindependent of the muscle mass but are directly related tothe intensity of the exercise. Subsequently, as the plasmavolume decreases during exercise of increased intensity, theplasma osmolality increases along with the concentrations of

47

sodium, potassium and chloride (Lundvall, Mellander,

Westling & White, 1972). _Increasing the intensity of exercise also elicits

certain cardiovascular changes such as increased heart rate,stroke volume, cardiac output, and oxygen extraction rate(Best & Taylor, 1985). The degree of vasoconstriction atthe onset of exercise is directly related to exerciseintensity, and this is associated with a decrease in skin

-

blood flow (Hirata, Nagasaka, Hirai, Hirashita, & Takahata,1984). In exercises of short duration, these peripheralvasoconstrictive effects related to intensity have virtuallyno influence on thermal equanimity, but in prolongedexercise situations, the effects of rising intensity aredetrimental to performance (Rowell, 1974).ggg; gi Exercise

Cycling exercise has been observed to elicit lower

oxygen uptakes (902) and higher blood lactate values thandoes running on a treadmill (Koyal, Whipp, Huntsman, Bray, &Wasserman, 1976; Hermansen & Saltin, 1969). Wasserman,

Whipp, Koyal, and Beaver (1973) attributed these findings toa smaller active muscle mass involved in cycling at anygiven exercise intensity. Another explanation was given byMatsui, Kitamura and Mizamura (1978) that the leg blood flowduring maximal cycling exercise was significantly lower thanleg blood flow during maximal treadmill exercise.

48

Genay (1979) investigated body fluid shifts duringexercise and found that the mode of exercise (bicycle,ergometer, treadmill, etc.) significantly influenced theshifts. A reduction in the plasma volume occurs duringcycling exercise (Harrison, Edwards & Leitch, 1975;Lundvall, Mellander, Westling, & White, 1972). Body fluidshifts are also affected by the posture of the cyclist(Diaz, Bransford, Kobahashi, Horvath, & McMurray, 1979).During short·term treadmill exercise, a reduction of plasmavolume and a hemoconcentration occurred, but with 20 min oftreadmill exercise at 76% 9Q2max no hemoconcentrationoccurred (Galbo, Holst & Christensen, 1975). Wilkerson,Guten, and Horvath (1977) using a similar protocol foundthat after 20 min of exercise levels in excess of 60% 902maxa hemoconcentration was obtained after prolonged exercise(>2 h), despite considerable water loss, littlehemoconcentration was found to occur in subjects studied byMaron, Horvath and Wilkerson (1977). These findings reflectinconclusive evidence concerning the conditions that mayinduce significant circulatory fluid loss in treadmillexercise.

Hydration ägage

Under most exercise conditions, sweat losses are

greater than the amount of water a subject can take in

0

49

during the activity, and a hypohydration state arises. Thisimposes multiple problems on the exercising human. Anincrease in the steady-state core temperature is broughtabout by increased heat storage due to an inability todissipate the thermal load (Nadel, 1977). Peripheral bloodflow decreases due to hypohydration, which in turn decreasesthe amount of convective heat transfer from active muscle aswell as transfer to the sweat glands (Nadel et al., 1980).Therefore, a decrease in evaporation results in furtherimpairment of other modes of heat transfer. During amarathon, Wyndham (1977) gathered data which provided abasis for predicting that a 5% water loss would elicit a 4l°C core temperature upon a runner's completion. This is

attributable to a decreased sweat rate which is attributableto the body's need to conserve water and prevent excessivelosses of fluids.

Hypohydration impairs both exercise performance andphysiological function (Harrison, Edwards, & Fennessy,1978). Development of hypohydration while exercising in ahot environment neutralizes the advantages of aerobicfitness and acclimatization. Aerobic capacity dissiminatesdue to an inability to attain the normal maximal cardiacoutput (and stroke volume) due to loss of water from thevascular compartment. At submaximal exercise intensities,

III

50 ·I

the heart rate increases to compensate for the impaired

stroke volume, but this is inadequate as intensity‘

approaches near maximal levels. The reduced cardiac outputcannot leads to insufficient oxygenation of the activemuscles and thus, performance decreases (Sawka, Francesconi,Young, & Pandolf, 1984).

In contrast, when an exercising subject is‘ hyperhydrated the plasma concentration of electrolytes are

diluted and osmolality is reduced slightly. Vascular watervolume is adequately maintained within the body and cardiacoutput can reach maximum capacity. Accordingly, theexercise heart rate and steady-state core temperature

decrease (Moroff & Bass, 1965; Nadel et al., 1980).Intracellular Fluid Compartment ang Extracellular FluidCompartment

The two main fluid compartments in the body are theintracellular fluid compartment (ICF) and the extracellularfluid compartment (ECF), the latter includes theinterstitial space and the vascular compartment. A water

permeable membrane separates these compartments and thethree main factors governing fluid shifts among compartmentsare: 1) gradient of colloid pressure; 2) tissue fluidpressure; and 3) hydrostatic pressure (of the blood).

51

Costill and Fink (1974) studied the effects ofhypohydration on the fluid compartments and found that wateris lost proportionally from each. At lower degrees ofhypohydration (2% body weight loss) the ECF is the space ofprimary losses, but as hypohydration increases thedistribution of water losses is equal from each compartment.During thermal hypohydration, a greater loss of Na+ and Cl-and a smaller loss of K+ occurs in the ECF than duringexercise hypohydration. Harrison, Edwards, Graveney,Cochrane and Davies (1981) suggested that if extracellularsodium chloride concentrations are increased, aredistribution of body water would have occurred at theexpense of the ICF. Also an increase in total body fluidwould have to occur since more fluid was retained as aresult of extracellular osmotic pressure, but since nochange occurred to the total body water and theintracellular water, the water and osmolality of theintravascular space could only have increased at the expenseof the interstitial space.

At the beginning of exercise, the changes in plasmavolume occur in the ECF with a temporary shift of water fromthe vascular space to the interstitial space without anactual loss of fluid from the body (Beaumont, Strand,

Petrofsky, Hipskind, & Greenleaf, 1973). If exercise is

52

maintained beyond 20 min, lymphatic circulation effectsreturn of some of this fluid to the vascular compartment.Electrolvtes

The major electrolytes involved in thermoregulation aresodium (Na+), chloride (C1-) and potassium (K+). Sodiumchloride is found in abundance in the extracellular fluidcompartment and is the ion having most influence onmaintenance of the vascular volume. Water loss duringsweating reduces the plasma volume which increases the NaClconcentrations in the plasma. The principle ions lost insweat are Na+ and Cl-. Heat exposure, exercise, and/orhypohydration (if fluid is not replaced) results in anarterial hypovolemia and a renal ischemia, which stimulatesan increased release of aldosterone. Aldosterone, amineralocorticoid, leads to the retention of sodium byincreased renal reabsorption (Costill, 1977). Myhre andRobinson (1977) stated that as long as fluids were replaced,plasma NaCl was not affected by prolonged heat exposure of 4hs, but when hypohydration occurred, NaCl was responsiblefor 90% of the osmotic activity within the fluid compartment(Myhre & Robinson, 1977).

Potassium is found in large abundance in theintracellular fluid compartment. Marathon running and evenrepeated days of exercise dehydration only produce slight

IIII

ss ?

decreases in K+ (Costill, 1977). With prolonged exertionthe intramuscular and plasma K+ ratio is significantlyaltered and this finding suggests a possible modification inthe muscle cell membrane (Beaumont et al., 1973). However,sweating has little effect on K+ concentrations in plasma ormuscle tissue (Costill, 1977).Osmolality

The hydration state of the body is the major factordictating the effects of osmolality. If the body isnormally hydrated, an osmolar equanimity exists and waterbalance is maintained among the fluid compartments. In ahypohydration state, hyperosmolality occurs due to thedecrease of water in the vascular fluid volume. Smallchanges in osmolality serve as a more potent stimulus forbody water conservation than small changes in the bloodvolume (Dunn, Brennan, Nelson & Robertson, 1970). Anychanges in osmolality correlate with changes in Na+, whichis the primary electrolyte determining the plasmaosmolality, and both of these changes correlate stronglywith decreased rates of evaporation (Greenleaf, vanBeaumont, Brock, Morse, & Mangseth, 1979). It is believedthat the increased plasma osmotic pressure accompanying

hypohydration and the reduced peripheral hydrostaticpressure stimulate the retention of electrolytes,

54 S Imaintenance of central blood volume, and decreased sweatrate (Greenleaf, Convertino, Stremmel, Bernauer, Adams,Vignau & Brock, 1977). The increase in osmolalitystimulates the osmoreceptors in the hypothalamus to increasevasopressin secretion, which increases the water

reabsorption in the kidneys and the eccrine sweat glands;this also stimulates the thirst sensation (Nielsen, 1974).Protein

Plasma proteins are the principle circulatory factorsdetermining colloid osmotic pressure and which resist theloss of fluid from the vascular space (Myhre et al., (1985).The movement of plasma proteins among fluid compartments is

_due to three factors: environmental temperature; the state

of acclimatization; and the proportion of the cardiac outputdistributed to cutaneous and muscle capillaries (Senay,1978). During heat exposure, shifts in plasma proteincontent are results of increased capillary permeability(Myhre & Robinson, 1977). Costill and Sparks (1973)observed an increase in plasma protein equal to the decreasein plasma volume. Harrison (1974) found no significantshifts of albumin from the vascular compartment during 2 hsof passive heat exposure with 10% decrease in plasma volume.

Regarding the effects of acclimatization on vascularprotein response to heat exercise stress, acclimatization

........------—-———————————————————————————————————————————————————”yvn

55

either alters the rate at which protein escapes from thecutaneous capillaries or modifies the available proteinpopulation residing within the cutaneous interstitial spaces(Senay, 1975). Therefore, the influx of proteins into thevascular volume occurs more rapidly after acclimatization.Rapid dilation and constriction of cutaneous vascular bedsby the massaging action of muscles causes an increased

Iperfusion and an increased protein influx to the vascularvolume (Senay, 1978).

Summary

The incidence of a heat-related injury occurring duringprolonged physical exercise is evident especially on hothumid days. The preceding sections have included importantliterature in several research areas. The initial sectiondescribed the clinical factors related to thermal injuries.The second section included the theoretical controls ofthermoregulation and related peripheral control factors.The third section presented the constitutional factors whichcould possibly modify temperature regulation. The nextsection initialed environmental factors which exert aninfluence on body temperature, and the final section dealtwith the individual factors modifying temperature control.Thus presenting an overview of the thermoregulatory system

along with any factor which could possibly modify thatsystem. ·

EFFECTS OF CHANGES IN PLASMA VOLUME,OSMOLALITY AND SODIUM LEVELS ON CORE

TEMPERATURE DURING PROLONGED EXERCISE IN HEAT

William S. Lackland, William G. HerbertFrancis C. Gwazdauskas, and Don R. Sebolt

Running Head: Effects of Hematologic Changes on CoreTemperature

William S. Lackland, William G. HerbertFrancis C. Gwazdauskas, and Don R. SeboltHuman Performance LaboratoryDepartment of Health, Physical Education and Recreation andDairy Science DepartmentVPI and SUBlacksburg, VA 24061703-961-6565

56

57 Ä

ABSTRACTe

Six adult males of similar body composition and aerobiccapacity were tested to study the effects of changes in

plasma volume (PV), osmolality (OSM) and sodium (Na+) oncore temperature (Tc) under three exercise-thermoregulatory

stress conditions. The protocol consisted of 120 min ofupright stationary cycling at 50% V02max under neutral (24°C, 50% RH) - euhydrated (NE), hot (35°C, 50% RH) —

euhydrated (HE), and hot-hypohydrated (HH) environmentalconditions. Venous blood samples were obtained at -30 min,0 min and at 15 min intervals through a 30 min recovery andwere analyzed for blood hematocrit and hemoglobin, and forplasma osmolality and sodium. Hematocrit and hemoglobinwere used to calculate relative changes in plasma volume.Tc showed qualitatively similar linear increases in thefirst 45 min of each trial. At 60 min, Tc in the NE trialplateaued at 37.9°C. In the HE trial, Tc continued to showa slight further increase after 45 min while in NE it becamesignificantly (p<0.05) lower at 45 min as compared to HE andHH; at 60 min of exercise, the core temperature of all threetrials differed significantly (p<0.05), with HH being thehighest (38.3°C). Percent change in plasma volume was notdifferent between trials, but did show the greatest decreasein all trials from 0 to 15 min of the exercise phase with at

°

saleast-4.3%. Osmolality was significantly different(p<0.05) between the NE (x = 283.3 mOsmo1/kg) and the HH (x= 292.5 mOsmo1/kg). Plasma sodium was significantly(p<0.05) higher for all intervals of HH (x = 137.9 meq/L) ascompared to the NE (x = 135.1 meq/L) and HE (x = 134.8meq/L). These data suggest that core temperature (Tc)

increase in moderate intensity endurance exercise is less

related to a decreased circulating plasma volume, but ismore strongly associated with rising osmolality,specifically the increase in the Na+ electrolyte, whichoccur with progressive hypohydration.

Index terms: core temperature; plasma volume; osmolalitygsodium; prolonged exercise thermoregulation; euhydration;hypohydration.

59 Q

Introduction

Heat injuries are a major problem when individualsengage in physical work or prolonged exercise in a hotenvironment. Environmental conditions, especially ambienttemperature and relative humidity, play a major role in thebody's ability to regulate internal body temperature. Asthe ambient temperature rises evaporation becomes the mainheat loss mode.

Another factor, which contributes to the rise in coretemperature, is the state of hydration. Early studies by(22,23) demonstrated that fluid restriction in a hotenvironment was associated with a continuous rise in bodytemperature under resting and exercising conditions, butwhen fluids were replaced, the internal temperature remainedconstant.

The hypothalamus is considered the control center forthermoregulation, interpreting neural and humoral inputsfrom various stimuli in the body (l) and adjusting effectormechanisms to keep dry body temperature constant.Disturbances due to external environmental conditions andinternal factors such as changes in body fluid volumes andsolute composition which directly relate to the state ofhydration may potentially have detrimental effects onthermal control mechanisms. Three clinical problems that

---———————-————-—--—————————————————————————————”_————'————"———"—————————‘“—”1

460can

be presented when exercising in heat are heat cramps,heat exhaustion and heat stroke. Heat stroke, the mostsevere heat injury, can cause widespread cellular damage in

vital organs and skeletal muscles (10,11).In the present experiment, the rise in body temperature

was determined in different environmental conditions andhydration states. The purpose was to assess the effects oftime—related changes in plasma volume and changes in thecomposition of blood, specifically osmolality and sodiumconcentrations on core temperature during prolonged exercisein heat.

METHODS

Subjects

Six young active adult males volunteered for thisstudy. Each was thoroughly familiarized with the proceduresand signed a written informed consent. Preliminary

measurements, taken to determine the presence of

cardiovascular exclusion criteria included a resting 12-1eadelectrocardiogram, heart rate and blood pressure.Subsequent pre-experimental testing included thedetermination of maximal oxygen consumption (ÜO2max) for

stationary cycling and body composition; only those with V0max between 40 to 60 ml•kg’1•min" and hydrostaticestimations of percent body fat between 8 to 20% were

61 |

accepted. An habitual physical training level equivalent torunning 15,000 to 20,000 m per week also was required.Additionally, the cycling workload vs oxygen consumption

relation for a range or submaximal intensities wasdetermined for each subject. This allowed calculation ofthe power output necessary for a 50% Ü02max, the desiredexercise intensity for the experimental endurance trials.Tggt Protocol

The experimental trials consisted of three different120 min bouts of stationary cycling with a 30 minpreliminary resting period included to establish baselinevalues and a 30 min recovery to establish return to ·

baseline. The environmental and hydration conditions ofeach trial were: exercise plus neutral/euhydrated (NE)environmental condition; exercise plus hot/euhydrated (HE)condition, and; a hot/hypohydrated (HH) condition. The NE

* condition imposed an average ambient temperature of 24 C anda 50% relative humidity. The average ambient temperaturefor the HE and HH bouts was 35°C with a 50% relativehumidity. Euhydration for bouts was achieved by having thesubjects drink a volume of water (room temperature)

equivalent to 1.0% of his body weight, immediately prior tothe preliminary rest period plus an equal amount during therest period and exercise phase, i.e., a maximum amount of

62 1

2.0% of body weight. The HH was with no fluids. At 15 minintervals, environmental conditions and subject's exerciseY02 values were monitored and adjustments were made in the

heat, humidity and/or workrate to keep these variablesconstant.

Measurements

Deep body temperature was monitored by a rectalthermocouple inserted 10 to 15 cm into the rectum. Bodytemperature changes were measured at 15 min intervals by a

telethermometer (Yellow Springs, Model TUC 46). Blood

samples of approximately 7.0 ml were collected withoutstasis at 15 min intervals from a 20 gauge teflon—catheterinserted into an antecubital vein. The hematocrit (Hct) was

measured in quadruplicate and corrected by a factor of 0.96for trapped plasma and by 0.93 to adjust for venous to wholebody Hct ratio (2). Blood hemoglobin was measured in

triplicate with the cyanomethemoglobin method. Relativechanges in plasma volume were calculated from the Hct andhemoglobin (Hb) values using the formula of Costill and Fink(2). From each plasma sample, the osmolality was measuredby a vapor pressure osmometer, and sodium concentrationswere measured by flame photometry.

——————————————————————·rrr_-——————"————————————————————————"’I"""FII"Il|

63StatisticalAnalysis

The data were analyzed to determine the within-trialand between—trial differences in core temperature (Tc), andthe hematologic variables of plasma volume (PV), osmolality(OSM) and sodium [Na+] for different environmentalconditions and hydration states. Analysis of variance(Table l) was utilized to determine if significantdifferences existed across time or between conditions foreach of the dependent variables. A Duncan's Multiple RangeTest was utilized in order to determine where differencesexisted within each trial for the dependent variables.Results

The physical characteristics for each subject are inTable 2. Only one subject was judged to be trained (30

mi•wk°‘), but all had reported having exercised on a regularbasis for several years.Rectal Temperature (T;)

During exercise Tr exhibited a gradual rise toequilibrium levels (Figure l). The overall treatment meandifferences for NE, HE, and HH were 37.7, 37.9, and 38.l°C,respectively. During both euhydration conditions (NE andHE), this thermal equilibrium was reached within the first60 min, however the NE equilibrium was reached at a lowertemperature (37.9°C). In the HE condition, the thermal

64 4

equilibrium was attained at 90 min (x=38.2r.1°C) and only amean increase of 0.2°C occurred over the last 60 min. Inthe HH condition, no early equilibrium occurred and Tr

showed a progressive rise to 38.7°C the final 30 min. ofexercise.

There was a gradual linear increase in Tr during thefirst 30 min of each trial, but at 45 min the Duncan'sMultiple Range Test determined in the NE trial that Tr wassignificantly different (p<0.0l) from the HE and HH trials.At 60 min Tr for all three experimental conditions wassignificantly different (p<0.0l) and remained significantthroughout the 120 min of exercise.Plasma Volume (PV)

A

Figure 1 shows that the greatest losses of PV in allexperimental conditions occurred during the first 15 min ofexercise with at least a (-4.2%) decrease. In the NE trial,PV decreased continuously through the first 60 min with a-7.8% decrement observed at 60 min of (-7.8%). ThereafterPV showed no further systematic change. PV was not affectedby treatment (p>0.05). Both the HE and HH conditionsresulted in a progressive decreases in PV similar to thatfor NE. _

65PlasmaOsmolalityn

Plasma osmolality did not vary significantly (p>0.05)as a function of time (Figure 2). Plasma osmolality wasaffected by treatment (p<0.01). Mean osmolality was 283.3,287.8 and 292.5 m0smo1/kg for NE, HE, and HH, respectively.Sodium Concentration [Na]

Plasma [Na+] during the NE trial exhibited a slowprogressive rise throughout the trial until stabilizing inthe final two intervals (Figure 2). Mean sodium levels were135.1, 135.7, and 137.9 meq/1 for NE, HE and HH,respectively. The greatest increase occurred during thefirst 15 min. Plasma [Na+] was significantly different(p<0.0l) over time. This basic pattern was observed in HE,_but from 15 min until the conclusion of the exercise, onlysmall fluctuations were noted. For the HH condition thelargest increase in [Na+] again occurred within the first 15min. The overall treatment mean differences for Na+ were135.1, 134.8, and 137.9 mEq/L for NE, HE, and HH,respectively. As with plasma osmolality significant

differences (p<0.01) were found between the two euhydratedconditions (NE and HE) and HH. Through application of aDuncan's Multiple Range test it was determined that thisvariation was due to treatment differences between the HHand the two euhydration trials (NE and HE). This differencewas exhibited throughout the entire 120 min of exercise.

. 66

Discussion· Nielsen (21) was the first to find that as deep body

temperature increased during exercise to reach a steadyplateau which was maintained for the duration of the

· exercise. That Tc never stabilized at a level equilibriumin the HH condition was attributed to the state ofhydration, since the HE trial did stabilize. Pitts et al.(82) was the first to demonstrate that the extent of the Tcincrease was affected by the water balance of the subject.The greater the subject’s level of dehydration, the greaterthe increase in body temperature would be; alternately, ifthe subject was hyperhydrated body temperature was reduced.Such findings also were substantiated by Moroff and Bass(l4), Ekblom et al. (4) and Greenleaf and Castle (7) whoattributed rising Tc in exercise after hypohydration toreduced sweat rates. Thus, heat loss by evaporation wasreduced, and core temperature increased. But when fluidswere replaced, the sweat rate was maintained and theevaporative process cooled the body.

The percent decrease in PV during the first l5 min ofthis study is in total agreement with the findings ofHarrison (9) and Greenleaf et al. (8). The PV decreaseresults from a transcapillary fluid flux into the workingmusculature, and during prolonged exercise the flux of

67 Ü

fluids is transient and followed by a gradual redistributingof body water (l2). During moderate submaximal exercise inthe upright position, the loss of PV is influenced byincreased hydrostatic pressure and probably systemic bloodpressure (5). Miles et al. (l3) noted a linearrelationship between the amount of PV lost from thevasculature and the exercise intensity (Z Peak V02) for botharm and leg exercises. Plasma volume decreased over time,but no differences between experimental condition werenoted. The decrease in PV is due to postural changes andexercise, and heat has little effect, if any at all (3).

In the present study, an 0SM response to the threedifferent experimental conditions was observed initially andwas maintained throughout the l20 min of exercise. Senayand Christensen (26) and Senay (24) reported correlationsbetween the rate of evaporative losses during dehydrationand both the plasma OSM and [Na+]. Senay and Christensen(26) also suggested that osmotic pressure could not act asan indicator of changes in body fluid volume. Such a non-thermal indicator along with thermoreceptor inputs mightprove a basis for heat regulation via effects at thehypothalamus. Nielsen et al. (20) gave a hypertonic salinesolution orally to prevent dehydration and imposed athermoregulation circumstance comparable to that produced by

68 Ä

dehydration alone. They showed that the effect of the stateof hydration on body temperature during work was related tothe plasma GSM rather than PV. Snellen and Mitchell (27)gave a hypertonic saline solution and observed a markeddepression of sweating. They reported that drinkingaffected thermoregulatory sweating in three ways: by thetemperature of the drink; by a volume effect; and by asalinity effect. Nielsen (18) confirmed these earlierfindings that plasma osmolality had a direct effect ontemperature regulation by acting peripherally on the sweatglands or centrally on the hypothalamus to shift the "setpoint."

Nielsen (19) reported that the [Na+] was the mostimportant factor in relationship to GSM. Sodiumconcentrations in the HH trial were significantly differentfrom the NE and HE experimental condition. Large increases

in both GSM and [Na+] of 4.1 mGsmol/kg and .8 mEq/L,respectively, were noted at 45 min. A central effect that[Na+] have on the hypothalamus is that increased [Na+] inthe blood determines the firing patterns of neurons withinthe hypothalamus (15). This [Na+] increase also stimulatesthe production of the antidiuretic hormone (ADH) andconserves body water at the kidney tubules (Senay &Beaumont, 25). The elevated concentrations effect another

696

peripheral factor, the sweat glands, causing a decrease inthe amount of cutaneous blood bringing water to these glandsand helping to conserve body fluids.

Therefore, in the present study plasma [Na+] was themajor factor in the increase in core temperature. Ourresults suggest that hypernatremia exerted a specific effecton the sweating mechanism to decrease the activity of thesweat glands and stimulated the hypothalamus to increasebody temperature. Findings by Greenleaf et al. (6) supportthis hypothesis in that the rise in Tr was related to a 5mEq/l increase in plasma [Na+]. In the present study duringthe HH trial, plasma [Na+] increased 4.5 mEq/l compared to3.1 mEq/l for NE and 2.9 mEq/l for HE. Thus, plasma [Na+]

·

was probably the major factor involved with the increase inTc. The large increase in plasma [Na+] is sufficient tohave a definite effect on the sweat mechanism (16). In thepresent experiment the decrease in the sensitivity of thesweat gland was not studied, but Neilsen and Greenleaf (17)assumed it was related to decreased activity in thethermoregulatory center in the brain or to a decreasedresponsiveness in the sweat gland.

y 70

References

1. Bligh, J. The central neurology of mammalianthermoregulation. Neuroscience, 4:1213-1236, 1979.

2. Costill, D. L. and W. J. Fink. Plasma volume changesfollowing exercise and thermal dehydration. J. ggg;.

Physiol. 37(4):521-525, 1974.3. Diaz, F. J., D. R. Bransford, K. Kobayashi, S. M.

Horvath, and R. G. McMurray. Plasma volume changes

during rest and exercise in different postures in ahot humid environment. J. ggg;. Physiol.: Resgirat.

Environ. Exercise Physiol. 47(4):798—803, 1979.4. Ekblom, B., C. J. Greenleaf, J. E. Greenleaf and L.

Hermansen. Temperature regulation during exercisedehydration in man. gggg Physiol. ggggg. 79:475—483,1970.

5. Greenleaf, J. E., W. van Beaumont, P. J. Brock, J. T.Morse and G. R. Mangseth. Plasma volume andelectrolyte shifts with heavy exercise in sitting andsupine positions. gg J Physiol 236:R206-R215, 1979.

6. Greenleaf, J. E., P. J. Brock, J. T. Morse, Beaumont, W.van, L. D. Montgomery, V. A. Convertino and G. R.

Mangseth. Effect of sodium and calcium ingestion onthermoregulation during exercise in man. In: Egg

Trends ;g Thermal Physiology Y. Houdas and J. D.Guici, ed. 1978, p. 157-160.

71

7. Greenleaf, J. E. and B. L. Castle. Exercise temperature

regulation in man during hypohydration andhyperhydration. Q. ggg;. Phqsiol. 30:847-853, 1971.

8. Greenleaf, J. E., V. A. Convertino, R. W. Stremel, E. M.

Bernauer, W. C. Adams, S. R. Vignan and P. J. Brock.

Plasma [Na+], [Ca2+], and volume shifts andthermoregulation during exercise in man. Q. gggg.

A

Physio1.: Resgirat. Environ. Exercise Physiol.43:1028-1036, 1977.

9. Harrison, M. A. Plasma volume change during work in a

hot environment. Q. ggg;. Physiol., London

39(6):925—93l, 1974.

10. Hart, L. E., B. P. Egier, A. G. Shimizu, P. J. Tandon,

and J. R. Sutton. Exertional heat stroke: The

runner's nemesis. Q ggg Mgg ggggg 122:1144-1150,

1980.

11. Kew, M. C., I. Bersohn, and H. C. Kent. Liver damage

in heat stroke. gg Q ggg. 49:192-202, 1970.

12. Lundvall, J., S. Mellander, H. Westling, and T. White.Fluid transfer between blood and tissues duringexercise. gggg Physiol. ggggg. 85:258-269, 1972.

13. Miles, D. S., M. N. Sawka, R. M. Glaser, and J. S.

Petrofsky. Plasmas shifts during progressive arm andleg exercise. Q. gggg. Physiol.: Resgirat. Environ.Exercise Phvsiol. 54(2):49l-495, 1983.

. 721

14. Moroff, S. W. and D. F. Bass. Effects of overhydrationon man's physiological responses to work in the heat.g. gggl. Physiol. 20:267-270, 1965.

15. Myers, R. D., and W. L. Veale. Body temperature.Possible ionic mechanism in the hypothalamuscontrolling the set point. Science 170:95-97, 1970.

16. Nielsen, B. The effect of dehydration on circulationand temperature regulation during exercise. g. Tgggg.

Bggl. 9(1/2):107-112, 1984.

17. Nielsen, B. and J. E. Greenleaf. Electrolytes andthermoregulation In: Qgggg, Biogenic amines ggg gggytemgerature: gygg. Pharmacology gi Thermoregulation.Karger, Basel, 1977.

18. Nielsen, B. Effects of change in plasma volume andosmolality on thermoregulation during exercise. gggg

Physiol. ggggg. 91:725-730, 1974.

19. Nielsen, B. Effect of changes in plasma Na+ and Ca++concentration on body temperature during exercise.gggg Physiol. ggggg. 91:123-129, 1974.

20. Nielsen, B., G. Hansen, S. 0. Jorgensen, and E.

Nielsen. Thermoregulation in exercising man duringdehydration and hyperhydration with water and saline.Intern. g. Biometer 15:195-200, 1971.

73

21. Nielsen, M. Die regulation der korpertemperatur bei nmuskelarbeit. ggggg. gggg. Phqsiol. 79:193-230,

1938.

22. Pitts, G. C., R. E. Johnson, and F. C. Conslazio. Workin the heat as affected by intake of water, salt, andglucose. Q. Physiol. 142:253-259, 1944.

23. Rothstein, A. and E. J. Towbin. Blood circulation andtemperature of men dehydrating in the heat. In:Physiology gf Mgg ig ggg Desert, edited by E. F.

Adolph. New York: Interscience, p. 172-196, 1947.24. Senay, L. C., Jr. Relationship of evaporative rates to

serum [Na], [K] and osmolality in acute heat stress.J. ggg;. Physiol. 25:149—l52. 1968.

25. Senay, L. C., Jr. and Beaumont van W. Antidiuretic

hormone and evaporative weight loss during the heatstress. Pfluger gggg. Rg;. Physiol. 312:82-90, 1969.

26. Senay, L. C., Jr., and M. L. Christensen. Variations

of certain blood constituents during acute heatexposure. J ggg; Physiol. 24:302-309, 1969.

27. Snellen, J. W. and D. Mitchell. Calorimetric analysisof the effect of drinking saline solution on whole-body sweating. Pflueger gggg. 331:134-144, 1972.

74•

Figure Legends

FIG l'. Mean core temperature (°C) changes before, duringand after 120 min of cycle ergometry at normal (24C, 50% RH)/euhydration, NE; Hot (35oC, 50%

RH)/euhydration, HE; and hot/hypohydration, HH

conditions. ¢ denotes time when NE wasstatistically different (p < 0.01) from HE and HH.·¢ denotes times when NE, HE, and HH are allstatistically different (p < 0.01). SEM = 0.38 forall time intervals in each condition.

Mean change of plasma volume (%) changes before,

during and after 120 min of cycle ergometer atnormal (24°C, 50% RH)/euhydration, NE; hot (35oC,50% RH)/euhydration, HE; and hot/hypohydration, HH,conditions. SEM = 1.03 for all time intervals ineach condition.

FIG 2. Mean osmolality (m0smol/kg) changes before, during

and after 120 min of cycle ergometry at normal (24°C, 50% RH)/euhydration, NE; hot (35°C, 50%

RH)/euhydration, HE; and hot/hypohydration, HH,conditions. SEM = 1.49 at all time intervals ineach condition.

Mean Na+ (meq/L) changes before, during and after120 min of cycle ergometry at normal (24OC, 50%

75

RH)/euhydration, NE; hot (35°C, 50%RH)/euhydration, HE; and hot/hypohydration, HH,conditions. ¢ denotes time when HH was

statistically different (p < 0.01) from NE and HE.SEM = 0.38 for all time intervals in eachcondition.

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77

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Chapter IVSUMMARY AND RECOMMENDATIONS FOR FUTURE RESEARCH

Prolonged physical exercise in a hot, humid environmentcan lead to exertional heat stroke. Exertional heat strokeis the most severe form of heat injury. Heat cramps and

heat exhaustion are other conditions brought on by heatstress. All of the injuries involve the loss of adequatebody fluids and/or electrolytes that produce an inability todissipate heat, and depending on the severity of the waterloss, a wide range of clinical manifestations may occur.

When exertional heat stroke occurs core temperature iscontinuing to rise without ever reaching an equilibriumlevel. The factors responsible for the excessive increasein core temperature are varied and even slight variations inthe stress placed upon the body can result in unexpectedresponses, leading to widespread functional and tissuedamage or even death to the participant. The problem isunderstanding the factors which lead to the ineffectivecontrol in the hypothalamus, the thermoregulatory center.Speculation has been given that a decline in circulatingblood volume, a rise in osmolality, or a large increase insodium concentration are possible causes for the lack ofequilibrium. The role of selected hematological factors(plasma volume, osmolality, and sodium level) is

84

85

investigated in an effort to understand the time course riseof core temperature.

The hypothalamus integrates neural stimuli which arereceived from peripheral receptors in various locationsthroughout the body. The receptors are controlled byinternal and external factors. Most internal receptors areeffected by the state of hydration of the body. The levelof fluids in the vascular compartment and cell and theconcentrations of electrolytes are controlled by thehydration state, and the sweat gland function and skintemperature range also are indirectly involved with thehydration state of the body. The intensity and duration ofthe exercise is another internal factor which involves themetabolic heat gain within the body and complicates the modeof heat loss. Other factors which can reduce the body'sability to dissipate heat are constitutional factors,including age, sex, body type, exercise capacity, physicaltraining and acclimatization.

External factors which affect peripheral receptors arethe environmental conditions including ambient temperature,relative humidity and wind velocity. These factors effectthe actual modes of heat loss and can reduce proper functionof the mechanism involved such as sweat gland function andskin temperature.

I

86 |

This study was undertaken to observe changes in thehematologic factors and the core temperature responses to

prolonged exercise in various conditions of thermal stressand hydration. The changes in PV, osmolality, and [Na+] arerelated to environmental stress and give a greaterunderstanding of the importance of hydration in a hotenvironment. Six adult male subjects of similar bodycomposition were selected to participate in this study. Allsubjects volunteered and signed an informed consent prior tothe study. All subjects received a preliminary trial 60 minat 50% V02max to acquaint them with the test procedures.The study consisted of three experimental conditions withthe same protocol for every trial. The control trialconsisted of 120 min of cycle ergometry (50% VQ2max) underneutral (24°C, 50% RH)/euhydration conditions (NE). Theother two conditions were administered in a hot environment4(35°C, 50% RH). Fluids were given in the hot/euhydration(HE), and no fluids were given in the hot/hypohydration (HH)trial.

The results of this study showed that Tc wassignificantly different (p<0.0l) in the HH trial from the NEand HE trials at 45 min. At 60 min all three trials becamesignificantly different (p<0.01) and remained this waythroughout the exercise period. Plasma volume in all three

l87

experimental conditions decreased over time but no treatmentdifferences were noted. Osmolality exhibited a treatmentdifference where the mean osmolality values at the beginningcaused an initial difference and did not diverge over time.The results from sodium concentrations [Na+] exhibited atime and treatment effect. The time effect was that overtime [Na+] showed an increase and the treatment effect was

”that in the HH trial [Na+] values were significantlydifferent (p<0.0l) from the HE and NE trials throughout.Conclusionsa

Low correlations did not allow the prediction of arelationship between the dependent variables, but regressionanalysis gave the ability to determine changes over time foreach dependent variable under the three conditions. Theeffects of hypohydration can be substantial and varyconsiderably between individuals. Subject variability wasthe major factor limiting any definite patterns of changewithin the present study.Recommendations ig; Future Research

The results of this investigation suggest certainchanges and additional procedures should be included forfuture research. If a follow up study is to be conducted, Ioffer several recommendations: a) use a larger sample size;b) add a neutral/hypohydration trial; c) insure the

T 88

measurements of all electrolytes in the blood which havebeen shown to relate to thermal stress.

Due to the small number of subjects, individualvariability produced a wide range of responses in eachtrial. Increasing the number of subjects would give moremeaningful physiological responses at each time interval andincrease the ability to interpret data in more precisedetail. Thus, a larger sample size would provide increasedstability and give more specific results. The initialvalues for plasma osmolality and plasma [Na+] in the HH weresignificantly different from the NE Trial, thus theinclusion of another trial, the neutral/hypohydration, wouldallow researchers a greater understanding as to whichfactor, environmental temperature or hydration, was

producing the lack of an equilibrium level in Tc duringexecise.

Plasma sodium is the greatest contributor to theelectrolyte pool involved in the osmolality of blood, butthe evaluation of plasma chloride, potassium and totalplasma protein would increase the understandings ofelectrolytes and other solutes in plasma osmolality. Theprocedural changes in blood collection would be to insurethe equipment and supplies the researcher uses the freedomto measure all electrolytes involved in thermal stressful

89,

situations. This would allow a detailed description ofchanges occurring within the osmolality measurement of theblood during fluctuations, and might demonstrate increasesin certain electrolyte values while others are decreasing toprevent changes in osmolality. ·Recommendations fg; ßggg Sgonsors ggg Runners

The recommendations for individuals that participate inprolonged exercise in a thermal stressful environment are infour areas: l) training, 2) acclimatization, 3)environmental conditions, and 4) state of hydration. Thetraining an individual is involved in during cold monthsshould gradually be incorporated into a summer program whenan individual's exercise capacity for training is 75% ÜO2max. The first weeks of a hot environment the individualshould reduce the strain of high muscle metabolism combinedwith increased ambient temperature by decreasing the percentÜO2max. Individuals should allow time for their body's toacclimate, which is accomplished within the first 2 weeks ofexposure, and reduce the time involved in the activity to aminimum after acclimatization has occurred. The individualsshould never try to push above the training level they haveset especially toward the end of an event. Thus, placingexcessive strain upon the thermoregulatory system. 4

90

In environmental conditions of a high ambienttemperature and high relative humidity, the individualshould avoid activity and try to train or race during thecooler times of day. Even if ambient temperature or therelative humidity are high, individuals should again try totrain before 8 am or after 6 pm.

When discussing heat injuries, probably the mostimportant aspect is the state of hydration. Prior toactivity an individual should insure adequate hydrationespecially of a prolonged nature. During a prolonged eventeven in a training run, the individual should place water instrategic points along the route. After the exercise,

hydration should continue, and a good way to know if properhydration has occurred is urinating within l5 to 30 minafter the exercise. Cool water should be used for thisprocess of replacing fluids but not cold because the gastricabsorption level decreases with cold liquids. Propernutrition and added salt at the table is adequate to replacelost electrolytes. The use of salt tablets should beavoided.

Other populations which should be made aware of theproblems of thermal stress include people who are young orover 60, overweight people, and people who are not fit.Through further research, a greater understanding of the

9lmechanismsand factors involved in thermoregulation will beable to assist in educating the public to the problemsinvolved during thermal stress.

1 92 ·l

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I

98 '

Miles, D. S., Sawka, M. N., Glaser, R. M., & Petrofsky, J.S. (1983). Plasma volume shifts during progressivearm and leg exercise. Journal pf Applied Physiology:Respiratory Environmental Exercise Physiology, 84(8),491-495.

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99

Nadel, E. R. (1985). Recent advances in temperatureregulation during exercise in humans. FederationProc., 44, 2286-2292.

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100 1

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I101

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102

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APPENDIX ADETAILED METHODOLOGY

103

104 1

METHODOLOGY

Introduction

The data needed to fulfill the objectives for thisinvestigation required three trials per subject. Thecontrol for this study was in a thermoneutral environmental,and the other two trials were in a hyperthermic exercisecondition. The exercise was performed on a stationary cycleergometer at a workload equivalent to 50% of theindividual's maximum Ü02 capacity (Ü02max), and lasted amaximum of 120 min. Data were collected during the pretestperiod at -30 min and at 0 min. Thereafter data werecollected every 15 min even during a 30 min recovery period.Subject Selection ang Screening _

From a pool of 15 adult male prospects, six subjectswere selected to participate in the study. Prior toparticipation in the study each subject was required to readand sign an informed consent which explained in detail theprocedures necessary for data collection during the testingand explained all the risk possibly involved. Approval fromthe University Board for the Protection of Human Subjectswas obtained prior to any testing. Each subject was given amedical examination consisting of a resting 12 leadelectrocardiogram; this was done to screen out anyindividuals with potential cardiovascular problems. A

|l

105 'functional capacity test (ÜQ2max) to insure an adequatefitness level for the study. A ÜQZmax between 40 to 60ml•kg"•min'1 was required along with an habitual traininglevel of 15,000 to 30,000 m per week and a percent body fatof 10 to 16%. These criteria insured a homogeneous subjectsample.

Preliminary Functional Testing Procedures

Since stationary cycling was the exercise modeofchoicefor the experimental trials, a Monarch cycleergometer (Model 868) was used for all Ü02max testing. Eachsubject wore gym shorts, socks, and tennis shoes. Prior tothe test, the subjects adjusted the height of the seat to aposition where their leg would be slightly bent when thepedal was at the vertical position. After a few minutes ofquiet, resting heart rate and blood pressure were taken byauscultation. A careful explanation of the test protocolwas given to each subject; each was asked to continueexercise until exhaustion. Each subject was then fitted toa mouthpiece and a Daniel’s two-way valve, which was coupledto a 3.81 cm, ID, flexible breathing hose of less than 1meter in length. The other end of the hose was connected toa Hewlett—Packard Pneumotach (Model A 7303A) which was usedto determine the ventilation rate volume (Te) in l•min").The mouthpiece was placed in the mouth and a nose clip wasplaced on the nose to occlude the nasal passage.

106 l· iPrior to the first exercise stage, the subject free

:wheeled the cycle ergometer for l min at a rate of 50 rpm. l

This pedal cadence was maintained by a metronome calibratedto 50 beats•min‘1. Immediately after the free wheelingperiod, l kg of resistance, which is the equivalent to aworkrate of 300 kpm•min'1, was applied to the wheel of theergometer. After 8 min the resistance was increased by anincrement of 0.5 kg load at 2 min intervals untilexhaustion.

At the end of each 2 min interval the oxygen content ofthe dry expired air was determined by a rapid responseApplied Electrochemistry Oxygen Analyzer (Model 5-3A). Thecarbon dioxide content was also determined by a rapidresponse Applied Electrochemistry Carbon Dioxide Analyzer(Model CD-3A). At the same time the volume of expired air

A (0a) was measured. The oxygen uptake was calculated foreach workload and the highest oxygen uptake was assumed tobe the ÜO2max. A work rate equivalent to 50% of the VO2maxwas assessed by a regression equation from the linearportion of the oxygen uptake vs work rate, and this workratewas then used as the steady-state exercise requirement foreach experimental trial. During the 002max test, a heartrate was taken by auscultation in the last l0 sec of each 2min interval to insure an accurate maximum heart rate atexhaustion.

Hydrostatic Weighing ProcedureSubjects were asked to refrain from food and drink for

lO hours before the weighing. Upon arrival at the labsubjects were asked to shower with soap to eliminate anybody oils which might hold air and eliminate any bodilywaste since both could lead to underestimation of bodydensity. Then each subject was weighed nude with a medicalbalance to determine the body mass. The weighing tank wasfilled half way with warm water (30—33°C) to minimizesubject discomfort. Prior to each test, a routine

calibration with a known amount of weight was conducted.With assistance each subject would carefully lower

themselves to a sitting position on a rectangular stainlesssteel basket. At each corner of the basket were load cellswhich transferred signals to a single channel Speedomax HAzar Recorder for a graphic readout. Each subject thenplaced a set of scuba weights around his ankles and laidanother set in his lap. These "lap" weights were to bemoved by the subject to the thoracic area as he reclined andforcibly (maximally) expelled air from their lungs. Thesubject stayed in the supine position motionless, as toprevent any artifacts on the recorded tracing, for

approximately l0 sec. This procedure was repeated a minimumof seven times to allow for learning the technique. An

1 108 éaverage of the final two attempts was computed as the actualunderwater weight.

Estimation of Percent Body Boo

Approximately the same percent body fat and bodysurface area were necessary in the subject set in order tominimize differences in heat storage tendencies. Measuring _each subject's height (cm) and body weight (kg) enabled

investigators to calculate body surface area. Hydrostaticweighing was the most precise technique for estimation ofbody density. After the body density was calculated, thepercent body fat was estimated from the equations below.Body Density Eguation:

BD = Ma .[Ma—Mw;I - (RV+VGI)Dw

where BD = body density

Ma = mass in air (grams)Mw = mass in water (grams)

Dw = density of water due to temperature

RV = residual volume; assumed to be a

constant 1300 ml.VGl= volume of gas in the gastrointestinal

tract assumed to be a constant 100 ml.

1109 1

a

Eguation gg; Percent (Z) ggg; gg; ggggg ggg; Densit;:% BF = 4.570-4.14Z X 100

BD

where BF = body fat

BD = body density.Exgerimental lgggl Conditions ggg Protocol

Prior to the actual study, a practice trial wasadministered to each subject to relieve anxiety, to minimizeany learning effect, and to acquaint the subject with allexperimental procedures. The practice trial was conductedover 60 min in a thermo—neutral environment with 50%relative humidity. Blood samples were not collected duringthe practice trial.

All experimental trials were conducted in a controlledenvironmental chamber between 0930 and 1300 hs to avoid anydiurnal effects or physiological responses, such as uponheart rate. Each subject's trials were randomly ordered andseparated by 1 wk periods to avoid any training effect.Also, the testing was conducted in late April and early Mayto avoid any acclimatization effect. Subjects were requiredto exercise during the cool part of the day (<22cC) andlimit activity to the criteria for the study. Subjects woregym shorts, socks and tennis shoes for each trial.

1 110 ll

The experimental trials consisted of four phases: 1)preparatory phase, 2) pretest phase, 3) exercise phase, and4) recovery phase. All subjects in the study were requiredto be in the Human Performance Lab at least 60 min prior to

testing. The first 30 min was the preparatory phase, wheresubjects were fitted with equipment necessary formeasurement of dependent variables. Also during this phase,each subject consumed the equivalent of 1% of his bodyweight in water of room temperature for the euhydrationtrials. The next 30 min was considered the pretest phase inwhich all baseline measurements of dependent variables wereobtained, i.e., 30 min and at time 0. During this phaseeach subject rested in a sitting position on the ergometer

within the environmental chamber. At 15 min intervals allexperimental measurements were taken, including cardiacoutput (0), heart rate (HR), blood pressure, skintemperatures (Ts; from thermisters), core temperature (Tc;via rectal probe), blood samples and thermograms. At theend of the exercise period each subject was weighed and therecovery phase began. At +15 and +30 min post-exercise,experimental measurements were obtained while the subjectsrested on the ergometer.

lll1

Experimental Trial Conditionsf

Each of the experimental trials were conducted in thecontrolled environmental chamber. The conditions ofenvironment and hydration were as follows:

1. Neutral euhydration. The ambient temperaturewithin the chamber was set at 24oC with a relativehumidity 50%. Euhydration was accomplished byhaving each subject consume 1% his body weight inroom temperature water during the preparatory phaseand 1% during the exercise phase, for a total of 2%of his body weight.

2. Hot euhydration. The ambient temperature was setat 35°C within the chamber and the relativehumidity was 50%. Euhydration was accomplished inthe same manner as in neutral euhydration.

3. Hot hypohydration. Ambient temperature again was35oC and a relative humidity of 50%, but no waterwas given during any phase of the trial.

Maintaining a Constant Environment and Workload

The environmental conditions and exercise workload wereconstantly maintained and if fluctuations occurred theproper adjustment was made. Every 15 min the environmentalfactors of ambient temperature and relative humidity withinthe chamber were checked.

112To

insure the proper exercise workload (50% V0gmax) wasmaintained, the heart rate (HR) and oxygen uptake measures

were checked every 15 min. The HR was monitored by a Vconfiguration of electrodes and displayed on a QuintonTelemetry system. The oxygen uptake was monitored by gasanalyzers, which were calibrated before each measurement.If the workload varied, the ergometer was adjusted.Measurement gf Dependent Variables

The core temperature was obtained by a rectalthermocouple se1f—inserted to a depth of 10 to 16 cm, andiall

changes were monitored on a Yellow SpringsTelethermometer (Model 46 TUC) (Saltin & Hermannsen, 1966).

_ All blood samples were collected from a_2O guage 3.18cm teflon catheter inserted in the antecubital vein by aregistered nurse. A pharmaseal K52 novex 3-way stopcockwith extension tube (2.3 ml) capacity was attached to thecatheter. To maintain patency in the catheter, a 0.01heparinized saline solution was used (every 15 min interval)before the blood sample (7 ml) was drawn. The heparinizedsolution was discarded and after the blood was taken a new(2.3 ml) amount of heparinized solution was infused into theextension tube and catheter.

Blood samples were obtained by using a 10 ml sterilesyringe. From the syringe a small amount was placed on a

113 I

Iclean slide and microcapillary tubes for Hct (4) and Hb (3)

:were filled from the slide. After the small amount wasplaced on the slide, the remainder of the blood was slowlyejected from the syringe into a vacutainer tube (10 ml)treated with crystaline potassium—ethylediaminetetraacetate(K+-EDTA) and placed on ice. After each trial the sampleswere centrifuged in a refrigerator 4 C Sorvall Preparatorycentrifuge at 10,000 RPM for 20 min. The plasma wascollected for each sample and stored in polypropylene tubesat -20 C for subsequent analysis for osmolality andelectrolyte (Na+ and Cl-) values.

Hematocrit (Hct) microcapillary tubes were centrifugedand values read (Appendix B), and hemoglobin (Hb) valueswere obtained (Appendix B). From these values, changes inplasma volume were calculated with formulas by Costill andFink (1974). The hematocrit was corrected by a factor of0.96 for trapped plasma and a factor of 0.93 to adjust forvenous to whole body Hct ratio.

Osmolality and the electrolyte of Na+ analyzed for eachtime interval (Methodology Appendix B). The mean resultsfor all the analyses are in Appendix C.

Statistical Analysis

The data were analyzed to determine the changes independent variables of core temperature (Tc), plasma volume

114 1_ b

(PV), osmolality (OSM) and sodium concentration [Na+] in theblood for different environmental conditions and hydrationstates. An analysis of variance was utilized to determineif significant differences existed between the dependentvariables during all three experimental conditions. Insteadof computing a separate variance for each trial-treatment

combination based on six observations, a combined estimateof variability was computed. An equal variance for theanalysis of variance was assumed, thus allowing for a moreprecise estimate of variance and more degrees of freedom forthe tests. A Duncan's Multiple Range Test was utilized inorder to determine where differences existed.

1

APPENDIX B

DETAILED METHODOLOGY

OF BLOOD PROCEDURES

115

1l6

PROCEDURES FOR CONTINUOUS VENOUS BLOOD SAMPLING

(CATHETERIZATION)

(Adapted from Goss, 1983)

1. Have the subject extend his/her forearm with the palm

up. The elbow and the back of the hand should rest on aflat surface.

2. Place a tourniquet securely around the upper arm.3. Locate antecubetal vein. NOTE: If vein is difficult to

locate have the subject alternately clench and relaxhis/her hand.

4. Cleanse skin around selected vein with Beta-Dyne oralcohol.

5. Insert sterile 20 gagge (5.08 cm length) teflon catheterinto antecubital vein.

6. Place a 2.54 cm x 2.54 cm sterile gauze pad under thatportion of the catheter extending out from the skin.

7.* Remove catheter needle and place sterile catheterextension tubing (25.4 cm) on the distal end of thecatheter.

8. Place a sterile 3-way stopcock on the distal end of thecatheter extension. NOTE: The catheter extension may

be shortened or omitted and the 3-way valve connecteddirectly to the catheter if the subject is to be engagedin stationary cycling or light to moderate treadmillwalking.

117

9. Release tourniquet.A

10. Secure catheter by taping the extending portion (distalend) to the skin. NOTE: For maximum stability narrowStrips of tape (0.64 cm) Should first be carefullywrapped clockwise and then counterclockwise around thecatheter projection and then in a similar fashion

'

wrapped around the circumference of the forearm.ll. Secure catheter system by taping the junction of the

I catheter and extension tubing to the skin. Foradditional stability 5.08 cm to 7.62 cm of the tubingsituated along the longitudinal axis of the forearmShould be taped to the skin. For best results tapeshould reach around circumference of the forearm.

12. Turn stopcock Valve to position 2 and attach steriledisposable syringe. Carefully draw blood out of Vein

> through the tubing and Valve into the syringe. SwitchValve to position 1. Remove and cap syringe.

13. Attach a sterile disposable Syringe containing 2 to 3ml of heparinized saline (2 drops heparin/5 cc saline)and switch Valve to position 1. Draw any remainingblood from the blood Sampling port. NOTE: If thisstep is omitted clotting of blood could interfere withsubsequent Sampling.

1 118 1

14. without removing syringe switch Valve to position 3 andcarefully draw a small (less than 1 ml) sample of bloodinto the syringe. Next, carefully inject heparinized

saline solution into the system (i.e., Valve tubing and

catheter) in order to maintain the potency of thecatheter. Switch Valve to position 1. Remove and capsyringe.

n

15. Attach sterile syringe and switch stopcock to position3. Draw off the heparinized solution plus 1 ml ofblood to insure that the subsequent sample is notcontaminated by the saline/heparin infusion. Switchstopcock to position 1. Remove and cap syringe.

16. Attach sterile disposable syringe and adjust stopcockto position 2. Draw off the desired volume of blood.Switch Valve to position 1 and cap syringe.

, 17. Rinse system with heparinized saline (see steps 13 and

14).

18. Repeat steps 15 and 16 and then 13 and 14 for eachsubsequent blood sample.

19. After the final blood sample has been taken, carefullyremove the catheter and immediately apply pressure

(with a sterile gauze pad) over the puncture area.20. Place a bandaid on the catheter insertion site. Watch

carefully for the development of a subdermal hematomabefore dismissing the subject.

119

Supplies for Blood Sampling Procedure

Item No. Required Supplies Cat. No. Cost

3-way sterile 50 American Sci 58965 $.64 ea.stopcocks Products 50 for

$21.66catheters 50 B-DSterile exten- 50 B-Dsion tubing

Sterile syringes 2110 American Sci 5cc $71.46/

Products 500

1066 $76.60/500

Tape 2 bx Whittaker Med.Sterile heparin

ISterile saline

Bandaids 50 Whittaker Med.Sterile gauze pads 50 Whittaker Med.Beta Dyne/alcohol Whittaker Med.Tourniquets 3 Whittaker Med.2 needles 1 bx 2/$.57/50

Faye List Equipment

- catheters - 20 gauge teflon75 - IV set up trays

120

4 box - alcohol wipes

60 - 3 way stopcock with extension tubing60 · 50 cc bag with .5% NaCl

- heparin

60 — minidrip chamber set ups— 5 cc syringes or 3 cc syringes— 10 cc syringes

18 boxes - heparinized test tubes 10 ml100 /vial - 20 — 20 ul hemoglobin pipette capillary tubes500 vial · 4 - hematocrit tubes

- disposable test tubes and caps

}121

DETAILED PROCEDURE EQ; HEMATOCRIT (gg;) DETERMINATION

Collect Soecimen

l. Put small amount of blood sample on a clean slide (usenew slide for each interval).

2. Place the end of a microcapillary tube in the sample.Blood will be drawn up into the tube. Allow the tube tofill at 2/3 full and remove from the sample. (Repeat 3more times for quadruplicate readings per sample).

3. Wipe off the blood on the external surface of themicrocapillary tube with a kleenex being careful not tocome in contact with the tip of the tube.

4. After the blood is in the tube, seal the opposite endfrom where the blood was taken in with a flame.

Centrifuge

5. Place an even number of sealed microcapillary tubes (2intervals, 4 interval) into a microhematocrit centrifuge(Model MB) for 10 min.

6. Remove microcapillary tubes after centrifuging and placeeach tube on the Hct stand in the proper interval slot.

Reader

7. While the next 2 intervals of tubes are in thecentrifuge, read the microcapillary tube just removedfrom the centrifuge on a micro-capillary reader (ModelCR)

122 “8. Slide the microcapillary tube into the slot underneathl

the magnifier with the sealed end down and in contactwith the edge of the holder.

9. Turn the adjust screw at the base of the holder untilthe lower edge of the red cells is directly at the edgeof the scale.

10. Slide the sample to the right, until the scale arm is atthe 100% mark (the plasma meniscus) and tighten thescale arm at this point.

ll. Slide the sample back to the left until the scale lineintersects with the red cell meniscus. Where the scaleline intersects read the Hct in %.

123 ‘

PROCEDU;E EQ; EE; QUANTITATIYE COLORIMETRIC DETERMINATION

QE EQEA; HEMOGLOBIN EE EEQEE EEQQQ(from Sigma Technical Bulletin No. 525, 1980)I. Reagents (for in vitro diagnostic use)

A. Drabkin's Reagent, QQQQ; EQ. Q;Q;;

l. A dry mixture, consisting of sodium bicarbonate,100 parts, potassium ferricyanide, 20 parts, andpotassium cyanide, 5 parts. Store in dark at

_

room temperature.

B. Drabkin's Solution

1. Reconstitute Drabkin's Reagent, stock No. 525-2with 100 ml water.

2. Add 0.5 ml 30% Brij-35 solution, stock no. 430AG-6, and mix well.

3. Filter if insoluble particles remain.4. Store in amber bottles at room temperature.

5. Stable for at least 6 months.*Caution: Drabkin's reagent and Drabkin's solution

contains cyanide.C. Brij-35 Solution, QQQQ; EQ. QQQ AQ;Q

1. Contains Brij-35, 30 gm/100 ml2. Store at room temperature.

D. Hemoglobin standard, QQQQ; EQ. 525-18

1. Lyophilized human methemoglobin

I' 124 p_

'2. Equivalent to 18 gm (r1%) hemoglobin per 100 ml

whole blood when reconstituted and usedaccording to this procedure.

3. Store in Refrigerator.E. Cvanmethemoglobin Standard Solution

1. Reconstitute vial of hemoglobin standard, stockno. 525-18 with 50.0 ml Drabkin's solution(Reagent A')

2. Mix well and allow to stand for at least 30minutes.

3. Stable for at least 6 months when stored inrefrigerator at 0-5°C.

II. Instrument and Materials Required ”

A. Instrument: Any filter photometer or

spectrophotometer that transmits light at 540 nm issuitable.

B. Materials

l. Test tubes: 10 ml.2. Pipets: 20 ml, sahli type or micro, 10 ml,

serologic.

III. Calibration.

A. Reconstituting the hemoglobin standard as directedyields the cyanmethemoglobin standard solution(Reagent E). This solution will yield an

125

absorbance equivalent to that of a whole bloodlsample containing 18 gm (tl%) hemoglobin per 100ml which has been diluted 1:251 with Drabkin'ssolution (Reagent B). Dilutions of the

cyanmethemoglobin standard solution with Drabkin'ssolution are used to prepare a calibration as

followsz

1. Prepare working standards by pipeting andmixing thoroughly the solutions indicatedbelow.

1 2 3 4 5Tube Cyanmethemoglobin Drabkin's Absorbance BloodNo. Standard Solution Solution, (A) Hemoglobin

Reagent E (ml) Reagent B (gm/100 ml)(ml)

1 0.0 6.0 0.02 2.0 4.0 6.03 4.0 2.0 12.04 6.0 0.0 18.0

NOTE: Diluted Standards are stable for as long as6 months when stored tightly capped andrefrigerated at 0—5°C in the dark.

126 (

2. Read absorbance of tubes 2-4 vs. tube l asreference at a wavelength between 530-550 nm.

3. Record absorbance valves in column 4 on chart.4. Plot a calibration curve of absorbance value

(column 4) vs. blood hymoglobin (gm/100 ml) incolumn 5. The curve is linear, passingthrough the origin.

NOTE: A curve should be constructed prior to eachassay session.

IV. PROCEDURE

A. Label two or more test tubes, blank, test l, test2, etc.

B. To all tubes add:

l. 5.0 ml Drabkin's solution (Reagent B)C. To Test add:

1. 20 ul whole blood, rinsing pipet 3-4 times withreagent.

2. Mix well.

3. Allow to stand at least 15 minutes at roomtemperature.

D. Place solution from blank, test l, test 2, etc. into (4) cuvettes.

E. Place cuvette tray into spectrophotometer.

i

127 ‘

lF. Read and record absorbance (A) of test Vs. blank as

reference at the same wavelength and in the sameinstrument as used in the preparation of yourcalibration curVe.

DETAILED PROCEDURE EQR OSMOLALITY DETERMINATION

Steps for the use of a Vapor pressure osmometer(Wescor, Inc., Model 5100).

Calibration

l. Process a 290 mmol/kg standard. Set the meter to 290using the calibrate 290 control.

2. Process a 1000 mmol/kg standard. Locate the instrumentreading of the left hand side of the calibrationnomograph. Then using the calibration 1000 controladjust the meter to read the corresponding set Value onithe right hand side of the calibration nomograph.

3. Repeat step 1. Then calibration is complete.Operational Procedure

4. Pipet an 8 microliter sample of plasma.5. Place sample on a solute-free paper disc.6. The sample slide is inserted into the sample chamber and

sealed.

7. The next four steps are electronically controlled andthe measurement proceeds automatically until finaldisplay on the panel meter 90 sec later. Stepselectronically controlled are:

128 I

a. equilibration and zero set (50 sec)b. maximum cooling—peltier effect (13 sec)c. dewpoint convergence (27 sec)

d. end of sequence and readout (total 90 sec)8. This procedure should be repeated in triplicate per

sample taken.

9. The readout is calibrated in units of osmolality,

mOsmo1/kg.

129I

DETERMINATION QL PERCENT CHANGE lä PLASMA VOLUME

Eguations Adogted from Costill ggg Elgg, lglß

= ' HctB

PVA = 100 (HbB/HbA) — l00(HbB/HbA) x HctA

Z PV = 100 (PVA - PVB)/PVB

PVB = The volume of plasma in 100 ml of blood beforeexercise

HctB = Z Hct before exercisePVA = The volume of plasma in 100 ml of blood aftgr exerciseHbB = Hemoglobin concentration in g•l00 ml°1 before exerciseHbA = Hemoglobin concentration in g•10O ml‘1 after exerciseHctA = Z Hct after exerciseZ PV = Z change in plasma volume.

130 A

ADETAILED PROCEDURE EQ; SODIUM DETERMINATION

Sodium concentrations were measured on a flamephotometer (Model 510).

I. Preparations:

A. Lithium Diluent

1) Dilute 510-022 lithium stock concentrate, 1500meq Li/1, 100 times with distilled water (final

concentration 15 meq/1). Store lithium diluentin plastic container.

B. Calibration Standards

1) Dilute all calibration standards 1:200 with thelithium diluent.

· 2) Dilute 510-020 flame standard - serium 140 meqNa/1 one part to two hundred parts of total

solution with the 15 meq Li/l lithium diluent.

C. Samples

1) Dilute 1 part sample to 200 parts of totalsolution with the 15 meq Li/1 lithium diluent.

2) Normal 0.5 ml sample is diluted to 100 ml withlithium diluent.a) normal concentration = 136-145 meq Na/1.

*Aspirate sample long enough for readings to assumetheir final value. 30 sec recommended between startand actual reading.

II. Detailed Sodium (Na+) Operation:

131 I

PA. Fill drain tube.'

B. Gas on — power on, get flame on display.C. Warm—up.

1) Aspiration lithium zero solution for 15 min.2) Set needle tip 0.16 cm clear of the bottom of

the sample cup.

D. Calibrate.

1) Aspirate zero lithium solution. With direct andrange Li depressed, adjust lithium zero to 0.00.

2) Aspirate calibrating standard. Adjust fuel flowfor a maximum reading. Set Li display to theconcentration of the lithium stock standard(1.50 meq/1).

3) Touch up. Zero on zero lithium solution.Calibrate on calibrating standard, at 30 sec.

E. Read unknowns.

1) Aspirate and read at 30 sec.2) Initially touch up zero and calibration every 4

to 5 samples. After 15 min of operation needfor zero and calibration occurs a lot less.

F. Turn off.

1) Aspirate distilled water for a few minutes.2) Turn off gas. When flame on display goes out

turn power off.

APPENDIX C

MEAN DATA TABLES

132

1 .L a

1 „. 1 „ 1:1 N N Q1-1 I M M M Ign 4- -1 QM N Q Q1-1 M M M

Q N ¤~ 1-1N N QIX M M M

I° •

c G M N61 N Q Q1-4 M M M

O• •,¤ Ln G N N‘A Q N Q QU 1-4 M M M

Ow • •3 G c~ 61 Qg c~ N Q Q¤_ M M M3 dl°‘ . ' c

' 0E Ln ¤~ 1-1 4- Ej N N Q QM M M 1:L

·‘¤

E- ° 1 >1g O c~ 1-1M**Q N Q Q . 111-1Q M M M umS LZ2. L1 _ .,"}B

+*C_Ln Q G G

1; Q wgN M gg.:1 L-1-•'Tö Tl ‘°„Ü' . .,71 WEQ N G GEMN N N II : --7M M M 61 LU• 1-* U.:HJ w-··•

• Q Lcn -•• 0L9,+-G 3·••NT U1 U} •

- WZgn 1 1 • qy1-1 N N N C U -*-*0M M M cu C Q CL0 O ·•'• Q3]

E ·¤ C L L-H-•¤ O 0 0100 m C ·•-• 1 *-1-L,: L Q -1-•~·••q;· 6.1 61 M -1- *3 ··-• ru -•· -··•1

. . . >, ae L [ 1;G N N N *1* .2 fü 7J Q) Q2M M M C 3 1. >1 E L-•··0 111 *3 L ·• -—*10 >1 O *5 ·••Eü 1*4 .1; O. Gl IO1 L 15 .1 >s L L61 61 1-1 1 1 L 1.11 Z 1- ww-G · ·

• | Q *‘ OM N N N I L 3 -•¤ -1- ~1- L-1 M M M 0 O O O 31-¤w Z Z Z -cC} 16 fü ·3 II II :1 : LG1-1 | --1 6: 0JI ru u.1 1.1.1 Z 0 1V·•·• > Z Z 2 Z EL Lu LU Z 011- Z Z Z cu L 0 'J 0 I-—

I

G ~1’•·-OLGgg .1.A L¤¢1·•‘\1III

L1 r·€G*1•·4|m .•.1-4 0N\G\|1II Ic3-e-1QL000

|>< 111

G H\~3‘0N •..1-t NQQIll

U] NNG*Q ..•1-1 NQN

m III

N° MG0W Q •.•Q Q* 0NN0 IIICOQ.

GIBMz gg ..•Q N NNN= III31-nO.>

-Q QNN1Q •••Q 0 NON_.

IIIQ

OO gg „..l_,xf INNUI.

2 III" I

· Zc NNN ll-O wgm <1·1:11:1 II 'III ¢• NI.I.| 1-I

U) OM0m ¥

LQ ··~1' · GFÜ TT] soZ5: *:1CIO OEw! C11-!6 QL'33C••·•0.’ZL.¤·1-•cLc ccc '¢"¤¤•¤I(ß

>,6;6"".‘:ßUCC3L>•U011.17:5cn >«0·1-•Cl¤"¢.:QI‘6s.m3>1<;1¤ :.;u.1:;M GGG ¤“J*‘

P-1 LjwwUOO‘*•0122:0Q)’ 3111111:•-tl ad 5m .:07 mu.1au:;1··-•| >2::zL 1.1.11.1;:1- 2:: I«¤..¤u¤c.1

I

I

Q Q QQ N Q NLG Q Q Q1-4 N N N

G M MG N Q QM Q Q ¢‘1-4 N N N

M Q U1Q M 1~ NQ Q Q{X N N N

N Q MO G N GN Q Q Q1-4 N N N ·

"' M G Q[Q • • •Q Ln N MIB r··4 Q Q Q

N N NClZ\ ,r-43 ¤~ M NE Q 1 • 1tt) Q G Q FÜO Q Q QE N N N

40QanC _ G M Nq 4} . • •D- N G Q MV! Q Q QQ N N NZäan••·• N Q M,-4 Q 1 • .GI Q G N MA Q Q QO N N NE IInC

G M Q• gg . 1 . _OW G Q Q GQ Q QQ N N N1-1Q QQ G "‘I- · C•-4

Q . „ 1 EM 1-4 Q Q IIQ Q Q QN N N • N _LU 1-4Q O

-4-Q Q x1'4,4} • . 1 1 Q«-• 1-1 c 1-4 Ih „.Q Q Q CN N N m C 'UQ O OE ·•·• C ·•·<

-4-* Q LQ tß C ·¢• Q~o c c .C L 0 -1-• ¤.• •-

-5 Q 1-4 Nc N Q 1-4 >« -4- L +1Q Q c~ +• .; 16 ‘¤ CN N N C ,1 L >q QQ LU "J .C Evi >4 O -1-*Q •'* ’° Q GUco 1:1 ~o L as 'B >• an· ·

• A L LI-I 2 I-G M Q Q Q ·•·‘ I-M a) cn ¤*~ L J ·•·• -•¤1 N N N 0 0 ¤ u-U! Z I I OQJ II Il II C1-4 •-4 0}Q B U Q IU LU LU Z Q·•‘• > Z Z'- 2 ZL Lu lu II- Z I 2 Q 3 O 'U Q

, I:-4 :3 a~ I

G G 6 N*-0 M M M:-4 :-4 :-4 :-4

M 6 NUI G In 0*M M M M:-4 :-4 :-4 :-4

M G 0G I-H 6 N

M M MX :-4 :-4 :-4•

N G NG G LQ 6*N M M M:-4 :-4 :-4 :-4

•

M N MLH G UI 6*G M M M:-4 :-4 :-4 :-4

L ' ·LI N gf N\ • : .O' Q U1 UI ¢*G ¤" M M ME :-4 :-4 :-4

IAG • 4*W CC WI G M GQ • : . g_Q Ih Ih III Q Gu: N M M M 4-41 :-4 :-4 :-4 ••-:-4_ '3= •3 >s-•4 N G G M*3 • • „ -4O UW I-0 G G ·(D Q M M M 0:-:G M M M ¤•4t¤

*52CD:-1QG

N G G GCpnq • • • -•¤••pQ.3 6 6 N InG I-H M M M GI- ~r :-1 :-• :-1 ¤EL·-4

(I4!QM

WGG M G • #5• . : Q aßG NT L3 N -:-4:})M M M M II··~ L:-4 :-4 :-• Q OO• N U).:IH :-4 L-• ·’ vi o 2..:N ~0 N +4 je• • n wnplH0 6 6 G • G ZM

N‘NY FÜ W uv •P‘

:-4 :-4 :-4 : CGG C Ü GLG O O L3• E ••¤4 C ·•4 @-4**' O L ‘*•U

:-4 N N G G C ·•·4 Q M-;·

• • L L Q -4- Q LQQ M~

LH -•- U -:-4 cu UaM M M >« ·•-• L. -•-e 5M M M 4* C GI 'U C LG: Ü L >« an -•-·~·•QI LH 'J L E ·•·•W >• C 4* ZEG :-4 Q Q. G OM G M L G 3 >4 G WLG ·

•· D. L Lu I L G'4-M »:· M In 3 -•-• I- 3I M M M L 3

·•·• # :-4**:-1 :-4 :-4 c: O O 4- mhh3 Z Z I O >G3 II :• II C EQM M G 3(U 3 LU LU = Ü "‘\/·•·• > Z Z 2 Z 'UL u.: u.: : OB.I- Z Z I G ..3 U '3 G V)-•

, !

A APPENDIX DDATA TABLES

i 137

{138 E

Table 11. Individual Weight Loss (Z)

TrialSubject NE HE HH

1 0.0 0.9 2.12 0.0 2.1 2.73 0.7 1.0 2.74 0.8 0.0 2.25 0.9 2.9 1.86 0.7 1.9 3.8

E:SD 0.5:0.2 1.5:0.4 2.6:0.3

NE = Neutral Euhydration, HE = Hot Euhydration,HH = Hot Hypohydration

r 1391

Table 12. Environmental Conditions of Neutral EuhydrationTrials

Ambient RelativeSubject Dry Temperature (°C) Humidity (Z)

1 21.5 49.02 27.1 45.43 25.1 55.64 22.5 _ 56.15 23.9 49.06 25.0 47.0

$E:sD 24. 2:1. 9 50. 35:4. 5

Values represent a mean of 12 observations taken persubject trial.

i

D 140 DI

Table 13. Environmental Conditions of Hot EuhydrationTrials

D Ambient RelativeSubject Dry Temperature (°C) Humidity (Z)

1 35.6 61.42 35.5 46.53 33.1 49.04 35.5 46.55 35.5 49.96 33.4 49.2

R:SD 34.8:0.2 50.5:5.4

Values represent a mean of 12 observations taken persubject trial.

I

I Z 141 LII

Table 14. Environmental Conditions of Hot HypohydrationTrials

Ambient RelativeSubject Dry Temperature (°C) Humidity (Z)

1 35.9 48.62 35.2 51.63 34.7 51.04 35.0 49.05 36.3 50.76 35.1 50.3

X:SD 35.4:0.6 50.2:1.2

Values represent a mean of 12 observations taken persubject trial.

Ü “

APPENDIX E

RAW DATA TABLES FOR EACH SUBJECT

14+2

I

I „I S'

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· 1-:-,,I Q-.}-:{ fI~I~mr~·r·~ SSO;

4 •• 4 4 • 4 4 4 4 4 4 4 4 • 4 4 •; ~•-4cx

CC C4. C'-N ' .. N-4III

,®·-·•I\4:q' Q —7wC‘-•·-!<\I IF4 4 4 4 4 4 4 4 4 4 4 4 4 4 • 4 4S -4so cc <'^<.*·-·I*^ ¤¤, C+C-1 1 4-4 gw ·-I N -••-I

. I.A1 I7::ÜE 7;;*:%2 I3 I Lnc\ TI ASC:V I; Q MI-*I~oC>~ O ~O·—~—I4-4c4 4 44 4 4 4 4 4 • 4 4 4 • 4 4 •~ _,_,,„,

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N ..- N —-I :~4Ü~/>:I‘:Q1 I I 1 Q44:7 { IE5;·:· 7 { IF":1:_ Q Qvxeznm4 • 4 4 • 4 • 4 4 4 4 4 4 • 4 4 4 _—

3 I-I**1 ON r'^<.°-I"'°‘ 99, =I7T'JJ! ' 444- N ·-•:*4; ¤- N L ··‘··· I I ‘

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4 4 4 4 4 4 4 4 4 4,_

2,* ggü:_-N •-—~ 4 *· ¢. ·•-1FSI I •-I N

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wg rx ~\ Q ~\\7—4 ··*\ Q aba;I ‘ .„ N -4 :4 —· NI apa--·-«,_4•Ix4«E,.::4.I;;I ,O€.„u¤¤:;,II IIL};I

QJI Inn° '°‘I A < A < A, Ilm4~ -4I °E7* 4.4 N+IE—II

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I :1 cr: ”‘~T··•I\T 9I 1 ·—- $*1 •-· N •— **41 T II .1

SNNTQC C ;‘1c¢1—-:=¤ CI5* • • • • • • • • • 1 1 • • • • •

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1 1 1—« N 1-1 N -7 f"$. I 1

, ' .f o c: ~:::>r·~<1· c'

^" • • • • • • • • « • • . 1

1 1,5 1.

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cx: ac c,-1 N ·- N 1- ~*I 1:1:1 1 QS;

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1 1 1- „-1 1 1;*::' 'cccu-mn :3 ·^<rr^··N C 1-^c~c~=^ C 2-1:--I

O ¤ • • 1 • • • • • 1 • • • •n1

Q c·^q•—1|r"^ N r‘*<r-·-~«? C\I1-3L-I - CY -1 N 1-- N_ :2*:*:I 1

I C·•l1_®$'%•—•® O ¥'^€D•···•·< C ~?$<'····· OI·•··*C: Lf§' • 1 • • 1 • • 1 •

~ 1QWNQCIOI L4 ·—

AI Ir^<.·•——1~w Q r^<r—•I<*W Q "^<r•-1«T C, Q1•-1 N •— N •- $*3 he;;-1 ' I '1.-:12-1:.1* ' ‘c¤:··1 1 1..1-:,*1 I ‘ 4:;1 1 E * ZZN,. <¤C>c~1-" :1* N¤oO1/N :3

1 •• • • • . • •

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I IQ•-14,1I I<DO<r~O O OOQQO:7:

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3 gb: -.:’ \-y1.ny\ QCII'. . „ - • •„ • „„ 1 -I 131-«1-auII1

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I -— N Mc-1 $*3 Q ¢^~v—— f"‘ 3*I 1..1E.:.1I I "" N "* NI SDLT.11 1 ·

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APPENDIX F, INFORPIED CONSENT

I 16+9

150 II

I· ILABORATORY FOR EXERCISE AND WORK PHYSIOLOGY :I

Division of Health, Physical Education and Recreation ICollege of Education

Virginia Polytechnic Institute and State UniversityBlacksburg, VA 24061

INFORMED CONSENT

I, , do hereby voluntarily agree andconsent to participate in a testing program conducted by thepersonnel of the Human Performance Laboratory of theDivision of Health, Physical Education and Recreation ofVirginia Polytechnic Institute and State University.

Title of Study: Effects of Endogenous B—endorphin andHydration State on ThermoregulatoryMechanisms During Prolonged Exercise in theHeat.

The purposes of this experiment include: 1) to establish acomprehensive model of thermoregulation in man duringprolonged work in the heat, integrating the time coursechanges in body fluids, hemodynamics and heat dissipation,2) to determine the possible role of the hormone b—endorphinon exercise thermoregulation, 3) to investigate the possibleeffects of B—endorphin on body fluid balance duringprolonged exercise in the heat.

I voluntarily agree to participate in this testing program.It is my understanding that my participation will include:

1. medical screening to determine by suitability forparticipation in this study,

2. a brief interview concerning by habitual activity,3. maximal oxygen uptake test performed on a bicycle

ergometer,

4. anthropometric measures including percent fat,(underwater weighing) height and weight, _

5. a maximum of four trials of prolonged cycling at aworkload equivalent to 50% of my maximal oxygen uptake.These exercise sessions will continue for a maximum of120 minutes. I understand that I am encouraged to

“ 151 1II

exercise to the end of each trial or to the point ofexhaustion.

a. the first trial will be an orientation trial inorder to acquaint me with the experimental protocol.lt will take place in a cool environment (25°C, 50%relative humidity) and last 60 minutes.

b. A trial (120 min duration) will also take place in acool environment (25°C, 50% relative humidity).Sweat losses will be replaced with water at 15minute intervals.

c. Another trial (120 min duration) will take place ina hot environment (36°c, 50% relative humidity).Sweat losses will be replaced with water at 15minute intervals.

d. The last type of trial (120 min duration) will takeplace in a hot environment (35° C, 50% relativehumidity). Sweat losses will not be replaced.

Note: The order of trials will be randomized.

6. During each of the aforementioned trials the followingmeasures will be taken at periodic intervals.a. cardiac output: This will involve the rebreathing

of a gas mixture containing a small amount of carbondioxide in oxygen for a period not to exceed 15seconds.

b. Blood pressure will be measured indirectly via theplacement of a cuff on the upper arm.

c. heart rate: Electrocardiographically determinedfrom a series of three electrodes placed upon thechest.

d. core temperature: Determined by a rectalthermocouple self inserted to a depth ofapproximately 10 cm.

Ie. perceived exertion: Subject reporting of the Iperception of effort based upon the Borg Relative

Perceived Exertion Scale. I6f. blood samples: obtained from a catheter placed in I

the forearm by a registered nurse.

i

I152 lg. skin temperature patterns: obtained from video

camera recordings of infra red radiation emittedfrom the body, and eight skin thermocouples taped onthe body at various anatomical locations.

I understand that participation in this experiment mayproduce certain discomforts and risks. I understandthat with any extended aerobic activity I will probablyexperience a general feeling of fatigue. In addition,due to the exercise mode (cycling, leg fatigue and legcramps may occur. Residual muscular soreness may bepresent following the trials and may persist for severaldays. During the exercise tests, especially theexhaustive bouts, I understand that there is a remotechance of dizziness and nausea. It is also understoodthat the region surrounding the catheter insertion sitemay develop a sub—dermal hematoma (slight swelling dueto fluid moving out of the vein into the surroundingarea).

Certain personal benefits may be expected from participationin this experiment. As a participant in the subjectselection process, I will be informed of the results ofthe medical screening. If cleared. to continue in thisendeavor, I will be informed of my body composition andphysical work capacity, i.e., fitness level.Additionally, at the completion of the study I will havegained knowledge relative to my capacity to performextended work in normal and heat stressful surroudnings.

I understand that any data of a personal nature will be heldconfidential and will be used for research purposesonly. I also understand that these data may only beused when not identifiable with me.

I understand that I may abstain from participation in anypart of the experiment or withdraw from the experimentshould I feel the activities might be injurious to myhealth. The experimenter may also terminate myparticipation should he feel the activities might beinjurious to myhealth.I

understand that it is my personal responsibility to advise Ithe researchers of any preexisting medical problem thatmay affect my participation or of any medical problemsthat might arise in the course of this experiment and Ithat no medical treatment or compensation is availableif injury is suffered as a result of this research. Atelephone is available which would be used to call the «

I _

•153 ;

community rescue squad for emergency service. A trainedteam of exercise technologists will administer eachtest.

I have read the above statements and have had theopportunity to ask questions. I understand that theresearchers will, at any time, answer my inquiriesconcerning the procedures used in this experiment.

Scientific inquiry is indispensable to the advancement ofknowledge. Your participation in this experimentprovides the investigator the opportunity to conductmeaningful scientific observations designed to improvethe safety of exercise and physical work in the heat.

If you would like to receive a copy of the results of thisinvestigation, please indicate this choice by marking inthe appropriate space provided below. A copy will thenbe distributed to you as soon as the results are madeavailable by the investigator. Thank you for makingthis important contribution.

I request a copy of the results of this study.

Date Time a.m./p.m.

Participant Signature

WitnessHPL Personnel

Project Director Dr. William Herbert Telephone 961-6565

HPER Human Subjects Chairman Dr. Don SeboltTelephone 961-5104

Dr. Charles Waring, Chairman, International Review Board forResearch Involving Human Subjects. Phone 961-5283.

I_ I

APPENDIX G

CORRELATION MATRICES

l5¢+

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155

Table 21. Correlation Matrices Between Core Temperature(Tc), Plasma Volume (PV), Osmolality (OSM),and Sodium Na+ in Different Environments andStates of Hydration

Normal/Euhydration

PV Na+ Tc

OSM 0.15 0.22 0.56*

PV 0.52* -0.24Na+ -0.05

Hot/Euhydration

PV Na+ Tc

OSM 0.29 0.37 0.58*

PV 0.56* 0.68*Na+ 0.53*

Hot/Hypohydration(HH)I

PV Na+ Tc {I

0sM 0.39 0.75* 0.37* EI

PV -.53* -0.55* ENa+

10.63* I

I

EI

Statistically significant correlation coefficient {^ (p < 0.01) {df = 34

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