hormonal response to carbohydrate supplementation at rest and after resistance exercise

7/29/2019 Hormonal Response to Carbohydrate Supplementation at Rest and After Resistance Exercise

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260

International Journal of Sport Nutrition and Exercise Metabolism, 2008, 18, 260-280

2008 Human Kinetics, Inc.

The authors are with the Dept. o Health, Leisure, and Exercise Science, Appalachian State University,

Boone, NC.

Hormonal Responseto Carbohydrate Supplementation

at Rest and After Resistance Exercise

Sean R. Schumm, N. Travis Triplett, Jeffrey M. McBride,and Charles L. Dumke

This investigation examined the anabolic-hormone response to carbohydrate

(CHO) supplementation at rest and ater resistance exercise. Nine recreationally

trained men randomly underwent 4 testing conditions: rest with placebo (RPL),

rest with CHO (RCHO), resistance exercise with placebo (EPL), and resistance

exercise with CHO (ECHO). The resistance-exercise protocol was our sets o

Smith machine squats with a 10-repetition-maximum load, with 90-s rests between

sets. Participants then consumed either a placebo or CHO (24% CHO, 1.5 g/kg)

drink. Blood was taken beore exercise (Pre), immediately ater testing (Post),

and then 15 (15P), 30 (30P), and 60 (60P) min ater drink ingestion. Blood wasanalyzed or cortisol, glucose, insulin, and total testosterone (TTST). Cortisol

did not change signicantly in any condition. Glucose concentrations increased

signicantly rom Pre to 15P and 30P during RCHO and Pre to 15P, 30P, and

60P in ECHO (p .05). Insulin concentrations increased signicantly rom Pre

to 15P, 30P, and 60P in the RCHO and ECHO conditions (p .05). There were

no signicant changes in TTST concentrations during RPL or RCHO. Both EPL

and ECHO demonstrated a signicant elevation in TTST concentrations rom Pre

to Post (p .05). During ECHO, TTST concentrations at 60P were signicantly

lower than Pre levels (p .05), but there were no signicant treatment dierences

in TTST concentrations at any time point during the EPL and ECHO conditions.Ingesting CHO ater resistance exercise resulted in decreased TTST concentrations

during recovery, although the mechanism is unclear.

Keywords: strength training, metabolism, nutrition

Resistance exercise has been associated with acute elevations in testosteroneconcentrations in both trained and untrained participants (Ahtiainen, Pakarinen,Alen, Kraemer, & Hakkinen, 2003; Ahtiainen, Pakarinen, Kraemer, & Hakkinen,2003; Chandler, Byrne, Patterson, & Ivy, 1994; Kraemer et al., 1999, 1990; Krae-

mer, Volek, Bush, Putukian, & Sebastianelli, 1998; Linnamo, Pakarinen, Komi,Kraemer, & Hakkinen, 2005; Raastad, Bjoro, & Hallen, 2000; Smilios, Pilianidis,Karamouzis, & Tokmakidis, 2003; Tremblay, Copeland, & Van Helder, 2004).


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Hormonal Response to Carbohydrate Supplementation 261

These acute elevations in testosterone typically persist or up to 30 min ater theexercise bout (Ahtiainen, Pakarinen, Alen, et al.; Ahtiainen, Pakarinen, Kraemer,& Hakkinen; Chandler et al.; Kraemer et al., 1999, 1990). It has been theorized

that repeated, acute elevations in testosterone associated with resistance exercisemight aect the overall adaptation to resistance exercise (Kraemer & Ratamess,2005). Dietary intake might also play an important role in the acute and chronicresponses to resistance exercise. Carbohydrate intake ater resistance exerciseappears to have positive eects on postexercise protein kinetics (Borsheim et al.,2004; Roy, Tarnopolsky, MacDougall, Fowles, & Yarasheski, 1997; Smilios et al.).In previous research, however, carbohydrate ingestion has been shown to be asso-ciated with decreases in testosterone concentrations (Chandler et al.; Kraemer etal., 1998). It is unclear whether it was the carbohydrate ingestion itsel that servedto trigger decreases in testosterone concentrations or whether it is an interactionbetween resistance exercise and carbohydrate ingestion (Chandler et al.; Kraemeret al., 1998).

One study indicated increased protein synthesis when participants ingested 1g/kg o carbohydrate ater resistance exercise (Roy et al., 1997). This was corrobo-rated in a later study by Roy, Fowles, Hill, and Tarnopolsky (2000), who ound thatcarbohydrate supplementation increased protein synthesis and decreased proteindegradation ater resistance exercise. Carbohydrate supplementation also increasesinsulin concentrations, which is thought to enhance amino acid transport into themuscle cell and thus contribute to increased protein synthesis or decreased protein

degradation (Ahtiainen, Pakarinen, Kraemer, & Hakkinen, 2003; Roy et al., 1997).These improvements in net protein balance with carbohydrate supplementationsuggest that carbohydrate supplementation might augment the recovery processater resistance exercise and thus help optimize adaptations to resistance training.The available evidence regarding carbohydrate supplementation and resistanceexercise suggests that there might be some benets to carbohydrate supplementa-tion in terms o protein synthesis.

As previously mentioned, carbohydrate ingestion might also infuence serumtestosterone concentrations (Ebeling, Stenman, Seppala, & Koivisto, 1995; Habito& Ball, 2001; Hjalmarsen, Aasebo, Aadvaag, & Jorde, 1996; Meikle, Stringham,

Woodward, & Memurray, 1990; Pasquali, Macor, & Vicennati, 1997). The rela-tionship between macronutrient ingestion and acute testosterone changes has beeninvestigated more extensively at rest than in exercise situations. There is evidencethat ingesting at might decrease serum testosterone concentrations, whereas ingest-ing protein and carbohydrate without at does not signicantly aect testosteroneconcentrations (Meikle et al.). Conversely, Habito and Ball ound that even low-at meals that contained protein and carbohydrate acutely decreased testosteroneconcentrations. There is also evidence that carbohydrate ingestion alone mightdecrease serum testosterone concentrations in older men (Hjalmarsen et al.). It isdicult to interpret the existing research because o diering macronutrient eeding

protocols and participant characteristics (Ebeling et al.; Habito & Ball; Hjalmarsenet al.; Meikle et al.; Pasquali et al.). Overall, the relationship between carbohydrateingestion and testosterone concentrations at rest is not completely understood.

There are ew data regarding the relationship between carbohydrate ingestionand testosterone concentrations ater resistance exercise. Kraemer et al. (1998)observed an acute elevation in testosterone concentrations with resistance exercise.


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262 Schumm et al.

They also demonstrated that testosterone concentrations dropped below baselinewith carbohydrate/protein supplementation taken 2 hr beore and immediatelyater exercise (Kraemer et al., 1998). This testosterone depression did not happen

with placebo ingestion ater resistance exercise (Kraemer et al., 1998). Chandleret al. (1994) ound similar patterns o testosterone changes with ingestion o car-bohydrate ater resistance exercise. They ound that testosterone concentrationsdropped below preexercise levels 30 min ater postexercise carbohydrate ingestion(Chandler et al.). This suggests that carbohydrate or mixed-macronutrient eedingmight indeed result in decreased testosterone concentrations when done imme-diately ater resistance exercise, although urther research is needed to validatethese ndings. Both Kraemer et al. (1998) and Chandler et al. noted that testos-terone concentrations were lowest when insulin concentrations were highest. Thissuggests an inverse relationship between insulin and testosterone concentrationswith eeding ater resistance exercise. Although insulin release can be triggeredwith ingestion o carbohydrate or protein or a combination o the two, amino acidavailability with protein ingestion might urther contribute other mechanisms oprotein synthesis (Borsheim et al., 2004; Chandler et al.; Roy et al., 2000, 1997).It has been theorized that an increase in protein synthesis or decrease in proteinbreakdown might result in an up-regulation o androgen receptor content, resultingin a decrease in circulating testosterone concentrations (Kraemer et al., 2006). Thisprovides a theoretical link between insulin concentrations ater exercise and circu-lating testosterone concentrations (Kraemer et al., 2006). To study the relationship

between insulin and testosterone, carbohydrate-only supplementation was necessaryto prevent any conounding or redundant eects o protein intake. It is not knownwhether carbohydrate ingestion has the same eect on testosterone in both restingand postexercise conditions because no research has been perormed with bothresting and exercise conditions in the same group o participants. Thus, the eectso carbohydrate ingestion on both insulin and testosterone concentrations need tobe better understood beore hormonal or cellular mechanisms can be targeted.

Based on the available research, we hypothesized that carbohydrate ingestionwould decrease testosterone concentrations both at rest and ater resistance exercise.The primary purpose o this investigation was to examine whether carbohydrate

ingestion resulted in changes in testosterone concentrations both at rest and aterresistance exercise. Another important purpose was to illuminate the relationshipbetween testosterone and insulin in resting and resistance-exercise conditions.

Methods

Study Design

Participants underwent one orientation session and one amiliarization sessionollowed by our testing sessions. The amiliarization session and all exercise ses-

sions were separated by 714 days. The participants were tested in random orderin each o the ollowing our test conditions: rest with placebo (RPL), rest withcarbohydrate supplementation (RCHO), exercise with placebo (EPL), and exercisewith carbohydrate supplementation (ECHO). Both the researchers and the partici-pants were blinded to the supplement condition. At each session ve blood drawswere taken: beore exercise (Pre), immediately ater exercise or an equivalent rest


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period (Post), and 15 (15P), 30 (30P), and 60 (60P) min ater supplement inges-tion (Figure 1). The participants ingested a carbohydrate supplement or placebobeverage immediately ater the second blood draw and then rested quietly or 60

min until the nal blood draw.

Participants

This study involved 9 recreationally weight-trained (minimum 1 year) men age1849 who served as participants (M SD; age 26.2 8.7 yr, height 174.5 6.8 cm,body mass 84.6 15.2 kg, 15.1% 5.35% body at, 167.5 35.4 kg 1-repetition-maximum squat, 1.98 0.3 one-repetition maximum [1RM]/body weight). Eighto the nine participants were between the ages o 18 and 26, with 1 at age 49. The1 older participant did not dier signicantly rom the group mean o the other8 in any hormonal or perormance variable and thus was included in the dataanalysis. All participants reported not having previously taken anabolic steroids,growth hormone, or related anabolic drugs. We used these criteria to eliminatevariable hormonal responses because o muscle-building-drug supplementation,training status, or gender. All participants were inormed o study procedures andsigned consent orms beore initiation o the study. The institutional review boardat Appalachian State University approved the study.

Orientation, Dietary Analysis, and Body Composition

At the orientation session participants were given instructions or the study, andmeasurements o height, body mass, and body composition were taken. Partici-pants were also tested or their 1RM in the Smith machine squat. Participants wereprovided instruction by a registered dietitian on the procedures or keeping ooddiaries or 3 days beore each exercise session. Participants were instructed tomaintain their normal dietary habits. There was no attempt made to manipulatediet because chronic dietary intake does not appear to aect the acute testosteroneor cortisol responses to resistance exercise (Volek, Kraemer, Bush, Incledon, &Boetes, 1997). Food records were kept to help explain any potential dierences in

baseline hormone levels. There were no dierences in total kilocalorie intake ormacronutrient distribution between conditions (results not reported). Participantswere instructed not to participate in strenuous exercise or 48 hr beore exercisetesting, not to eat or 12 hr beore exercise testing, and not to ingest caeine oralcohol or 24 hr beore exercise testing. Body composition was determined usingdual-energy X-ray absorptiometry (DEXA; Hologic QDR, Bedord, MA, USA),with the same technician perorming all the scans. A total-body scan was perormedor each participant. DEXA calibrations were perormed daily and beore eachscan with a calibration block rom the manuacturer. In a separate amiliarizationsession participants were tested or their 10-repetition maximum (10 RM) in the

Smith machine squat.

Strength Testing

Participants were rst tested or their 1RM in the Smith machine squat during theorientation session using the protocol described by McBride, Triplett-McBride,


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Figure

1

Timelineofeventsateachtestings

ession.Pre=preexerciseorprerestperiod;Post=postexerciseorpostrestperiod;15P=15

minafter

beverageingestion;30P=30minafterbeverageingestion;60P=60minafte

rbeverageingestion;RE=resistanceexercise;CHO=carbohydrate;

PL=placebo.


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Davie, and Newton (2002). They were given a number o warm-up trials using30% (810 repetitions), 50% (46 repetitions), 70% (24 repetitions), and 90%(1 repetition) o an estimated 1RM rom the participants recommendation. The

resistance was then increased to elicit a 1RM within three or our maximal eorts.Adequate rest was allowed between all trials (35 min). Squats were perormedto a 90 knee angle determined with a goniometer. A piece o tape visible to theparticipant was put on the Smith machine column such that the bottom edge o thebracket attached to the bar was even with the tape when proper depth was reached.All testing sessions were perormed using the squat depth previously describedand were supervised by a certied strength and conditioning specialist. During theseparate amiliarization session, 10RM was determined by starting with ~80% o1RM and increasing or decreasing resistance as needed to determine 10RM. Theparticipants also perormed our sets o Smith machine squats with 90 s o restbetween to establish the resistance adjustments that would be necessary to maintainsets o ~10 repetitions during the testing sessions.

Testing Sessions

Participants reported to the neuromuscular laboratory in the morning ater havingasted or the previous 12 hr. This helped ensure that no acute dietary variableswould aect hormone concentrations. All testing sessions or each participant wereconducted at the same time o day to minimize the infuence o diurnal variationon hormone concentrations. On reporting to the laboratory in the morning or eachexercise session, participants handed in their ood diary and were weighed. They satquietly or 10 min beore undergoing an initial 10-ml blood draw. All blood drawswere taken rom the antecubital orearm vein with participants in a seated position.Both right and let arms were sampled to maintain viability o blood draws. Aterthe initial blood draw, participants either began the resistance-training protocol orrested or 10 min, which is approximately how long it took to complete the protocol.In the exercise conditions, participants perormed our sets o the Smith machinesquats to volitional ailure. The rest period between all sets and exercises was 90 sand was closely monitored. This resistance-training protocol was selected because

it has previously been shown to acutely increase serum testosterone concentrationsimmediately ater exercise (Kraemer et al., 1998). The resistance or each set wasadjusted to maintain ~10 repetitions per set. The resistance and number o repeti-tions were recorded or each set at every exercise session to track the total workperormed in each o the resistance-exercise conditions.

Participants did not consume anything at any time during the exercise phaseor equivalent rest phase o any o the our testing sessions. Immediately ater theexercise protocol, or at the end o the equivalent rest period, a second blood samplewas taken. Immediately ater the second blood draw, the participants ingested acarbohydrate beverage or placebo beverage. The carbohydrate beverage was a 24%

carbohydrate solution made with Gatorade Thirst Quencher (Gatorade, Chicago,IL, USA) with added maltodextrin (Carbo Gain, Now Foods, Bloomingdale, IL,USA) that provided 1.5 g/kg o carbohydrate. A 24% carbohydrate solution at adose o 1.5 g/kg has previously been associated with a decrease in postexercisetestosterone levels (Chandler et al., 1994). The Gatorade Thirst Quencher wasmixed to the standard concentration o 6% carbohydrate, and then maltodextrin


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was added to increase the carbohydrate content to 24%. The placebo beverage(Gatorade, Chicago, IL, USA) was an equal volume o fuid favored with anarticial sweetener to match the taste o the carbohydrate beverage with identical

electrolyte composition. The participants then rested quietly or 60 min ater drinkingestion. During that period blood samples were taken 15, 30, and 60 min aterdrink ingestion (Figure 1). A 60-min rest period was chosen because changes inserum testosterone levels have been evident in previous research within or at 60min ater exercise or supplementation (Chandler et al.; Kraemer et al., 1998).

Blood Collection and Analysis

Blood was collected with a 20-gauge needle and a Vacutainer blood-collectionsystem. The blood was allowed to clot and then centriuged at 3,000 g or 15

min. The serum was then removed and stored in microcentriuge tubes rozen at80 C until subsequent analysis. The serum was analyzed or total testosterone,cortisol, and insulin in duplicate via commercial assay kits (DRG InternationalInc., Mountainside, NJ, USA). Total testosterone was analyzed using DRG kitEIA-1559 with an intra-assay variation o 2.9%. Insulin was analyzed using DRGkit EIA-2935 with an intra-assay variation o 3.8%. Cortisol was analyzed usingDRG kit EIA-1887 with an intra-assay variation o 2.1%. In the current investiga-tion, each participants samples were always analyzed within one kit to removethe interassay variability. Serum was also analyzed or glucose and lactate using aYSI 2300 STAT glucose and lactate analyzer (YSI Incorporated, Yellow Springs,OH, USA). Hormonal data were not corrected or plasma volume shits becausehormone concentrations represent exposure at the tissue level. Hydration statuswas not quantied, although it appeared to have a negligible eect on biochemicalvariables because there were not dierences in baseline hormone levels betweenany o the conditions.

Statistical Analysis

Hormone responses were analyzed using multivariate analysis o variance withrepeated measures. When signicance was ound, ollow-up paired t tests wereperormed with a Holms sequential Bonerroni procedure to adjust signicancelevels. Pearsons correlation coecients were determined or biochemical vari-ables. The signicance level or all statistical tests was set atp .05. All statisticalanalyses were perormed using a statistical sotware package (SPSS, Version 12.0,SPSS Inc., Chicago, IL, USA).

Results

Testing-Session Characteristics

The mean resistance, percent o 1RM, and mean repetitions perormed or eachset are outlined in Table 1. Although the mean resistance did decrease or eachset, it was not signicantly dierent rom the rst set until the ourth set (p < .01).This was to ensure that the desired number o repetitions was maintained. Some


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participants reported nausea and eeling ill, but all completed the protocol. Therewere no signicant dierences in any o the perormance variables between thetwo conditions.

Total Testosterone

There were no signicant dierences in baseline (Pre) total testosterone concen-trations between any o the our conditions. In the RPL and RCHO conditions,total testosterone concentrations did not change signicantly rom Pre levels ineither condition (see Figure 2a). There were also no signicant dierences in totaltestosterone between RPL and RCHO at any time point. In the EPL and ECHOconditions, total testosterone was signicantly elevated (p = .007 and p < .001,respectively) rom Pre to Post in both conditions (see Figure 2b). With EPL, totaltestosterone concentrations returned to baseline by 15P and remained there or theremainder o the postexercise period. With ECHO, total testosterone concentrationsdropped signicantly (p = .003) below baseline at 60P (see Figure 2b). Despite

these dierent patterns o change ater exercise, there were no signicant treatmentdierences in total testosterone concentrations at any time point during the EPLand ECHO conditions.

Insulin

There were no signicant dierences in baseline (Pre) insulin concentrations in oramong any o the our conditions. There was a signicant main eect (p = .001)o carbohydrate supplementation on insulin concentrations, with the carbohydrateconditions (RCHO and ECHO) having higher overall insulin concentrations than the

placebo conditions (RPL and EPL). Insulin concentrations increased signicantly (p< .01) above RCHO Pre concentrations at 15P (p = .004), 30P (p = .001), and 60P(p = .002; see Figure 3a). At the 15P, 30P, and 60P time points insulin concentra-tions were signicantly higher (p = .005,p = .001, andp = .002, respectively) inthe RCHO condition than in the RPL condition. With RPL, insulin concentrations

Table 1 Testing-Session Characteristics, M SD

Mass (kg) % one-repetition maximum Repetitions

ExerciseSet 1 130 28 78 5 10.1 1.5

Set 2 121 28 72 5 9.7 1.0

Set 3 109 28 65 5 9.7 1.0

Set 4 97 26 58 6* 8.7 3.6

Placebo

Set 1 127 23 76 6 10.0 1.3

Set 2 118 26 70 4 9.9 0.3

Set 3 109 28 65 6 10.1 1.1

Set 4 99 31 58 7* 10.0 0.0

*Signicantly less than Set 1.


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did not change signicantly. With EPL, insulin concentrations were signicantly

higher at 15P (p = .002) and 30P (p = .001) than preexercise baseline (see Figure3b). With ECHO, insulin concentrations also increased above baseline at 15P (p= .015), 30P (p = .001), and 60P (p = .001). Insulin concentrations in ECHO werealso signicantly higher (p = .001) at 60P than in EPL. Although insulin concentra-tions were elevated in both RCHO and ECHO, concentrations appeared to increasemore rapidly in RCHO.

Figure 2 Serum total testosterone (TT) (a) at rest and (b) with resistance exercise,M SE. RPL = rest with placebo; RCHO = rest with carbohydrate; EPL = exercise withplacebo; ECHO = exercise with carbohydrate. *Signicantly dierent rom correspondingPre value.


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Figure 3 Serum insulin (a) at rest and (b) with resistance exercise,M SE. RPL = rest withplacebo; RCHO = rest with carbohydrate; EPL = exercise with placebo; ECHO = exercise withcarbohydrate. *Signicantly greater than corresponding Pre value. #Signicantly greater thancorresponding RPL or EPL or value.

GlucoseThere were no signicant dierences in baseline (Pre) glucose among any o theour conditions. There were signicant main eects or exercise (p = .033), time(p = .027), CHO (p < .001), and CHO Time (p = .043) interactions with serumglucose concentrations. Serum glucose concentrations also increased signicantlywith carbohydrate intake both at rest and ater exercise. In the RCHO, glucose


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concentrations were signicantly increased (p .05) at 15P (p < .001) and 30P (p= .002) but had returned to baseline by 60P (see Figure 4a). Conversely, RPL didnot result in any change in glucose concentrations. At the postexercise time point,

there was a signicant (p = .001) increase in glucose in both the EPL and ECHOconditions (see Figure 4b). With EPL, glucose remained signicantly elevated (p =

Figure 4 Serum glucose (a) at rest and (b) with resistance exercise, M SE. RPL =rest with placebo; RCHO = rest with carbohydrate; EPL = exercise with placebo; ECHO =exercise with carbohydrate. *Signicantly greater than corresponding Pre value. #Signi-cantly greater than corresponding RPL or EPL value.


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.001) at 15P but had returned to baseline at 30P. With ECHO, glucose concentrationscontinued to rise until 30P and remained signicantly elevated (p = .002) at 60P.

Cortisol

There were no signicant dierences in baseline (Pre) cortisol concentrationsamong any o the our conditions. Cortisol concentrations showed a nonsignicantdownward trend over time in the RPL and RCHO conditions (see Figure 5a). In

Figure 5 Serum cortisol (a) at rest and (b) with resistance exercise, M SE. RPL =rest with placebo; RCHO = rest with carbohydrate; EPL = exercise with placebo; ECHO =exercise with carbohydrate. No signicant changes or dierences in cortisol levels.


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EP and ECHO conditions, cortisol tended to rise ater exercise similarly at the15P time point with both conditions, but these increases were not signicant (p =.63; see Figure 5b). Despite these dierences in the overall trends, there were no

signicant dierences in cortisol concentrations between any o the our conditionsat any time point resulting rom large variability in cortisol levels and the cortisolresponse to exercise.

Lactate

There were no signicant dierences in baseline (Pre) serum lactate concentrationsamong any o the our conditions. Carbohydrate supplementation caused a signi-cant increase in lactate concentrations at rest but not ater exercise. In the RCHOcondition, lactate concentrations were signicantly (p .01) above baseline at 30P

and 60P but remained at baseline concentrations in the RPL condition (see Figure6a). Carbohydrate ingestion did not appear to have the same eect ater exercise.In both EPL and ECHO, lactate concentrations peaked immediately ater exercise,ollowed by a decrease, although they remained signicantly above baseline at 60 P(see Figure 6b). This pattern was the same with both EPL and ECHO conditions.

Correlations

There also were no signicant correlations between any o the independent (exercise,rest, carbohydrate, placebo) and dependent (total testosterone, insulin, glucose,

cortisol) variables. Although peak insulin concentrations occurred at the sametime point as the lowest total testosterone reading in the ECHO condition, therewere no signicant correlations between insulin and total testosterone at any timepoints in any o the our conditions. Overall, total testosterone was not correlatedwith glucose, insulin, lactate, or cortisol.

Discussion

The primary nding o this investigation was that carbohydrate intake ater resis-

tance exercise resulted in decreased total testosterone concentrations (24% belowpreexercise baseline) 60 min into recovery (see Figure 2). Total testosterone willbe reerred to as testosterone throughout the discussion. Thus, there appeared tobe some interaction between acute resistance exercise and carbohydrate supple-mentation that resulted in a depression o testosterone that was not as pronouncedat rest in healthy young men. When comparing all time points, there was nosignicant correlation between insulin concentrations and testosterone concen-trations, as had been theorized in some previous investigations (Chandler et al.,1994; Kraemer et al., 1998). Similar to much o the previous research regarding thehormonal responses to resistance exercise, EPL resulted in a signicant elevation

o testosterone o 18% and 23% in ECHO immediately ater exercise (Ahtiainen,Pakarinen, Alen, et al., 2003; Ahtiainen, Pakarinen, Kraemer, & Hakkinen, 2003;Chandler et al.; Kraemer et al., 1999, 1990, 1998; Linnamo et al., 2005; Raastadet al., 2000; Smilios et al., 2003; Tremblay et al., 2004). Ater this acute elevationo testosterone, concentrations ell back to near baseline by 30 min post in both theECHO and EPL conditions, which was also consistent with previous research in


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Figure 6 Serum lactate levels (a) at rest and (b) with resistance exercise,M SE. RPL= rest with placebo; RCHO = rest with carbohydrate; EPL = exercise with placebo; ECHO= exercise with carbohydrate. *Signicantly greater than corresponding Pre value.

which testosterone concentrations typically returned to baseline within 3045 minater exercise (Ahtiainen, Pakarinen, Alen, et al.; Ahtiainen, Pakarinen, Kraemer,& Hakkinen; Chandler et al.; Kraemer et al., 1999, 1990, 1998; Linnamo et al.;Raastad et al.; Smilios et al.; Tremblay et al.).


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In the RPL condition, testosterone showed no signicant changes over thecourse o the session, which would be expected given that the relatively short dura-tion o the testing sessions would not allow or any signicant diurnal variations in

testosterone to take place. Carbohydrate supplementation did not appear to havean eect on testosterone at rest because there were also no signicant changes intestosterone concentrations in the RCHO condition. These results are dierentthan those o Hjalmarsen et al. (1996), who ound that testosterone concentrationsdecreased with an oral glucose load. The most likely reason or these dierences isthat the participant populations are very dierent. Hjalmarsen et al. used older men(mean age 62 years) with chronic obstructive pulmonary disease, and the currentinvestigation used younger, healthy men. Conversely, Meikle et al. (1990) ound nodierence in testosterone concentrations in young, healthy men ater placebo or alow-at protein/carbohydrate supplement (51 g protein, 146 g carbohydrate, 1 g at)but ound a signicant decrease in testosterone concentrations ater an isocaloricprotein/carbohydrate supplement with higher at content (17.9 g protein, 67.5 gcarbohydrate, 50.4 g at). The diculty in interpreting these results is that both theat and protein content diered between the two supplement conditions and thusdierences in testosterone response could be a result o added at or less protein.The results o the current research taken with the results rom Meikle et al. suggestthat at is the primary mediator o acute changes in testosterone concentrations atrest because both carbohydrate and protein/carbohydrate combinations have yieldedlittle acute impact on testosterone concentrations.

The testosterone results ater the acute eect o exercise are similar to thoseo Kraemer et al. (1998) and Chandler et al. (1994), who ound that supplementa-tion immediately ater resistance exercise resulted in testosterone concentrationsthat dropped below baseline 3060 min ater exercise. This eect appeared to bemediated by the ingestion o carbohydrate, protein, or a combination o the two.Kraemer et al. used a carbohydrate/protein supplement, and Chandler et al. testedprotein, carbohydrate, and carbohydrate/protein supplements and reported similarndings. The unique nding in the current investigation was that these same trendswere not seen in the same group o participants when they were given carbohydrateat rest. Again, this suggests some type o interaction between resistance exercise

and carbohydrate that resulted in decreased testosterone concentrations in theexercise recovery period.This leads to a question o why testosterone concentrations appear to be

aected by carbohydrate ingestion ater exercise but not at rest. Fluctuations intestosterone can be caused by changes in testosterone output, testosterone uptake,or shits in plasma volume. Increases in testosterone concentration immediatelyater resistance exercise might be largely related to shits in blood plasma volume(Ahmadizad & El-Sayed, 2005; Collins, Hill, Cureton, & DeMello, 1986; Kraemer,Kilgore, & Kraemer, 1993; Kraemer, Kilgore, Kraemer, & Castracane, 1992).One possibility is that the carbohydrate beverage was absorbed more quickly and

increased plasma volume to a greater extent than the placebo beverage, resultingin a lower testosterone concentration at 60P. This seems unlikely because higherconcentrations o carbohydrate do not acilitate gastric emptying or expansion oplasma volume, and the total volume and electrolyte content o the placebo andCHO beverages were identical (Murray, Bartoli, Eddy, & Horn, 1997). Despitethis, dierences in plasma volume between conditions cannot be ruled out. The


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current investigation does not provide a denitive answer as to what the mechanismsare or decreases in testosterone concentrations with carbohydrate ingestion aterresistance exercise. Based on previous investigations, it is dicult to tell whether

decreases in testosterone are caused by decreased output.One study showed that concentrations o luteinizing hormone (LH) did not

change with supplementation ater resistance exercise despite decreases in testos-terone, and another investigation ound a signicant decrease in LH with eedingater resistance exercise (Chandler et al., 1994; Kraemer et al., 2006). It is alsodicult to tell whether LH responded to testosterone concentrations or vice versa.Another possible scenario is that changes in testosterone with carbohydrate inges-tion ater resistance exercise were caused by increases in testosterone uptake. Onepotential explanation was an increase in testosterone uptake at the muscle level.One possibility was an interaction with glucose and/or insulin that caused an up-regulation in androgen-receptor expression or binding anity, which could serve todecrease circulating testosterone concentrations. A recent study ound that eedingater resistance exercise increased androgen-receptor content and decreased serumtestosterone concentrations compared with a water-only condition (Kraemer etal., 2006). With eeding those researchers ound that testosterone dropped belowbaseline starting at 20 min postexercise, whereas in the current investigation wedid not see a depression o testosterone concentrations until 60 min postexercise(Kraemer et al., 2006). It should be noted that they used a mixed-uel eedingcontaining carbohydrate, at, and protein, whereas the current investigation used a

carbohydrate-only eeding (Kraemer et al., 2006). This is one potential explanationor the dierences in testosterone decrease between the two studies. Nonetheless,this does lend support to the idea that an up-regulation o androgen receptorstakes place with eeding ater resistance exercise and that this might be related todecreases in circulating testosterone concentrations (Kraemer et al., 2006). Giventhis evidence and the act that carbohydrate ingestion has been shown to avorablyaect protein kinetics ater resistance exercise, it seems plausible that androgen-receptor expression could be avorably aected (Borsheim et al., 2004; Kraemer etal., 2006; Roy et al., 2000, 1997). It seems logical that insulin mediates the eects ocarbohydrate eeding, whereas other mechanisms might be at work with protein or

amino acid eeding (Borsheim et al.; Roy et al., 2000, 1997). What is not completelyclear is exactly how manipulating total kilocalories or macronutrient content couldaect these potential mechanisms. Despite what is known, the current investigationdid not directly measure plasma volume, testosterone production, or testosteroneuptake, so the mechanisms at work remain somewhat speculative.

In addition to testosterone, glucose and insulin responded to carbohydratesupplementation dierently ater resistance exercise than at rest (see Figures 3and 4). Plasma glucose concentrations were signicantly above baseline immedi-ately ater exercise in both the EPL and ECHO conditions. In the EPL condition,glucose stayed above baseline at 15P but then returned to baseline at 30P and 60P.

With carbohydrate eeding, glucose concentrations continued to rise until 30Pand remained elevated at 60P. Kraemer et al. (2006) ound elevations in glucosepersisting until 50 min ater mixed eeding, with glucose returning to baseline at60 min posteeding. Chandler et al. (1994) showed signicant elevations o glucoseat 30 min posteeding, but levels had returned to normal at 60 min. The pattern oglucose elevation in the ECHO condition also diered rom the RCHO condition,


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in which glucose levels returned to baseline by 60P (see Figure 3). It is dicultto explain this persistent elevation in glucose in the ECHO condition, especiallybecause recent evidence suggests that resistance exercise improves glucose toler-

ance (Venables, Shaw, Jeukendrup, & Wagenmakers, 2007). It is possible thatdierences in plasma volume between the exercise and resting conditions explainsome o the dierences because resistance exercise can cause plasma volume shits(Ahmadizad and El-Sayed, 2005; Kraemer et al., 1993, 1992). Based on the insulindata, it appeared that lower insulin levels in the ECHO condition at 15P and 30Pthan in the RCHO condition might have allowed glucose to remain in circulationlonger with ECHO (see Figures 3 and 4). Insulin also responded dierently tocarbohydrate ingestion at rest compared with exercise, with a more rapid insulinresponse to carbohydrate eeding at rest (see Figure 3). Previous investigationshave also ound elevations in insulin 60 min ater eeding ater resistance exercise,although they had more pronounced elevations in insulin earlier in the posteedingperiod (Bloomer, Sorzo, & Keller, 2000; Chandler et al.). It seems plausible thissomewhat blunted insulin response was caused by the resistance training itsel,because Bird, Hons, Tarpenning, and Marino (2006) saw insulin concentrationsincrease or 1530 min ater eeding during a 60-min resistance-exercise session.It is dicult to interpret what mechanisms are at work because the investigationsin this area have used dierent resistance-exercise protocols and dierent eedingprotocols in many cases (Bloomer et al.; Chandler et al.; Kraemer et al., 1998).

It is also interesting to note how insulin concentrations might be related to

testosterone concentrations. Peak insulin concentrations occurred at the same timeas the lowest testosterone reading (60P). Despite this, insulin and testosterone didnot appear to have this same inverse relationship throughout the ECHO conditionor any o the other conditions. The results in the resting conditions (RPL, RCHO)were in agreement with those o Ebeling et al. (1995), who ound hyperinsuline-mia did not result in any change in testosterone concentrations in young, seden-tary men. These results suggest that insulin might only be related to testosteroneconcentrations in exercise recovery situations. Because there was no correlationbetween insulin and testosterone in either the RPL or RCHO condition, it appearsthat insulin does not markedly infuence testosterone concentrations at rest in

young, healthy men. During resistance exercise, insulin does not appear to directlymediate testosterone concentrations, because they were signicantly elevatedimmediately ater exercise with very little change in insulin concentrations, giventhat both would be aected by any plasma volume shits (see Figures 2b and 3b).Ater exercise, though, insulin concentrations rose sharply rom 30P to 60P andtestosterone concentrations decreased during that same time period in the ECHOcondition (Figures 2b and 3b). Although insulin concentrations did not appear tobe related to testosterone concentrations overall, it is still possible that insulin isan indirect mediator o testosterone concentrations in specic circumstances, suchas ater resistance exercise.

There has been no research done on potential mechanisms o the interactionsbetween insulin and testosterone. The available data rom the current investigationand previous research seem to suggest an indirect link between insulin andtestosterone because insulin clearly does not aect testosterone concentrations inall situations (Bloomer et al., 2000; Chandler et al., 1994; Ebeling et al., 1995).Again, a theoretical link between the two is androgen-receptor expression (Kraemer


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et al., 2006). Regulation o testosterone appears to be mediated by a complexinteraction o exercise state and eeding state that is not well understood. It shouldalso be noted that these changes in blood testosterone concentrations and perhaps in

androgen-receptor levels with eeding may or may not result in any physiologicallysignicant enhancement o the overall adaptation to resistance exercise.

Another noteworthy nding was the lack o signicant dierential eects oncortisol concentrations with carbohydrate ingestion. The inormation regardingcortisol concentrations with supplementation and resistance exercise is also notentirely clear, although there is evidence that suggests that supplementation aterresistance exercise might not signicantly aect cortisol concentrations (Krae-mer et al., 1998; Williams, Ismail, Sharma, & Jones, 2002). It is noteworthy thatthere was a signicant exercise main eect, with cortisol concentrations beingsignicantly higher overall in the exercise conditions. This was not unexpectedbecause resistance exercise has been previously shown to acutely elevate cortisolconcentrations (Ahtiainen, Pakarinen, Kraemer, & Hakkinen, 2003; Kraemer et al.,1999; Raastad et al., 2000; Smilios et al., 2003; Tremblay et al., 2004). There wereno signicant dierences between time points in the ECHO and EPL conditionsbecause o a highly variable cortisol response to exercise. In addition, becausecortisol was not signicantly dierent between the EPL and ECHO conditions, itdid not appear to play a signicant role in mediating testosterone concentrationsater resistance exercise. Like cortisol, lactate did not appear to be related to tes-tosterone concentrations based on the patterns o change. As would be expected,

there was a main exercise eect, with higher overall lactate concentrations in theexercise conditions than the resting conditions. In the RCHO condition lactate con-centrations were signicantly above baseline at 30P and 60P, but lactate remainedat baseline in the RP condition. This might have been the result o a shit in uelutilization to glucose with carbohydrate ingestion, which in turn resulted in higherlactate concentrations (de Sousa, Simoes, Oshiiwa, Rogero, & Tirapegui, 2007). Inthe EPL and ECHO conditions, the lactate response to exercise and the decreasein lactate ater exercise ollowed very similar patterns, with no apparent eect ocarbohydrate ingestion.

The results o the current investigation overall demonstrated that carbohydrate

intake ater resistance exercise results in a decrease in testosterone concentrationsby 60 min into recovery. Based on their patterns o change, cortisol and lactatedid not appear to be related to this decreased testosterone concentration during therecovery period. Changes in serum glucose and insulin at rest did not result in anychanges in testosterone. The relationship between glucose and insulin and testos-terone ater resistance exercise is not as clear, however. Other potential mechanismsthat might infuence testosterone concentrations ater resistance exercise includetestosterone production by the testes or adrenal cortex, hepatic or muscle bloodfow and subsequent uptake o testosterone, or androgen-receptor binding, butthese mechanisms can only be speculated on because they are beyond the scope

o the current investigation.In conclusion, depression o blood testosterone concentrations with eeding

ater resistance exercise has been demonstrated in multiple investigations includ-ing the current one (Chandler et al., 1994; Kraemer et al., 2006, 1998). Althoughit has been theorized that this testosterone depression ater eeding with resistanceexercise is related to androgen-receptor expression, insulin levels, or both, the


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278 Schumm et al.

mechanisms at work are still uncertain (Ratamess et al., 2005; Kraemer et al.,2006). It is also uncertain precisely how each o three major macronutrients mightdierentially aect these mechanisms. It appears that glucose and insulin kinetics

might be aected by resistance exercise ollowed by carbohydrate ingestion. Futureresearch in this area should ocus on urther examining the mechanisms at work inthe hormonal changes ollowing eeding ater resistance exercise.

Acknowledgments

We would like to thank the participants who made this study possible. The authors would

like to thank the graduate students, aculty, and sta who worked very hard in all areas

o this study, including data collection, laboratory biochemistry, and data analysis. This

study was supported by the Vaughn Christian Grant rom the Department o Health,

Leisure, and Exercise Science at Appalachian State University and grants rom theCratis D. Williams Graduate School and the Oce o Student Research at Appalachian

State University.

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