ORIGINAL ARTICLE

Richard A. Ferguson áMargaret D. Brown

Arterial blood pressure and forearm vascular conductance responsesto sustained and rhythmic isometric exercise and arterial occlusionin trained rock climbers and untrained sedentary subjects

Accepted: 24 February 1997

Abstract Cardiovascular responses to sustained andrhythmic (5 s on, 2 s o� ) forearm isometric exercise tofatigue at 40% maximal voluntary contraction (MVC)and to a period of arterial occlusion were investigated inelite rock climbers (CLIMB) as a trained populationcompared to non-climbing sedentary subjects (SED).Blood pressure (BP), monitored continuously by Fina-pres, and forearm blood ¯ow, by venous occlusionplethysmography, were measured and used to calculatevascular conductance. During sustained exercise, timesto fatigue were not di�erent between CLIMB and SED.However, peak increases in systolic (S) BP were signi®-cantly lower in CLIMB [25 (13) mmHg; (3.3 (1.7) kPa]than in SED [48 (17) mmHg; (6.4 (2.3) kPa] �P < 0:05�,with a similar trend for increases in diastolic (D) BP.Immediately after sustained exercise, forearm conduc-tance was higher in CLIMB than SED �P < 0:05� for upto 2 min. During rhythmic exercise, times to fatiguewere two fold longer in CLIMB than SED [853 (76) vs420 (69) s, P < 0:05�. Increases in SBP were not di�erentbetween groups except during the last quarter of exercisewhen they fell in CLIMB. Conductance both during andafter rhythmic exercise was higher in CLIMB than inSED. Following a 10-min arterial occlusion, peak vas-cular conductance was signi®cantly greater in CLIMBthan SED [0.597 (0.084) vs 0.431 (0.035) ml á min)1 á100 ml)1 á mmHg)1; P < 0:05]. The attenuated BP re-sponse to sustained isometric exercise could be due inpart to enhanced forearm vasodilatory capacity, whichalso supports greater endurance during rhythmic exer-cise by permitting greater functional hyperaemia in be-

tween contraction phases. Such adaptations would allfacilitate the ability of rock climbers to perform theirtask of making repetitive sustained contractions.

Key words Blood pressure á Forearm blood ¯ow áIsometric exercise á Training á Arterial occlusion

Introduction

Physical training results in many well-documented car-diovascular adaptations that serve to make the systemmore e�cient and play a part in the increased ability toperform strenuous exercise.

During exercise, sympathetic vasoconstriction acts todivert blood from areas of non-working tissue toworking muscles and contributes to the rise in bloodpressure (BP) which may help to increase perfusion tothe working muscles (O'Leary and Sheri� 1995). It hasbeen previously demonstrated that sympathetic neuraladjustments to isometric exercise are not in¯uenced bythe level of aerobic conditioning (Seals 1991). However,it was reported by Somers et al. (1992) that a forearmendurance training protocol resulted in an attenuationof the muscle sympathetic nerve activity (MSNA) duringisometric exercise. A reduced output of MSNA follow-ing training may be expected to transcribe to a reducedBP response to isometric exercise, yet Somers et al.(1992) failed to observe a reduced pressor response aftertraining. They attributed this to insu�cient BP mea-surements which, since they were made by sphygmo-manometry and could only be obtained at minuteintervals, may have missed more transient changes. Amore recent report by White et al. (1995) described anattenuation of the pressor response during 2 min of in-voluntary isometric exercise of the calf following atraining intervention consisting one-legged heel raises.Therefore, it appears that certain types of training mayindeed reduce the magnitude of the pressor response toexercise.

Eur J Appl Physiol (1997) 76: 174±180 Ó Springer-Verlag 1997

R.A. Ferguson áM.D. BrownSchool of Sport and Exercise Sciences, University of Birmingham,Edgbaston, Birmingham B15 2TT, UK

R.A. Ferguson (&)Neuromuscular Biology Group,Department of Exercise and Sport Science,Manchester Metropolitan University, Hassall Road,Alsager ST7 2HL, UK

A reduced pressor response after training could bedue to an attenuated MSNA. This would reduce oppo-sition to metabolic vasodilatation facilitating functionalhyperaemia. It could also be due to a more e�ectiveactive vasodilatation of the muscle vascular bed. Studieshave indeed shown enhanced vasodilator capacity im-mediately following ischaemic exercise in the forearms oftennis players (Sinoway et al. 1986) and in the lower legof endurance-trained subjects (Snell et al. 1987) and agreater reactive hyperaemia in the forearms of manualcompared to sedentary workers (Smolander 1994).

Modern sport climbers epitomise highly trained ath-letes. Rock climbing involves intense sustained and in-termittent isometric forearm muscle contractions whichmay provide an e�ective training stimulus to induceadaptations to the muscle vascular bed and to themuscle sympathetic neural adjustments during exercise.Thus, the present investigation sought to examine thecardiovascular responses to speci®c stimuli using eliterock climbers as the trained population in comparison tonon-climbing sedentary subjects. Arterial BP and fore-arm blood ¯ow were measured in response to sustainedand rhythmic isometric handgrip exercise to fatigue andalso following arterial occlusion to produce reactivehyperaemia. Preliminary data have been presented inabstract form (Ferguson et al. 1996/1997).

Methods

Subjects

A total of 15 healthy male subjects took part in the study. Five eliterock climbers (CLIMB), mean (SEM) age 22 (0.8) years, were re-cruited from a local rock climbing centre. The climbers had anaverage of 7.4 (1.2) years of climbing experience and climbed anaverage grade ranging between F6b and F7c+ with the best climbsranging between F7a and F8a+. These levels of climbing arewithin the top 10% of graded di�culty in competitive sport rockclimbing. Ten matched sedentary subjects (SED), mean age 20 (1.5)years, were recruited from the general University population. Re-quirements for the sedentary subjects were they had not partici-pated regularly in any form of physical training for at least12 months prior to the study. All subjects completed a generalhealth screening questionnaire and gave written informed consent.The study had approval from the Ethics Committee of the Schoolof Sport and Exercise Sciences, University of Birmingham, and theSouth Birmingham Health Authority.

Physiological measurements

Arterial BP and heart rate

Arterial BP and heart rate (HR) were continuously monitoredusing the Finapres Blood Pressure Monitor (Ohmeda), with a ®n-ger cu� positioned around the middle ®nger of the contralateralhand which was maintained at heart level. This provided a non-invasive beat-to-beat estimate of the arterial waveform from whichsystolic, diastolic and mean arterial pressures were derived. Pres-sures and heart rates were evaluated at rest and at intervalscorresponding to 25, 50, 75% of exercise duration time and im-mediately at the end of exercise (100%: END). At each of thesetime points systolic blood pressure (SBP), diastolic blood pressure(DBP) and HR from ten consecutive waveforms were averaged.

Forearm blood ¯ow

All blood ¯ow measurements were carried out by venous occlusionplethysmography using mercury-in-silastic strain gauges (Whitney1953), with the strain gauge positioned around the widest portionof the forearm. In order to exclude blood ¯ow to the hand, 30 sprior to blood ¯ow measurements a distal occlusion cu� around thewrist was in¯ated to 200 mmHg (26.6 kPa). Blood ¯ow was mea-sured by rapidly in¯ating, using a semiautomatic in¯ation pump,the proximal occlusion cu� around the arm above the elbow tobetween 40 and 50 mmHg (5.3±6.7 kPa) for about 3 s. Multiplerecordings were made as required with one complete recording (i.e.in¯ation and de¯ation) taking approximately 5±8 s. Vascularconductance was then calculated as limb blood ¯ow divided bymean arterial pressure (DBP plus one-third pulse pressure).

Experimental protocol

Three experiments were carried out in a randomised order in alaboratory maintained at a temperature close to 20°C. Each subjectarrived in the morning and all experiments were carried out in asingle day. The morning session was devoted to habituation of thesubject to the procedures of measurement and experimentation.Su�cient periods (> 60 min) between each experiment were givento allow adequate recovery.

Sustained isometric handgrip exercise

All climbers and ®ve of the sedentary subjects participated in thisexperiment. The subjects rested supine with their left arm sup-ported in a speci®cally designed forearm ergometer. The forearmwas supported at both the wrist and elbow which allowed attach-ment of occlusion cu�s and mercury-in-silastic strain gauge asdescribed. Maximal voluntary contraction (MVC) was obtained byinstructing the subject to pull on the handgrip as hard as possible.MVC was determined as the maximum force the subjects generatedduring three attempts sustained for 2 s performed 2 min apart.From this the target force of 40% MVC was calculated and dis-played on a pen chart recorder for the subject to observe. After aminimum of 20 min rest baseline measurements of BP and blood¯ow were taken. Three to four resting blood ¯ow measurementswere taken and averaged. The subject then performed a sustainedisometric handgrip contraction at 40% of MVC which continueduntil volitional fatigue. This was de®ned at the point where thesubject expressed a desire to stop or was unable to maintain thedesired contraction force. Throughout the exercise the subject wasencouraged not to perform Valsalva or straining manoeuvres. Thedistal occlusion cu� around the wrist was in¯ated upon advice fromthe subject that termination/fatigue was imminent. When con-traction ceased, duration of holding time was recorded and blood¯ow was measured within 5 and 15 s and further measurementsevery 15 s for 2 min.

Rhythmic isometric handgrip exercise

Four climbers and four sedentary subjects participated in this ex-periment. The subject was instrumented, MVC determined andbaseline measurements taken as described above. The subject beganhandgrip exercise at 40% of MVC at a frequency of a 5 s con-traction followed by 2 s of relaxation. Timing was made audible bya metronome. Every minute during the exercise the subject wasinstructed to stop so that a single blood ¯ow measurement could betaken, this procedure lasting a maximum of 5±8 s, after which thesubject continued exercising. The distal occlusion cu� around thewrist was not in¯ated during these measurements. Exercise con-tinued until volitional fatigue, at which point the subject expresseda desire to stop or was unable to maintain the desired contractionforce. When contraction ceased, exercise time and blood ¯ow weremeasured as described above.

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Post-occlusion reactive hyperaemia

All 15 subjects participated in this experiment. The subjects restedin a supine position. The left forearm was supported in a pronatedposition by foam pads. The occlusion cu�s were attached to thewrist and upper arm and the mercury-in-silastic strain gauge po-sitioned and calibrated. After a minimum of 20 min rest baselinelevels of BP and blood ¯ow were taken. The proximal occlusioncu� around the upper arm was in¯ated to 200 mmHg (26.6 kPa)for 1 min followed by de¯ation and immediate measurement of asingle hyperaemic blood ¯ow. This served as a priming stimulus forvasodilatation (Patterson and Whelan 1955) as well as an indica-tion of the subject's post-occlusion blood ¯ow. This allowed timefor adjustment of baseline recordings prior to the 10-min occlusion.The arm cu� was then in¯ated to 200 mmHg (26.6 kPa) for10 min. After rapid de¯ation forearm blood ¯ow was measuredwithin 5 and 15 s and then every 15 s thereafter for 2 min.

Analysis

All data is presented as mean (SEM). Statistical analyses werecarried out by 2-way analysis of variance (ANOVA) for repeatedmeasures and independent t-tests where appropriate. A 5% level ofsigni®cance was set.

Results

Sustained isometric handgrip exercise

Forearm forces generated during MVCs were not sig-ni®cantly di�erent between climbers and sedentarysubjects, being 715 (34) N for CLIMB and 635 (55) Nfor SED. Holding times to fatigue were also similar forthe two groups, being 140 (11.1) s and 122 (14.2) s res-pectively (not signi®cant, NS).

Resting SBPs were 124 (3) mmHg [16.5 (0.4) kPa]and 136 (6) mmHg [18.1 (0.8) kPa] in CLIMB and SED(NS), respectively, with peak SBPs occurring at fatigue(END) reaching 149 (8) mmHg [19.8 (1.1) kPa] and184 (8) mmHg [24.5 (1.1) kPa] respectively �P < 0:05�.These represented increments above rest of25 (13) mmHg [3.3 (1.7) kPa] and 48 (17) mmHg [6.4(2.3) kPa], (P < 0:05, Fig. 1A). Resting DBPs were72 (6) mmHg [9.6 (0.8) kPa] and 72 (4) mmHg [9.6(0.5) kPa] for CLIMB and SED (NS), with peak DBPsalso occurring at fatigue reaching 101 (5) mmHg [13.4(0.7) kPa] and 108 (6) mmHg [14.4 (0.8) kPa] respec-tively (NS). Although there was an apparent trend forincrements in DBP to be lower throughout exercise inCLIMB than SED this did not reach accepted levels ofsigni®cance (Fig. 1B). Resting HR values were 59 (4)and 60 (3) beats á min)1 increasing to 113 (14) and 98 (5)beats á min)1 at the end of exercise in CLIMB and SEDrespectively, which, although slightly higher in CLIMB,did not reach signi®cance.

Resting forearm blood ¯ows were 5.3 (0.8) and 4.4(1.3) ml á min)1 á 100 ml)1 in CLIMB and SED (NS).Peak blood ¯ow values attained during the 2-min post-exercise period were 44.1 (3.1) and 28.0 (2.4) ml ámin)1 á 100 ml)1, respectively �P < 0:05�. At rest, meanvascular conductances were similar in the two groups

[0.06 (0.009) vs 0.048 (0.016) ml á min)1 á 100 ml)1 ámmHg)1]. Immediately post-exercise, conductance hadincreased four fold in SED but 7.5-fold in CLIMB(Fig. 2). Thus, with a lower mean arterial pressure at theend of exercise, conductance was much greater in CLIMB[0.439 (0.028) ml á min)1 á 100 ml)1 á mmHg)1] than SED[0.265 (0.028) ml ámin)1 á 100 ml)1 á mmHg)1] (P<0.05).Conductance remained signi®cantly higher in CLIMBthan SED throughout the entire 2-min post-exercise pe-riod during which measurements were made (Fig. 2).

Rhythmic isometric handgrip exercise

MVC forces obtained prior to rhythmic exercise were730 (7) N for CLIMB and 660 (65) N for SED. Thesewere again not di�erent between groups nor from thoseobtained prior to the sustained exercise protocol, sup-porting the repeatability of MVC determination betweenexperiments. However, exercise times to fatigue forrhythmic contractions were almost double in CLIMB[853 (75.6) s] compared to SED [420 (68.9) s] �P < 0:05�.

Fig. 1 Changes from resting values in systolic (A) and diastolic (B)blood pressure during sustained isometric handgrip exercise to fatigue.*P < 0:05; climbers vs sedentary

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As with sustained exercise, SBPs and DBPs were ta-ken at time points representing rest, 25, 50, 75 and 100%(END) of the exercise times. With the large di�erences inexercise times to fatigue between groups it must beemphasised that the percentage duration points repre-sent similar relative, rather than absolute, time points.Resting SBPs and DBPs were similar to those obtainedin the sustained exercise experiment. The peak SBPsattained during rhythmic exercise were 158 (10) mmHg[21.0 (1.3) kPa] and 174 (9) mmHg [23.1 (1.2) kPa] inCLIMB and SED respectively, and, although apparentlylower in CLIMB, were not signi®cantly di�erent. Whilepeak SBP was reached at 100% of duration to fatigue inthe SED group, it occurred at 75% in CLIMB. There-after, between 75 and 100% of duration time SBP de-clined, although this was not signi®cant �P � 0:08�.Peak DBPs occurred at fatigue in both groups and werenot signi®cantly di�erent. The mean increments in SBPand DBP also show these changes (Fig. 3A, B) anddemonstrate a trend for increases in DBP, but not SBP,to be lower in CLIMB than in SED throughout exercise.Resting HR were similar to those measured prior to thesustained exercise. Peak HR occurred at the end ofexercise, reaching 84 (1) beats á min)1 in CLIMB and107 (4) beats á min)1 in SED �P < 0:05�.

There were large variations in vascular conductancemeasured during rhythmic exercise, probably arisingfrom di�culties in keeping the forearm still during thebrief intervals required to make blood ¯ow measure-ments. However, as Fig. 4 shows, conductancethroughout tended to be higher in CLIMB than in SED.During the post-exercise period blood ¯ows were sig-ni®cantly greater in CLIMB, ranging between 38.7 (4.9)and 48.9 (9.3) ml á min)1 á 100 ml)1 compared to SED,24.3 (5.7) to 28.6 (3.4) ml á min)1 á 100 ml)1 �P < 0:05�.

Fig. 2 Forearm vascular conductance at rest and following sustainedisometric handgrip exercise to fatigue. *P < 0:05; climbers vssedentary

Fig. 3 Changes from resting values in systolic (A) and diastolic (B)blood pressure during rhythmic isometric handgrip exercise to fatigue

Fig. 4 Forearm vascular conductance at rest, during and followingrhythmic isometric handgrip exercise to fatigue

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Post-occlusion reactive hyperaemia

Blood ¯ows at rest were 3.8 (0.8) and 3.0 (0.4) ml ámin)1 á 100 ml)1 in CLIMB and SED respectively (NS).The highest level of blood ¯ow attained upon release ofthe 10-min arterial occlusion was 50.2 (6.7) ml á min)1 á100 ml)1 in CLIMB compared with 38.5 (3.6) ml ámin)1 á 100 ml)1 in SED, which did not quite reachsigni®cance. Mean arterial blood pressures (MAP),which at rest were 87 (3) and 88 (3) mmHg [11.6 (0.4)and 11.7 (0.4) kPa] in CLIMB and SED, respectively,did not change either during the 10-min occlusion orduring the 2-min post-occlusion period during which¯ow was measured. Because of this, it can be assumedthat the changes in ¯ow to the forearm are entirely dueto vasodilatation of the muscle vascular bed.

Calculated vascular conductance at rest and at timedintervals during the 2-min post-occlusion period is shownin Fig. 5. There were no di�erences in resting values butconductance was signi®cantly higher in CLIMB thanSED for 60 s following release of the occlusion cu�(P < 0.05). The time course of post-occlusion conduc-tance changes as shown in Fig. 5 disguises the fact thatpeak conductance was attained at di�erent time pointsafter occlusion release for di�erent individuals. For mostof theCLIMB group, peak conductancewas reached laterthan that for SED where it occurred almost immediatelyupon occlusion release. Taking peak conductances forindividuals revealed that mean peak conductance forCLIMB was signi®cantly higher [0.597 (0.084) ml A

Ämi-

n)1 á 100 ml)1 á mmHg)1] than for SED 0.431(0.034) ml á min)1 á 100 ml)1 á mmHg)1] (P < 0.05).

Discussion

This investigation sought to determine the e�ects oftraining status on the arterial BP and vascular conduc-

tance responses to forearm isometric exercise and arte-rial occlusion using elite rock climbers as the trainedpopulation compared to non-climbing sedentary controlsubjects.

There was no di�erence in MVC between the CLIMBand SED subjects which may be due to the small numberof subjects in each group. However, this is surprisingand is in contrast to results of Grant et al. (1996) whoreported signi®cantly greater MVCs in their climbingsubjects compared to non-climbing controls. Watts et al.(1993), however, suggested that elite climbers may notneed to develop high levels of grip strength since it wasindicated that the strength to body mass ratio was moreimportant than absolute grip strength. Unfortunatelybody mass was not measured, and thus it cannot bedetermined whether any di�erence in the strength tobody mass ratio exists between the two groups of sub-jects in the present investigation.

There was no signi®cant di�erence in holding time tofatigue during the sustained exercise between theCLIMB and SED subjects. This is also surprising as itmay be thought that climbers would be able to continueto maintain grip for a greater length of time than non-climbers. Previous investigations have demonstrated anegative relationship between MVC and relative en-durance such that stronger individuals have the lowestisometric endurance and those with lesser maximumstrength possess superior relative endurance (Carlson1969; Carlson and McCraw 1971). Therefore, as climb-ers seem to be no stronger than sedentary subjects, thereare no potential detrimental e�ects on the ability tomaintain sustained contractions, which would be theconsequence of a greater strength. In contrast to sus-tained exercise, however, times to fatigue during rhyth-mic isometric exercise were twofold longer in theCLIMB compared to the SED subjects.

There was a clear attenuation of the BP responseduring sustained isometric handgrip exercise to fatiguein the trained individuals. Exercise intensity and dura-tion are known to have a profound in¯uence on thepressor response. Therefore, since there are no di�er-ences in MVC or exercise time between groups, the ef-fects on BP observed cannot be attributed to thesefactors. There were no signi®cant di�erences betweenCLIMB and SED subjects in either SBP or DBP duringrhythmic isometric handgrip exercise. There was atrend, however, for SBP to drop during the latterquarter of the exercise. This could be consistent with thesustained exercise SBP response described above. To theauthor's knowledge, the only other study that has re-ported a pressor response attenuation in trained indi-viduals was that by White et al. (1995). They measuredthe BP responses to both voluntary and stimulatedcontractions of the triceps surae before and after a 5- to6-week training period. The training resulted in a sig-ni®cant attenuation of the SBP response during thevoluntary contractions and also during the 2-min post-exercise circulatory occlusion period in the trained limb.DBP was also reduced during both voluntary and

Fig. 5 Forearm vascular conductance following 10 min of arterialocclusion. *P < 0:05; climbers vs sedentary

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stimulated exercise as well as during the post-exerciseocclusion.

The present data, and results from White et al.(1995), could be consistent with reports describing re-duced e�erent activity in the form of attenuated MSNAduring contractions in trained limbs, as measured bymicroneurography techniques (Somers et al. 1992).Factors that contribute to the level of MSNA and thusthe pressor response include the level of metabolitebuild-up in the muscle that stimulates muscle chemore-ceptors. Therefore, it is conceivable that a reduced af-ferent input to the pressor response is brought about bya reduction in metabolic by-products causing less stim-ulation of chemosensitive a�erent nerve endings. Theperipheral e�ects of endurance training are well docu-mented (Holloszy and Coyle 1984). Metabolic adapta-tions include less lactate production and greater musclebu�er capacity. These latter adaptations would result ina lesser accumulation on H+ ions, one of the manymetabolites that stimulate the chemosensitive nerveendings. The present study's subject population wereelite rock climbers who are probably not highly aero-bically trained due to the relatively low maximal O2

uptake � _V O2max� reported for this group, i.e.�55 ml á min)1 á kg)1 (Billat et al. 1995). Although it isdi�cult to describe the trained status of climbers, thehigh intensity and ischaemic nature of rock climbingpresumably induce adaptations within the skeletalmuscle and vascular bed. Whether fewer metabolic by-products are produced as a result of the intenseischaemic contractions of the forearm when climbingcan only be speculated upon. It may be possible, how-ever, that even if metabolic adaptations do not occur theattenuated pressor response may be due to the a�erentnerve endings themselves being desensitised to the build-up of metabolites.

The present study was unable to distinguish betweencentral and peripheral components of the pressor re-sponse since no comparison between voluntary andelectrically evoked contractions was made. White et al.(1995), however, suggested that there is no central ad-aptation to training as BP responses to isometric exercisein untrained contralateral limbs were unchanged. In anycase, the pressor response attenuation reported is incontrast with a previous report that demonstrated un-changed BP responses to isometric exercise in trainedindividuals despite a training-induced reduction inMSNA. Somers et al. (1992) attributed the failure todetect any BP attenuation to their measurement tech-nique, i.e. semi-automated sphygmomanometer record-ings whereby only one recording per minute was made.

Two previous investigations have reported thattraining does not culminate in MSNA attenuation dur-ing isometric exercise. Seals (1991) reported the increasein total minute activity of MSNA to be 161% for trainedendurance athletes compared to 204% in the untrainedsubjects during isometric handgrip exercise, this di�er-ence being insigni®cant. Satio et al. (1993) compared

MSNA between the dominant and non-dominant fore-arms of racket sport players and reported no di�erencesin the MSNA between the forearms. Both these studiesrecruited mainly endurance-trained individuals whichmay suggest that endurance training, per se, does notin¯uence the MSNA response to isometric exercise,whereas other training paradigms may indeed reduce themagnitude of the MSNA response.

The blood ¯ow and conductance results during andfollowing both sustained and rhythmic exercise clearlydemonstrate an enhanced forearm vasodilator capacityin the trained climbers. This supports previous in-vestigations describing enhanced vasodilator capacitiesfollowing arterial occlusion and ischaemic exercise intrained individuals, i.e. Sinoway et al. (1986), Snell et al.(1987) and Smolander (1994), and also the results fromthe post-arterial occlusion in the present study. Thechanges in vascular conductance could be attributed tostructural adaptations of the local vascular bed, e.g.increases in the number or cross-sectional area of thecapillary bed or the arteriolar vessels having a greatercapacity to accommodate blood ¯ow, or functional ad-aptations such as alterations in the myogenic, metabolic,neural or endothelial control of the muscle vascular bed,or both. There is indeed evidence from animal studiesthat endothelial-dependent dilator function is enhancedby training (Delp et al. 1995). We have described anattenuated pressor response which may be the result of areduced MSNA activity. Reduced MSNA ultimatelyleads to less sympathetic vasoconstrictor activity thusallowing greater dilatation and blood ¯ow. Whatever themechanisms involved, a greater vasodilator capacitywould enable a more e�cient substrate supply and me-tabolite removal during any rest period in a climb, andcould contribute to the climbers' ability to maintainsustained and repetitive high-intensity contractions overlong periods of time. This has been clearly demonstratedduring the rhythmic exercise.

In conclusion it can be seen that elite rock climbersare suitably adapted for the nature of their sport. Theyare not signi®cantly stronger and thus their submaximalstatic holding time is not reduced during exercise butthey have a twofold improvement in endurance perfor-mance during rhythmic isometric exercise. They alsohave an attenuated BP response to static exercise whichmay be caused by either a desensitisation of the a�erentnerves or a reduced build-up of metabolites causing lessstimulation of chemosensitive a�erent nerve endings inthe muscle. They demonstrate superior peripheral vas-cular characteristics in that they have an enhanced va-sodilator capacity in the forearm, as demonstrated byboth post-occlusion and post-exercise hyperaemia con-ductance. This may in part be due to less active sym-pathetic vasoconstrictor activity. Furthermore, if there isa reduced metabolite build-up then the enhanced vaso-dilator capacity may be due to additional mechanismssuch as augmented release of endothelial-derived relax-ing factor.

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Acknowledgements The authors gratefully acknowledge the assis-tantship of Mr Tom Blakely and Miss Alison Fowler. The researchwas supported by the School of Sport and Exercise Sciences,Faculty of Science, The University of Birmingham.

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