CARDIOVASCULAR RESPONSES IN

RUNNERS, POWER ATHLETES, BODYBUILDERS,

AND HEALTHY SEDENTARY SUBJECTS

Thomas Leslie Babits National Library Bibliothèque nationale 1*1 of Canada du Canada Acquisitions and AcquisÎîions et Bibliographic Services services bibliographiques 395 Wellington Street 395. nie Wellington OttawaON KlAW OccawaON KlAW canada Canada

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RUNNERS, POWER ATHLETES, BODYBUILDERS,

AND HEALTHY SEDENTARY SUBJECTS

Thomas Leslie Babits

A Thesis Submitted in Conformity with the Rcquirements for the Degree of Master of Science Graduate Deparaent of Community Heatth University of Toronto

Copyright by Babits 1996 Across a wide range of health and fitness, a linear relationship exisu between Gmax and VO2peaL Gmax values have not been obtained for thox eiite aîhietes whose performance is dependant on teaching their highest possible V-max, or in bodybullders. V02max, Gmax, and MAP,at rest and fouowing caifergometry at submaximai and maximal workloads, in age and sex matched eiite middle distance mers (ER), body builders (BB), power athletes (PA) and healthy sedentary subjects (HS) was compared. Grest was simiificandy higher in BB than in ali other groups, whïie Gmax was higher io BB and ER than PA and HS. A strong linear relationship was found in BB (r = 0.94, p < 0.002) between Gmax and Grest, but not in any of the other groups. A strong linear relationship was found, across the non-resistance trained groups (ER, HS) (r = 0.84, p < 0.0001). This study shows that within the vascuiature of trained muscle, adaptive processes involved in body building are quaiitatively similar to to those found in ER, and different fiom those resulting fiom a traditional strength training model. -v of my Gr- This thesis couid not have bcm pricpared without the help of many colleagues, family, and friends, 1 would iike to aii the membof my thesis eumiaoton cornmittee; Dr. L. Goodman, Dr. B. Goode, and Dr. S. Thomas, who worked on my behalfon such &or& notice. 1 greatly respect the care talren in suggesting improvements, which have clearly strengthened the work. 1 was fortunate to be accepted by Dr. Jack Goodman following my project proposal and a disappointing initiai Cxpctience at graduate school, As my supervisar, he patiently handled my Occasionai over zcalou~~~ess,and helped to shape the thesis. Speciai thadcs are extcnded to Dr. Müa Plyley, who not only helped with the development of the ideas and writing of the thesis, but yeam aga, rekindled my fascination with the potcntial of the human body, and brought rcason to the wodd of science. Instrumentai in the completion of this thesis wu the encouragement and fhkof my fellow graduate students. 1 would espaally Wrc to th& Rich Evans, and Dr. Russ -le. Their support was truly invaluable. Russ in particth bas grealy influenced the ideas in the thesis. This thesis would not have been possible without the support of my family, especiaiiy rny parents, George and Kathy Babits. For nearly thirty yaus they have devoted themselves to ensuring 1reœive a baiancd and meaningful education, and that 1 stxive for excellence in the areas 1 chose. This work repmsents your efforts as much as it does mine. Thank you. Finaliy, 1 wouid like to thank my most patient and understanding de, Trisha. The thesis has been a part of our entire marrieci life together, and with ail the changes in iife that have occurred over the past theyears, her love and support was instrumental in its completion. Another dream attained.. .thanks!

to Maximal Ischemic CalfErgometry ...... 62 4.4.4 Rcsting Vascuiar Conductance and msomal Vasadar Conductance ...... -62 4-5 Vascular Conductance vs . Aerobic Power ...... -70

Chapter 5: Diussion

Major Findings ...... -73 Subject Characteristics ...... 74 Blood Pressure and Heart Rate Responses to CaifErgometq ... 75 M;uamal Aerobic Power ...... -77 Vascular Conductance ...... ,., ...... -78 5.5.1 Sources of Error ...... -78 5.5.2 Resting VdarConductance ...... -80 5.5-3 Response to Submu

Conclusions ...... -92

Recommendations for Future Research ...... ~...... 94

References ...... -95

Appendu 1 Approval by the Review Cornmittee on the Use of Human Subjeets ,...... O...... o..o...... 106 Appendix 2 Informed Consent ...... 107

Appendix 4 Heart Rate and Blood Pressure Data ...... 109 Appendb 5 Resting Blood Flow Meuutes , ...... Il0

Appendis 6 Submasimd Blood Flow Measures ...... UII...... lll

Appendis 7 Maximil Blood Flow Measures ,...... œ...... ,. 1 12 Appendb 8 Aathropometric Murores ...... 113 Appendis 9 The Sipificance of Bodybuilding ...... -114

vii LIST OF TABLES

page

Table 2.1 Hypathetîcai VOpax Improverncnt ...... -6

Table 2.2 Manmal Oxygen Consumption Values in Elite Runners ...... 10

Table 4.1.1 Subject Characteristics ...... 53

Table 4- 1.2 Training Pattern Summary ...... -54

Table 4.3.1 Maxhd Oxygcn Consumption test Rdts ...... -60

Table 4 Heart Rate and Blood Pressure Data ...... 109

Table 5 Resting Blood Fiow Mmes ...... Il0

Table 6 Sub- Blood Flow Measures

Table 7 Maximai Blood Flow Measwes LIST OF FIGURES

Figure 2.3.1

Figure 2.3.2 Total Peripherai Resistance at Vûpax

Figure 4.2.1 30 second Average Heart Rate Foiiowïng Calf Ergometry

Figure 4.2.2 30 Second Average Mean Arterial Pressure Foiiowing Calf Ergometry

Figure 4.4.1 Blood Flow at Rest

Figure 4.4.2 M&hd Blood Flow

Figure 4.4.3 VdarConductance at Rest

Figure 4.4.4 Maximai Vascuiar Conductance

Figure 4.4.5 Gmax vs. Grest in Elite Runners and Power Athletes

Figure 4.4.6 Gmax vs. Grest in Body Builders and Healthy Sedentary Subjccts

Figure 4.4.7 BFmax vs. BFrest in Body Bdders and Healthy Sedentay Subjects

Figure 4.4.8 Years of Training vs. Grnax in Body Builders

Figure 4-4.9 Years of Training vs. Gmax in Elite Runncrs

Figure 4.5.2 Gmax and Maximal Oxygen Collsumption

Figure 4.5.1 MaWnal blood Flow and Maxhai mgen Consumption

Figure 5.3.1 Gmax and Mruamal Oxygen Consumption

Figure 5.6.1 Maximal Aerobic Power vs. Gmax The purpose of this study was to chaacterize maximum oxygm uptake, skeletal muscle blood flow and blood pressure rcsponses at rest and foilowhg both submaxirnal and maximai caif ergometry in attiletes who have undergone one of two forms of mistance training @owa training or bodybuilding) and endurance training, mmpared to heaithy untrained individuais.

It has been clearly demonstrated that across a wide range of health and fimes, a strong hear relationship exists berneen the maximal vascular cooductanœ (G max) of the cal& and maximal oxygen uptake (V02max) (Reading, 1993, Snd, 1987). However, for high aber atbietes, in which athletic performance is dependent on the development of the greatest possible maximum oxygen uptake, maximai Iowa leg vascular conductance may reflect the structurai maximum for the system. Therefore, the nlationship betwem maximum oxygm uptake and lower leg muscle vascular conductance might weii dtviate from the ob~avedlinear relationship 2 established among sedenw or mildly active and 'mduranœ trainedt individuais (Reading et ai., 1993; Snell, 1987). It is weii known that many practitioners of taditid strcngth Paiaing models, such as long, triple, and high jumpers, develop inmases in muscle bu& and strength (Hakkinen et al., 1981; MacDougall et al., 1980; Young et al., 1983). Rumers too, typically mode1 th& &stance eaining regimens on such programs.

There is evidence tint the adaptive pnnz~~esinvolved in bodybuilding wt only lad to increases in muscle bulk and strength, but may also promote signifïcant increases in aerobic fwiction through adaptive changes within the musde tissue (Shantz, 1982; Tesch and Larsson, 1982; Tesch et aï, 1989, Bcii and Jacob, 1990). Additiondly, the volume of high force muscular contractions pcrhrmed during bodybuilding ellicits high blood flows (Wallœ and Wesch, 1987), which may result in a high G max. There is a paucity of data describing pcripheral blood flow and training, especially conœming the ieiationship of muscle bldflow to maximum oxygen uptake in specifc training groups. nierefore, this study wiii provide: 1) a more complete understanding of the the contribution og maximal vascular conductance to maximum oxygen uptaloe; 2) an examination of the effits of the different models of training on the cardiovasculat responses to exercise; 3) evidence suggesting the optimal methai of rrsistance trainhg for endurance athletes. 1.3 SpCeaii Objectives

The objectives of the prcsent study were: (1) to compare healthy,cmtniaed individuals with sex matched, elite ninaws, body builders and power aîhletes with regard to maximum oxygen uptakc (VOpax), siccletai muscle blood flow, and vascuiar conductance at nst, imm~lyfoilowing sub-maximai exercise, and immediately foliowing cxacis to cxhaustion, and (2) to examine the relationship between maximal aerobic power and Mscular conductance in these groups.

1.4 Hypotbeses

1) Body buiiders WUdemonstrate higha maximai vascular conductance and lower blood pressure than power athletes, elite nmners, and healthy Eedeatary subjects in response to maximal caif ergometry.

2) Qite rumen wiU demonstrate a higher maumal oxygen amsumption, and body builders will demonstrate a lower maximal oxygen consumption than would be predicted by maximaI vascular conductance in acoordana to the relationhip established by healthy sedentary and endurance trained individuals. One of the clafsic debates in the field of ex- physiology bu beai the question of which wmponent(s) of the oxygen transport system limit(s) maximal oxygen uptake (VO;! max). The vafiables involved in the oxygen tcansport and utiihtion system an be grossly repyat+d into central and paipherai components: the central components are gaieraiïy considemi to k those componats associami with the heart, lungs, and large vessels, white the paiphaal components are those which are involved with control of blaxi flow, ciiffision, and metabollism in the active muscle tissue. The major focus of research in this area has been on oxygen uptake during an acute bout of maximai exercise (Sdtin and Strange, 1992). The cardiovasculv correlate of Ohm's Law states that the flow (cardiac output) is quai to the pressure (mean utgial) divided by the rrsistance (total peripheral). Since the circulatory system is a closed loop system, the SOlCaUed central and peripheral oomponaits are intricately linked, Le. they are interdepeadmt. It is due to this simple faa that an answer to the question of which factor(s) limit(s) V@ max is so elusive. The more important question for the general population, and the cruciaï question for the cornpetitive distana runner concems what limits the degree of improvement in V02 max? While the answcr to this question may not be as simple as the centrai vs. pcripheral argument, it does represent a way of systematically investigating the adaptive changes with imhhg. IP an hprovement in V@ max Limiteci by the capacity of the heart to grnerate the cardïac output rcquireû to provide sufficknt blood flow to the exercising tissues? Or conversely, das a limitation in the priphaal vascuiature to accept freely the blood flow hto the exeicising tissues result in a ceiling for V02 max improvemmt? A scrics of most interesthg obsemtions, and a potential answer to this question, aui be found in the littie understood cardïovascular i&ptaîicms that occur with body building training,

2.1.2 Limits to hmeases in Mnximnl Aerobic Power

Healthy individuais of any age can expect an incnase of 5 to 15% in VOpax with training (Daniels et al., 1978b). Smith and O'Danneil (1984) demonstrated an increase in VOpax of 14% following 36 weeks of ninning training. Interestingly, most of the imprwement occurred within the first 12 weeks, and aIl of the change had occurred by 24 weeks. Most exercise physiology textbooks describe a maximum of 5 to 20% improvemeat in Vopax foUowhg endurance training irrespective of training frequency or the length of the training periud. (Brooks and Fahey, 1985; Guyton, 1991; Nmkes, 1991). However, since the typical VOpax value for a young untrained male is 40 to 45 ml (kg min)-l (Macnab et al., 1969; Staron et al., 1983; Simoneau et al., 1985), a 5 to 15% improvemmt would not be adequate to achieve the high Wues measured in ebathletes (table 2.2). Since most training stuclies are conducted over weeks or months, whercas dite athletes will have ofmi been engaged in training for rnany years or evai decades, this analysis may be somewhat simplistic. In addition, it is vay dificult for training studies to duplicate the extreme tmhkg intensity to which a high performance athlett would be comrnittcd. Indeed, thae is some evidence to suggest that with high-intensity and a long-tam training cornmitment (>2 years), improvements of up to 50% cm k achieved (Saitin et al., 19'77). Although changes in V%max among established dite runncrs are usually Iess on a prantage-basis than in previously seüentary subjects, Muiia and Cm (1991) anedotally repmted obseming an iiicuise in VOpax hm4695 to 5525 ml (min)-1 (+18%), in an elite middle distance merover a SCiVen month paid. Table 2.1 considm a hypotheticai training effea based on various degrees of improvement in V02max in a healthy de, weighing 83.3 kg, with an initial VO~maxof 45 ml (kg min)-1, and a body fat pemtage of 19% (figures basal on mean data from Staron et al., 1983):

Table 22

Vemax Improvement vûynax (ml (kg min)-1) v0ymi.x (ml (kg min)-l)* 10% 49.5 54.5 20% 54.0 59.4 40% 63.0 69.3 * with a body fbt correction of -10%

Clearly, an improvement of 20% in V02max would not be suffiCient for the average male to develop an aerobic power comparable to that found in eiite athletes; however, an improvement in the orda of 40% is more iihly ncccssary.

It would seem that there is a lirnit to the extent that V%max can k impved with training, and that the values seen in eiite athietes may be partly because of genetics, and partiy due to intensive trainhg ova a pcriod of y-. A gaietic endowment for a high V-mvr may manifest itself as a reJpoar to training. In other words, some pople rnay respond to training to a gmta degree than moat others. In conclusion, although the evidence is mixed, there is a distinct possibility that with appropriate training over an extcnded priai, some people may be able to in- in- thev VOpax from that indicative of a normal, heaithy, sedentaq individual (45-50 ml (kg min)-l) to the 70 ml (kg mi& range reprrsentative of elite mers,

2.1.3 Mdmal Aerobic Power and Testhg ModPility

Maximal aerobic power values are usdy higher when larger muscle masses are used, (McArdle and Magel, 1970; Pechar et al., 1974; Pannier et al., 1980; Shephard et al., 1988). Subsequently, V-max vaiues reportai using cycle ergometry tend to k 7-1196 lowa than those reported using a treadmill (McArdle and Magel, 1970; Pechar et ai., 1974; Shephard 1977; Pannier et al., 1980; Shephard et al., 1988) Typidy, in studies such as these, the subjects tended to be from a non - higNy trained population. Withers et ai. (1981) have shown that elite mers score higher @

2.1.4 Muamril Aerobic Power and RmhgPuiormance

The cmdation betwecn Vûpax and Nnning p&onaarice ranges hm0.08 to 0.9 1 (McConneli, 1988). While the relationship may be stronger across a broad range of aerobic fitness, within a group of elitc mers, the range of VOpax values is quite smaii, and therefm, VOpax is not a good predictor of performance. Within the grwp of 26 elite mers listed in table 2.2, there is no correlation between pafonnance and VOpax (Nœkes, 1991). in a study by Costill et al. (1976b), some of the greatest rumers at the time wminvestigated to fïnd out what physiologicai mechanism(s) was responsible for their outstanding endurance performances. They concluded that there was no wmlation Ween VQmax and performance; however, depite these fhdings, there is strong evidence that V0,max is very important to running performance, and in kt, the relationship may not be a causal one, but spcific to the performance duration. This evidence is outlined in the remainder of this section. Per€ormance pdktîon Running economy (RE), or what is oft~ded efficiency, is the amount of oxygen raquued for an individuai to maintain a specific submaumal running velocity (Daniels, 1974). It has been suggested that RE is a very good predictor of running performance. It has ken show in severai stuclies that the more accomplished the mer, the better the running economy (Noakes, 1988). Ahhough great rniddle and long distance running performance may require an individual ta have a VO~maxof 70 ml kgel nidor higher, among those with V@mu values of such magnitude, performance is best predicted by Nnniag economy.

rable 2.2 Maximum Oxygen Coasum@n (VOpax)VPhia in Eüte Endurance AthleSes (from Nohs 1991)

VOpax vaiue Major Performance (ml min-1 kg-1) Dave Bedford 85.0 10 km WR 1973 Steve Prefon taine 84.4 1 mile 354.6 Gary Tuttle 82.7 2: 17 marath011 Kip Keino 82.0 2 hn WR 1965 Don Lash 81.5 2 mile WR 1937 Craig Vugin 81.1 2: 10:26 marathon Jim Ryun 81.0 - 1 mile WR 1967 Steve Scott 80.1 1 mile 3:37.69 Bill Rodgers 78.5 2:09:27 marathon Matthews Temane 78.0 21.1 km WR 1987 Don Katdong 77.4 2:11:15 marathon Tom OIReilly 77.0 927 km ina6day rra John Landy 76.6 1 mile WR 1954 Alberto Sm 76.0 Marathon WR 1981 Johnny Halberstadt 74.4 2: 11 :44 marathon Amby BUTfÔot 74.3 2: 14: 28 marathon Cavin Woodard 74.2 48-160 km WR 1975 K~MYhh0~ 74.2 2: 11 : 36 marathon Bruce Fordyce 73.3 80 km WR 1983 Grete Waitz 73.0 marathon WR 1980 Buddy Edelen 73.0 marathon WR 1963 Peter Snell 72.3 1 mile WR 1964 Zithuiele Sinqe 72.0 2:O8: 05 marathon Frank Shorter 71.3 2: 10:30 marathon Willie Mtdo 70.3 2:08: 15 marathon Derek Clam 69.7 marathon WR 1969 The onset of plasma lactate accumulation (OPLA) has ben shown to be highiy wrrelated to maximum running velocity ova long distances moahts , 1991). OPLA is related to the highcst stady state perœntage of V*max thu can be tolerated. When this criticai intensity is surpasvd blood lactate begins to accumulate in an exponential matter (Fatrcii et ai., 1979). Coyle et ai. (1988) elucidated the fkctors responsible for a high iactate threshold (LT). The two factors most stnmgiy related to the LT werc years of eXpene~3t(r = 0.75; p < 0.01) and percent type 1 muscle fiben (r = 0.55; p < 0.05). Running economy can k combined wiîh LT as a powaful prediaor of endurance running performance through the measurement of nrnning velocity (v) corztsponding to OPLA (Farrell et al., 1979) or the onset of blood lactate (OBLA) (Sjodin and Jacobs, 198 1). Sjodin et ai. (1982) showed that the metabolic changes bmught about by the introduction of a twenty minute treaddl run at a blood lactate of 4 mm01 1-1 into the training program of weii trained male distance mers resuited in an incnase in VOBLA. Although there was no statistid increase in V02max foiiowing the VOBLA training, all but two of the subjects exhibited an hcrease (2.35 ml kg1 min-1). It is interesthg to note that the two mers who did not demonstrate an increase in VOpax were the oniy two 800 m numers in the group; the 0th- speciplind in longer distances (Sjm et al., 1982). Subsequentiy, 0th- investigators have ah dissociated improvements in LT or VOBU and VOpax (Denis et ai., 1982; Yoshida et al., 1982; Smith et al., 1984; Gaesser et ai., 1984; Hurley et ai., 1984; Gaesser et ai., 1986; Gacsser and Poole 1988). The Role of Musck Power Scrimgeour et al. (1986) found that the maximai horizontai running speed durhg a level running treadmill VOpax test was the best predictor of ninnuig performance (r = O.72), even for ultramarathon running. Whiie high lactate thresholds are strongiy assoaated with a high perccntage of slow twifch fibres

(Coyle et al., 1988). high VOpax roies migre high pomt ou- (Jones. and McCartney , l986), poyibly making the two incompatible (La Fontaine a al., 198 1; Noakes, 1991). If this were the casc, then athletes cornpethg in short ddm, high power output evmu, where there is little concem with steady state raobic metabolism, and therefore LT, may actually achiwe higher V02max scores. In fâct, Costiii r ai. (1976a) nported thu mi& distance ninnas have a lowa percentage slow twiteh fibres than distance mers, and that 800 m performance is inversely reW to the percent slow twitch area (this may explain Sjodin's (1982) finding of no increase in VOBU in 800 m runners afkVOBU training). More directly, it has been show that elite rniddle distana mers (1.500 to 10,000 meters) had V0pa.x scores 5 ml kg-1 min-1 greater than elite marathoners (Pollock, 1977); the marathoners however were 2 ml kg01 min-1 more efficient at 19.3 km/hr. It has been reported that integated electromyographic activity (LEMG) during hcremental exetcise is highiy comlated (r = 0.92, p<0.001) to the blood anaerobic threshold (Nagata et al. 1981). It may well be possible that elite middle distance running requires the development of the type IIa fibers. It is quite logical that the type Ila fibers have the potcntial to perfimn at higher force outputs for sufficient duration to be amducive to successfui middle distance running pefiomance, and yielding higha VOpax values. Specificaiiy, type IIa fibres are capable of being both highly oxidative and highly giycolytic (Essen et al., 1975; Hoiloszy et al., 1982; Faulkner et al., 1986), and therefore, would have the capability of producing much higher powa out- than type 1 fibers for a much longer time than type IIb fibers (Faulkner et al., 1986). Jones and McCarmey (1986) have demonmatcd a strong linear rektionship between VO@ and total work done in a 30 second maximal power test. In addition, Martin and Cœ(1991) have suggested that by using four npeated V02max tests, one can genarte a "mean sustainable VO/maxa, and that the duraiion of the piaieau is an important indicptor of anaerobic work tolaance. Therefm, it seems quite convincing that withb a group of elite mers, VOpu may in part reflect an interplay of musck powa and oxidative factors. B has been shown that iipolysis is inhi'bited by elevatad bloai lactate lenls md et al., 1974). CmverSly, PFK may be inhibited by endunna aauYng. When ATP, CP, and citrate levels are hi@, PFK is inhibited and FFA is utilized as an energy source, (GoMck and Hermansea 1973). Therefore, it seems possible thaî training the type 1 fiber apability only would be advantagwus for the marathoner due to the glycogen Jpving cffect of increased lipolys*. However, this could limit glycolytic activity, and therefore limit VOpax and middle distance @ormance. In kt, it may weii be that V@max is related to a speafic power output. In other words, if the race distance is tao short, then the htors limiting performance may have more to do with anaerobic power and capacity. On the other hand, if the race is too long, the race performance may be more dependant on Nnning economy and LT. Interestingly, in a study of &te middle distance runners (Lacour et al. 1989), only the 3,000 metcr specialists showed a correlation ôetween V@rnax and race performance. Meanwhile Yoshida et ai. (1990), hm th& assessrnent of the relative contributions of V-max, VOBLA, vLT,RE, and ansietnhic peak and mean power in coiiegiate fernale distance mers (800 m, 1,500 m, 3,000 m), revealed that only anaerobic peak and mean power w~gatt anaerobic test) were signif~cantly related to 800 m running mormance. V02mnx, on the otha hand, was a good predictor of 3,000 m perfbmance (r = 0.67, p < 0.01). but not oi%nifcantly relateci to 800 m and 1,500 m pcrf~œ. Svendenhag and Sjodin (1984) measurcd the Vqma of track athlctes hmthe Swedish national tam. They found thaî those athletes who participate in the 5,Oû m and/or 10,000 m events had the highest values of acrobic power followed by the 1,500 m and 5,000 m r~lllers,and then the marathoners. The marathoners were, however, higher than the 800 m andfor 1,500 m nmncts. Three conclusions can be made kmthe forcgoing: 1. VOpax is an important measure relatai to running performance in that it provides an upper lirnit for aembic metabolism hm which fractonal masuns corresponding to racing durations can k effectively utilued. In this way, it is a vaiuable tool for assessing ninning potential. 2. Additionally, it seems possible ihat the contractile pmperties of the muscla may be responsibk for settïng the limit of oxygai utiiization. For short middle distance Nnning performances (1,200 m and shorter), the maximal contribution of anaerobic pwer and capacity hmthe type II muscle nbas is criticai, whereas for distance running pe&mance, the contribution of the type 1 fibers dominate. This may explain why elite rniddle distance running performance (-y 3,000 m to 10,000 m) is more more directLy iinked to Vemax. 3. For the individuai elite runner, the relative (conected for body weight) V%max score is most important as it represcnts an excelient measure of fitness. Any change in relative V~maxover the in an individuai is ükely to be reflected in a change in running @ormance potaitial. It would obviously k to a mer's benefit to attempt to incna~eVO~max over time, thereby upwardly adjurting any performance prediction equations, and more importantiy, the ptrformanccs themse1ves. Therefore eiite middle disîance mers are most Wly to rrpreseat a physiological model of optimued VOpax.

Resistance training is weli hown to lad to increpscs in strength and musde power (Schmidtbleicher, 1992). Many endurance athletes, including elite mers, have utilized modest resistance trajning programs, both at times of injury and as a reguiar part of their training program, in the klief .that strength gains would help prevent injury andlor improve performance. Since ninners are very concemed about keeping their body mass as low as possible (rationale as demmsîrated in table 2.1, and explained in 2.1.4), one of the most significant rcasons not to engage in an mbitious resistana training programs has been the fear of muscle hypertrophy and the resulting weight gain which would ensue.

Concumnt strength and endurance training in previously untrained individuals erns to irnpede strength dewelopment, but not VOpax or short term endurance (Hickson, 1980; Dudley and Djamil, 1985; Hunter et al., 1987). In contrast, when endurance trained individals added strength training programs ta their overall training regimens, no impedanœ to strength development was obferved (Hunter et ai., 1987), and endurance performance wu impnmd (Hickson a al., 1988). Sale et al. (lm),uoed a single leg model in previously untrained males and fernales, to examine strength and endurance training interactions. Strerigth training, in addition to endurance txainïng, rrsulted in the same improvement in 1RM as strength training done, and rcsulted in a greater irnpmvemait in muscular endurance than endurance training alone or strength training alone. A slightly greater thigh girth was alro found among the strength + endurance naining pup. It is of interest to point out that the reshtance training protaml was emilv to a bodybuilding type (6 sets of 15-20 repetitions maximum with 2 minute xests betwœn sets). Nelson et al. (1990) found that concurrent strength and endurance training resulted in a similar degree of hypanophy as seem with strength training alone.

Additionaüy, the strerigth gains from concumnt training was fwnd to be rimilar to those who only strength traùied (Beii et al., 1990). Thus, both studies indicate that concurrent endurance minhg does not irnpede gains in strength. Wediffering resistimce training protocols make it ciifficuit to draw conclusions, the evidence suggests that (i) the addition of sa~ngthtrauiing to the program of an endurance athlete would increase strength, mwukendurance, and muscle girth, and (ü) that the effect on V02rmx =mains unclear, although probably neutral. Although muscie comprises approxhately 40% of body mas, it dves approximately 20-21 96 (1,260 ml) of cardiac output at rest (Vander et al., 198!5; McArdle a al., 1991). Dhg maximal exacise however, active muscles an receive up to 88% (26.400 ml) of cardiac output. Witùin a muscle tissue, blood flow can increase by a brof up tu 30 times or more. This shift in the distribution of cardiac output is accomplished thmugh a cornplex rrgulatory systcm involving neurogenic, humoral, and 1d ccmtrol mechanisms (RoweU, 1986; Guyton, 1991, pp. 185-198). Accordhg ta Ohm's Law, blood flow is dercnnined by the relationship of the pressure gradient and the resistance:

Q = (Pl -P2) IR

where Q = flow, (Pl - P2) = change in pressure, R = resistance

Specificaiiy, Ohm's Law states that the blood flow is directly proportiorial to the pressure difference, and inversly proportional to the resistanœ. Vascula. conductance is a measure of blod flow through a vesse1 for a given pressure clifference. In this way, it is the inverse of resistance: a

conductance = 1 / Resistance

As TPR cannot be directly measured, it must k calcuiated as the quotient MAP 1

Factors infhiencing vasculrue conductance The three factors which afféct the conductance of a given vessel or set of vessels include: (i) the degree of lam.vs turbuient flow, (fi) the blood viscosity, and Ci) the diameter of the vessel(s) . Laminar and turbulent fiow: Flow in the arterioles is Iaminar (streamIined or linear). The molecules in the center of the vessel fiow more quickly than do the molecules closer to the vesse1 waiis. This is termed a 'parabolic ve1ocity' flow profile. In contrast, under certain conditions, such as whm flowing blood passes a rough surface, or makes a fharp turn, the flow becornes turbulent. in turbulent flow, some of the molecules will be flowing crosswise (ïmward and outward), thgcby causing eddy currents. Within eddy currenu, some molecules will actuaily travel opposite the direction of flow, and therefore, produce an in- in the ovdfiction and an increasc in resistance to the flow. Although rough surfaces are not nonnally present inside the arteries, theromatous piques may k a contzibuting factor to the incnased TPR seen in people mth atherosclerosis. Turbulence has been found to increase in direct pmprtion to the velocity of blood flow, and the diameter of the blood vusel (Guyton, 1991). In rcsponqe to exercise, arteriolar diameter is incfeased to accommodate an increased hw, and the velocity in any given vesse1 is incnased due to a -ter driving pressuxë gradient. These factors canaibute to an increase in rcSiStanœ with rising blood flow. Viscosity : The viscosity of bloai is constant under normal conditions. Changes in hematocrit have the most simcant effkct on blood viscosity. This is because layers of suspended red blood œiis 'carcss' each other as they move dom the vessel, and thereby cause fiction. Factors which affect hemuocrit inclde pathologicai states, such as anernia and polycythemia, and transient states, such as dehydration. Under nomai conditions, th- does not seem to be any ciifference in blood viscosity between endurance trained individuals and healthy untrained individuais (Wood et al., 1991). Vesse1 Calibre: The diameter of the vessel is perhaps the most important factor affecthg resistance as it is capable of npid change, thereby altering the flow of blood to a tissue. It is in this way that the blood flow is matched to metabolic need. The effect of even a smail change in diameter greatly influences flow because vascular conductance increases with the fourth power of vesse1 radius. Two thirds of TPR is provided by the arterioles. Sina these vessels are -le of a four-fold dilation, and based on the fourth powa relationship of vessel radius and flow describeci by Poiseuille's law, arterioles could increase flow by a fktor of 256. Obviously arterioles play the major role in controliing blood flow. There are other important structures downstream from the arterîoles which play an important role in regulating blood flow to tissues and individual ceus. Metarterioles and precapillary sphincters cmtrol the flow of blood into and within a capillPry network in such a way that under nod conditions, blood does not flow continuously through a giwn capillary. This is termeci 'vasornotion'. Ovedcontiol of blood fïow The mechanical fgctors which effect blood flow have been discussed above, however, the factors which regdate the degree of vasoconstriction in the arterioles, and the pattern of vasocrnistricfion in mctarbzioles and pracaplllary sphincters arc complex. It is the complex interaction of alî mechanisms that dows for the precise matching of blood supply to œll nds. A system controiled centrally wouid be unable to provide for thïs precise matching.There are several recent nviews of blood flow control mechanisms which are quite comp&enEive (Granger et al., 1988; Reading 1990; Shephard and Plyley, 1992). The key regulating factors are of neurogenic, humoral, and local origias. Neural Contra1 It is well known that nwral control of blood flow involves both sympathetic and parasympathetic branches of the autonamic nervous system. Arterial baroreceptors and chemofeceptors constantly monitor artaial blood pressure and blood volume (Guyton, 199 1, pg. 198). In addition, ergofeceptors in skeletal muscle also sead afferent nerve traffïc to the brain stem. where they are pmassed, and adjustments to the levels of activity of the sympathetic and parasympathetic ncrves is made (S hepherd, 1987). Sympathetic outflow acts on the cardiovascular system through two basic types of adrenoreceptors. They are classifieai as the a and Badmergic. The a-adrenergic receptors are present on the sympathetic resistance and capacitance vessels, and their activation results in the contraction of the smwth muscle tissue surrounding these vessels. At rest, the smwth muscle in a vesse1 waU is constantly slightly contracted as it receives a sîeady discharge hmthe sympathetic fibers. This is caiied 'basai me'. Vasodilatation can be achievad by rcducing the sympathetic activity. B-adrenergic receptors are cIasnfied as either Bi- anci &r. When 82 receptors are activitated, there is a duction of intra-celiular caicium, disengagement of intracei.lu1a.r proteins, and therefore vasdilatation via a relaxation of the smooth muscle tissue (Meisheri, 1982).

Hormonal Factors Hormones are relcascd into the systernic cucuiation in response to a vYiay of stimuli including changes in blood pressure, the two most active agents during exercise king adremlin and n0dred.h. They are released from the adrrnal medulla as a result of sympathetic discharge. Nondrraalllr acts as a ~socanstrictm by acting on the p-recepton in the vesse1 MU. Adrenaün can act on either the p- receptors, in which case the vesscls vasoconstrict, or on the Bpeœptors auhg vasodilatation. The vasculature of mat tissues in the body are supplie. with p- receptors (cereb-al tissue is a nome exception), while only the smooth muscle of vessels found in skeletal muscle, bmchi, and caidiac muscle, contain h-receptors (Shephard and Plyley , 1992).

Lmd Controi Dilatation of the resistance vdsoccm immediately with the contraction of muscle (Corcondilas et al., 1%4), and is proportionai to the strength of the contraction (Waüoe and Wesche, 1988). The pzecise mechanism(s) that are responsible for the adjustments in dilatation are controversiai (Grauger et al., l988), however they include: incrtlscs in hydrogm ion concentration, potassium, inorganic phosphate, and osmolarity, as weil as Mous piostaglandin's, adenosine nucleotides, and adenosine (Granger et al., 1988). The Eactors which initïaîe vasodiiatation may be ditfkmnt than the factors that maintain it since artcria upstrearn from the dilating artenols also relax, suggesting a possible neural componen t.

2.2.2 Blood Fîow to Active Musde

During endurance exercise, neural wntrol mec:hanisrns act to maintain mean blood pressure. As exercise becornes progressively. more intense, a progressive elevation of mean blood pressure is achieved. This is accomplished by a decrease in flow to inactive siceletal muscle tissue, a decrease in bloai flow to the viscera (Clausen, 1976). Flow ta active muscles incfeascs through the effects of local control mexhanisms such as decnaSed oxygen partialprtssure, heat, and lealrage of potassium ions, which are responsible for the dilatation of the tesistance vessels (ar&erioles)(Grangeret al., 1988). During exercise with a smaU muscle mas, it has beai shown that there is a relatively larger increase in heart rate than with a large active muscle mas, and that at an equal work *output, thcre is a more pronounced rise in sympathetic tone

(Astrand et al., 196%. Sirniiarly, it has kai show that ami work leads to a greata increase in total peripheral rrsistance than with leg work, possibly caused by vasoconstriction of the relatively larger arterioiar bed in the legs (Bevegard ad Shepherd, 1966). Clausen (1976) showed that maximal oxygen intake is inversely reiated to systemic vascular Rsstance. More recently , a relationship established ktwcen maximal oxygen uptake and maximal vascuïar conductance of the calf muscle (Sneil et al., 1987, Reading et al., 1992). Therefore the degree to which vasodilatation can be induced in the siceletal muscle vasculaavlt is associated with maxiarnl oxygai intake. It is unknown whether theis a fiuictionat or a stnicairal diffkrenct in the skeletal muscle vascuiattm between endurance trained and sedmtary subjects. AdditionaUy, work by Shephard et ai. (1988) has suppiid strcmg evidcnce that as active muscle mass increases, the limitation of oxygen uptake moves hm a peripheral to a centrai dcpadency. It s&ms that there is a threshold amount of active muscle rnass that if not achieved, will ldto local muscle fàctors resulting in fatigue. If this thrcshold is achieved, then the limitation for oxygen consumption will be more dependent on the central delivery of oxygen.

Blood flow is usuaily expressed in units of ml of flow per 100 ml of muscle volume. Normal Rsting values for bldflow tend to be in the range of 24 ml min-1 100 ml-1 of muscle volume. Vascular conductance is caicuiated by nonnaliting the blaod flow by the driving pressure. Normal nsting vascular conductance values are very close to 0.04 ml min-1 100 ml-1 mmHg-l. Measmement of blood flow has recently been extensively reviewed (Bernstein 1985; Reading, 1990; Hutchison, 1994). There are a varkty of methods avlilable which mureci-ly , or reflet, the rate of bldflow through muscle (Clausen, 1971; Anderson et al., 1983). Venous occlusion plethsmogaphy has been shown to be a reliable non-invasive technique for measuring rdng and post-exercise blaxi flows on srnall lirnbs, such as the caif (Sneil et al., 1987; Weber et ai., 1988;. Hepple, 1992; Reading a al., 1993). The basic principle of the technique is that when the thigh cuff is inflated, venous blood is prwented from flowing out of the calf while arterial bldcontinues to flow in, producing a volume change in the Sze of the caif in proportion to the arteriai blood inflow. The use of a mercury or gallium-indium strain gauge saisor to dctst the changes in the volume of a limb has Mer improved the application of venous ocdusion pkthsmography (Hughm, 1988). Vascular conductance can be caiculatPA using this technique by dividing the blood flow by the sïmultaiaeously obFaincd mean rrtgipl bldpressue (MAP). One signifiant limitation of sûaïn gauge vmus occlusion plethsmography concerns the interpietation of dues achieved immedutely following submaximal exercise. Walloe and Wesch (1988) studied the magnitude and time course of adjustments in blood flow during and akquadriceps exercise, using a rapid pulsed doppler uitrasound technique. Theu data revealed an inverse exponential decline in blood flow irnmediately foiiowing exercise, with a 3096 reduction after 5 seconds, and 50% after 10 seconds, Therefore, the pst exercise measurement is not truly reflective of the actual blood flow during exercise, but it still provides valuable information, providing that the time betwem the cessation of exercise and the flow measurement is consistent. The one exception to this limitation is when maximal ischemic exercise is performed. Ischemic conditions are created by infiating the proximal (thigh) cuff to occlude blood flow to the caif (>22Omm Hg). Maximal exerck is defined as an inability of the subject to continue to contract the calf (usuaily limited by discomfort or pain). Under such conditions, reactive hyperemia ensues, and maximal vasodilation is acheived (Snell et ai., 1987). Conway (1966) has show that an intra-arteriai infusion of ATP yields the same blooâ flow as reactive hyperemia. AdditionaUy, following maximal ischemic exercise, the blood flow values remains elevated for severai minutes; in fact, it may even rise during the fht 20-30 seconds foiiowing the ischemic episode (Sneii et al., 1987). Sin= vascuiar conductance is detefmined by the luminal site of the artcrioles, precapillary sphincters, and metarterioles to a lessa extent, changes in vascuk conductance in mpcmst to exercise reflect the change in the cross-sectionai area of the arteriolar bed. therefore, strain gauge plethsmography, using the maximal ischemic exerciSt technique, can prwide an accuratc reflection of the maximum +ty for Mscular conductance (G max) under these controIled conditions. 2.3 Vasculai. Conductance and Wbdc Body Oxggen Consumption

Andersen and Saltin (1985) have show that Vq2 mur is limitcd by the Capacity of the heart to pump blood. They used a constant infusion thermodiluticm technique to measure qdceps blood flow during sevd gnded exache loeds, including peak flow during maximal exmise. Thch fmdings of a mean blood flow of 248 ml min-1 100mloomllmusck mus would requise a cardïac output of mer 41 L -1, assurning an active muscle mas of 15 kg and shunting a flow of 4 L min-l to the non-exercising tissues (thmre&icalargument based on Rowell, 1988). A maximum blood flow of these proportions clearly indicates that the ability of the muscle to accept such a large blood flow when a iarge muscle mas is active as would be the case during runniag, is fàr in excess of the ability of the huvt to pump such large quantities of blood. This conclusion is logicaiiy deduced as weii, since it has long been known that maximal cardiac output is closely lïnked to V* max (Jones, 1988). Although the prevailing Mew of the scientific community is that central processes are limiting, there is ample evidence to suggest that a more complex interplay of central and peripûeral f&ckmoccurs than previously realiad (Green and Patla, 1992). 2.3.2 The P0Ssib.i of a BMF10w UtedPcripherPI Limbtion to

As wouid be expected, elements rcpreseriting the centrai and periphaal contributions are evident in the V02 equaticm from the Fick equation (fig. 2.3.1). in which cardiac output (Q) defines the total transport capacity of the system, a central wmponent, and the -0- mixed veaous oxyggt Mcrc~~ce,(a-* m.),i.c the extraction, represents the pripherai component. Assuming normal respiratory fimction, 02 transport is dependent upon myavdial hmction, blood volume, hematocrit and q binding capacity. The extraction is detamincd by the balance between the intracellular oxygen utililiition (metabolic rate) and the oxygen availability , which is a function of Lod muscle bldflow, capillary blood volume, and diffusion. Consequently, mean transit time of blood through the capillana, is negatively correlateci with V-max (Kayar et al., 1994). While b1d flow and mean îransit time are closely reiatsd (both a,in part, dependent upon the design characteristics of the miCrOCiTCuiatory bed), mean transit time is determined primarily by the density of capillary suppiy (Saltin, 1985), and blood flow in the rnidulation is dependent on the balance between the pressure head and the ability of the artmoles to dilatte (Ohm's law at the local level). The size of the arterioliu bed is reflected numeridy by the conductance, Le. the amount of bldflow when nonnalucd for the driving pressure.

Figure 2.3.1

Vamax = Cardiac Output (MBP + TPR) X (a-va content) If the ability of the hart to dekbld to the exercising tissues, Le. Q, acdylimits V@ mu, and not the ability of the pcripherai vascuiature to accqt the bldfreely (as demonstrated by Andersen and Saltin (1985)), then we would not expect any signifiant changes in the periphd vascuiaturc afkr endurance trauiing. However, significant changes in the periphd circuiatim do occur as evidenced by an in- in the numba of capillaries in the muscle tissues which has been weU documentcd as a mmmonly occuring adapstion to endmance îraining (Hudlicka et al., 1992). Much les is known about the changes which occur with regard to arterioiar structure and fiindon. Clausen (1976) published a rcview papr in which he compiied 125 vaiues hmthe various human studies in which V% max, mean blood pressure (MBP) and Q had been detemhed at maximum exercise. Fmm the data, he plotted the V@ max data against calculated values for total penpheral resistance (where TPR = MBP + 0); the relationship was found to k hyperbolic in nature (fig . 2.3.2), and the wonequation determincd wuy = 11.8 / x0-72 (r = 0.87, p < 0.001). Clausen also plotted the mean values for a number of subject groups hmthe various studies, including studies involving exercise or bed rest interventions which known to aiter V% max. The derived regression line described above fit these data quite weU (fig. 2.3 -2). ~8PnrârOmar

Figure 2.312 Total Peripheral resistance at VO2max Maximal oxygen consumption (V-max) in relation to total peripheral resistance (TPR) at V@max (MBPmax / Qmax) basexi on V%max, Qmax and MBPmax values from the iiterature. The left-sided panel displays 125 individual vdues. Subjects included top trained young athletes, well erained middle aged athletes, young and middle agad heaithy men and women, and patients with CAD and patients with essential hypertuision. Subjects with the highest VO;?max values had the lowest TPR values, whiïe subjects with the lowest V-max values had the highest TPR values. The right-sided panel gives group mean values from intervention studies where changes in V02max were induced by training or bed rat, by beta rceptor blockade, or different types of exercise. Any intervention that changed VOzrnax, changed it in accordance with the regression line y = 11.8 / ~0.~2(r = 0.87, p C 0.001) denved from the 125 individual vaiues shown on the left-sided panel. (Clausen, 1976). The relationship betwem VOy mu and TPR is sipnincant for several nasons. It clearly shows that a deneast in TPR is accompanied by an hcrease in V% max. Furthermon, ui the weiï-ttained athletes (uppcr left corner of the graph), a srnall decrease in TPR cbnesponds to a large change in V@ mu. Since ~a~~~~nstriction in the non-exercising tissues during maxUnal exercise is not significantly modified by training (Clausen, 1976; 197'7). a daxaise in TPR at maximum exkacan only be achieved Uuough alterations in artenolar fwrction in the exaciping muscles. Any decrease in resistance, therefore, must be due to a functionai increase in the ske of the arteriolar bed, attained àtha by incnuing the number of artenoles andh by developing a greater degree of dilation in eristing arterioles.

2.3.3 The Ur& Between Muscie Blood Flow and Maximal Aerobic Power

More recently, a strong relationship has been established ktween V% man and lower leg maxirnal vascular conductance (G max) in weU trained and untrained men (Sneil, 1987), and in male endurance trained and untrained men, and congestive heart failure patients (Reading et al., 1993). These studies have show that across a wide range of fitness, higher levels of V@ max are associated with higha levels of maximal vascuiar conductance in the lower kg, suggestive that an increase in G rnax as a result of endurance training produces a concomitant increase in V02 max. The endurance aained subjests in the study by Reading a al. (1993) were defïned as those participating in a regular physicai activity program - not elite by any standard. The VO;! mur of these subjects was 48 ml 4-1 rnid as measured on a cycle ergorneta, and the mean G max was 0.65 ml min-1 100 ml-l tissue mmHg-l pressure. This mean G max was only slightly less than that found by Snell (1987) 5.2 Subjed Charaderistics

As can be seen in table 4.1.2, the athlete groups saidied were distinct in how they trained for their sport. The pwer group, coasisting of track and field jumpers and decathietes, were chosen because of the high priority they place on fi- @asonal corzespondenœ with the University of Toronto Jumps coach: Car1 Georgevski). These athletes Waly presmt a better modei for a cardiovascuh study than those athletes usually used to represent a power trained muscle, such as throwers and Olympic and power liftcrs. Such athletes are not conœmed about propebg their own body weight, and therefore are less concerned about maintainhg a low fat body mass and overail fim.Furthamon, in the power group utüued in this study, the volume of supplementary aerobic activity and running, albeit mostiy short distance, contrasts weli with the body builden wbo avoided such acîivities. Therefore, any aerobic adaptations sem in the body builders which are greater than those seen in the power group could k attrïbuted directly to the mode of resistance aaining employed. The modes of resïstance aaining employed are markedly different between the two resistance trained groups. Although the volume of training was not quantifieci, table 4.1.2 clearly shows that a much larger number of repetitions are perfonned by body builders than by power athletes. The total time spent resisiance txaining was similar in the two groups. Additional leg work was done by the power athletes through plyometric training. If a structurai / fiinctional limit to O max cxists, then it wouid k ex- that those athietes for whom the highest possible V02 max is cnrinl for succcss will lie closest to that lunit (Rowd, 1988). The VOL max - G max relationship for the range involving the sedentary and 'trained' individu& has been established, it is unclear as to the nature of the rciationship in the dite, durance athiete. CIearly, Roweii (1988) would prcdict that the relationship of V02 rmx and G rnax in the elite endurance athlete shodd have a much grcater slope than that observed with the sedentary and 'trained' individuais described by Sneil (1987) and Reading a al. (1993). A greater dope for the V02 max - G max relationship in the elite endurance athiete wouid be suggestive of a leveiing off of the structwai / functional vascular adaptation, and iikely , a pahision limitation. 2.4 Training Metbods and RdPted Adaptations in Elite Athletes

2.4.1 Elite Runners

Training In generai, any runner whose priniary competitive event is 800 m or longer has traditionally been wwed u an endurance athlete, yet the 1eagth of cornpetitive distances in ninning races exCYiPdS the marathon, a race of 42.2 km. In kt, the metabollïc demands and muscdar limitations presented by these activities are quite different, and so is the training program in which these athletes patticipate. As was clarified in the review of V0,max and running performance, the middle distance events (1,500m - 10,000m) seem to be more directiy dependent on VOpax. This is intuitive, based on the type of training employed, since middle distance mers spend a signifiant portion of th& overall training volume at high velocities using various forms of intaval training. This intensity element is a higher priority tban absolute volume of training, which is the haümark of the marathon cornpetitor. Consequently, a greater portion of training volume is spent by rniddle distance runners at intensities at or even above VOpax, as measured by heart rate (Janssen, 1987; Martin and Coe, 1991; Ne,1991). The training year of a wmpetitive middle distance meris highly periodized. Approximately 60% of the year is in the preparatory phase of training, and is characterized by a relatively higher volume and lower interisity training. Aithough training programs vary, many ninners continue to engage in intend training, utilizing sessions which are more volume-based with work to rest ratios &y exceeding 1.5: 1, usuaiiy in the range of 2:l or 3:l. Such sessions may be performed twice per week. A third 'hard' &y is included either in the forrn of a long run, a 'tempo' Xun, or a race. The reiative intaisity of 'muwery' runs (oh ded'easy' runs) on altemate days is highest during this period. As the cornpetitive season approachcs, there is a gradurl priority shin from volume to intensity. In general, 'tempo' rwis become shorter in length, and races are introduced und they occur with a fhquency of at least once every week (not always at distance of specialization). At this point, the aining prognuns of the various distance specialists begins ta diverge, but the diffèrence in tralliing baweai the specialists is primarily one of volume vs. intensity. The 800, l,MO, and even 3,000 m mers devote a gmt deai of th& hard training donsta developing anaerobic power and capacity interspers4d on aïternate days with fecovcry runs. A typical set may aLe the mers through a velocity range of klow race velocity, usuaiiy at or near V02max (a 'wann up set': e.g. 4 X SOO rn with l:15 min. rat), to repeated msnear maximal velocity for the given distance (e.g. 8 X 200 m with rats ascending hm 1 min. to 5 min.). Since such training probably mmits fibers repeatedly, it is liUy that this training stimulus is responsible for the inverse relationship betwetn 800 m perfomance and ST% (Saltin et al., 1976a). At the longer end of the cornpetitive spectrum, 10,000 m rumers taper theh volume of training more slowly, and only deal with high intensity (anaerobic) training through races or through a high intensity repetition at the end of a trainhg session (e-g. 6 X 800 m with 1:W min. rest + 2 X 800 m with 3:ûû min. nst). Adaptations Adaptations to running training bave beai discussed in section 2.1. It s&ms reasonable that fikr type +c adaptations occur depending on training stimulus wmbined witb genetic différences and may account for the ditferences seen in VOpax among elite athietcs. If the fàctors thzt lead to V-max are viewed as a series of interdependent resistances, then it would be logical that physical training designeci to impmve VOpu would lead to a 'fine mg'of the entire system, limited by the rnost unchangeable resistance. Structures which are adaptable wouid not be maintaincd with a structurai CapeCity greater than the fiinctional demands placcd on it. Therefm, they would Iürcly appear to limit VOymax. Unadaptable stnictures on the otherhand, would exist with excess capacity in orda to k able to accommodate any poterrtial adaptation in aembic capacity (Lindftcdt et al., 1988).

Tmhhg: the bodybailclhg mdhod nie primary objectives of body building are to increase muscle mas, to produce symmetry, and to produce definition so that individuai musdes can be visiially separated fiom each other (ï'esch, 1992). Within the body building community, there are a variety of training strategies, which have evolved ova the years based on the experiences of succesdul comptitors. This is, in part, because science has not yet been able to idaitify clearly a Spccinc &stance training protoc01 which is optimal for muscle hypertmphy (Tesch et al., 1989). in generai, bodybuilders tend to see their trainhg as "breaking down" the muscle. During recovery between training sessions, they believe that the muscle protein is king 'rebuilt', and that due to supercompensation, a larger muscle will be developed. As a mult, much of the curent emphasis in body building has revolved amund supplern~~~tingrecovery nutritionally with the aid of extensive vitamin and vnino acid suplemaitation. It is weli documentcd that fofceîùl contractions, -y ecœntric contractions, result in delayed muscle soreness; analysis of biopsies provides evidence to support that actual mriscle damage to contractile proteins occm (Abraham, 1977; Tiidus and

buzz~,1983; Fnden et al.. 1983). Based on the 'break dom and buiid up thmry', it ems logicai to many bodybuilden that the pater the 'break dmu, provided that there is adequate ~ecovery, the greater the murle growth. Subsequently, bodybuildm typicaiiy employ training pmtocols which utilire submaximd contractions that lead to concentric contraction Mure between 6 and 12

repetitions. Each set lssu appr~ximattly30 seco~lds,followed by a 60 second rest, Le. a work to rat ratio of 1:2. This effort is rrpcetcd 3 or more times for any given exercise. Additional exercises activating the svae muscle group are then prformed, u> that in 30 minutes, approximately 20 sets are perfonned on one muscle pup(Tesch and Larsson, 1982; Dudley, 1988). Aàaptations Bodybuilden do not show greater incrrves in systolic or diastolic blood pressure than untrained controls when performing nSstana. exercise with high relative or absolute waghts (Fkck and Dean, 1987). In fact, resting blood pressure in body builders bas been reportai to be the same or lower than in untrained controls, and showed a much lower rate pressure product (Coliiander and Tesch, 1988; Urhausen et al., 1989). Very little is known about the circulatnry adaptations which nsult hmchronic body building wg.This is h large part, due to the problem in categorizing resistance training. It is now rrcognued that the morphologid changes which mur as a result of resistanœ training Vary greatly depending on the laad used, the number of repetitions pet set, the numôer of sets, and the length of the rest period behwai repetitions and sets. As these training variables are rnanipulated to produce diffmnt training regimais, several distinctive levels of adaptive stress an be applied to the muscle. Most training studies have employed a 'standard" rcsistance training protocol both for simplicity andlor dstency with the existhg litcraturc on resistance training (Vogel, 1988). However, the type of nsist~ncetraining performed by bodybuilders is thought to resdt in slreldal muscle structurai adaptations which are smilar to those seen foiiowing endurance training (Tcsch and Larsson, 1982). During graded cycle ergometry, bodybuiiders have been shown to exhibit a lowa heart rate and systolic blood pressurr for uiy ghm worLload men compnrrd to studcnts U-h, 1992). This is a response si& to that found in endurance trained subjects, and indicates an enhanced capacity for aaobic work. From the limiteci data avaiiabIe on the adaptive nsponse of siccletal muscle to body building training regirnens, one can oaly speculate on the circulatory adaptations at the level of the muscle. Again, it must be emphasized that b bring about alterations in the flow capacity of the muscle, Le. to bring about adaptations in arteriolar structure / function, the aaining involved in body building must adequately stress the cardiovascuiar system. It has been show that bodybuilders have an in- in the number of capillaries per muscle fiber (Shantz, 1982; Tesch and Lasson, 1982; Tesch et al., 1984; Bell and Jacobs, 1990), and an increase in the oxidative capability of the fan huitch fibers (Tesch et al, 1989). The same study showed that bodybuildm had a greater citrate synthase activity within the slow twitch muscle fibers. These studies are supported by Ingjs's endurance training study in which it was shown bat the capillary supply to a given fiber is more closely related to its mitochondriai content than to its fi& type (Ingjer, 1979). This shdy shows that a high percentage of slow twitch fibres, as found in elite endurance athletes, wouid not be necceJJary for a muscle to be highly capillarized. These changes by themselves do not necessanly indicate an increased capacity for blood flow. It has also been reportecl that recovery hmhtiguing excrcise, simiiar to that employed by bodybW1dcrs, is strongly relatai to the muscle's respiratory capacity and to the capdhy blood nipply (Tesch and Wright, 1983; Ivy et ai., 1982). In addition, signifiant findings wac reported by Waüoe and Wesch (1988), who demoastrated that blaod flow through a muscie is directiy related to the tension of the contraction, and that it was increascd when the relaxation phase was show than the contraction phase, and that near maximal flow rates wcre achicved within a few contractions. These findings implicate the high npetition, multiple set, low test Ûaining regimen employed by bodybuilden as king extrcmely messful on the pripheral varulature. However, it is unhown whetkr bodybuildm exhibit high peripheral blood flows and bigh G max values.

2.4.3 Power Athlets

Training: the cbdcaï stiength method The primary objective of power training is for the neuromuscular system to be able to produce the greatest possible force within a given time period. The relationship between maximal force and movement speed is expressecl as a force- time curve. In a general serise, as the extemai load decrcases, a movement can be perfomed more quickly, and the relative -contribution of maximal strength diminishes. In this do,the rate of force gaieration is the predominant faMi (Schmidtbleicher, in Komi (ed. ), 1992). In track and field cornpetition, high, long, and triple jumpers, as weU as decathletes, are prunarily concernai about moving their own body weight, a mas which is far less than their 1 repetition maximum (IRM) load. Since most forms of resistance training resuït in some degree of hypmophy, the jumper, in contrast to the thrower, cannot afford to increase muscle mass without positively adjusting the whole body force the curve. In contrast to bodybuiiders, powa athietes use dstance aaining as a means of improving their relative power (work 1 tune 1 body mass). The resïstance training mode1 utüued by jumpers is modeled on the program followed by olympic Mers. This program involves few repetitions with f&ly high loads, with full recovery between sets. The emphasis is on exetcises for the legs, such as squats and luges, but also include the match, clean and jerk, and some basic uercises for the upper body. This training is heavily supplemented by plyomebics, medicine bail work, and perfomhg the jump activity itself. Jumping rarely ex& three days per week, and a maximum of tmnty jÿmps are paformed performed within one hout. Therefore, an average of one maximal contraction is perfimned every thne minutes. In contrast to the jumpers described above, it should be noted that since the lifters are training for an event that is more directiy ddepddent on th& lRM, they use resistance training as the prllnary mode of training (Garhammer and Takano, 1992). The one signifiant difference may be that thae is a greater degrre of hypertrophy. So ded "pure" power training of the legs, such as jumping, resuîts in smaller increases in maximum strength and musde hypertmphy, but har a gmua effcct on the rate of force development than san with ciassicai strrngth training (Hakkinen and Komi, 1986). Mnximal strength and power are not separate entities however, as maximal strength pmvides the basis for power development. It is for thLF mason that jumpen utiiize both "pue' powa training as weU as maximai strength training. Adaptations There is ample evidence to support a detrimental effect of power lifting training on systernic cardiovascular parameters. Heavy resistance training seems to subject the athletes to more extreme blood pressures, with values greatcr than 300 mmHg being reported (IbkcDougaii et ai., 1985; Fleck and Dan, 1987). The Pdrptive response to such high vascuiar pressults indude Uicre9ses in Iefi ventricular wrll thickness and cardiac mass (Fïeck, 1988), and may occur at the expense of heart volume (Longhwst et al., 1980; Brown et al., 1983; Morganroth, 1975) . In addition, this form of training typidy resuits in muscle hypertrophy (Hakkinen et ai., 198 1; MacDougaii et ai., 1980; Young et al., 1983). primarily of the fast twitch fïôer types (Hakkïnen et al., 1981; Young et al., 1983). Fast twitch fibers are associated with lower leg blood fhws (Frisk-Hoimberg M. et al., 1981). Since there is no apillary nwforrnaticm during this form of training, the capillary density decrrases, resulting in a grepta mondistance (Tesch et al., 1984). There is also a concomitant reduction in the skeletal muscle mitochondrial fractions (Mac-ugail et al., 1980; Luthi et al., 1986). These adaptations indicate a decrcase in aerobic power. Longitudinai studies utüizïng a smüar type of Paining as that employed by power liftm have reporteâ either no change (Hickson 1980; EIickson et al., 1980; Stamn et al., 1984), or a decrease (Gettman and Poliock, 1981), in VO;! max. Thus, the cardiovascular and ceiiular adaptations which have been reported for power lifting indicate a reduceû aaobic capacity. If this is the case, then one wodd expect that this type of training rnight mult in a denased G max in relation to Vqmax. in a typicai bodybuiiding training sessions the oxygm consumption wili rise to no more than 50% of maximum (Seais and Wberg, 1984)- One can speculate that regstance training, utiiizing fewer sets and rcpctitions, as well as a longer rest period, would mult in a relative oxygen ~~~lsumpti~bwhich is lower than that seen with bodybuilding. Previous reports indicating a lack of improvement in VqZmax in response to RSstance training have suggested that this is due to the lack of an adequats centd circulatory stress, as reflected by the low dative rate of oxygm consumption (Dudley, 1988). Howeva, during graded cycle ergometry, bodybuilders demonstrateci the same or slightly lower blood lactates at eacb work load when compared to untrained wntrols. Weight Liftas and power lifterp, on the other hand, had higher blood lactates for any givai workload flesch, 1-987). These findings may, in part, be explained by evidence of selective hypertqhy of fast twitch fibers in mpnrto traditionai resistance training programs (Prince et al, 1976; Hakkinen et al., 1981; Tesch and Lamon, 1982; Young et al., 1983). In contrast, bodybuilding scems to result in the h~pertrophyof both fiber types (Tesch et al, 1989), probably due to the exhaustive 'endurance' nature of Mybuilding. Such training is likely to &te aii fiber types. In one case, Tesch and Larsson (1982) examined the muscle fibers of three elite body bdders and found no hypertmphy of either fast twitch or slow twitch fibers. Additionaily, the bodybuilders were found to have a very low percentage of Fï'b fibers (45% for the vastus lateralis and 3% for the deltoid). As the authors speculatsd that their peculiar finding were indicative of hy~erplasia,it is unfortunate that they did not maMecapiliary dmsity and diffiision distance. and CQ~(1984) bave ded the neurornusculal, answabic, and aerobic @ormana chaactenstics. . of bcdybuiïdczs snd compprrd thcm to those of C powerliftcrs. Itwas showntbattherrwas nodi&rrwe in fikrtypedbtribution and isomcûic forrz produchi011 pa unit body weight, but there wat simcant ciifferences in the to 30%, 60%. and 90% force production. Thcy Plso fouad a sigmficant di£fkrmœ in V* max values with 42 and 51 ml min-1 kg01 fa the power 1iRen and bodybuiiders, rcqcctivtly. Thme data iadicaft that despite no differt~lœsin fiba type distribution and iso&c mgth, the bodybuildcrs had an devatcd Perobic capacity and grniter power. Tesch et aï. (1989) fond a gr- citrate syntbase activity in the slow twitch nbaJ of bodybuilden thn in powa lifters, and a greatcr myokmPJe activity in the fist twitch fibas. It is intcrcsting to note that the citrate synthase actïvity was lowa in the bodybuilders than it was in the untrained subjccts. Furthermore, it rpp*w that the bodybuilders, unüke the powa liftas, have developed an inaaisal VOy max comparai to that of dentary individuals menet al., 1984; Shephard et al., 19û4). Thae is a pwcity of data cm the cirnilptory adaptations to nsistance training in general, and body building in particuiar. A recmt rcview of cardiovascular adaptations to nsistance training (Fieck, 1988) concluded with a cal1 fot more rrsearch to idcntify the nature of thesc adaptations with considdon of the diber and type of athlete (Le. bodybuilder, powa ahk&). There does not s&m to be any published data on muscle blood flow in resistance trainai subjects. The infirenttiai evihœ hmthe m&w prescntd above suggtsts that therit may k signifiant incrcascs in peak shletPl muscle blood fiow and corductance as a resuît of the type of training a body builda would engage in. Powa athletes would contrast well with body builders sina tbcy nprrsent a mode1 of taditionai nsistlnatnlliiagmcthods. Fuitbamorr,trackandficldjunipasmd~ would be an ideai powa athlctt group for a study utiliPng calf crgometry to asscss skeletal muscle blood flow and trdmiu V@max tcsting, sina their training focuses on improving power (work / the) relative to body mas, specifically in muscles involved in running (c.g .p1anta.r flexofs). Eütc mers provide a calf musde model of the most highly endurance trained. From the relationship established betwcm Gmpx and Vozmax, it muid be postulatcd that this group would have the highest-Gmax values. If a ptnpheral perfusion limitation to VOpax casts, then the ~mshipbetwœn Gmax and VOpax in elite ruwas should display a steepa slope thin untrained and les well traiaed groups. The V* max and G max of 37 male nibjects cmshthg of 7 body buiïdcrs, 10 elite numas, 11 powa atbktcs, and 9 daMary aibjectp wu examinad. AU teshg was done Pt the University of TmtoLifksty1t Laborotory- AU subjccts anrc fiœ nOm madicatim. None of the athlttts had bccn uacising for twenty four &ours prior to the lab tests.

Age was not incldeci in tbe selccticm criteria as the priority was to &tain the highesî calikz 91hlcccs possi'ble. It was cxpcdai that any variation in age will not k so gnat as to k a COIIfou~ldingfactor. AU abjects signed the informed consent appved by the Office of Resear& Services at the University of Toronto (appendix l), and wae asked to complete a standard physicai activity readincss qutsfionairt (PAR-Q) @or to the testing. AU athletes wcre askcd to cornpletc a dctailcd ~~rmanctand training qucstionairc (appendix 2). 3.1.1 Heatthy Seden-

AU healthy sedcntary (HS) subjccts wne rccniitcd hm the gend univenity community. Al1 were fîee of medication, and had not been engaged in prior regular physical activity or training programs for at least two y-. Regular physical activity was dehed as any exercir program which elevated heart rate above 60% of maximum, and/or involved any form of mistance training, and required three sessions a week.

3.1.2 Elite Runners

EIite middle distance mnners (ER) were recruited from local running clubs.

Inclusion critena were îhat they must have been training for competition for at Ieast 2 years, and racing competitively at distances between 800 m and 10,000 m at a national level.

3.1.3 Power Athletes

Power athletes (PA) were remited from the University of Toronto Track and

Field Club. Inclusion criteria were that they must have been . training for competition for at least 2 y-, and competing at national andlor international competitions. PA subjects were considemi as jumpers (Iong, triple, high), or decathletes. Body Buildcrs (BB) war ncmitcd from local bodybuilding clubs. Inclusion criteria wert tbat they must ha.ken training faavn two years in prcparation for cornpetition. No aaemp was made to scrrcn subjects for Steriod use.

33 Maximai AerobkPower Testing

Ail laboratory testhg was perfiotmed on one &y within a two hou paiod. Maximai aerobic tcsting foiiowcd blocxi flow testing on a caif ergorneter. V@ mu wu oôtpwd through opn circuit spirometry duing an incnmtai exercise test ta exhaustion on a motordziven tiedmill. FoJiowing estabkimeat of a cornfortable treaddl specd, the dope was incrcYcd by 2% evq2 minutes for 8 minutes foîiowed by 1% haaises in dope evay 1 min. until the subject became exhausted. Test termination was determined by subject exhaution, and the RER (> 1.15). acheivement of an age priadicteri maximum heart rate, and a pl?tcau in V@ (an incnase of less than 1 mi kg-1 min4 with an inaase in work luad of 1%) wac used as criteria ta vaify that a manmal value was attained (McCoiineli, 1988). Expi. gases were coilected evay 15 seconds in a mixing chamber. The fraction of cxpired oxygcn (FE~Z)wu demmined using an oxygai analyser with a zirconium dioxide ~hcmicald (Amtek) which is heatai to piecuely 700

OC. The fiaction of corbm dioxi& (FEC~~)was determined by a fàst rtsp01lst carbai dioxide analysa (Jacger) dgnon-dispasive infnred absorption. A hrated mmpling lb insures thrt the conest amount of gas sampk, with its aagianl water vapour coatmt, is dram nOm the mixing chamber. Vc11tilation mcasurements aiac pdormad by insgrrd air aoWing Wugh a turbine flow-metcr caztridgc (PIC Morg~n). In this devia, Ur spins a Wcai impeiicr qporkd ai cushion-mountai sapphk jewei bearings. Four ,infiaredlight bauns cross the fiorneter bore in the path of the impuer. These light beams ut ~6~uentiallyintempted as the implEa 10- and produce fan trains of digital pulses. Flow rate adtotal volame can k detedned by processiag these pulses. The turbine blade has a vcry smnll mas (0.005 grams), and theref-, any changes in air direction or velocity wexe detect6d. Caiibration: The gas aiialypas wac turned on at least 30 minutes pria to cach calibration to dow the ce11 to hat and equilibrate. Anaiysers wae caliirated with known oxygm and carbon dioxick amcentrations immcdiptcly befon and foilowing cach test. During the cal'braticm ptocedust, the thne delay bctwœn the volume signal and the exhaied gas transpt to the analyser is determinecl and introduced to the program. Volume caiibration was accornpiisbed using a 3-liter calibratuf syxinge prior to and afkr each test, AU cardiorespiatory data wcre collected and analyzed by a d-automatcd metabolic cart (P K Morgan) with on-line cornputer. Blocxi flow to the caif was measUrcd using vaous occlusim strain gauge plethysmography (SGP) as desaibed prcvidy by this labonitory (Reading a al., 1992, 1993). Subj- wae plred in a siipint position with the right fa(or jumping fmt) on the calf ergorneter pedai, with the calf elevated appmximatdy 25 aatimekss. Shoulda rcstrabts wae adjusied to position the lowa leg to siightly less than horiurataî in order to facilitate venous retuni. Subjects rcmained in tùis position for 15 to 20 minutes to ailow for acclimatim and SGP setup. A blood pressure sin ("exclusion cm) wu pl& around the MUe and iaaatcd to a pressm of 220 mmHg to ment bloud Mmarailpting in and out of the foot. A second cuff @xclusioafflD, placcd amund the thigh just above the kme, was rapidly inflated to 60 rnmEg, and the change in volume of the leg was measured over the first scven scc01lds of data collection via an indium-gdliwn strain gauge (Mediasonics Mode1 SPG16) plrcd vound the gmitest chamference of the right calf (or jumping leg), and was applicd with a teasion of approximately 10 gm in order to msun skin contact around the atire calf. The sixain gauge was electnidy calibrated with a square wave dcflcction of 1% @or to each daacquisition session. The indium-gailium stmh gauge technique bas ôecn prcviously show to be diable (Reaâing , 1990).

Systemic blood pressure and hmrate was estimptrd from racordcd beat to bept signais during the strain gauge measuriemmt using a Fi2300 autornated blood prrssun monitm (Ohmeda). The FiiÿiPrcss utüizes the Peaaz method of nm- invesively measuring the amplete arterM wavefoim at the fhgertip. It is basai on thecaiapttbatifaaexrermllyapp1idprrssurrisequaltot&PItcrirlprwsut, thae will be a zen> tninsmuraï pressure and the artcries wül not cbange in Boc. Thdbrc the blood volum in those artcries u4.i not change, and this cunstant blood volume will becorne the sa point for a -O lo0p. As the bldvolume varies hm the set point, the savo loop is drivm to incrca~tor draase tbe pressure of the fingad. ~cuffprcssureismepniradwingan~c~~sd~~tr, and the mting si@ is dispiayed as the priaial panirr. The Finepnss uses two mcthods for sctting and main-g the set point. The htis caiid tbe 'raw> start-up odjusmient'. 1t caasWIs of Jtqipiag the cuff prrssurr thn>ugh various pnssurrs and measuring the magnitude anci shapc of the waveform at each level. If the prrssure is WOWdiasbIic pk,the resulting waveform is smali because t&e artmiai waU is oonstantly unda tension. if the cuff piessure is above systolic pressme, the the utaial waU wiil be wlïapsai, and 1&rr wiU be virtdîy no pullcatile componmt. Somewhcxe khuccn these two pnsairrs wiil be a point where the rcsulting puisatim wiU be relatively large because the aaerial wall expericnas both compression aad teasion. The computcr measwts and interprets these waveforms, and &cas the intial set point. Once the set point is established, the seumd methd, caïïed the =O-self adju~tment,is used. It involves the ~amedacision by the cornputer (to dightly djut the piessure based on the waveform), but ai a single bat ôasis (my 10 to 70 beats, depcnding on the magnitude of the lut adjusbnent). AU ciata collectuï as part of the caif blood flow p-1 wu obtained through an automated cm-line wlicction and processing syJt#n usiag a WATSMART data acquisition unit and custam writtai software. 3.33 BWFlow Data Ad@s

Blood flow (BF) data analysis was Mtated by a custom Mimn analysis progr~mwith samples taken at 100 Hz. A blood flow curve wos aisplaycd on the monitor which visuaüy rcpreserited the indgand demeashg crlf volume (Mow and outflow phase during thigh Cun inflation and deaation). The sofhme ddatedtheslope hmtwopoints sdcacd at tbescgion ofthecurve whercthae appeard to be the fiutest incr*ue in caif volume. Any artifkt hmthe thigb cuff when it was tumai cm could be casiiy sem and avoideb during tbe sclcdon of the points for dope calculation. Systolic and diastolic blood pressures, mean vteriaJ blood pressure (MAP), and harr ntc were calculatni simuitaneously. Conductance caiculations wae made by the software as the bld flow normalued for simuitaneous MAP, where G = BF / MAP. Systoiic and diastolic bload pressures, MAP and HR were also calculatd using the abve rnethod for the entire 45 second perid.

Cllf blood fiow was meansurrd @or to the maximum oxygen consumption testing. The blood fbw measuremmt technique was performed thrœ times: whiie the subject was at rest, after submaximal cxerciSt, and aftcr maitimpl khemic ex&, using a spcQaUy designcd calf ergomcter which provides to plaatar flexion (Reading a al, 1992). nie atacise protoc01 uscd caasistcd of oo~ltinuous,rhytûmicai, plantar flexion aac*c on the calf ergorneter. Blood fiow was asstsred immediucly upon cessation of the ex&. Sub- exerck was PerfORlldd hwdhtdy foiiowing the reSaag data acquisition. Work through the movcxncnt of a 5 kilogram lmâ mwd cm by continuou, rhythmicai, plantar &àoa at a fque~lcyof once pcr second for a duration of 2 min. The maximal exexcise protocml was desigDed to eücit a maximai ischemic

~espo~lst.It was pafOrmed apprr,ximatciy 5 to 10 min. foliowing abmaximai ex- data aquisition. Mnximpt blood flaw fi,lïowîng isehemic ex- was zuxomplisbed thmugh the inflation of a blood pressure cuff around the thigh (>220 mmHg) to prtvat flow CO the alf. With the thigh cuff SUinflatcd, the subjea resteci fa 2 min., foUowcd by vigorous, rhythmicai, piantar fiexion ex- at an initial cadena of 60 rpm, with a 30 kg load, and matinuing to volitionai Eatigue.

AU data wen anaIzyed using a one-way ANOVA to compare responses among the four groups. A post-hoc test (Duncan's muitiple ange) was used to identiry ciifferences betweem SpeEinc subgroups bllowing the ANOVA. Withia each pup, hear regmsion anaîysis (ïaiJr squares mefhod) and simple eornlaton coefficimts were usaï to exnmint aie relationship bctwem the foiiowing variables: VO;Z max and G mu, VO2max and BFmax, Gmax and Grest, and Gam and years of training. Statisticai significance was daaminsd as pups, aU grwpa wac simiiar in age. Significant differemes in body mus war found betwcm BB and ER comparai to HS or PA. As wodd be expcçtcd ER had a Iowa body mass than ail otha groups, while PA wae talla than aii otha groups. The .mats which apck and field athtetts consdacd th& prirmry wents are alsa W.

Table 4.2 is a training sumnmry of the pthlete groups. AU athletes utüized a periodized training progrm. Each athlett was asked to report typid training pa#erns ow the put yar. Nme of the athletes indicatdd a ïapse in trainhg aii Y==- AUPthlae~ejrceptfafive~ersppitici~in~stancetrainiagonarrgulPr basis. Thcsix~whodidpatticipatcinIGSiStaLIatrainingrcporicdthat &tance training wu newundertab#i duhg cornpetitive pbasesof th& training. In addition, the nmnas did not tmd to participate in additionai anobic dvitics.

PA on the otha hand tended to participate in O variety of di&tat dcactivitics.

Tabk 4.1.1 Sobjccr 0 œ Values art means * SEM

n

Age (Y==)

--y-@@

Height (cm)

Cornpetitive Event

a-pC0.m (VS. HS), b=p<0.05 (vs. ER), c=p

While PA pdcipated in an extcaSive NMing prognm, aait of it mu aduranœ oriented. The Arrathlats trainal the slme way as the jumpers, but taadal to spmd more total timc training whai caiculatad on a wœkly basis. Table 4.1.2 Training Pattern Summary Values are means & SEM

Years of Training 9.1 f 1.6

Running 1111 1 11/11 117 Mean Volume = 85 kmlwk High Intensity Intermittent (40m - 10-15 min Intermittent and Continuous 300m) IContinwnis (warm-up only) Continuous for warm-up 5-7 dlwk 4-5 d/wk 2 d/wk

Ot her Aerobic Cycling - 31 1 1 Pool Running - 21 1 1 Cycling - 717 ~ctivities Pm1 Running - 11 1 1 Cycling - Ili 1 Stairmaster - 117 Swimming - III I Basketball - 31 1 1 1 5-Omin Basketbalt - 111 1 Wrestling - 11 1 1 **always asy** Hockey - 11 1 1 Bobsledding - 11 1 1

Resistance Training 61 1 1 1111 1 717 10-15 W~S 1-10 reps 6-10 nps 1-3 sets 2-6 sets 3-5 sets lexercise 2-3 d/wk 154hrs /session 2-4 txacises /muscle 0.5 -2 hr /session 2-6 d/wk 1-3hr /session (+ extensive plyometrics) 4-7 dlwk Tables containhg heart rate and blood pmmmc daîa at rest, pst submaximal exefcist, and post mrxirml ischemic caifcrgomety can k fodin the appendices. Post submaximaZ measmes were made 2 t~ 32 samds foilowing caif ergomctry withamsusaf~aadahpCtitionnttof60paminu~.Pdst~~ were made 5 ta 35 seconds foiiowing calf ergometry with a 10kg mass and a seif dcttrminad rcpcfition rate, kmhîaî by volitionai îkîiguc.

At nst, tbcn was a tendeacy for ail pups ta show a higha systolic and a lower diastolic blwâ press- than the l2Ommag and 80mmHg normally expectcd for this ag= grow HS tcnded to have the highest mean arterial blood pressure dues and BB the lowest. Body buiîders tendeci to bave a lower mean nrtmal pnsain although this différence was found not to be significant (figure4.2.2). Signifiant diff;crtnces were observai f;ar kart rate bdwem ER and aii other groups (p <0.01), which is amsistent with their high volume of chrcmic a~durancetraining (figure 4.2.1). ERM a significantlylowcrheprtaitethan aU ahagroups @<0.01). HS tmded to hvethe highest mean Paerinl prcsswc. In ccmbast, BB exhibitcd the lowest MAP.

While ER demonstrated a lowa haut rate than ail otba groups, the differetlces were not Statisticaily -tt BB had a lower MAP following the .raaximal ischemic calfcrgomcûy protoc01 @<0.05) whm wmpnrrd to each of PA,ER and &S. The MAP among PA, ER, and HS wu very mnnlY (figure 4.2.2).

4.3 Maximai Aerobic Power

Accordhg to the criteria, aU subjects demOIISfrafbd a maximum eff- Table 4.3.1 depicts the data obtained from the VCQmax testing. A signifïcant diffcltllœ @<0.001)was found hemHS and ER in aôsuîute vg~max(i.e. IXII min-1). WheaV~max,wp~txpressedptfalogrambodymass,ERwosfo~tobe oignificantly diffc~clltfrom aU other groups (p <0.0001). Nane of the other groups were found to be signXcantly dinkmt hmeach other. Maximrl hcart nta at VOpax wae not mcordd for BB duc to tachnid difficulties with the heart ratc monitor. ER and PA showed 1- haut rates at V@max thn HS @

Figure 4.2.1 30 Second Average Heart Rate Following Calf Ergomety a=p4.05 (vs. HS). b-pcû.05 (vs. ER). c-pQ.05 (vs. PA) 130.00 -

120.00 --

A 2 110.m --

V1 P -e looao -- -gt: 4 r ,U9 90.00 --

80.00 --

I Rcs t Submûx Max

Figure 4.2.2 30 Second Average Mean Arterial Pressure Following Cal f Ergomety @.O5 (vs. HS), -.OS (vs. ER). tqAI.05 (vs. PA) Tabk 4.3.1 Maximal Oxygen Consumption Test Results Values are means f SEM

n 8 1 I 11 7

V@ (ml (min)-') 3531 & 173 4606f 98. 4061 f226 3971,f 233

V02 (ml (kg min)-1) 45.151 1.86 71.04f 1.W 50.741 1 .57b 44.7313.24b

HR @ min) 192f 2 18312a l85f 1.a NIA

RER (VC% / V*) 1.263 f0.020 1.15 1 &o.025a 1 .220*0.018Y 1.126f 0.010" a=p

Tables amtaining blood flow and amductance measmes at mit, and following both submaamal and maximai ischemic caif ergometq can be found in ihe appendices.

4.4.1 RdngBbod Flow and Vascular Condudance

Figures 4.4.1 and 4.4.3 depict resthg blood flow and vascuiar conductance observations at nst. BB bd a signifïcandy higba blood fiow (4.7f 0.41 ml (min 100 ml)-1) than HS (3.6f 0.24 ml (min 100 ml)-1,p

Submnrrimal blood flow and Msnilar ductance wae not signiticantly dinhent between groups- 4.4 Bboa Flow and VeConductance in Response to MrmimPl

Figuns 4.4.2 and 4.4.4 dcpict bloal flow and vascular conductance observaîicms foiiOWlIlg maximai iscbemic alf ergometq. ESexhibitai the lowest values foi maximai blood flow (54.5k3.00 ml (min 100 ml)-1) and Gmvr (0.456*0.022 ml (min 100 mi mm~~n')mm~~n')l).ER hPd a sipnifiic.antly hi* m+ximol blood flow (87.1 IS.28 ml (min 100 ml)-1, p~0.001)and Gmax (0.721 f0.û38 ml (min 1ûO mi mmHg)'l, pCO.OOO1) than HS, lad PA (68.5i3.90 ml (min 100 ml)-1 and 0.570&0.034 ml (min 100 ml mmHg)-1 rtspectively, p<0.05). PA had a sigdïcantiy higher Gmax than BS @ < O.û!j). BI3 hd a sisaificantly bighcr maximai blood fiow (89.1k6.49 ml (min 100 ml)-1, p

4.4.4 RcstiDJ Vssciilnr Conductance and Miubd Vlise9lsr Conductance

Linear rrgreJsion analysis revealexi a strong relPtmohip in BB betwcm vascuiar conductance and Gmax (rz0.94, p <0.m) (Fig. 4.4.6). as well as betwan resting BFiesr and BFmax (Fig. 4.4.7). Tbac was no relationslip betweer~ resting Msaila coadudsulce and Gmax, or BFrest and BFmax in Qther the HS, PA, or ER (Fig. 4.4.5, Fig. 4.4.6, and Fig. 4.4.7).

abc

Rgure 4.4.3 Figure 4.4.4 Vascular Conductance at Rest Maximal Vascula r Conductance a=pa.05 (vs. HS), b=p9.05 (W. ER), c=p

Figure 4.4.5 Grna.\- vs. Grest in Elite Runners and Power Athletes Figure 4.4.6 Gmax vs. Grest in Body Buüders and Heaithy Sedentory Subjeds Figure 4.4.7 BFmax vs. BFrest in Body Buiidcrs and Healthy Sedentary Subjcds

4.5 Vascuiar Condudance vs. Aerobic hwer

Figure 4.5.1 depiao the nhtiOIlShig kov&n maximal blood flow adVopax. Inter-group anaiysis mealed a non-s@Mbnt rclationship. The relatianship betweai Gmpx and VOpax was dightly strongu, but was also not sigdficazlt (figure 4.5.2). However, a strong positive lin- tclatiodipktwcm V@rnax and Gmax was found (r=O.W. p <0.0001) wben the non-res&mœ traincd proupr wac analy=f scpaately- One BB subject had a Vûpax value of 58.3 mi (min kg)-l which is over 30% higher than the mean for BB. A strong negative rclatianship was fomd behukn Vamax and Gmax (r=-0.88, ~~0.03)within the BB group whn bisone outlia was removed (n =6). 60 80 100

BFmu (mi (100ml min)")

Maximai Blood Fiow and MaximaJ Oxygen Consunption - a SED a ER PA BB

Figure 4.5.2 Gmpx and Maximal Oxygen Cansumption The matjor -8s of this pmject are: 1. Blood pressure at rest, and in responst U, submiuimal and maximai caif crgomctry, was lesJ pronOUMXd in body buildm than in powa athletes, &te ru~ers,and halthy ScAcntary subjects. 2, Maximal acrobic pwer in &te runners was sigdicantly highcr than in the healthy seda~taryor rcsistance traincd groups. None of the 0th- thrœ &roups were dinmt fiom each other. 3. Rcsting wnilar conductance wu greata in body buiiders than in any of the other groups, none of which wae di&rent from each otba. 4. Maximai Msailar conductance was greater in body builders and &te rumas üian in power athfctes or haltby sechtary subjccts. Power athlctes had a gr*rter maximal vascuiar amductancc than hcalthy saientaq subjects. 5. According to the established reiatiollshjg betweea VOpax and Gmax, dite mers hd a higha VOzmax than wouid have bœn prrdicttd by Gmax. Convasiy, body buildas hrd a lower VOpax than wouid have prcdictad by Gnru. As can bc secn in table 4.1.2, the athlete groups studicd were distinct in how tbey traincd for their sport. The powia group, amîsthg of tmck and field jumpas and decatthletcs, wcre chosen because of the high priority they phcc on fitncss @ersonal comspondace witn th UnlvCfSity of Toronto Jumps carh: Car1 Georgevshi. These athletts Wypresent a ôctter model for a UUdiovascuîar study than tboae

athktcs usually ustd to rrpre~cnta power traincd musde, such as tbwers and Olympic and power liRm. Such athletes are not ccmcerned about propdbg thir own body wught, and thdbre arc les amœmed about maintainhg a low fit body mass and overail fitaess. Fuahermaore, in the powu puputilized in this study, the volume of supplemmtary aerobic dvity and running, albeit mortly short distrace, cmtrasts well with the body bdders who avoided such activities. Thcrefm, any aerobic adaptations seen in the body buiiders which arc gxeater tban those seen in the powcr grwp wuid be attributcd dirstly to the mode of rtsistance aPining employed. The modes of rtsistance trPining cmployed are markeûiy different betwcm the

two resistuice traUied groups. Although the volume of trpiaing was not quantined, table 4.1.2 clcarly shows that a much larger number of repetitions arc @O& by Mybuiiders than by power athietcs. The total time spcnt resistana training was

zmÜnr in the two groups. Additional kg work was &me by the powa atmhietes through p1yon;etric training. Most shdies bave rbown thpt highly Wgth traincd aîbietes arhibit average or lowa than average systolic and diastolic blood pressure (meck, 1988; Fkck et ai., 1989; Goldberg, 1989; Stone a al., 1990). Training studies bave supported this obscmaîîon as a trainkg adqtaticm (Fkk, 1988; Goldbag, 1989; Stone et al., 1991). This study has shown a consirtcnt mdaicy towafd a Iower blood pressure both at rest and in mpomc to caif egometry in the bodybuilders maiparcd to any of the otha groups. This tcadency was mgest foliowing rmxirml ischernic calf ergometry (figure 4.2.3). In net, the in- in man iutezhl pressure in the body builders (fiom 82.7i2.7 mmHg to 103.3*4.5 mmEIg) was Only 20.6k3.6 xmnHg. Powa athlaes, on the derhami, exhi'bitad an incrca~ehm 88.6k2.6 mxnHg to 1l8.9*2.8 mmEg, an in- of 30.3k2.7 mmtig. The similar response of mean aaaial pressure to the maximai calf ex- protocol among healthy seden-, &te runners, and powa athietes dewnstratcs a prryor nsponse which b different hm that of the body builders, and suggcsts that bodybuilding training results in alterations in the pressor nspoase to such exaeise. These hdings support those of Fleck and Dean (1987) in which lower priwsor re.sjKmses were ckmonstrated by bodybuilciers during exaçiccs cdsting of dumb-bell ov&ead press and one legged knee extension than was sœn in untrainad amtrols or in novice mgth trained subjacts. A duced mean arterhi presstue, espcaplly if acheived primady through changes in diastolic blood prrsure, wouid iadicaîe a daxeasd rislr of pmaae induccd carâïac h-y. Indeai, the edarged lefk ventricular mess sscn in bodybuiiders is due not only to an in- in diastolic posterior left ventticular Wall thickness (PWI'd) and intraventriiailnr septum waU thickncss @VSd), as in pomr athletes, but plso beCglLIt of an increasad chamber size @eligipimi9 et al., 1988). Unfiy,intkpresatstudytbeworkdoaeduxingtaemaximaiaCaCiSC bout was not quantifiecl, and tbenefozt, the catcgorical nature of the worldopdr dots not aliow for a statisticai YialytU krweai groups. indecd Tesch (1992) showad tint during gndcd cyde ergometry, balybuilders have a lower heut rate and systolic blood prrssure for pny given workioad whm coqmecl to studmts (Tesch, 1992). Because the submaximal workïnaAs wae -, th& finding mry be explaineci by a lowcr relative worklad in the bodybuilder grnup. Straiga muscle fibrs wouîd ritsult in a lower portion of those fibas (tbcrefozt, a lower number of motor units) Mgin oida to producc a ghm amount of force. This would Wy trigger a lower pressor rwpoasc than in subjects with walpt nkrs.

Thae are two rrpsoiu thpt it is unïikciy that a Iowa relative workld is tbe cause of the obsc~edlowa pressor respoase in th body buüders in this study. Fintlyy it ca~be anecdotally repoasd that during the maximai ischemic protoco1, mon work was &ne by the body buiiders thaa any othr graip. since more rrsstive weïght was quired to fabigue those suôjccts Mthin a reasonable the. Secondly, ach subject continued until volitionai Eitigue, thercfm providing a maximai effort immediately prier to the donof crgometry. The rtsufts are ntco supportai by &ers who found a RPP following sûmgth training in prcviously untrauied coiïege aged mala (Stone et pl., 1991), indidg a possible hypotauive effect of rtsistance training. VOrm fdin the heaithy lQcACntary group (45.2k1.86 ml (min kg)-l) was within the range ucpcctd as fouad by ocbas (48f 8 ml (min kg)-l)(~hephud, 1992). Thev~~tsfort&~tcmnnasandpowaPthletwverePlsou expacd. As was extensively outiincd in Section 2.1, it was expctrd that dite

middle distance ~UMCIS wddhave O much bigha VOpax than aU otha groupa. Therefbrc, the rcsult of 71 ml (min kg)-1 compares well to the nnge outlined in the fiterature fot such athldcs (7&75 ml (min kg)-l) (N',1988). The powa athletes' value of 50.7*1.57 mi (min kg)-l compares well to the nnge found in the iikzatqc for powcr track and fieid athlctes (4û-52 ml (min kg)-1 for sprinters, 50-55 mi (min kg)-l for long jumpcrs, and 6065 ml (min kg)-1 for multi-evcnt aîhietes) (Newnann, 1988). The VOpax found in th body buiidcrs in this shdy is slightïy lower than wodd have ban expsdcd hm the literaturc (44.7k3.7 mi (min kg)-1 in this study cornparal to 51 ml (min kg)-1 found Haldrinen and coiitaguts (1984). A possible explanation for this différence is that the body builders in this study wac al1 in the prepPratory phase (buiid-up) puid of training and wae concemeci only with building m-ucle mars and not a low body fu. niey thacfore tended to have a relativdy (to cornpetitive season) high fkt weight. 5.5 Vascular Conductance

There are five potential sources of emx with the data aquisition system useû to qantifaîe icstllig aud pst exdsebld flm 1. fitruigofthesh.ainpuige~oundtûecaif 2. assumption that thc caL€ is cyhdricai 3. tempcmhm smsitivity of the strain gauge 4 varying iimb cornpartment slle 5. finapress mcmitor 6. unbllinded expaimcntcr

1. The sepin gauge must be appiied with a slight (approximately 5-15 gnm) stnetch so as to aisure contact with the appendage. This stretch ans applid and fidi contact was always acheived. FuRhermore, the gauge tubing laigth shouid be matched as cldy as possible to the caif gUtli. Shce caif gUths vary amoung individuais, a systematïc arm may exist. Calf girths hmthis study are supplied in appendix 8. 2. In a cylinder, the cross-section is uniformly circular. Theriefort, any change in the ciK:umf~aiœis directiy piooortional to the change in cylinder volume. Tberfbxe, the theory of strain muge plethsmography is dependent on the assumption that the caif is a cyfiadcr (Sumner, 1985). Any change in saain gauge rtSiStanœ (circumferaice of the cplf) is dirr*ly pmpoitid to the cbange in volume, providd that the CirCWIlfercllce of the Iunb is the stme as the length of the rtrain gauge. Tbecrou~~~~afthealfmnynatbe~yarmly,~~~it,adirrct rciationship must involve a systemptic emx depadiag cm the deviatïcm in sbPp hmtbat of a cylinder. 3. The gaîiium indium in Nbkr strain gaugc has a slight omiperature SCDSiîiviîy of 0.056% pcr OC (Hokamon et ai., 1975). This means tbot an incrcPse in temperame of 10 OC would rwult in a enor 0.56%. Tbc tcrnpemture in the was moaiiorcd and rmiPiasd at 19-21 OC. Inaaucs in ane temperature wexe iikely minimal due to the smaü muode nature of the exefcisc, the short duration of the exgcist, and the rest intend between the exercise bouts. Any &in tcmperanire effkcts on the stmh gauge wme mraimiIsd.. . duc to the low tempcaaut smsitivity of the gallium indium straïn gauge usai. 4. The calf cornpartment sire may change with the unequai expansion of dinacat perts of the caif. The skin ovcriying the muscuhr cornpartment of the caif will obviously atp~admore thPn the skin overlying the tibia. It has bœn found that unequai expansion of tlie limb does not effs* the accuracy of the resuits (Sumner, 1985). 5. A potenfiai ineccurpcy in the blood pressure mcasuremat using the Fia4prrsr monitor. The fhgatip b an extrcmity and is useâ in rcsistanœ training. Subjects werc acclimated, and rom tempeaatwt was coosistent, therefiwc tempaoture was an unülPly source of mer. The thickness of the skin may Plso contribute to mor in blocxi pressam measurement. nie mistance traincd trained groups in Pyricular may have bai thickcr skïn due to tbe havy work done woth dieir hanch. Finger tip skin thichess was not mcasud. The hand was held in a rtlaxd manncr at the level of îhe heart in order to aisure no variana in elevation or intia-muscular P- P- 6. In the present study, the expimenter wu unbhded when blood fbw analysis was performed. Therefore, the posibiiity exists that data aquisition and analysis was biased despite the best efforts of the experimenter. Strict attention to the measuremeni criteria was used when determinhg the dope selection.

One surprising and signifiant finding of this study was that of a significantly @ <0.001) higher resting ~xularconductance in the body builden compared to al1 other groups,

5.5.3 Respoose to Submaximal Caîf Ergornetry

The submaximal exercise load did not reveal any significant differences between groups. There are two possible reasons for these findings:

1. Precise control of the workload was not possible, as some individuals exhibited difficulty in maintainhg the steady rhythmic contraction Frequency set by the metronome. Furthemore, despite Our criteria of a 15cm deflection of the load, some subjects exceedeû this criteria by a greater or lesser degree. Combined with the expected intersubject variabiiity, and a srna11 but fmite, variation from data analysis, ail groups exhibitexi a high standard deviation in blood flow and conductance. 2- Post exercise blood fIow data is Wrely dependent on more than the supply of oxygen; other local vaso-regulatory factors, such as the clearance of rnetabolic waste, arc also of imporÉance. It may be upctai that any training inddœîlular i.mpmvemaits in musde functicm wouid ieaùt in a decnaJcd submaximaï blood flow. However, such adaptations may be achievcd umcomittent with an improvement in the nisodibtory rrspoast to exetcise. Such changes wouM not k mrealed with the methods employcd in this shdy. An cxamination of the pmccsses involved in rrcovery hm such suômaxirml aracise bouts would have to be necessarymdistinguishbdween~possibilities.

Maximû vasailu cmàuctance was signincantly highcr in the elite mers cornparrd to the powa athlctcs and heaithy SriACntary subjects (dite runncrs vs heaithy sedentary; p~0.0001,dite mers vs power athletes, p

training program. Additioaally, becpus these nthlcta trPin primPrily for jumping powa, and thezefare prfm extensive Myataciscs involving the caif, it was arpded that some enhmccment of caif musdc functim would be rrflectd in the

@phetal blood flow rncpsiirrs. 1t was theref-, not sinparing tbat the power athletes hacl a siBnificantly hi* maximal vascuk conducfance than the healthy sdentaq Jubjects @<0.05), and cxhibitad a tmdary fm a àighcr blood flow (68.5I3.9 vs 54.5f 3.0). Despite almost identical blood flows (87.1 k5.3 for the dite nmnas vs 89.1 f6.5 for the body buiidcrs), the body builders exh'bitaï a hi* (ah not Pignificant) conductance (0.72*0.04 for the &te runaers vs O.8lf 0.05 far the body buil-). In this study, a rather limited sample (n=7) of body builclers was cvalultevl, and themforc, it is possible that a lpga numk of subjccts might bave yicldad a signifiant differcllce.. Furthermm, thrœ of the =en body buildcr abjects wae level VIi cornpetitors (Le. municipaVregional), and theref-, had a avely shorter training history. Interestingïy, these subjects plso exhibitecl the lowest maximai vascuiar amductana vaiucs. Figure 4.4.8 clcarly shows tbat a Jtrong iinear nlationship (r=O.ûû) allsts bawcen the number of years of eaining and maximal vascuiar conductance. nie relatidp b&mm the ycars of expeRmce and Gmax demonstrates an rrecnciatitm betweai traini~gand Gmax among the body buiiders, but not the dite ninaa~(figure 4.4.9). This indi- thrt if a structurai enlargemmt of arteriok structure crn occur in responte to training, then it would more Wrely bc reflected in body buildcrs with a long training history. 5.6 The Possibüity of a Strudud Increase in the C~16s-Sediod Area of the Arterioiar Bed

5.6.1 The Conductance - Mean Arterid Pressure Relationship

In the body builciers examined in this study, thcrc was a tendenq for lower blood pressures at rest. Previousiy, low levels of resting bld pressure have kai reported ammg strength train& individuah. Possible explanations off- include a decre. body fat, a decnased level of body salt, and aiterations in the sympathoadrenai drive (Fieck, 1988; Goldberg, 1989; Stone et al., 1991). This study provides data on biood pressure at r#t and foilowing both submaximaî and maximal exercise of a srnaIl muscle rnass, as weli as corresponding vascular conductance data. Perhaps an aitemative intcrpretation for the lower blood pressure seen in the body builders can be used to interpret the observations in the cuntnt investigation.

Vanhees et al. (1992) found a deçreased arm musck blood flow (resting brachial artery blood flow), despite an unchanged cardiac output, after running and cychg endurance training in previously untrained subjects. In addition, an earlier investigation nported a 36% higha resting blwd flow @ t0.001) in the brachial eryof wheel chair confinexi paraplegics compareü to age matched able bodied controls (Shenberger et al., 1990). Furthennore, an increaSeC resting muscle blood flow, perticularly in the fist twitch red muscle fibers, has beai found in rats following training (Armstrong and LaugM, 19W). Therefore, it would seem possible that aAa training, cardiac output at rest may k rrdistributed in fivour of the trained muscle tissues. Since bodybuilding involves a concerted effort to develop aii skektal muscles, it rnay be pumd that thac would be a hyperkinetic blood flow at rest to all muscle tissues, potentially dting in an elevated cardiac output. Although cardiac output was not measurai in the prrsait study, it has been shown both in literature cited above and through the obsc~eddata on the resting heart rate of the baiy buikks in this study, that it is unIilrelly that carâiac output in- by an order of 36%. Vanhees et al. (1992) did rmt pmsent a hypothesis for the mechaniSm involved in the redistribution of cardiac output. One possible answer lies with the sympathetic nenrous system. Although it is clcar tbat physicai training dccmws sympathetic activity in hypertensive subjects mji, 1992), many siudies have show an increase in resting epinephrine levels of hdthy subjects foiiowing physical training (Kjacr et ai., 1984; Uhmann et al., 1984; Kjacr et al., 1985; Svaidahag et al., 1985). Additionally, end organs have spscinc independerit thresholds for responsc to circulating hormones flnjii, 1992). In the unique case of body builders, an increase in sympathetic tone thughout the body may act as a balance to an increased structural size of the artenolar beû in trained muscle in an attempt to maintain TPR at constant levels, with cardiac output rernaining at near normal levels. One major implication d this theq is that nsting blood flow may be in excess of metabolic demands. Such a situation is plausible considering vasornotion, which ailows for more or les bld flow, depmding not only on demand, but also supply . The lower blood pressure may refiect a pncticai compromise in bodybuiiders between further increases in sympathetic tom and increases in the fiindonai site of peripheral skeletal arttrioks at rest. In the face of a raiucd TPR, a decrmst in mean arterial pressure would maintah catdiac output according to Ohm's Law. Consistent with this premise, a signifïcantiy higher vascular conductance was seen at rest in the body buiïders compared to the other groups @<0.001). The three otha groups were not dB-t fkom each otha. The fkct that body builders train aïi muscle groups equally suggests that the vascuiar amductana measd in the calf is probably representative of the other muscle tissues in this subject group. Furthermore, the body buiiders did not participate in an extensive aaabic conditioning program which cbuld otherwise have been implicated in an increascd calf muscle vascular conductance relative to tk other muscles. Arteriolar neoformation has been well documented in.animals (Hudlicka et al., 1992), so it scans likely that it could occur in humans as weiï. The possibility that an increased arteriolar stnicture is rcsponsible for a decreased resting TPR in body builders is indirectly supported by the findings of Egan et al. (1987), who implicated structural changes in the arterioles as the teason for an increasui vascular rieactivity in @y hypertensive individuais. It was found th nonnotensives and hypertensives required the same amount of an intra-arterial infusion of norepinephrine to &tain a 30% increase in f0r"arm vascuiar resistance, indicating that p-receptor sensitivity was not different between the two groups. Greater resistmce at maximum vascu1a.r contraction was aiso seen in the hypertensive subjects despite no difference in p-receptor scnsitivity. The authors spéculateci that this was probably due to a smailer vascular lumai prior to the vasoconstrictive intervention. Ba& on this evidence, it could be hypothesited that a hypotensive effect would be seen in subjects with a very large artezioiar structure, assuming p receptor sensitivity was not significantly modifieci. Therefore, a decrrascd blood pressure could also reflet a larger arterioiar bed hespective of changes in sympathetic stimulation. The present study corroborates Reading et al. (1993) and Snell et al. (1987) in that a higher Gmax and V02rnax was observed in the elite runners than in healthy sedentary subjects, in the presence of simüar blood pre~surr~.However, the body buiiders exhibited a G max quai to that of the dite runners, with no positive correlation to VOpax, and a lower mean vtaial pressure responr io maximal ischemic caif ergomary. This suggcsts tbat a structural increase in the crw sectional Sue of the arteziolar bed is an adaptation to cbnic bodybuilding training. Since the tendency for hubulant blood flow increases in direct proportion to the velocity of flow, as weil as the sire of the vessel, a structurai adaptation may k preferential to a fhctional one in response to training stimuli. In other words, if maximal or near maximai blood flow is reguiarly elicited, it may well be advantagrnus to have a mer number of v&s available than to have fewer vessels regularly diiated to a maximal diameter.

The stnrcural versus functional adaptive response in the arterioiar bed is not neccessarily the mein elite runnm as found in the body bdders. Although several adaptive responses within and between muscle fibers are of a similar nature, others are dinerent as evidenced by the hding of a similar Vqmubetween body builders and healthy sederitary subjects. Intaestingly, a study which examined muscle blood flow in the rat during different spe& of running concludeci that the increase in muscle blood flow during exercise was diiectly reiated to the extuit of the fast oxidative glycoIytic fiber population rccruited (Laughlin and Armstrong, 1982). Furthemore, the smng positive linear relatimship ôetween yanof aining and Gmax indicates that improvements in Gmax are a stinig adaptive repense specific to bodybuilding. There are major diffhnces in the trainhg stimuli involveci in running and body building. Baseci on the fïndings of Walloe and Wesche (1988), that the rate of blood fiow is proportional to the foroe of contraction, it is possible that during body building, which typicaily utilizes a set of ten to f%œn repe!itions to muscle Mure, maximal flows are eiiicited, whereas they arc not during running. Furthamon, during a typicai training set, the body buiiders do not allow the muscle to relax between the eccentric and concentric phases thereby crcating an ischemic intra- muscular environmait Such stimulation is Waly to elicit a sïgnificant eve hyperemia post exacir. This is intuitive in that body builders rely on 'pumping up" through the use of such ischemic sets immediately priot to posing in trainhg or in cornpetition. On the other hand, during nmning the force exencd in each contraction is likely below the level achieved during body building, and therefoie, in response ta running training, there rnay be a functionai optimization within the structurai limitations. Finally, evidence for structurai changes in the arterioles of bodybuildm is given in the strong linear rehtionship (rz0.94, pC0.002) found between Grnax and Grest (Fig. 4.4.6). Within the otha groups, no signifïcant relationship was exhibitai (Fig . 4.4.5). In order to exunine the possibility thu this reiationship rnay just be a reflection of the man ar

Figure 4.5.2 depicts the relaiicmship between V02max and Gmax in all groups. It cari be seen that the rclationship within the body buiiders graup is quite différent than that secn within the other groups. In faa, a signifiant negative reiationship (r--0.88, p<0.03) wu found between V@max and G max when one subject with an exceptidy high VOpax was exciuded; this is pmbably the duea result of an increased muscle rnass with incdyears of training and performance level. The muscle mass hcrcase of the body builden was disproportionately in upper body muscles, and therefoic, lihly resulted in the lower VO;?rnax (exprrsscd relative to body mass). An alternative interpretation is that the body builders have a lower extraction of oxygen relative to Grnax, than any 0thgroup. The dissociation of V@max and Gmax in the body builders compareci to the healthy sedentary 's and elite rumen as illustrateci in figure 4.5 .2 clearly shows that the body buiiders are differerit hmthe other groups, including the power auiletes. They tend to have a lower Vmrnax than would be predicted hmtheh Gmax. Based on this finding, it may k concludeci that Gmax can be incdwithout a sirnultanmus increasc in V-ma. Figure 5.6.1 illustrates that acmss a wide specttmm of endurance fitness, when body builders, elite mers, and heart Mure subjects are excluded, a linear relationship exists between VOpax and Gmu (r=0.86, p < 0.000 1). The data for the healthy sedenmy subjects hm the present study fit very weU with the prediction equation derived hmthe other pups. It is interesthg to note that the data hmthe power athletes also fit very weii to the prediction equation, despite the extensive training program these subjects have participated in over several yeus. The three groups which deviated from the trendline wmthe elite ru~ers,the body builden, and the heart fhiiure patients in the Jtudy by Reading (1990). Reading attributed the dewiatim from the line in the hcart fidure subjects to a cardiac limitation to VOymax. This is an uniiicely explanation for the body buiiders. It is more likely that the body buiïders bave a pana extraction of oxygai for a givai Gmax, and therefore, att unable to acirieve the predicted Vamax, On the otherhand, the elite mers in the priesent study waindeed elite relative to the endurance trained subjects uosd in bodi Reading (1990) or SneU (19û7) snadies. Therefore, it is quite possibie that these subjects fâii above the prediction equation because they are able to extract more oxygen for a given Gmax. 0.2 0.4 0.6 0.8 1.O Gmax (ml (100ml mmHg minrl)

Figure 5.6.1 Relationship betweeii maximol vasculor conduct~nceand maximal rerobic powcr. JRs Reading1Q90; PS=SnelCe+.lT1 98% JR-€HF~~~aiiurc,Radin6 1998; nSP treafthy sedentary, for the cumtinvestigation. The line indicates the best fit for the &ta of Snell et al. (1987) and Reading (1990). Conclusions

The first hypothesis of this study was accepted:

1. Body builders demonstrated a higher maximal vascular conductance and lower blood pressme than power athletes, &te runners, and healthy sedmîary subjects in response to maximal caif ergometry. Additionally, body builders demonstrated a higher peripherai varular conductance at rest than &te mers, powa athletes, and healthy oedentary subjects.

The second hypothesis of this study was also accepte&

2. Elite mers demonstrated a higher maximal oxygen consumption, and body buiiders demonstrated a lower mwmal oxygen umswnption than would predicted by maximai vascula. conductance by the relationhip established by healthy sedentary and endurance trained individuals-

In conclusion, the fïndings of a very high maximal vascular conductance in conjunction with a Iowa mean arterial pressure in body builders, indicates a hemodynarnic adaptation qualitatively similu to that observeci with chronic endurance training. The type of mistance training employeü by body buiiders may elicit vascular adaptations which are quite différent hmthe traditional resistance training methods employed by body builders. Future dstana training studies examining the training adaptations in muscle, and cardiovascuhr responses to exercix, wiü have to rt-evaluate the rc9stanœ training mcthod employai. .. The data hmthe dite mers bas shown an opWuaiion of oxygai extraction for a given maximai vascuiar conductance. The body builder data has show a poorer extraction of oxygni for a given maximal vascular conductance. This is

evidence of a central limitation to maximal actobic power in this group. In cantrast to the body bdders. the power athlefe data suggests that the type of training they employ has not dissociatecl the relationship bttween mPumal oxygen consumption and maximal vascular conductance. Recaiiing the the association of total pedpheral rrsis*iace and maximal oxygen consumption show by Clausen (1976). combined with the data fian this study and the work of Reading (1992) and Snell (1987), it can k ponilated that the size of the arteriolar structures within active musde tissues influences total peripheral fcsistance even though maximal blood flow rates within those active muscles are probably not achieved during maximal or ncar maximal oxygen cbnsumption (Anderson and S~M, 1985). This suggests an alternative interpetatition of the signifïcance of maximal vascuiar condutance. PerIiaps during maximal or near maximal whole bdy exercise, a higher maximal conductance aiiows for a greater blood flow prïo~ to an elevation of systernic bldpressure. Remmendations for Future Rese9ilch

Due to the ktthat this study WPS cross-sectional by design, direct proof of a structurai enlargement of the arterioIar bed should k the main obje~tiveof future sîudies. The cardiOreSpiratOry and catdiowscuk adaptations muking from body building, power naining and high htcnsity endmance ninning were examined in subjects who had participated in spcitic extensive trainhg piognuns ova a phod of years. This study clearly demonstrates a necd for a longitudinal exetcise naining study involving various groups utiiizîng the two distinctive types of resistanœ training. Previous studies which attempted to detemine whether rrsistance mg alone could increase VOpax may have Wed buse they did not use the bodybuilding method of resïstance training. Venous occlusion plethsmogrpphy should be utilucd in wnjunction with the skeletal muscle biopsy technique to examine the structurai changes in the Sre of the arteriolar bed. Since the elite ru~ersexhibited both a high blood flow and a larger Gmax compaRd to the heaithy sedentary subjats, it may weii be that Gmax plays a role in the improvements seen in Vopax. Therefore, further studies on Gmax and its role as a possible predïctor of the microcirculatory -se to endurance trainiag should be wnducted. Further resistance training studies should be conducted to examine the various strength training methodc, since the adaptive rr~ponsescan k dramatically different. Abraham W.M. Factors in deiayed musck SOZCLI~SS. Md Ski. Sports. 9: 11-20, 1977.

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University of Toronto

OFFICE OF RESEARCH SWVlCES

P~O~WOV~~b y ~çvicw cornmm on the Use of HU~L-

Principal ln~e~gator : Dr. J. Goodman. Physical and Health Education

Tide : Peripheral Blood flow and Maximum Oxygen Consumption in Elite body Builders, EIite Oistance Runners, and Healthy Sedentary Subjects

Review Cornmittee : Dr. SI Thomas. Rehabilitation Medicine Dr. R. Goode. Phytical and health Education Professor R Hewitt, Religious Studies

Oocumenu Subrnined to Review Cornmittee : Study oudine. consent form

Subjects : Eiite iunners. alite bodybuilders, and age matched healthy sedentary subjects

Procedures : As descriïed in the anached consent form

Method for Obmining Consent : Consent forrn as anachad. Subjects are to be given a copy of the form to keep.

Remarks

Date of Approval : May 3. 1993

*During oie course of the research. any significant deviations from the rpproved protocol andfor any unanticipatad devaiopmenfs within the rssearch stiould be brought to aie anention of the Office of Reisaarch Services.

cc: Review Comminee Professor 8. Kidd Susan Pilon Executive Officer Human Subjects Review Cornmittee APPENDIX 2

lnformed Consent

Sthod of Physical and Heatth Education University of Toronto Lowtt Lcg Musde Maximal Conductance and Muimat Oqsen t'pmkc in EIite Runaers, Eiïtt Body Buiidus. and Heaithy Sedeataq Subjectr

Sipa:~ Date: APPENDIX 3

Performance and Training D4t~Questionaire

b Physical Data 1 Weight: Date d -lu of most rrrrnt Body Composition Tan:

I Heighc Date urd rcsulu of m~trecent Extrcis Tests:

rn L Best Achievcments During the Past Twelve Months 1

1

Plme Describe Your Training: Hovr -y yars imve pu bsm training for pur sport?

kiswtr the follo~ingwith regards io running Ovuthe pSowrlve e. How anay dip per wdc? How -y houn per &y? Howr much volume?

Dacr your program inel& my lJJitiana1 wtivitia (cg. cyding or swimmïng? If ycs. plme &rtrik: Table 4 IIeart Rate and Blood Pressure (30 sec Average) Values are means f SEM

At Rest Hart Rate (b min- 1) 6713~ 501:3ac 72k3 66f 3 MAP (mmHg) 95.1 k4.6 90.7I2.1 88.6I2.6 82.7I2.7

1;ollowing Submaximal Cal f Ergometry Heart Rate (b niin- 1) 74k 1.9 . 59f 2.7ac 72 f2.9 75 *4.9b MAP (mmHg) 101.413.7 99.6I3.0 99.3I3.8 88.2I3.6

Follow ing Maximal Cal f Ergomet ry Hart Rate @ min-1) 81.3f 2.0 67.4f 4.0 74.8k4.2 77.6f 4.0 MAP (mmHg) 119.7I2.9 120.4*4.8 1 18.9&2.8 103.3*4.5~~ a=p

C1 3

The Sificance of Bodybuilding

Body building is ofkn portrayed as a fige sport, where the eathusiasts are sccn as physicai anomalies, and the spon is perceived as bang riddled with the abuse of anaboiic steriods and extreme surgicai altcrations. Most importantiy however, it is not an olympic sport, and kks the international organization necctssary for 1egitihtion. As such, it has not been as exterisively studied as have other spom, such as, track and field. The intent of this study was not to aiter the papuiar view of the sport, but rather to elucidate the cardiovascular training adaptations resuiting from the training methods employed by bodybuilding enthusiasts. The followhg adaptive responses may be obtained from body building training: 1. an increased resistancœ to fatigue (Tesch, 1987). 2. a decreasrd arterial lactate concentration in reqionse to effon pesch, 1987). 3. an increased resting vascdar conductance (this study). 4. a positive alteration in resting blood pressure and pressor response to effort (this study). 5. an increased maximai vascuiar conductance (this study). 6. an increased capcïty for aerobic work in previousiy untrained individuais (Shantz, 1982; Tesch and Larsson, 1982; Tesch et al., 1989; Belï and Jpcobs, 1990; Tesch, 1992). 7. an in- strength and powa in those not previousiy strrngth trained. The changes oulincd above wouid benefit muiy groups of active and prwiously inactive individuais,

Runners Many resistance training programs in which nmncn participate have not fully utiiized body building as a resistance training method. One reasan may have been sïmply that this type of training is diffIcult to jw to the endurana atblete because of the time required for both singie training bouts, and to achieve the volume of work necessary to promote the appoprinte muscular changes. Such a iarge volume of training time and effort might weii k at the arpnst of the endurance activity itself. However, body building training would benefit mers in many ways. First of ali, they would gain at least the same amount of strength and paua that are gained during a traditional resistaace trainiag program. More importanîîy however, this study has shown that these gains can be made without negative effi on the cardiovascular symm. A more ambitious rcsistance training prognm might yield even greater gains in mgth and power dong with additional cardiovascuiar adaptations. These gains in strength and power codd be dmropsd whiie simultana>usiy improving muscuiar endurance. Fast and slow fiber types would adapt in ways which would positively alter the lactate response to various workloads. In this way, benefid changes to the lactate threshold wouid OCCUT, which wouid benefit middle and long distance ninners. Power Athletes

Power athletes muid employ the bodybuilding method without any dctrimeiit to power performance (Hakhncn a ai., 19W). The cardiovasculaf bemfits, such as a lowered mean aagial pns~uie,rcsuiting hmthe bodybuilding method, versus the power training mdbod, are an added benefit for heaith reascms. Furthmore, in many power events musculat endurance is abvq important This is oôvious far events such as the 20m and 400 m et,but aiso has value for jurnpers, since it wodd aiiow a -ter volume of training in a given &on @asaul correspondence with University of Toronto Tnck Club jumps coach; Car1 Georgevski). The multi evmt athîetes arc a special group which would pertiaps reap the greatest benefit of ail hmthe bodybuilding mahod. The dccatholon congsU of eight track and field events which arc considefed popowerwcnts. The other two are the 400 m and the 1,500 m. Conquently, deCathaletes tend to follow the powa athlete training mode1 described in 2.4.3, and 1,500 m performances tenâ to be below what would be expectsd (as evideriœd by the fict that the decathîon performance in this cvent is a lower fiaction of normal event sp&c athlete performances). The bodybuilding method may provide a means for these athletes to improve on the weakest part of th& paformance, and stiU maximize th& power development . The lower VOpax saxes rrponod fm untrained individuais in rrspoase to cycle ergometry cornparrd to treadmU running has kai amibuted to a mumilu iimitation of the quadriceps muscle (MacNab and Conga, 1966; Sheppard, 1977). It seems klythat muscie fûnctim limitations are more Sgnificant at lower fitness levels, such as in çedenîq el-y populati011s. It is likdy that in these îndividuals, the relative muscle straigth (96 1RM) re~uiredevai for basic activity is so great that blood flow is occluded, and glywlytic fiben an recruited (Edgertcm 1978); therefore, a hrge amount of venous lactate is produœd, rcsuiting in prernature fatiguing of the whole muscle. The bodybuilding method of resistana aPining rnight help to relieve this limitation by incnving absolute stnmgth, vascuiar conductance, and the oxidative capbility of aii fiber types, aU at the same the.