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Dissociation of peak vascular conductance
and V
˙
O
2max
among highly trained athletes
RUSSELL T. HEPPLE,
1
THOMAS L. BABITS,
2
MICHAEL J. PLYLEY,
2
AND JACK M. GOODMAN
2
1
Department of Medicine, University of California, San Diego, La Jolla, California 92093-0623;
and
2
Faculty of Physical Education and Health and Graduate Department of Exercise Science,
University of Toronto, Toronto, Ontario, Canada M5S 2W6
Hepple, Russell T., Thomas L. Babits, Michael J.
Plyley, and Jack M. Goodman. Dissociation of peak vascu-
lar conductance and V
˙
O
2max
among highly trained athletes. J.
Appl. Physiol. 87(4): 1368–1372, 1999.—Previously, a strong
relationship has been found between whole body maximal
aerobic power (V
˙
O
2max
) and peak vascular conductance in the
calf muscle (J. L. Reading, J. M. Goodman, M. J. Plyley, J. S.
Floras, P. P. Liu, P. R. McLaughlin, and R. J. Shephard. J.
Appl. Physiol. 74: 567–573, 1993; P. G. Snell, W. H. Martin,
J. C. Buckley, and C. G. Blomqvist. J. Appl. Physiol. 62:
606–610, 1987), suggesting a matching between maximal
exercisecapacityandperipheralvasodilatoryreserveacrossa
broad range of aerobic power. In contrast, long-term training
could alter this relationship because of the unique demands
for muscle blood flow and cardiac output imposed by different
types of training. In particular, the high local blood flows but
relatively low cardiac output demand imposed by the type of
resistance training used by bodybuilders may cause a rela-
tively greater development in peripheral vascular reserve
than in aerobic power. To examine this possibility, we studied
the relationship between treadmill V
˙
O
2max
and vascular con-
ductance in the calf by using strain-gauge plethysmography
after maximal ischemic plantar flexion exercise in 8 healthy
sedentary subjects (HS) and 28 athletes. The athletes were
further divided into three groups: 10 elite middle-distance
runners (ER), 11 power athletes (PA), and 7 bodybuilders
(BB). We found that both BB and ER deviate from the
previously demonstrated relationship between V
˙
O
2max
and
vascularconductance.Specifically,foragivenvascular conduc-
tance, BB had a lower V
˙
O
2max
, whereas ER had a higher
V
˙
O
2max
thandidHSandPA.Weconclude that the relationship
between peak vascular conductance and aerobic power is
altered in BB and ER because of training-specific effects on
central vs. peripheral cardiovascular adaptation to local
skeletal muscle metabolic demand.
muscle blood flow;strain-gauge plethysmography; bodybuild-
ing; resistance training; maximal aerobic power
A STRONG LINEAR RELATIONSHIP between peak vascular
conductance of the calf and maximal aerobic power
(V
˙
O
2max
) has been described previously by our labora-
tory (19) and by others (25), suggesting a matching
between whole body maximal aerobic function and
peripheral vascular reserve in skeletal muscle. Con-
versely, prolonged physical training of specific routine
by high-caliber athletes may cause an alteration of this
relationship because specific adaptations occur in re-
sponse to the unique demands of different types of
training. For example, traditional resistance training
programs promote increases in both muscle strength
and muscle size (i.e., hypertrophy), with little or no
change in skeletal muscle capillary supply or muscle
fiber oxidative capacity in young adults (29), and may
reduce the reactive hyperemic blood flow response (5).
In contrast, the type of resistance training used by
bodybuilders is qualitatively different, promoting mod-
est increases in both capillary supply and oxidative
capacity (4, 27, 28), in addition to increasing muscle
strength and size. These muscle adaptations arise
because of the high metabolic and blood flow demands
of the multiple-set, high-repetition, and high-intensity
muscle contractions that are characteristic of the resis-
tance training used by bodybuilders (BB) (28). Because
thesemusclecontractions represent activation of only a
small percentage of total body muscle mass at any one
time, the stress placed on the central circulation to
provide blood flow (i.e., cardiac output) would be much
less than that required by endurance types of activity,
such as running. We hypothesized that the modality of
training used by BB leads to structural and/or func-
tional changes in the peripheral vasculature that are
independent of changes in maximal central circulatory
function, resulting in a lower V
˙
O
2max
for a given peak
vascular conductance compared with that normally
seen. In contrast, we reasoned that the training em-
ployed by track and field jumpers and decathletes
[power athletes (PA)], which includes traditional resis-
tance training to maximize power relative to body mass
in those muscles used in running and jumping, in
addition to running training, would result in higher
V
˙
O
2max
and peak vascular conductance but an un-
changed relationship between these variables com-
pared with healthy sedentary subjects (HS). Similarly,
the nature of training employed by highly trained
endurance runners (ER; e.g., racing distances of 800–
10,000 m), which includes a significant proportion of
interval running at intensities greater than or equal to
V
˙
O
2max
, was expected to result in an even greater
peripheral vascular reserve and systemic V
˙
O
2max
but a
maintained relationship between these variables com-
pared with HS. To evaluate this, we determined peak
vascular conductance in the calf after maximal isch-
emic plantar flexion exercise and whole body V
˙
O
2max
on
the treadmill in BB, subjects representing a wide scope
of aerobic power (HS and ER), and practitioners of
traditional resistance training (PA).
The costs of publication of this article were defrayed in part by the
payment of page charges. The article must therefore be hereby
marked ‘‘advertisement’’ in accordance with 18 U.S.C. Section 1734
solely to indicate this fact.
8750-7587/99 $5.00 Copyright
r
1999 the American Physiological Society1368 http://www.jap.org
METHODS
Subjects. Thirty-six male subjects, including 7 BB, 10 ER,
11 PA, and 8 age-matched HS, were studied at the University
of Toronto Cardiovascular Regulation Laboratory. The PA
were included to compare the effect of traditional resistance
training vs. the resistance training used by BB (see below).
Details of the experimental protocol were explained, and
informed consent was obtained from all subjects. Screening
included completion of a physical activity readiness question-
naire, and an interview to obtain details of training history,
before the study began.
The HS, recruited from the general student body of the
University of Toronto, had not been engaged in regular physical
activityortrainingprogramsforatleast2yrbeforethestudy.The
ER were recruited from local running clubs and had been in
training for competition distances from 800 to 10,000 m for a
minimum of 2 yr. The PA were recruited from the University of
Toronto Track and Field Club and had been in training for
national and/or international jumping and/or decathlon competi-
tion for at least 2 yr. The BB, recruited from local bodybuilding
clubs, had beentrainingforcompetition for aminimumof2 yr.
All athletes periodized their training, and none indicated a
lapse in training in the year before the study. All athletes,
with the exception of five of the ER, participated in some form
of resistance training on a regular basis. The six ER who did
participate in resistance training reported it to be seasonal
(i.e., during noncompetitive phases of training) and only
supplemental to a training regimen dominated by running.
Running was in most cases the exclusive aerobic activity of
the ER, whereas PA tended to participate in a variety of
different aerobic activities. PA had an extensive running
program;however,none of it was enduranceoriented, consist-
ing of short (⬃10 min) low-intensity warm-up runs and short
interval sets (40–300 m) with long recovery periods. The type
of resistance training used by PA and ER consisted of 1–2
exercises per muscle group, with each exercise having 1–3
sets of 6–12 lifts by using moderate-to-heavy weight for both
upper and lower body muscle groups (i.e., a traditional
resistance training approach). Whereas all of the PA and BB
performed resistance exercises specifically for the lower leg
(i.e., calf muscles), this was true in only 4 of the 10 ER. BB
only used aerobic activities to lose body fat (e.g., in prepara-
tion for a competition) and always at very low intensities. BB
resistance training consisted of 2–4 exercises per muscle
group, with each exercise having 3–5 sets of high repetitions
(6–100) performed to the point of muscle failure (character-
ized by the inability to perform another repetition throughout
thefullrangeofmotion)forbothupperandlowerbodymuscle
groups. As such the total resistance training stimulus for a
given muscle group, including the calf muscles, was much
greater in BB than in both PAand ER.
V
˙
O
2max
. V
˙
O
2max
was determined by using open-circuit spi-
rometry during an incremental exercise test to exhaustion on
a motor-driven treadmill (model 1864, Collins). Subjects
warmed up for 2 min at a self-selected speed, after which
speed was held constant while the slope was increased by 2%
every 2 min for the next 8 min, and by 1% for each additional
minute thereafter until voluntary exhaustion. Heartrate was
monitored by using a Polar heart rate monitor. Expired gases
were sampled at 15-s intervals, passed through a mixing
chamber, and analyzed via an infrared CO
2
monitor (Jaeger
CO
2
-test) and an O
2
analyzer (Ametek S3-A). Ventilation was
measured with a ventilation monitor (Morgan Ventilometer
Mark 2) connected to a pneumotachograph on the inspiratory
arm of the mouthpiece. All cardiorespiratory data were
collected and analyzed with the aid of a semiautomated
metabolic cart (Morgan) on-line with a microcomputer. Crite-
ria for acceptance of V
˙
O
2max
included attainment of three or
more of the following: 1) minute ventilation ⬎115 l/min; 2)
respiratory exchange ratio ⬎1.15; 3) heart rate ⫾10 beats/
min of age predicted; and 4) a plateau in O
2
uptake (increase
of ⬍2ml·kg
⫺1
·min
⫺1
with an increase in workload) (18).
Strain-gaugevenousocclusionplethysmography.Bloodflow
to the calf was measured by using venous occlusion strain-
gauge plethysmography at rest and immediately after sub-
maximal (data not presented) and maximal ischemic plantar
flexion exercise on the dominant leg, as described previously
(19). Briefly, a blood pressure cuff, placed around the ankle,
was inflated to a pressure of 220 Torr to occlude blood flow
from the foot. A second cuff, placed around the thigh just
above the knee, wasrapidly inflated (⬃1s)to60Torr,andthe
change in volume of the leg was measured over a 14-s cycle
viaanindium-galliumstraingauge(modelSPG16,Mediason-
ics) placed around the calf at the position of widest girth.
Beat-to-beat systemic blood pressure and heart rate were
recorded during the blood flow measurement via a finger cuff
placed on the left index finger (with the hand at the level of
the heart) by using a Finapress 2300 automated blood
pressure monitor (Ohmeda). The data-collection period was
42s(3⫻ 14-s cycles), and data were processed (at a sampling
frequency of 100 Hz) on-line with a microcomputer by using a
WATSMART data-acquisition unit and software customized
to our system, allowing simultaneous collection of blood
pressure, heart rate, and blood flow measurements. Blood
flows were calculated from the slope of the line made by three
manually selected points on the ascending portion of the
blood flow vs. time tracing. The corresponding vascular
conductance for each blood flow measurement was calculated
as the quotient of blood flow and mean arterial pressure
(MAP ⫽ systolic blood pressure ⫹
1
⁄3
pulse pressure). Muscle
and adipose mass in the calf were estimated by using the
equations of Clarys and Marfell-Jones (8), as described
previously (19).
The calf plantar flexion exercise protocol consisted of two
stages performed on a specially designed ergometer (19). The
first stage consisted of a moderate-load (5-kg) exercise per-
formed at a frequency of 1 Hz for 2 min. Five minutes later,
the second workload was preceded by 2 min of ischemia
inducedby inflating the thigh cuff to 220Torr to prevent blood
flow to the calf.After this, with the thigh cuffstillinflated, the
subject performed the second stage of plantar flexion exercise
with a heavy load (30 kg) at a frequency of 1 Hz until
volitional fatigue, which was characterized by dull ischemic
pain in the calf muscle and ⬎25% reduction of the range of
motion(19).Bloodflowmeasurementswereobtainedimmedi-
ately (starting within 5 s) after each stage. Peak blood flow
and conductance were taken as the highest of the three
readings obtained after the maximal ischemic exercise stage.
Criteria for accepting a blood flow measurement as maximal
was that it exhibit a decrement ⬍10% between the first to
third measurements (i.e., a sustained hyperemic response).
Statistical analysis. Data were analyzed by using one-way
ANOVAand Student-Newman-Keuls post hoc test to identify
differences between groups. Linear regression analysis was
used to examine the relationship between V
˙
O
2max
and peak
vascular conductance and to interpolate V
˙
O
2max
at a common
peakvascularconductance(70ml·min
⫺1
·10ltissue
⫺1
·Torr
⫺1
)
in each subject. Values are presentedas means ⫾ SE.
RESULTS
Body mass was significantly greater in BB than all
other groups, whereas body mass in ER waslower than
in all other groups (Table 1). As expected, V
˙
O
2max
1369VASCULAR CONDUCTANCE AND V
˙
O
2max
IN COMPETITIVE ATHLETES
(ml·min
⫺1
·kg
⫺1
) was higher in ER (71.0 ⫾ 1.2
ml·min
⫺1
·kg
⫺1
) than in the other groups (Table 1). In
addition, PA (50.7 ⫾ 1.6 ml·min
⫺1
·kg
⫺ 1
) had a higher
V
˙
O
2max
than did HS (45.1 ⫾ 1.9 ml·min
⫺1
·kg
⫺1
) but not
BB (44.7 ⫾ 3.2 ml·min
⫺1
·kg
⫺1
). The blood flow and
blood pressure responses at rest and after the maximal
ischemic plantarflexionexercisearepresentedin Table
2. The BB had a lower resting MAP (83 ⫾ 2 Torr) than
did HS (99 ⫾ 5 Torr) and a greater resting blood flow
and vascular conductance than did the other groups.
The peak blood flow and vascular conductance in both
ER and BB were higher than in PA and HS. Although
BB demonstrated a greater estimated calf muscle mass
(2.11 ⫾ 0.11 kg) than did ER (1.74 ⫾ 0.05 kg), there
were no differences between groups in the ratio of
estimated adipose mass to muscle mass of the calf
(Table 2).
The relationship between peak calf vascular conduc-
tance and V
˙
O
2max
obtained for healthy subjects in
previous studies representing a broad scope of aerobic
power (19, 25) along with the values for each group in
the present study are shown in Fig. 1. For a given
vascular conductance, theV
˙
O
2max
in PAand HS wasnot
different from that shown previously (19, 25). Addition
of these results to the previous data (19, 25) yields the
followingregressionequation:V
˙
O
2max
⫽ 21.12⫹ (0.488⫻
peak vascular conductance) (r ⫽ 0.79, P ⬍ 0.001). By
using this regression equation to predict V
˙
O
2max
at a
vascular conductance of 70 ml·min
⫺1
·10 l tissue
⫺1
·
Torr
⫺1
ineachsubject, a higher V
˙
O
2max
inER(70.0 ⫾ 1.7
ml·min
⫺1
·kg
⫺1
) and a lower V
˙
O
2max
in BB (39.5 ⫾ 4.2
ml·min
⫺1
·kg
⫺1
) than in both HS (57.0 ⫾ 1.9ml·min
⫺1
·
kg
⫺1
) and PA(57.1 ⫾ 2.4 ml·min
⫺1
·kg
⫺1
; P ⬍ 0.05) was
revealed.
DISCUSSION
We found that compared with healthy subjects who
demonstrate a widerange of aerobic power (19, 25) (HS
and PA of present study), both highly competitive ER
and BB deviate from the previously described linear
relationship between maximal aerobic power and calf
muscle peak vascular conductance. Specifically, we
observed that ER have a higher V
˙
O
2max
than would be
predicted from their peak vascular conductance,
whereas BB have a lower V
˙
O
2max
than would be pre-
dicted from their peak vascular conductance. It is
suggested that this result is a consequence of the
different training regimens and their effect on the
balance between central vs. peripheral cardiovascular
adaptation to muscle metabolic demand.
Venous occlusion plethysmography was used to non-
invasively determine peak vascular conductancein calf
muscle after exhaustive ischemic exercise. This ap-
proach provides peak blood flows that are markedly
lower than those reported for the quadriceps during
knee extensor exercise by direct methods (2, 20), which
may reflect the difference in site of measurement
(quadriceps vs. calf; for review see Ref. 16) and/or
methodological issues [see Reading et al. (19) and Hiatt
Table 1. Descriptive subject data
HS PA ER BB
Age, yr 25.1⫾ 1.3 23.0⫾ 1.1 24.8⫾ 1.4 26.9⫾ 1.5
Height, m 1.73⫾ 0.04 1.87⫾ 0.02† 1.79⫾0.01 1.74⫾0.02
Body mass, kg 78.5⫾ 3.1 79.6⫾ 2.9 64.9⫾ 1.0† 89.6⫾ 3.3†
V
˙
O
2max
,ml·min
⫺1
·
kg
⫺1
45.1⫾ 1.9 50.7⫾ 1.6* 71.0⫾ 1.2† 44.7⫾ 3.2
Values are means ⫾ SE. V
˙
O
2max
, aerobic power; HS, healthy
sedentary subjects; PA, power athletes; ER, endurance runners, BB,
bodybuilders. *P ⬍ 0.05vs.HS. †P ⬍ 0.05vs. all other groups.
Table 2. Blood flow and blood pressure responses at
rest and after maximal ischemic plantar flexion
exercise
HS PA ER BB
Estimated calf
muscle mass,kg 1.84⫾ 0.09 2.01⫾0.08 1.71⫾ 0.05 2.11⫾0.11§
CalfA/M, % 23⫾ 220⫾222⫾ 316⫾1
MAP
rest
,Torr 99⫾595⫾ 494⫾383⫾2*
BF
rest
,
ml·min
⫺1
·100
ml
⫺1
3.6⫾ 0.2 3.5⫾ 0.3 3.2⫾ 0.2 4.7⫾ 0.4‡
G
rest
,
ml·min
⫺1
·10
l
⫺1
· Torr
⫺1
3.6⫾ 0.3 3.6⫾ 0.3 3.4⫾ 0.2 5.9⫾ 0.3‡
MAP
peak
, Torr 117⫾4 120⫾ 2 122⫾ 6110⫾4
BF
peak
,
ml·min
⫺1
·100
ml
⫺1
54.5⫾ 3.2 68.5⫾ 4.1 87.1⫾ 5.6† 89.1⫾7.0†
G
peak
,
ml·min
⫺1
·10
l
⫺1
·Torr
⫺1
45.6⫾ 2.3 57.0⫾ 3.6 72.1⫾ 4.0† 80.7⫾5.6†
Values are means ⫾ SE. A/M, ratio of estimated adipose mass to
musclemass;MAP
rest
,meanarterial pressure atrest;MAP
peak
,mean
arterial pressure after ischemic exercise; BF
rest
, resting calf blood
flow; BF
peak
, peak calf bloodflow; G
rest
, resting vascular conductance;
G
peak
, peak vascularconductance.*P ⬍ 0.05vs. HS, †P ⬍ 0.05vs.HS
and PA. ‡P ⬍ 0.05vs. all other groups. §P ⬍ 0.05vs.ER.
Fig. 1. Relationship between maximal aerobic power (V
˙
O
2max
) and
peak vascular conductance in the calf muscle in healthy subjects
across a broad scope of aerobic power and training backgrounds.
Regression line includes previous data from healthy subjects (19, 25)
and the healthy sedentary and power athletes of the present investi-
gation [V
˙
O
2max
⫽ 21.12 ⫹ (0.488 ⫻ peak vascular conductance); r ⫽
0.79, P ⬍ 0.001].
1370 VASCULAR CONDUCTANCE AND V
˙
O
2max
IN COMPETITIVE ATHLETES
etal. (11) fora discussion ofthese issues]. Differences in
peak vascular conductance between individuals have
been interpreted as reflecting differences in the ana-
tomic structure for conducting blood flow [e.g., arterio-
lar number and/or dimensions (3, 5, 26)], and/or an
altered vasomotor response to exercise due to the
balance between myogenic control (e.g., sympathetic
drive) and local regulatory (e.g., nitric oxide release)
factors (9, 19).
Differential effects of resistance training and endur-
ance training on vascular conductance. Endurance
training and traditional forms of resistance training
have been shown to affect the muscle blood flow re-
sponse in different ways. For example, an augmented
muscle peak vascular conductance has been found after
both whole body endurance training (17) and small-
muscle-group endurance training (10, 24). In contrast,
a reduction in reactive hyperemic blood flow has been
shown after 4 wk of high-intensity resistance training
of the calf, perhaps the result of muscle hypertrophy
without concomitant vascular growth (5). Unfortu-
nately, the impact of these adaptations on the relation-
ship between V
˙
O
2max
and peak vascular conductance
was not considered in these studies.In this respect, the
results for HS and PA in the present study are consis-
tent with previous studies showing a strong relation-
ship between V
˙
O
2max
and peak vascular conductance
(19, 25) (Fig. 1), and show that the type and/or volume
of resistance training used by PA does not alter this
relationship. The relationship between peak vascular
conductance and V
˙
O
2max
shows that, as V
˙
O
2max
in-
creases, peripheral vasodilatory reserve also increases.
Inother words,ratherthan increasingthe proportion of
vasodilatory capacity utilized as V
˙
O
2max
is increased,
vasodilatory capacity is increased in proportion to
V
˙
O
2max
such that the scope of the vasodilatory reserve is
maintained. Nevertheless, it is also noteworthy that
long-term physical training may cause a dissociation of
the relationship between peak vascular conductance
and V
˙
O
2max
as illustrated by the responses of the ER
and BB. In this respect, the response of ER in the
present investigation is quite different from that dem-
onstrated by the study of Snell et al. (25), in which the
runners demonstrated the same response as other
healthyindividuals. The training history(anaverage of
9.1 ⫾ 1.6 yr of training) and small variability in the
V
˙
O
2max
seen in the ER subjects of the present investiga-
tion suggest that they were more highly trained than
werethose of thestudyof Snell etal.,which may inpart
account for the deviation of our ER subjects’response.
BB perform training that evokes repetitive and large
hyperemic responses in the exercised muscles (30);
however, because of the limited volume of muscle active
at any one time, the training does not stress maximal
cardiac pumping abilities (22). Thus we might expect
that the relative adaptation in the peripheral vascula-
ture would be greater than that of the central circula-
tion with BB training, which would account for the
lower V
˙
O
2max
relative to peak vascular conductance in
these athletes.Aunique effectof BB resistance training
on skeletal muscle adaptation, compared with more
traditional resistance training paradigms, is supported
by the somewhat greater capillarity and oxidative
enzyme activities reported previously in this popula-
tion (27, 28) compared with the reduction in hyperemic
blood flow seen after more traditional high-intensity
resistancetraining (5). In thisrespect,BB training may
more closely resemble the adaptation to rock climbing,
where muscle contractions are submaximal but are
maintained for prolonged periods of time and where
forearm peak vascular conductance has been shown to
be higher than in nonclimbers (9). Further evidence
that the high peak vascular conductance in BB is a
function of their training is supported by the strong
correlation between the number of years of training
and peak vascular conductance in BB (r ⫽ 0.80, P ⬍
0.05).
Physiological basis of peak vascular conductance.
The high peak vascular conductance response in BB
could reflect anatomic and/or functional differences in
the peripheral vasculature induced by their training
behavior. It is worth noting that the literature of
animal studies supports the possibility that an in-
creased size of the arteriolar bed may result from a
chronically elevated blood flow (i.e., as occurs with BB
training) (for review see Ref. 12). In addition, it has
been suggested that the greater peak vascular conduc-
tance after training of small muscle groups (10, 24) and
in athletes compared with sedentary subjects (25) is
secondary to an increased diameter and/or number of
the resistance vessels (23) rather than changes in
sympathetic vascular control (24) or nitric oxide medi-
ated vasodilation (10). In this respect, the only mod-
estlygreatermuscle capillarizationandoxidativecapac-
ity found previously in BB compared with practitioners
of more traditional resistance training paradigms (27)
do not preclude more significant growth in the arterio-
lar resistance vessels with BB training because ele-
vated blood flow per se (as occurs during BB training) is
not thought to be a major cause of angiogenesis (14, 21)
but is thought to induce both arteriolar proliferation
and increased vessel diameter (15). This explanation
may also account for the response observed in ER in
whom V
˙
O
2max
was significantly greater for a given peak
vascular conductance. Specifically, whereas we would
expect the chronically elevated blood flows during
running training to induce arteriolar proliferation
and/or enlargement (as is suggested by their greater
peak vascular conductance compared with HS and PA),
adaptations in capillary growth and mitochondrial
structure may be relatively greater consequent to the
intramuscular environment [e.g., intracellular hypoxia
(6, 14)] created when running at intensities greater
than or equal to V
˙
O
2max
. Indeed, a greater capillariza-
tion in endurance-trained subjects is well described
(e.g., Refs. 1, 7) and is thought to play an important role
in the greater V
˙
O
2max
in this population (13).
Conclusions. In summary, we observed that both
competitiveBBand ERdemonstrateanalteredrelation-
ship between peak vascular conductance in the calf
muscle and whole body V
˙
O
2max
, compared with HS
representing a broad scope of aerobic power. Specifi-
1371
VASCULAR CONDUCTANCE AND V
˙
O
2max
IN COMPETITIVE ATHLETES
cally, ER have a higher V
˙
O
2max
and BB a lower V
˙
O
2max
compared with both HS and PA at a similar vascular
conductance. It is suggested that this result is a
consequence of the unique cardiovascular demands of
long-term running training and the type of resistance
training routinely used by BB and the subsequent
adaptations in central vs. peripheral cardiovascular
structure and/or function.
This work was supported by a grant from Sport Canada, Applied
Sport Research Program.
Address for reprint requests and other correspondence: R. T. Hepple,
Dept. of Medicine, 0623A, Univ. of California, San Diego, 9500 Gilman
Dr.,LaJolla, CA92093-0623 (E-email:rhepple@ucsd.edu).
Received 5 February 1999; acceptedinfinal form 27 May 1999.
REFERENCES
1. Andersen, P., and J. Henriksson. Capillary supply of the
quadriceps femoris muscleofman:adaptive responseto exercise.
J. Physiol. (Lond.) 270: 677–690, 1977.
2. Andersen, P., and B. Saltin. Maximal perfusion of skeletal
muscle in man. J. Physiol.(Lond.)366: 233–249, 1985.
3. Bassett, D. R., W. J. Duey, A. J. Walker, E. T. Howley, and V.
Bond. Racial differences in maximal vasodilator capacity of
forearm resistance vessels in normotensive young adults. Am. J.
Hypertens. 5: 781–786, 1992.
4. Bell, D. G., and I. Jacobs. Muscle fibre area, fibre type &
capillarization in male and female body builders. Can. J. Sport
Sci. 15: 115–119, 1990.
5. Bond, V., Jr., P. Wang, R. G. Adams, A. T. Johnson, P.
Vaccaro, R. J. Tearney, R. M. Millis, B. D. Franks, and D. R.
Basset, Jr. Lower leg high-intensity resistance training and
peripheral hemodynamic adaptations. Can. J. Appl. Physiol. 21:
209–217, 1996.
6. Breen, E. C., E. C. Johnson, H. Wagner, J.-M. Tseng, L. A.
Sung, and P. D. Wagner. Angiogenic growth factor mRNA
responses in muscle to a single bout of exercise. J. Appl. Physiol.
81: 355–361, 1996.
7. Brodal, P., F. Ingjer, and L. Hermansen. Capillary supply of
skeletal muscle fibers in untrained and endurance-trained men.
Am. J. Physiol. 232 (HeartCirc.Physiol. 1): H705–H712, 1977.
8. Clarys,J. P., and M.J. Marfell-Jones. Anthropometric predic-
tions of component tissue masses in the minor limb segments of
the human body. Hum.Biol.58: 761–769, 1986.
9. Ferguson,R.A., andM. D. Brown.Arterial bloodpressureand
forearm vascular conductance responses to sustained and rhyth-
mic isometric exercise and arterial occlusion in trained rock
climbers and untrainedsedentarysubjects.Eur. J. Appl. Physiol.
76: 174–180, 1997.
10. Green, D. J., N. T. Cable, C. Fox, J. M. Rankin, and R. R.
Taylor. Modification of forearm resistance vessels by exercise
training in young men. J.Appl.Physiol. 77: 1829–1833, 1994.
11. Hiatt, W. R., S. Y. Huany, J. G. Regensteiner, A. J. Micco, G.
Ishimoto, M. Manco-Johnson, J. Drose, and J. T. Reeves.
Venous occlusion plethysmography reduces arterial diameter
and flow velocity. J. Appl.Physiol. 66: 2239–2244, 1989.
12. Hudlicka, O., M. Brown, and S. Egginton. Angiogenesis in
skeletal and cardiac muscle. Physiol.Rev.72: 369–417, 1992.
13. Ingjer, F. Maximal aerobic power related to the capillary supply
of the quadriceps femoris muscle in man. Acta Physiol. Scand.
104: 238–240, 1978.
14. Ito, W. D., M. Arras, D. Scholz, B. Winkler, P. Htun, and W.
Schaper. Angiogenesis but not collateral growth is associated
with ischemia after femoral artery occlusion.Am. J. Physiol. 273
(Heart Circ. Physiol. 42): H1255–H1265, 1997.
15. Kamiya, A., and T. Togawa. Adaptive regulation of wall shear
stress to flow change in the canine carotid artery. Am. J. Physiol.
239 (Heart Circ. Physiol. 8):H14–H21, 1980.
16. Laughlin, M. H., R. M. McAllister, and M. D. Delp. Heteroge-
neity of blood flow in striated muscle. In: The Lung: Scientific
Foundations, edited by R. G. Crystal, J. B. West, E. R. Weibel,
and P. J. Barnes. New York: Lipincott-Raven, 1997, p. 1945–
1955.
17. Martin,W. H., III, W. M.Kohrt, M. T. Malley, E. Korte, andS.
Stoltz. Exercise training enhances leg vasodilatory capacity of
65-yr-oldmen andwomen. J.Appl.Physiol. 69:1804–1809,1990.
18. McConnell, T. R. Practical considerations in the testing of
V
˙
O
2max
in runners. Sports Med. 5:57–58, 1988.
19. Reading, J. L., J. M. Goodman, M. J. Plyley, J. S. Floras,
P. P. Liu, P. R. McLaughlin, and R. J. Shephard. Vascular
conductance and aerobic power in sedentary and active subjects
and heart failure patients. J.Appl.Physiol. 74: 567–573, 1993.
20. Richardson, R. S., D. C. Poole, D. R. Knight, S. S. Kurdak,
M. C. Hogan, B. Grassi, E. C. Johnson, K. F. Kendrick, B. K.
Erickson, and P. D. Wagner. High muscle blood flow inman: is
maximal O
2
extraction compromised? J. Appl. Physiol. 75: 1911–
1916, 1993.
21. Roca, J., T. P. Gavin, M. Jordan, N. Siafakas, H. Wagner, H.
Benoit, E. Breen, and P. D. Wagner. Angiogenic growth factor
mRNAresponses to passive andcontraction-inducedhyperperfu-
sion in skeletal muscle. J.Appl.Physiol. 85: 1142–1149, 1998.
22. Seals, D. R., and J. M. Hagberg. The effect of exercise training
on human hypertension. Med. Sci. Sports Exerc. 16: 207–215,
1984.
23. Silber, D. H., and L. I. Sinoway. Reversible impairment of
forearm vasodilation after forearm casting. J. Appl. Physiol. 68:
1945–1949, 1990.
24. Sinoway, L. I., J. Shenberger, J. Wilson, D. McLaughlin, T.
Musch, and R. Zelis. A 30-day forearm work protocol increases
maximal forearm blood flow. J. Appl. Physiol. 62: 1063–1067,
1987.
25. Snell, P. G., W. H. Martin, J. C. Buckley, and C. G. Blom-
qvist. Maximal vascular leg conductance in trained and un-
trained men. J. Appl. Physiol.62:606–610, 1987.
26. Takeshita, A., and A. L. Mark. Decreased vasodilator capacity
of forearm resistance vessels in borderline hypertension. Hyper-
tension 2: 610–616, 1980.
27. Tesch, P. A. Skeletal muscle adaptations consequent to long-
term heavy resistance exercise. Med. Sci. Sports Exerc. 20:
S132–S134, 1988.
28. Tesch, P.A.,A. Thorsson, and B.Essen-Gustavsson. Enzyme
activities of FT and ST muscle fibers in heavy-resistance trained
athletes. J. Appl. Physiol. 67:83–87, 1989.
29. Tesch, P. A., A. Thorsson, and P. K. Kaiser. Muscle capillary
supply and fiber type characteristics in weight and power lifters.
J. Appl. Physiol. 56: 35–38, 1984.
30. Walloe, L., and J. Wesche. Timecourseandmagnitudeof blood
flow changes in the human quadriceps muscles during and
following rhythmic exercise. J. Physiol. (Lond.) 405: 257–273,
1988.
1372 VASCULAR CONDUCTANCE AND V
˙
O
2max
IN COMPETITIVE ATHLETES
