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1 Laboratoire de
Physiologie-Biologie du Sport, ABSTRACT Pickering, Gisèle P., Nicole Fellmann, Béatrice
Morio, Patrick Ritz, Aimé Amonchot, Michel Vermorel, and Jean
Coudert. Effects of endurance training on the cardiovascular
system and water compartments in elderly subjects. J. Appl. Physiol. 83(4): 1300-1306, 1997.
plasma volume; ejection fraction; extra- and intracellular fluids
INTRODUCTION AGING IS ASSOCIATED WITH a continual change in all body
systems. Research over the last 20 years has shown that some of these declines, such as that in maximal oxygen consumption
( METHODS Subjects
A maximal exercise test, body composition, water compartment volumes,
and echocardiography, determined before training (T1) and described
below, were repeated after 2 mo (T2), at the end of the 4 mo of
training (T3), and 4 mo after subjects had stopped training (T4).
Maximal Exercise Test and Anaerobic Threshold
The
effects of endurance training on the water compartments and the
cardiovascular system were determined in 10 elderly subjects [age
62 ± 2 yr, pretraining maximal oxygen consumption
(
O2 max)/kg = 25 ± 2 ml · min
1 · kg1
body wt]. They trained on a cycloergometer 3 times/wk for 16 wk
(50-80%
O2 max,
then 80-85%
O2 max). They were
checked at 8 wk, 16 wk, and 4 mo after detraining. Training improved
O2 max (+16%) and
induced plasma volume expansion (+11%). No change in total body water,
extracellular fluid, interstitial and intracellular fluid volumes,
fat-free mass, and body weight was detected in this small sample with
training. Body fat mass decreased (
2.1 ± 2.2 kg).
Echocardiography at rest showed increased fractional shortening and
ejection fraction and decreased left ventricular end-systolic dimension
(P < 0.05). Blood volume expansion
correlates with cardiac contractility and has an impact on cardiac
function. These improvements are precarious, however, and are
completely lost after 4 mo of detraining, when elderly subjects lose
the constraints and the social stimulation of the imposed protocol.
O2 max), can be acted
on and slowed down by endurance training (11, 15). Aging is associated
with a decrease of blood volume (BV) (4) and total body water (TBW)
(23), a proneness to disturbances in water balance, homeostasis
impairment while in extreme situations, and alterations in renal
function (22), the perception of thirst (17), and cardiovascular
performance (8). Although exercise-induced hypervolemia in young people
is now well established (3, 7), studies in older subjects are fewer and
controversial. Whereas Hagberg et al. (14) did not demonstrate any BV
change after 9 mo of training (70-85%
O2 max), Carroll et al.
(1) showed an increased BV (+12%) in subjects after 26 wk of training
(70% O2 max).
Information on the global changes in water during chronic endurance
exercise is also scarce: in older healthy subjects, Goran and Poehlman
(10) showed increased TBW linked to increased fat-free mass (FFM) after
8 wk of endurance training at 60-80% O2 max. On the other
hand, endurance training has positive effects on the cardiovascular
system, especially on heart rate (HR) (13), ejection fraction (EF), and
diastolic filling at rest and during exercise (16). In our global
understanding of the effects of training on the water compartments and
cardiovascular system in healthy elderly subjects, a few points are
still incomplete: 1) water changes
in the extra- and intracellular compartments,
2) the link between exercise-induced
increased BV and the concomitant cardiac benefits, and
3) the evolution of these parameters
with detraining. The purpose of our study was therefore to determine whether 4 mo of individualized training modify global and compartmental hydration in elderly subjects, induce plasma hypervolemia, and if so,
how such training affects cardiac function. We were also interested in
following the water and cardiovascular consequences of the interruption
of a supervised protocol and the detraining, if any, that it may
induce.
O2) was
measured continuously by open-circuit spirometry and averaged every 30 s with the use of the automated one-line system. The test was
considered as being maximal when three of the following four conditions
were fulfilled: constant O2
despite 30-W increment increase; maximal HR
(HRmax) near theoretical
HRmax
[HRmax = 220 age
(yr)]; respiratory quotient >1.1; and exhaustion of the
subject.
Earlobe blood samples were taken at the end of each step and 3 min
after the end of the test for blood lactate concentration ([La]) measurements (Analox LM5). Measured maximal
variables
{O2 max, maximal aerobic power (MAP), maximal expiratory ventilation
(Emax), and maximal [La]
([La]max)}
were used as baseline results (T1). Lactate threshold
(Lat) was determined, and the
corresponding HR threshold (HRt)
was used as a guideline for subsequent individualized training. Each subject came to the laboratory on a second
occasion for determination of body composition and water
compartment volumes.
Anthropometry
Body weight (BW) was measured on a mechanical scale (Ceba) to the nearest 0.1 kg, with subjects wearing light underwear. Height was measured to the nearest 0.001 m. Skinfold thicknesses were measured at four sites on the left side of the body (triceps, biceps, subscapular, suprailiac) in triplicate with a skinfold caliper by the same person, as described by Durnin and Womersley (5). Body density was estimated by using these results in the equation of Durnin and Womersley, adapted to >50-yr-old subjects (5)
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4.5) × 100 (26) and converted to FFM: FFM
(kg) = {[1 (%BF/100)] × BW
(kg)}.
Blood Parameters
Fasting blood samples were taken for hematologic and biochemical analyses. Hemoglobin concentration [Hb], hematocrit (Hct), mean cell volume (MCV), and mean cell hemoglobin concentration (MCHC) were measured on an H3 Technicon (Beckman). Red cell mass (RCM) was calculated as (BV × Hct) and total hemoglobin (tHb) as BV × [Hb]. Plasma Na+ concentration ([Na+]) was measured by specific electrode and protein concentration ([Prot]) by the biuret method (Hitachi 911, Boehringer). Glucose and urea were measured by glucose oxidase and urea oxidase, respectively (Hitachi 911). Plasma osmolarity (mosmol/l) was calculated as 2 × [Na+] + urea concentration ([urea]) + glucose concentration ([glucose]).Water Compartments
Plasma volume (PV), extracellular water (ECW), and TBW were measured as follows. PV measurement. A catheter was inserted into an antecubital vein of fasting volunteers, and PV was measured with use of the Evans blue dye technique (9). An accurately weighed amount of 2.5 ml Evans Blue solution from sterile 5-ml ampules (at 5 mg/ml concentration) was then injected. Ten milliliters of saline were flushed to rinse the catheter, and blood samples were drawn 5, 7, 10, 15, and 20 min after injection. Evans blue concentrations of standard and plasma solutions were calculated from 620-nm and corrected 740-nm optical densities measured on a Unicam 8625 UV/VIS spectrophotometer (Unicam, Cambridge, UK). Time 0 concentration was calculated by back extrapolation of the dilution curve with time (T) and was used to calculate PV. BV was calculated as PV/(1 Hct).
Variations of PV (%) were also calculated from Hct and
[Hb] according to the equation (27)
![{(1 − Hct T/1 − Hct T1) × [Hb] T1/[Hb]T} −1](/content/vol83/issue4/fulltext/1300/img004.gif)
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20°C. Volunteers continued fasting for 6 h
but were permitted light activity within the laboratory (reading,
watching TV, and so on). Samples were later analyzed by means of
high-performance liquid chromotography as described by Miller et al.
(18) by using a diode array detector (Partisil 10 SAX column, Whatman
International, Maidstone, UK). Protein-free plasma samples were
obtained after centrifugation by using a MPS1 micropartition system
(Amicon, Epernon, France); ECW was calculated from the plateau
concentration of plasma bromide (18).
TBW measurement.
TBW was measured with the
2H2O
dilution technique (20, 24). Urine specimens were collected before oral
administration of an accurately weighed dose (0.15 g/kg BW) of
2H2O
(99.9% enriched, Sigma Chemical, Poole, UK) and 4, 5, and 6 h
afterward. 2H enrichments were
measured with the zinc-reduction technique on an Optima dual-inlet mass
spectrometer (VG Isotech). 2H
dilution space was calculated from plateau enrichments in
2H, and TBW was considered 4%
smaller than the dilution space.
Interstitial fluid volume (ITW) and intracellular water (ICW) were
calculated as
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Echocardiography
Echocardiographic and pulsed-wave Doppler studies were performed on six subjects only at rest by using a Vigmed 750 model imaging system with electrocardiographic recording electrodes. Parietal measurements were made through parasternal slits and aortic flux Doppler measurements through an apical slit. All measurements were averaged from at least three successive beats. All echocardiographic and Doppler measurements were made by a single observer, who was unaware of the fitness level and age of the subjects. The following variables were measured or derived: fractional shortening (FS; %); EF (%); left ventricle end-diastolic and end-systolic diameters (EDD and ESD, respectively), interventricular septal diastolic dimension (IVSD), and left ventricular posterior wall diastolic thickness (PWD), all in millimeters; stroke volume (SV; ml); and cardiac index (CI; l · min1 · m2
body surface area).
Training
The exercise program comprised supervised bicycling on a Monark cycloergometer 3 times/wk for 16 wk and consisted of a moderate-intensity training period (T1-T2), followed by a high-intensity training period (T2-T3). All training sessions began with a 10-min warm-up and ended with a 10-min cooling-down session at the HR corresponding to 50% of the subject'sO2 max. After the
first 2 wk with subjects training at 50% of
O2 max for 20 min, a
25-min-long interval training period (with 5 min at a HR 50% of
O2 max and 5 min at
HRt, respectively) was applied for
6 wk. From week 9 to
week 16, intensity and length of
training were gradually increased, with the same interval training
pattern at a higher intensity for 35 min (with 5 min at
HRt and 5 min above it,
respectively), with care taken, because of the high value of the
thresholds, that subjects always stay ~10 beats below
HRmax as a safety measure.
HR was continuously recorded with a commercially available device (Sport Tester PE4000 Polar Electro, Kempele, Finland), and blood pressure was checked before and after exercise.
Detraining
After 4 mo of training (T3), subjects were completely discharged and strongly recommended to keep training as regularly as possible. Some of the subjects even purchased an ergocycle, and all were very enthusiastic and willing to maintain vigorous physical activity. They came back to the laboratory 4 mo later for reassessment. Their activity between T3 and T4 was evaluated via a questionnaire that showed that they had not succeeded in maintaining vigorous physical activity and that they had replaced the 3 h of training/wk by sedentary leisure activities immediately or in the month after the end of the protocol. They had not joined any exercise clubs or associations and had a sedentary type of schedule comparable to the one they had when starting the protocol. The period from T3 to T4 is indeed a "detraining" period: it reinforces the analysis and the validity of the effects of training and is counterproof of the training period.Statistical Analyses
Data analysis was performed with the Statview statistical package (Abacus Concept, Statview). Statistical differences were established by using a repeated-measures analysis of variance design with a confidence level of P < 0.05; when an overall difference was found at P < 0.05, individual stages were compared by using the nonparametric paired Wilcoxon test, with a significance level of 0.05. All data were expressed as means ± SD.RESULTS
Anthropometry (Table 1)
BW was maintained constant all through training and detraining. FFM did not increase significantly (+1.3 ± 2.9 kg; P = 0.09), but BF decreased between T1 and T3 (2.1 ± 2.2 kg, i.e., 2.3 ± 2.9%;
P < 0.05). After 4 mo of detraining,
BF was back to its pretraining value.
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Bioenergetics (Table 2)
O2 max (l/min and
ml · min1 · kg1
BW) did not vary significantly between T1 and T2, but increases between
T2 and T3 were significant: +175 ± 123 ml/min (i.e, +10 ± 8%;
P < 0.01) and +2.6 ± 2.0 ml · min1 · kg1
BW (i.e, +10 ± 8%; P < 0.01).
The overall O2 max
(l/min and ml · min1 · kg1
BW) training gain between T1 and T3 was +237 ± 152 ml/min (i.e., 14 ± 8%; P < 0.01) and +3.8 ± 2.1 ml · min1 · kg1
BW (i.e., +16 ± 8%; P < 0.01),
respectively. There was no correlation between pretraining
O2 max
(ml · min1 · kg1
BW), which indicates the initial degree of fitness, and the
%O2 max (ml · min1 · kg1
BW) gain from T1 to T3.
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MAP (+20 ± 15 W, i.e., +16 ± 10%;
P < 0.01) and
Emax
(P < 0.05) increased, whereas
HRmax and
[La]max were
maintained constant. Lat did not
change significantly between T1 and T3
(%O2 max 77 ± 9%)
nor did corresponding HR (133 ± 12 beats/min).
After 4 mo of detraining,
O2 max
(ml · min1 · kg1
BW) decreased by 14% (P < 0.01) and
came back to its T1 value, as did MAP and
Emax.
Water Compartments (Table 3)
Between T1 and T3, PV, hence BV, increased with training: +263 ± 80 ml (i.e., +11 ± 3%; P < 0.01) and +286 ± 120 ml (i.e., +7 ± 3%; P < 0.01). Calculated PV change (+10 ± 4%) was similar to the change (+11 ± 3%) measured with Evans blue dye dilution. PV and ECW were not measured at T4 to lighten the tests, and therefore ICW and ITW could not be calculated. We calculated PV at T4 on the basis of changes of Hct and Hb from T1 values.
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TBW, ECW, calculated ITW, and calculated ICW did not change
significantly with training. BV (liters) and
O2 max
(l/min) at T1, T2, T3, and T4 show a good correlation
(P < 0.01, r = 0.814 at T1), but we did not show
a relationship between the increases in BV (%) and
O2 max (%) from T1 to
T3.
After 4 mo of detraining, PV and BV decreased (239 ± 204 ml, i.e., 9 ± 6%;
P < 0.01) and (276 ± 185 ml, i.e., 6 ± 4%; P < 0.01), respectively, and were back to pretraining values, whereas there
were no significant correlations between %changes from T1 to T3 in TBW
and O2 max, and TBW and
BV.
Blood Parameters (Table 4)
From T1 to T3, [Na+], [Prot], and plasma osmolarity were maintained, whereas total circulating Na+ and protein increased (P < 0.01 and P < 0.05, respectively). RCM (1.81 ± 0.6 liter), MCV (91.4 ± 4.8 fl), MCHC (32.9 ± 0.08 g/dl), and Hb (597 ± 215 g) were maintained, whereas [Hb] and Hct decreased (P < 0.01).
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After 4 mo of detraining, [Na+], [Prot], and plasma osmolarity did not change, but Na+ and protein masses, Hct, and [Hb] were back to pretraining values.
Cardiovascular Parameters (Table 5)
Resting (136 ± 18/84 ± 8 mmHg) and maximal (Table 2) systolic and diastolic blood pressures did not change with training and detraining. The resting HR decrease was not significant [86 ± 14 beats/min (T1) vs. 82 ± 14 beats/min (T3)]. Echocardiography (T1-T3) showed a significant increase in FS (+20 19%; P < 0.05) and EF (P < 0.05) and a concomitant decrease of ESD (P < 0.05). All other cardiac parameters studied were maintained. At T4, ESD, FS, and EF were not significantly different from pretraining values.
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Variations of FS (%) and EF (%) correlated well with BV changes (%)
between T1 and T3 (r = 0.885, P < 0.05 and
r = 0.904, P < 0.05, respectively) (Figs.
1 and 2).
) and
changes in blood volume (BV; %) with 4 mo of endurance training.
%) and changes
in %BV with 4 mo of endurance training.
DISCUSSION
The short and intense endurance-training protocol we proposed to our
healthy sedentary subjects improved their aerobic and cardiac
functions. O2 max
improvement (+16 ± 8%, T1-T3) is within the range of published
studies [from 10 to 28% (15)]. However, our protocol is
shorter than most, extending up to 1 yr of training and/or with
more training sessions per week. Studies report different training
programs, with the intensity on the basis of
O2 max or HR reserve,
and exact comparison with our protocol is difficult because its
intensity is based on the anaerobic threshold HR and not on
O2 max alone. Our
protocol has showed that a short but individualized training
period leads quickly to improvements in exercise capacity and a
significant gain in MAP of 20 W, corresponding almost to one step of
the maximal exercise test protocol. Most of the
O2 max
increase took place during the high-intensity (T2-T3) period (+10 ± 8%); this stresses the fact that a high level of intensity is required
to get any valuable
O2 improvement. We
studied the influence of the initial level of fitness (pretraining O2 max) on the
O2 max improvement and
found it was not a determining factor in these sedentary subjects as in
the study of Kohrt et al. (15). Among central and peripheral mechanisms
proposed for the increase of exercise capacity with training, we
focused on the concomitant changes of resting cardiovascular and BV
parameters. FS and EF increased with training and correlated well with
exercise-induced BV expansion. Detraining, however, led to a return to
pretraining values of
O2 max, BV, FS, and EF,
thus stressing the benefits and the responsibility of the imposed
protocol in changing cardiovascular and BV variables.
With training, the cardiovascular axis has to accommodate progressively a 7% BV expansion. Echocardiographic assessment of the left ventricle at rest, apart from increases of FS and EF, shows a concomitant decrease of ESD. This implies a better emptying of the ventricle with each systole at rest and improved inotropic effect. Age-associated incomplete emptying of the older heart can thereby be improved by short-term training for an elderly sedentary population. The good correlation between resting FS and EF and exercise-induced BV changes translates the direct and proportional impact of the increased preload and stretch on the cardiac myocyte. The increased preload was probably accompanied by an increased end-diastolic pressure (not measured), and although resting EDD shows only a tendency to increase and SV was not significantly modified, the results reflect the Frank-Starling relationship. The heart, with its permissive role, accommodates the increased BV by an augmentation of contractility, probably also through improved local cardiac oxidative mechanisms. Studies have shown that elderly subjects rely more than the young on the Frank-Starling mechanism, especially to increase cardiac output during exercise (21): reliance is more marked in elderly men than in women (8) because men make greater use of this mechanism at rest (8).
On the other hand, ESD, HR, and EF are catecholamine-mediated
cardiovascular parameters, especially during exercise (21). Resting HR
did not decrease significantly, probably because of the shortness of
the protocol and also because of the size of the sample. The resting
decreased ESD and increased EF might reflect the evolution
of the resting sympathetic nervous system activity with training toward
an enhancement of this sympathetic control. Increased resting
circulating catecholamine levels and decreased 
-adrenergic
responsiveness are associated with aging and/or adaptations to
physical inactivity. Repeated solicitations of the sympathetic system
with adaptation to chronic physical exercise must modify resting
sympathetic nervous system activity. Norepinephrine and epinephrine
concentrations have been reported as being maintained (1) or increased
(19) with training. Modifications of catecholamine receptor number or
affinity and Ca2+-coupling
proteins could also be adaptations to training and induce improvement
of the heart's -adrenoreceptor responsiveness. Training would
thereby shift, even partially, the reliance of elderly subjects on the
Frank-Starling mechanism to an enhanced catecholamine-mediated control.
The study of Ehsani et al. (6), with a 12-mo-long protocol, gives
different resting cardiovascular results with increased EDD and
maintained EF and ESD, implying an enhanced Frank-Starling mechanism.
These results might differ from ours because of the length of the
study, a larger BV increase (not measured), or the gender of the
population (11 men).
Maintained thicknesses of the PWD and the IVSD rule out any heart hypertrophy with this short training protocol. Training had no detrimental effect on resting and maximal blood pressure, despite attenuation of high-pressure baroreceptor sensitivity with aging (2). There might also have been a reduction in peripheral resistance because of increased muscle vasodilation. Most of the FS increase took place when subjects were training at moderate intensity, tending to indicate that training at and around anaerobic threshold improves cardiac function better than strenuous high-intensity exercise.
Another physiological adaptation to endurance training is the lowered
[Hb] and Hct. Expanded PV without change of RCM is the major contributor to this hemodilution. This hemodilution decreases the
oxygen-carrying capacity of the arterial blood, but compensatory mechanisms have been proposed, such as an increased oxygen delivery to
the muscles because of the lower affinity of Hb for oxygen, decreased
blood viscosity that favors perfusion, and improved blood flow to
muscles with training. The good correlation between O2 max (l/min) and BV
(liters) (i.e., T1 = P < 0.01, r = 0.81) at each stage of the
protocol shows the concomitant increases of
O2 max and of
hemodilution with training; however, we did not find any correlation
between the relative increases of BV and
O2 max (as percentages
of the pretraining values), but the wide individual variability and the
size of the sample might be explanatory factors.
The exercise-induced plasmatic hypervolemia (+11%), hence BV expansion (+7%), represents the only fluid modification with training among the water compartments. It is accompanied by maintained [Na+] and [Prot] and increased total circulating protein and Na+. Na+ conservation was very effective in our study despite literature (22) describing progressive renal Na+ conservation defects and reduced aldosterone levels with age, which argue in favor of a limitation of water and electrolyte retention. Na+ retention via an aldosterone-feedback mechanism must have diluted intravascular proteins, triggered liver control on oncotic pressure, and increased albumin synthesis, holding water in the intravascular compartment. In our study, PV expansion is definitely not the consequence of increased global water expansion, as suggested by some authors (3).
We did not use a control group of young subjects in our study but assumed that the same techniques used by other investigators (4, 17) provide results comparable to those in our study. When our elderly volunteers in the pretraining stage are compared with younger populations (4, 17), they are in a hyperosmotic hypovolemic state, with higher plasma osmolarity (although within physiological range) and lower BV. Elevation of thirst plasma osmolality threshold and impaired perception of thirst (17), attenuation of cardiopulmorary volume-pressure baroreflex function (2, 12, 25), and loss of interaction between cardiopulmonary and aortic-carotid reflexes (25) have been described in connection with aging. Despite this age-associated decline of functions, elderly subjects can adapt to training as well as do the young. Exercise-induced hypervolemia is accompanied by maintained electrolyte concentration and also hormone concentration (1) and is perhaps associated with a resetting of volume receptors (1, 3). Plasma osmolarity has been maintained with training; this could be accompanied by a decrease in the thirst plasma osmolality threshold, as observed in young athletes with training, but we have no data on thirst ratings and perception with training in our population.
Although the good electrolyte and protein homeostasis proves the
adaptation of elderly subjects to training, no changes in TBW, ECW,
ICW, and FFM were detected. These results are probably linked to the
small size of our sample. Although the skinfold-thickness measurement
method is weak in the elderly population and prone to random error
because of variations in skin elasticity and compressibility, a
decrease of BF (2.1 ± 2.2 kg;
P < 0.05) took place with training. The maintained TBW can only attest that the weight changes with training, although not significant, are largely because of fat loss.
After patients were outside the protocol for 4 mo, evaluation showed
that they had completely lost all their aerobic
(O2 max), BV (PV), body
composition (BF), and cardiovascular (FS, EF, ESD) improvements, with
results similar to those in the T1 stage. Although high motivation and
good will were evident at the end of the endurance training period, it
is difficult for sedentary healthy elderly subjects to maintain
training outside the frame of the protocol, and the 3 h/wk devoted to
training are rapidly replaced by nonphysical leisure activities. BV and
thus cardiac improvements are rapidly lost, and the subjects return to
their initial state after 4 mo of detraining. The maintenance of
exercise is especially difficult in the sedentary population, which is
instinctively slower and more reluctant to join training groups on a
long-term basis.
In conclusion, our study has shown that 4 mo of individualized training
that enhances O2 max
improves the resting systolic function of the heart in healthy
sedentary elderly subjects. This improved cardiac contractility is
correlated with the exercise-induced BV expansion. Global and
intracellular body hydration are not modified by training in this small
sample, but elderly subjects manage to adequately preserve their
electrolyte homeostasis. These gains are of a precarious nature and
cannot be maintained outside the social stimulation and friendly
competitiveness of the imposed protocol. The subjects rapidly lose all
the cardiovascular and aerobic benefits strenuously acquired over 4 mo
of vigorous individualized training.
ACKNOWLEDGEMENTS
We warmly thank our subjects for highly enthusiastic participation in this protocol. We also thank Dr. B. Beaufrère for his support, Dr. B. Dastugue for biochemical measurements, Dr. J. Bonhomme for hematology measurements, and Dr. B. Citron for allowing the use of the echocardiography equipment. We are indebted to Liliane Morin for nursing assistance, Paulette Rousset and Michel Delaitre for technical assistance, and Colette Cohendy for secretarial support.
FOOTNOTES
Address for reprint requests: J. Coudert, Laboratoire de Physiologie-Biologie du Sport, Faculté de Médecine, 28 Place H. Dunant, 63001 Clermont-Ferrand France (E-mail: Physio.sport @u-clermont 1.fr).
Received 12 February 1997; accepted in final form 12 June 1997.
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