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10.1152/japplphysiol.00630.1999.—Some recent studies of competitive athletes have shown exercise-induced hypoxemia to begin in submaximal exercise. We examined the role of ventilatory factors in the submaximal exercise gas exchange disturbance (GED) of healthy men involved in regular work-related exercise but not in competitive activities. From the 38 national mountain rescue workers evaluated (36 ± 1 yr), 14 were classified as GED and were compared with 14 subjects matched for age, height, weight, and maximal oxygen uptake (V˙o 2 max; 3.61 ± 0.12 l/min) and showing a normal response (N). Mean arterial Po 2 was already lower than N ( P= 0.05) at 40% V˙o 2 max and continued to fall until V˙o 2 max (GED: 80.2 ± 1.6 vs. N: 91.7 ± 1.3 Torr). A parallel upward shift in the alveolar-arterial oxygen difference vs. %V˙o 2 max relationship was observed in GED compared with N from the onset throughout the incremental protocol. At submaximal intensities, ideal alveolar Po 2, tidal volume, respiratory frequency, and dead space-to-tidal volume ratio were identical between groups. As per the higher arterial Pco 2 of GED at V˙o 2 max, subjects with an exaggerated submaximal alveolar-arterial oxygen difference also showed a relative maximal hypoventilation. Results thus suggest the existence of a common denominator that contributes to the GED of submaximal exercise and affects the maximal ventilatory response.

We have previously reported a reduction in exercise-induced hypoxaemia following polyunsaturated fatty acid supplementation (PUFA). Although this might have been explained by increases in membrane fluidity, a clear explanation could not be provided due to potentially confounding influences of series-2 prosta- glandin mediated effects resulting from PUFA. In this investigation, ten master athletes [mean age 48.1 (SEM 6) years, maximal oxygen uptake (V˙O2max) 3.39 (SEM 0.21) l · min−1] completed a maximal cycling test (Ctrl) which was repeated after the administration of 150 mg of indomethacin to inhibit prostaglandin synthesis, both before and after 6 weeks of 3.66-g PUFA · day−1. Cardiorespiratory parameters were obtained simultaneously with brachial arterial blood sampling for partial pressure of oxygen in arterial blood (PaO2), partial pressure of carbon dioxide in arterial blood (PaCO2), pH, oxygen saturation in arterial blood and lactate concentration determinations. A significant decrease in PaO2 (mmHg) from rest [93 (SEM 1.5)] was observed for exercise intensities of more than 40% V˙O2max in Ctrl reaching 75.9 (SEM 2.1) at V˙O2max. PUFA resulted in a 5.0 (SEM 0.68) mmHg upward shift (P < 0.05) in the PaO2–oxygen uptake relationship, reducing the difference in partial pressure of oxygen between alveolar air and arterial blood (P(A−a)O2) at V˙O2max [Ctrl 36 (SEM 1.6) vs PUFA 33 (SEM 2.2) mmHg] while PaCO2, remained unchanged. Indomethacin had no effect on either PaO2, ideal partial pressure of oxygen in alveolar gas or P(A−a)O2 in either Ctrl or after PUFA. In contrast, the fall in pH was significantly reduced after indomethacin while V˙CO2, PaCO2 and lactacidaemia remained unchanged. These observations confirm an effect of PUFA on exercise PaO2 behaviour which does not appear to be mediated by the influence of a series-2 prostaglandin.

Exercise-induced hypoxaemia (EIH) has been associated with an oxygen diffusion limitation. Because polyunsaturated fatty acids (PUFA) administration can modify cell membrane fluidity, we hypothesized that the importance of EIH could be reduced after a 6-week PUFA diet. Resting pulmonary functions and a maximal cycling test were performed before and after the diet, in eight master athletes [48 (SD 6 years)]. The partial pressure. of O2 in arterial blood (PaO2), alveolar ventilation (\(\dot V_A \)) and ideal alveolar-arterial oxygen partial pressure difference (P(Ai−a)O2) were obtained at each exercise intensity. The extent of EIH at maximal exercise was significantly lower after PUFA [PaO2 −17.2 (SEM 1.9) vs −12.9 (SEM 2.2)]. Before PUFA,\(\dot V_A \) accounted for 50% of the variance in the fall inP(Ai−a) for intensities below 80% maximal oxygen uptake (\(\dot VO_{2\max } \)) andP(Ai−a)O2 for 60% between 70% and 100%\(\dot VO_{2\max } \). After PUFA, the reduction in EIH was highly correlated (r2 = 0.85;P < 0.001) to resulting changes inP(Aii−a)O2 and resting pulmonary diffusing capacity\((D_{L_{CO} } )/\dot V_A \) but not with changes in ideal alveolar partial pressure of oxygen. The improvement in EIH following PUFA could be related to an increase in alveolar-arterial oxygen conductance following improved pulmonary diffusion.

The aim of this study was to test (a) three methods to estimate the quantity of lactate accumulated (QLaA ) in response to supramaximal exercise and (b) correlations between QLaA and the nonoxidative energy supply assessed by the accumulated oxygen deficit (AOD). Nine rowers performed a 3-min all-out test on a rowing ergometer to estimate AOD and lactate accumulation in response to exercise. Peak blood lactate concentration [(La)peak ] during recovery was assessed, allowing QLaA(m1) to be estimated by the method of Margaria et al. Application of a bicompartmental model of lactate distribution space to the blood lactate recovery curves allowed estimation of (a) the net amount of lactate released during recovery from the active muscles (NALR max ), and (b) QLaA according to two methods (QLaA(m2) and QLaA(m3)). (La)peak did not correlate with AOD. QLaA(m1), QLaA(m2) and QLaA(m3) correlated with AOD (r = 0.70, r = 0.85 and r = 0.92, respectively). These results confirm that (La)peak does not provide reliable information on nonoxidative energy supply during supramaximal exercise. The correlations between AOD and QLaA(m2) and QLaA(m3) support the concept of studying blood lactate recovery curves to estimate lactate accumulation and thus the contribution of nonoxidative pathway to energy supply during supramaximal exercise.

Lower amounts of circulating anabolic hormones are thought to accelerate the age related decline in muscle mass and function. Replacement therapies are promising interventions but there are problems with these therapies. Thus alternative strategies should be developed. The age related changes in hormonal status may be probably influenced by exercise. The purpose of this study was: a) to confirm with other methods, more adapted for elderly people, the results of a previous study that has shown relationship between physical activity (PA) and quadriceps muscle function with dehydroepiandrosterone sulphate (DHEAS), insulin like growth factor-1 (IGF-1). Quadriceps muscle power (Pmax) is measured in this new work with a recently developed leg extensor machine and, b) to complete the results of the first study examining simultaneously the relationship between PA, Pmax and cardiorespiratory fitness (VO2max) with DHEAS, IGF-1 and testosterone in a group of healthy elderly people.Fifty independent, community dwelling elderly subjects (25 mens and 25 womens) aged from 66 to 84 volunteered to participate in the study. PA was evaluated by the questionnaire and expressed using two activity indices: mean habitual daily energy expenditure (MHDEE) and the daily energy expenditure corresponding to leisure time sports activities (Sports Activity). Pmax and optimal shortening velocity (vopt) were measured on a Ergopower dynamometer. The Pmax was expressed relative to body mass, Pmax/kg (W kg-1), and relative to the mass of the two quadriceps muscles, Pmax/Quadr (W.kgQuadr-1). VO2max has been measured during a maximal treadmill exercise.In women, IGF-1 correlated significantly with MHDEE (r = 0.54, P = 0.004), Pmax/kg (r = 0.54, P = 0.004) and Pmax/Quadr (r = 0.46, P = 0.02), whereas DHEAS with MHDEE (r = 0.54, P = 0.004), Sports Activity (r = 0.65, P0.001), VO2max (r = 0.46, P = 0.02), Pmax/kg (r = 0.46, P = 0.02) and Pmax/Quadr (r = 0.55, P = 0.004). No such correlation was found in men.These findings confirm that in healthy elderly women physical activity, cardiorespiratory fitness and quadriceps muscle function are similarly related to levels of circulating DHEAS and IGF-1 suggesting a favourable influence of exercise on anabolic hormonal production in the elderly.

Breathe Right (BR) external nasal dilator have become increasingly popular over the past few years, however, the physiological basis for using BR remains unclear. We have examined whether alteration in nasal ventilation would influence the metabolic cost of submaximal running.Metabolic cost was estimated in 10 male endurance triathletes by measuring heart rate (HR) and exercise perception by measuring the rate of perceived exertion (RPE) during submaximal field running. The protocol consisted of 5 min of running at 80% of their maximal aerobic velocity (MAV(f), previously determined under field conditions) for three randomised experimental conditions, separated by a 10 min rest. The conditions were normal nasal ventilation (N), no nasal ventilation (using a nose clip) (NC) and with a BR.Running with the BR or with NC did not significantly influence HR (N: 173+/-7, BR: 173+/-8, NC: 172+/-7 beat x min(-1); F=0.01, p=0.99) or RPE (N: 12.1+/-1.7, BR: 11.8+/-1.9, NC: 13.2+/-0.8; F=1.88, p=0.18). We conclude that alteration in nasal ventilation produced by using BR or NC do not influence HR or RPE in a group of triathletes running 5 min at 80% of MAV(f).The present study tended to demonstrate that both nasal ventilation would not influence the total metabolic cost, and that the BR device is not advantageous during high intensity exercise.

The relationship of oxidative stress and the anti-oxidant defence system to maximal oxygen consumption (VO2max) and habitual physical activity was assessed in 26 elderly men (71.0 +/- 4.2 years) and compared to that of 12 young men (22.1 +/- 5.1 years). Physical activity was assessed by a questionnaire. Malondialdehyde (MDA), plasma total anti-oxidant status (TAS), the levels of red blood cell (RBC) superoxide dismutase (SOD) and glutathione peroxidase (GPX), as well as serum GPX activities were determined under resting conditions. The older and young men had similar TAS and RBC SOD, while MDA, RBC GPX and plasma GPX were higher, and RBC SOD/GPX ratio was significantly lower in the older men. Neither MDA nor anti-oxidants were associated with any of the physical activity/aerobic capacity measures in the elderly men. We conclude that in healthy elderly men with a good nutritional status, indicators of the anti-oxidant defence system are not lower in comparison with young men. Increased RBC and plasma GPX coupled with a high level of lipid peroxidation marker may indicate an adaptation of anti-oxidant defences to sustained oxidative stress. Furthermore, the results of the present study suggest that the level of habitual physical activity and aerobic capacity have no major influence on the resting balance between radical generation and blood anti-oxidant potential in healthy older men.

A population of 120 healthy voluntary subjects of both genders aged 16-88 was studied using the QAPSE (Saint-Etienne Physical Activity Questionnaire) with the purpose of investigating the factors influencing the relation between MHDEE (mean habitual daily energy expenditure) and VO2max (maximal oxygen uptake) to elucidate the factors accounting for individual variation. The mean of MHDEE obtained was 12,181.9 +/- 4041.9 kJ.d-1. The mean VO2max obtained was 39.9 +/- 13.8 ml.kg-1.min-1. A strong relationship between MHDEE and VO2max (r = 0.916; N = 120; P0.0001) was found. Further, MHDEE seemed to be the greater determinant in the variation of VO2max (89.35%). Other variables were found to be involved in the relation between MHDEE and VO2max for a smaller, but still substantial part: age (6.92%), PAST (exathletes who had considerably reduced or stopped their training) (2.45%), body mass (0.85%), and gender (0.43%). Two variables regarding maximal intensity of activity were not included in the multiple-linear regression analysis. These results suggested that the most important factor in the variation of VO2max is the total quantity of energy expenditure and not only the maximal intensity that could reach the subject.

The purpose of this study was to evaluate the various factors involved in the performances of three groups of swimmers with disabilities. These factors were average VO2max (Av-VO2max) measured during swimming and gliding factors measured by the passive drag. Thirty-four swimmers with disabilities were assigned into three groups ranging from more disabilities to fewer disabilities. The first group (G I) included 13 subjects in wheelchairs, the second group (G II) 10 subjects walking with technical aids, and the third group (G III) 11 swimmers with disabilities walking without any help. For G I, the performances and Av-VO2max were lower (P0.05) than for G II and G III while the passive drag was higher than for G III (P0.05). The performances, Av-VO2max, and passive drag were not statistically different between G II and G III. Some of the swimmers had a pronounced amyotrophia of the lower extremities (i.e., reduced volume of inactive muscles). The height from the top of the head to the beginning of the bilateral amyotrophia was called "height without amyotrophia" (HWA). In the whole group, passive drag was not related to the mass or the height but to the ratio mass/HWA (r = 0.71, P0.01). However, within each group, passive drag was mainly related to the mass (r = 0.63, 0.78, 0.62, P0.01, for G I, G II, and G III respectively). Performances of a 100-m and 400-m swim were mainly related to Av-VO2peak (r = 0.81 and 0.79, P0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

To investigate the effect of the ingestion of arginine aspartate (AA) in the decrease of the exercise-induced accumulation of ammonia in plasma, 11 voluntary subjects took part in a cross-over study where AA effect was tested against placebo. Both treatments were randomly administered in a double-blind procedure. To ensure the subjects would be able to present reproducible exercise-testing results during repetitive sessions, they were involved before the experiment in a cycle ergometer training program during 8 weeks. This training determined a significant 14% increase (P less than 0.001) in maximal oxygen uptake (VO2 max). The treatments were administered during 10 days and the two treatments were separated by a 10 day-wash-out period. A 45 min-cycle ergometer test was performed at 80% VO2 max during the 10th day of each treatment to measure plasma ammonia (p[NH4+]) and total blood lactate (b[lact]) concentrations at rest and at the 15th, 30th and 45th min of exercise (determinations of changes from rest; delta p[NH4+] and delta b[lact]). Both concentrations were unchanged between AA and placebo at rest but a significant lesser delta p[NH4+] was found under AA at the 15th min of exercise only (P less than 0.05). On the other hand, an order effect was found for delta p[NH4+] between the two periods of randomized treatment that was interpreted as a remaining training effect. This effect was highly significant at the 30th and 45th min of exercise (P less than 0.001). It was concluded that AA effect was minor with regard to the training effect. As it was not located at the same time of exercise, AA effect would not consequently have the same functional origin (postulated increase in the peripheral clearance of ammonia) than those of training (decrease in muscle production of ammonia).

The relationships between anaerobic glycolysis and the average velocity (\(\bar \upsilon\)) sustained during running were studied in 17 top level athletes (11 males and 6 females). A blood sample was obtained within 10 min of the completion of major competitions over 400 m, 800 m and 1500 m and the blood lactate concentration [1a]b was measured. In both male and female athletes [1a]b was related to the relative performance, as expressed as a percentage of the athlete's best \(\bar \upsilon\) of the season. Over 400m, r=0.85 (P

Thermal balance was studied in 11 boys, aged 10-12 years, with various values for maximal oxygen uptake (VO2max), during two standardized sweating tests performed in a climatic chamber in randomized order. One of the tests consisted in a 90-min passive heat exposure [dry bulb temperature (Tdb) 45 degrees C] at rest. The second test was represented by a 60-min ergocycle exercise at 60% of individual VO2max (Tdb 20 degrees C). At rest, rectal temperature increased during heat exposure similar to observations made in adults, but the combined heat transfer coefficient reached higher values, reflecting greater radiative and convective heat gains in the children. Children also exhibited a greater increase in mean skin temperature, and a greater heat dissipation through sweating. Conversely, during the exercise sweating-test, although the increase in rectal temperature did not differ from that of adults for similar levels of exercise, evaporative heat loss was much lower in children, suggesting a greater radiative and convective heat loss due to the relatively greater body surface area. Thermophysiological reactions were not related to VO2max in children, in contrast to adults.

The purpose of this study was to consider which characteristics are related to a high velocity in water during swimming. The study was performed on 13 of the best competition swimmers of the region of Lyon (France). The collected data were:\(\dot V_{O_2 } \) max, measured during leg-work (\(\dot V_{O_2 } \) max LW), during arm-work (\(\dot V_{O_2 } \) max AW), and the hydrodynamic resistances measured when the swimmers were towed at the speed of 1.80 m/sec. The cardiac output was measured for four of the subjects. The swimmers were characterized by a mean\(\dot V_{O_2 } \) max LW of 56 ml/kg/min and by a high value of the ratio\(\frac{{\dot V_{O_2 } \max {\text{ }}AW}}{{\dot V_{O_2 } \max {\text{ }}LW}}\) which reached 99% for three of them. There was a very high correlation (r = 0.90 and 0.91) between the mean speed calculated from the best performances in competition swims of 400 m and 1500 m and a value which is thought to express the aerobic energy available to the swimmer: $$\dot V_{O_2 } \max water:\dot V_{O_2 } \max {\text{ }}AW + \frac{{\dot V_{O_2 } \max {\text{ }}LW - \dot V_{O_2 } \max {\text{ }}AW}}{6}$$

To compare the results obtained by incremental or constant work load exercises in the evaluation of endurance conditioning, a 20-week training programme was performed by 9 healthy human subjects on the bicycle ergometer for 1 h a day, 4 days a week, at 70-80% VO2max. Before and at the end of the training programme, (1) the blood lactate response to a progressive incremental exercise (18 W increments every 2nd min until exhaustion) was used to determine the aerobic and anaerobic thresholds (AeT and AnT respectively). On a different day, (2) blood lactate concentrations were measured during two sessions of constant work load exercises of 20 min duration corresponding to the relative intensities of AeT (1st session) and AnT (2nd session) levels obtained before training. A muscle biopsy was obtained from vastus lateralis at the end of these sessions to determine muscle lactate. AeT and AnT, when expressed as % VO2max, increased with training by 17% (p less than 0.01) and 9% (p less than 0.05) respectively. Constant workload exercise performed at AeT intensity was linked before training (60% VO2max) to a blood lactate steady state (4.8 +/- 1.4 mmol.l-1) whereas, after training, AeT intensity (73% VO2max) led to a blood lactate accumulation of up to 6.6 +/- 1.7 mmol.l-1 without significant modification of muscle lactate (7.6 +/- 3.1 and 8.2 +/- 2.8 mmol.kg-1 wet weight respectively). It is concluded that increase in AeT with training may reflect transient changes linked to lower early blood lactate accumulation during incremental exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Two groups of human subjects were submitted to a 20-week endurance training program (1 h a day, 4 days a week, 70-80% max VO2). The first group (G20) consisted of eight 22 +/- 3 years male students, the second group (G60) was composed of seven still very physically active elderly male subjects (62 +/- 4 years). Training significantly increased max VO2 by 15% in G20 and 7% in G60. Muscle samples taken from the vastus lateralis muscle before and after training were histochemically stained for fibre-typing (myofibrillar ATPase), capillary supply and fibre area measurements (amylase PAS and NADH-TR). Fibre-type distribution was unchanged with training. Capillary density (cap X mm-2) increased significantly in both groups from 316 +/- 42 to 396 +/- 73 in G20 and from 308 +/- 48 to 409 +/- 55 in G60. This enhancement of capillary supply was linked to the proliferation of capillaries in G20 where the number of capillaries in contact with ST and FTa fibres (CC) significantly increased from 4.6 to 5.9 and from 4.8 to 6.1 respectively. No significant changes in fibre areas were found in G20. On the contrary, G60 did not show any significant sign of capillary growth (CC unchanged) whereas fibre areas significantly decreased in ST (6,410 to 5,520 micron 2) and FTa fibres (5,830 to 5,090 micron 2). A methodological evaluation of fibre-area measurement was described, with confirmation of the data. It was concluded that this study may illustrate the trainability of skeletal muscle of elderly men in a possibly different way to that seen in a younger age group.

The purpose of this review is to analyze the different factors which intervene with respect to the ability to perform intense exercises of long duration. This ability implies : (a) a high level of maximal oxygen uptake (Vo 2 max) and (b) a great endurance, i.e. the capacity of maintaining for a long time a high percentage of this Vo2 max. First of all, the values Vo2 max usually recorded on normal subjects are given, as well as those of subjects specially trained for endurance events ; then the factors which condition a high level of Vo2 max are described. These factors consist on great capacity in all of the links of the oxygen transport system. These capacities appear to be essentially dependant on the genetic endowment, but their maximal size can only by attained through intensive training. Endurance can be defined as the maximal period of time during which a given percentage of the Vo2 max can be sustained. The values recorded on normal subjects and on those specially trained for endurance events are given, and then the factors conditioning a high level of endurance are studied. Endurance appears to depend on the feeding of muscular fibers with energentic substrates. Training permits the muscles to store large quantities of glycogen. It also seems to enable the organism to increase the percentage of energetic substrates made up by lipids. This latter ability in associated with an alteration of the endocrine reactions induced by exercise. Finally, endurance is accompanied by an ability of the body to store and to eliminate the heat produced during exercise.

Eleven laboratory-pretrained subjects (initial\(\dot V_{O_{2max} } \)=54 ml·kg−1·min−1) took part in a study to evaluate the effect of a short endurance training programme [8–12 sessions, 1 h per session, with an intensity varying from 60% to 90% maximal oxygen consumption\((\dot V_{O_{2max} } )\)] on the responses of blood ammonia (b[NH4+]) and lactate (b[la]) concentrations during progressive and constant exercise intensities. After training, during which\(\dot V_{O_{2max} } \) did not increase, significant decreases in b[NH4+], b[la] and muscle proton concentration were observed at the end of the 80%\(\dot V_{O_{2max} } \) constant exercise intensity, although b[NH4+] and b[la] during progressive exercise were unchanged. On the other hand, no correlations were found between muscle fibre composition and b[NH4+] in any of the exercise procedures. This study demonstrated that a constant exercise intensity was necessary to reveal the effect of training on muscle metabolic changes inducing the decrease in b[NH4+] and b[la]. At a relative power of exercise of 80%\(\dot V_{O_{2max} } \), there was no effect of muscle fibre composition on b[NH4+] accumulation.

The effect of a 22.5 week training program on the fuel-hormone response to prolonged (1 h) high intensity (85% maximal aerobic power, MAP) of six male subjects was studied. The training program consisted of pedalling 1 h per day, four days a week, a bicycle ergometer at 80% of their MAP. It resulted in a 14.3% increase in Vo2 max (P less than 0.01). Training did not significantly alter the RQ neither the blood glucose and lipid values measured at the end of a 1 h exercise requiring 85% of Vo2 max. At the end of the exercise blood level of norepinephrine was unchanged; in contrast, that of epinephrine was significantly (35%; P less than 0.01) reduced at the end of training. These results lead to the conclusion that during high intensity submaximal exercise there is no consistent relationship between the epinephrine blood level and mobilization or metabolic utilization of energy substrates in trained subjects.

The influence of endurance-training on hematocrit, plasma vasopressin, renin activity, and aldosterone changes at rest and at the end of an exercise performed until exhaustion at a given and constant relative work-load (87% of maximal oxygen uptake) has been studied in four untrained subjects submitted to a 5-month training. At the end of this period, maximal oxygen uptake increased of 15.2% (p less than 0.01). Hematocrit at rest slightly rose after training, and if exercise constantly induced increases in hematocrit before (p less than 0.001) and after training (p less than 0.005), the per cent increase after training was lower than before (p less than 0.05). Comparison between the importance of weight loss and hematocrit variation showed that when untrained subjects become trained the variation of hematocrit after exercise becomes smaller while weight loss is more important (p less than 0.01). Plasma renin activity (PRA), aldosterone (Aldo) and vasopressin (AVP) levels, compared to control values, displayed a significant increase after exercise before as well as after training. Control values remained unchanged after training for aldosterone and AVP, but were significantly lower (p less than 0.05) for PRA. This latter observation could be explained by the change in blood volume induced by exercise.

The influence of exercise on blood borne substrates in relation to plasma catecholamine (CA) levels has been studied in untrained subjects (eight men and eight women). Subjects pedalled a bicycle ergometer for 20 min at a workload approximating to 80% maximal aerobic power. During exercise women reacted similarly to men except that their weight loss and hematocrit were significantly lower. At the end of the bicycling test, plasma dopamine (DA), norepinephrine (NE) and epinephrine (E) concentrations increased similarly in both groups. There was no significant difference in blood energy substrates between men and women except that the plasma free fatty acid (FFA) level was significantly higher in the female. When fitness levels were similar, the previously reported sex-related difference in response to exercise seemed to disappear. The lack of correlation between blood borne substrates variations and CA changes raised the question whether other hormonal factors combined with CA could play a role in the mobilization of energy substrates during exercise.

Six healthy subjects, aged 35.8 +/- 4.4 years, volunteered to participate in a 40-week training program on a bicycle ergometer [three 60-min sessions per week at 80%-85% of maximal oxygen uptake (VO2 max)]. Before training and at the 10th, 20th, 30th, and 40th weeks of the training program, plasma testosterone, cortisol, and androstenedione concentrations were measured at rest (t0) and at the end (t60) of a 1-h endurance exercise requiring 85%-90% of VO2 max. Training resulted in significant increases of anaerobic threshold (12.6%) and VO2 max (7.3%). The training program did not significantly alter the resting values of plasma testosterone, androstenedione, and cortisol; in contrast, the exercise responses (delta = t60-t0) of testosterone, androstenedione, and cortisol were increased. The highest amplitude of these responses was reached at the 30th week for cortisol and androstenedione and at the 40th for testosterone. These results suggest that long-term training enhances both testicular adrenal and responses to endurance exercise. The possible role of hormonal changes in the mobilization of energy substrates during exercise is discussed.

The H.R./\(\dot V_{O_2 }\) relation was checked in 20 healthy male students performing exercises of different intensities at sea level and in acute moderate hypoxia. This hypoxia was induced by breathing a wet oxygen nitrogen mixture (\(FI_{O_2 } \) = 0.15) at the ambiant pressure.