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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.

To describe the time course of plasma volume alterations and the changes in the plasma concentrations of hormones regulating water balance in relation to a marathon race, six experienced marathon runners (five men, one women) aged 28 (SD 6) years were studied during and for the 3 days following a treadmill marathon run at 68 (SD 5) percent of maximal oxygen consumption. Haematocrit, haemoglobin, plasma protein (Prot) and electrolyte (Na+, K+) concentration, osmolality (osm), plasma concentrations of renin (Ren), aldosterone (Ald) and atrial natriuretic peptide (ANP) were determined at rest in a sitting position (T(-30)), and then after 30 min in an upright posture (R(0)), while running a marathon at 10 km (R(10)), 30 km (R(30)) and 42.2 km (R end), and after the marathon at 30 min (T(30)), 60 min (T(60)), 120 min (T(120)) and 24 h (TD(+1)), 48 h (TD(+2)) and 72 h (TD(+3)). The changes in plasma volume (PV), Prot, osm and Na+ observed during the race were nonsignificant. Significant increases in plasma concentration of K+ [4.8 (SD 0.6) vs 5.5 (SD 0.6) mmol*1(-1); P0.01], Ren [38(SD 57) vs 197 (SD 145) pmol*1(-1); P0.02] and Ald [175 (SD 142) vs 1632 (SD 490) pmol*1(-1); P0.01] were observed at R(end). A significant increase of ANP (P0.05) was only found after R(10). Body mass significantly decreased by 2.0 kg (P0.01) during the race in spite of the ingestion of 1.46 (SD 0.34)1 of a 5 percent glucose solution. Urinary volume and Na+ excretion dropped significantly after the completion of the marathon in comparison with the day before [2600 vs 1452 ml*day(-1)(P0.02) and 161.3 vs 97.1 mmol*1(-1) (P0.05)]. At TD(+1) and TD(+2) a significant increase in PV was noted, compared to T(-30). The lack of a decrease in PV during the marathon may have been due to the production of 402 g of metabolic water and by the release of 1280 g of water stored in glycogen complexes in muscle and liver. Thus, the hormone response during the marathon may have been due to the effects of the exercise itself and not to the effects of dehydration. The postmarathon PV expansion may be explained by a protein shift to the intravascular space and by renal sodium retention.

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.

This study was designed to discriminate, according to their accuracy, between eight pulse oximeters (PO) using a realistic evaluation performed by means of a moderate exercise to provide artefacts and thus represent a typical clinical situation. Accuracy was assessed by calculating error on saturation (EOS) as the difference between simultaneous measurement of non-invasive (SpO2) and invasive functional (SfO2) arterial blood oxygen saturation. An index of homogeneity of EOS (InH), calculated using a Lehmann analysis, was chosen as a representative of error dispersion, leading to a statistical classification; the influence on error introduced by the drift of EOS with SfO2 was thus eliminated. We obtained a clear-cut separation of the eight PO (Datex Satlite (DA), Kontron 7840 (KO), Nellcor 200 (NE), Novametrix 505 (NO), Ohmeda 3700 (OH), PPG-Hellige (PP), Physiocontrol 1600 (PH), and Radiometer Oxi (RA] into two statistically different subgroups by comparing their InH standard deviation (SD). There is a highly statistically significant difference between the accuracy measured for the high precision subgroup with an InH SD ranging from +/- 1.6 to +/- 1.9% SaO2 (DA, PH, and RA), and that measured for the low precision subgroup whose InH SD ranges from +/- 2.8 to +/- 5.0% SaO2 (NE, OH, NO, KO, PP). These results suggest that, in our clinical conditions, there is a wide range of inhomogeneity of error from one PO to another. The error introduced by the drift of EOS with SfO2 should be considered separately.

This study validated the laboratory testing used to monitor on water training. The purpose was to test that reference heart rates (HR) determined during an incremental test elicit comparable blood lactate levels ([La](b)) during a 30 min on water rowing.Blood lactate profile were determined during incremental graded exercise in 14 national and international level oarsmen. The HR corresponding to [La](b) of 2 and 3 mmol x l(-1) were determined (HRLa2 and HRLa3 respectively). The rowers then performed a 30 min training session in a boat. Training intensity, as assessed by HR monitors, had to range between HRLa2 and HRLa3. Field [La](b) (Laf) and HR (HRf) were measured at the end of the training session.Laf was 2.13+/-0.49 mmol x l(-1) (range: 1.43-3.07) and did not differ significantly from 2 mmol x l(-1). HRf (162+/-7.4 beats x min(-1)) ranged from HRLa2 (159+/-9.5 beats x min(-1)) to HRLa3 (171+/-9 beats x min(-1)). HRf was not significantly different from HRLa2.It was concluded that the HR determined during the laboratory testing are valid for monitoring on water training in highly trained rowers.

The purpose of this study was to determine the importance of leg strength and stiffness relative to i) 100 m sprint performance, ii) mean speed on the three phases of the 100 m race (30-60-100 m) and iii) the speed differences between these phases.Nineteen regional to national level male sprinters competed in a 100 m race. Video analysis was used to determine mean velocity parameters. Two subgroups were created since some of the runners decreased their velocity during the third phase (G1), whereas others maintained or accelerated it (G2). Leg strength (concentric half-squats - counter movement jump) and stiffness (hopping) were determined. Simple (r) and multiple regressions (R) were used.The mean performance over 100 m was 11.43 sec (10.72-12.87 sec). The concentric half-squats were related to 100 m (r=0.74, p0.001) and to the mean speed of each phase (R=0.75, p0.01). The counter movement jump was related to 100 m (r=0.57, p0.05) and was the predictor of the first phase (r=0.66, p0.01). The hopping test was the predictor of the two last phases (R=0.66, p0.05). Athletes who had the greatest leg stiffness (G1) produced the highest acceleration between the first and the second phases, and presented a deceleration between the second and the third ones.The concentric half-squats test was the best predictor in the 100 m sprint. Leg stiffness plays a major role in the second phase.

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.

In chronic congestive heart failure (CHF), attenuated heart rate response to exercise, a manifestation of chronotropic incompetence (CI), contributes to limiting exercise capacity. The present study was thus conducted to evaluate the respective role of chronic attenuation of cardiac vagal tone associated with depressed baroreflex sensitivity or affected cardiac sympathetic responsiveness in CHF patients with CI. Spontaneous cardiac baroreflex sensitivity (BRS) assessed by sequence method and spectral- and time-domain analysis of heart rate variability (HRV) were analysed in 21 chronic CHF patients. All patients performed a symptom-limited exercise test with measurement of gas exchange. Chronic incompetence which was defined as failure to achieveor =80% of the heart rate reserve (%HRR) given by (HRpeak - HRrest)/(predictive maximal heart rate - HRrest) was observed in 14 (66%) patients. There was no significant difference in age, heart rate, peak oxygen uptake or left ventricular ejection fraction between the patients with and without CI. Although there was no significant difference in BRS, low frequency power of HRV in normalized units (LFnu) and SDNN were significantly lower in CI patients. Percentage of HRR correlated significantly with LFnu on 15 min (r=0.64, P0.005) and, with LFnu on 24 h (r=0.52, P0.01), SDNN (r=0.48, P=0.03) and SDANN (r=0.48, P=0.03), but not BRS (r=0.04, P=NS). Autonomic nervous system derangement is a complex process in CHF. The role of basal depressed cardiac sympathetic tone seems to contribute more closely than depressed baroreflex sensitivity to the impaired heart rate response to exercise frequently observed in CHF patients.

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.

The hyperoxia-improved tolerance to maximal aerobic performance was studied in relation to exercising muscle metabolic state. Five students were submitted to four different tests on a cycle ergometer, each being conducted under normoxia and hyperoxia (60% FiO2) on separate days: Test 1, a progressive exercise until exhaustion to determine the maximal work load (Wmax) which was unchanged by hyperoxia; Test 2, an exercise at Wmax (287 +/- 12 W) until exhaustion to determine the performance time (texh) which was elevated by 38% under hyperoxia but exhaustion occurred at the same arterial proton and lactate concentrations; Test 3 (S-Exercise test) consisted of cycling at Wmax for 90% normoxic-texh (4.8 +/- 0.5 min under both O2 conditions) then followed by a 10-s sprint bout during which the total work output (Wtot) was determined; Wtot was elevated by 15% when exercising under hyperoxia; Test 4 (M-Exercise test) consisted also of cycling at Wmax for 4.8 +/- 0.5 min with blood and muscle samples taken at rest and at the end of the exercise to compare the level of different metabolites. During hyperoxic M-Exercise test, glycogen was twice more depleted whereas glucose-6-phosphate and lactate were less accumulated when compared with normoxia. No significant differences were observed for pyruvate, phosphocreatine and muscle/blood lactate ratio between the two conditions. Conversely to normoxia, levels of ATP, ADP and total NADH were maintained at their resting level under 60% FiO2. These data lead us to suppose a higher oxidation rate for pyruvate and NADH in mitochondria, thereby lowering the metabolic acidosis and allowing a better functioning of the glycolytic and contractile processes to delay the time to exhaustion.

The increased sympathetic activation that occurs in obstructive sleep apnoea (OSA) may play an important role in associated morbidity. We investigated the effect of long-term (3 month) nasal continuous positive airway pressure (CPAP) on the autonomic nervous system assessed by heart rate variability (HRV). Fourteen patients (12 men), mean age 61.4 +/- 8.1 years, with OSA underwent continuous synchronized electrocardiographic and polysomnographic monitoring. The apnoea/hypopnoea index (AHI) decreased from 50.6 +/- 13.7 to 2.2 +/- 2.5 events h-1 after CPAP. HRV analysis showed significant decreases in low frequency (LF; from 7.12 +/- 1.06 to 6.22 +/- 1.18 ln ms2 Hz-1; P0.001), high frequency (HF; from 5.91 +/- 0.87 to 5.62 +/- 0.92 ln ms2 Hz-1; P0.05) and LF/HF (from 1.21 +/- 0.12 to 1.11 +/- 0.15 ln ms2 Hz-1; P0.001) when the patients were asleep. The decrease in LF/HF was prolonged into the daytime (from 1.33 +/- 0.22 to 1.24 +/- 0.21 ln ms2 Hz-1; P0.001). Treatment of OSA by CPAP significantly reduced the parameters of cardiac sympathetic tone, a favourable effect.

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.

During both the cool and hot periods of the dry season of the Sahelian climate, sleep patterns of four African sportsmen from Niger (23 +/- 0.8 years old) were studied after square-wave cycle ergometer exercise. The sleep patterns were studied in the sedentary (Baseline) condition and under two exercise conditions, with and without rehydration. All conditions were randomly assigned. The exercise programme consisted of 3 sequences of cycling, beginning with 10 min at 30% of maximal aerobic power (MAP), followed by an exhaustive supramaximal effort (130% of MAP), and ending with a 10 min recovery at 30% of MAP. Polysomnography was recorded for 2 consecutive nights in each condition. One adaptation night, to familiarize the subjects to the polysomnography protocol, preceded the first session. Baseline slow-wave sleep (SWS) and REM sleep were high. In the hot season, there was an overall increase in SWS (p0.02), due primarily to an increase in Stage 4 (p0.01). Stage 2 sleep decreased (p0.01). This effect was also observed after exercise with rehydration, but was absent in the non-hydration condition. This distinction between the rehydrated and non-rehydrated condition is thought to be due to the greater stress which may accompany an exercise-induced relative dehydration. REM sleep decreased after exercise in the cool season (p0.001), but equalled baseline levels during the hot season. The results suggest a combined action of hyperthermia, water balance and stress, and are further supportive of an underlying hypothalamic control of human sleep.

The objective of this study was to design and validate a working tool for the objective evaluation of daily energy expenditure (DEE) by means of a simple, noninvasive method: the QAPSE (Saint-Etienne Physical Activity Questionnaire), a questionnaire about physical activity (PA) over a period of 7 d (168 h). This eight-page questionnaire is designed to provide a complete picture of the subject's habitual PA without any restriction concerning the activities investigated, nor any specialization in relation to health components. It investigates the five areas of PA during daily life: work or way of keeping occupied, leisure activity (sports and nonsports activities), housework, basic everyday activity, moving about from place to place. Assessment of physical activity was conducted in 115 healthy volunteer subjects of both sexes aged 20-88. The values of mean habitual daily energy expenditure (MHDEE) obtained varied between 6,510 and 24,331 kJ.d-1. The MHDEE were in agreement with the data reported in the literature for various groups differing in respect to level of activity, sex, and age. The study demonstrated the reproducibility of the QAPSE (r = 0.997; N = 20; P0.0001). Its validity was tested in a comparative study between MHDEE and caloric intake (r = 0.576; N = 20; P0.01).

The effects of 7 weeks of sprint training (repeated 5-s all-out sprints) on maximal power output (Wν, max) determined during a force-velocity test and a 30-s Wingate test (Wpeak) were studied in ten students [22 (SD 2) years] exercising on a cycle ergometer. Before and after training, muscle biopsies were taken from vastus lateralis muscle at rest for the ten subjects and immediately after a training session for five of them. Sprint training induced an improvement both in peak performances by 25% (Wν, max and Wpeak) and in the 30-s total work by 16%. Before sprint training, the velocity reached with no load (ν0) was related to the resting muscle phosphocreatine (PCr) stores (r=0.87, P < 0.001). The training-induced changes in ν0 were observed only when these PCr stores were lowest. This pointed to a possible limiting role of low PCr concentrations in the ability to reach a high velocity. The improvement in performances was linked to an increase in the energy production from anaerobic glycolysis. This result was suggested in muscle by the increase in lactate production measured after a training session associated with the 20% higher activity of both phosphofructokinase and lactate dehydrogenase. The sprint training also increased the proportion of slow twitch fibres closely related to the decrease in fast twitch b fibres. This result would appear to demonstrate an appropriate adaptive reaction following high-intensity intermittent training for the slow twitch fibres which exhibit a greater oxidative capacity.

The sickle cell trait (HbAS) does not seem to affect exercise performance. It remains unclear, however, whether the capability to sustain repeated brief maximal effort and recovery by HbAS subjects, is also preserved. To study this, nine HbAS and nine matched controls underwent on two different occasions, a series of four, approximately 2-min duration, maximal cycle exercise tests separated by 20-min recovery periods of either absolute rest (P) or light pedaling (A) as well as an incremental test to exhaustion. In all tests, work performed, heart rate, blood hematocrit, lactate, and serum creatine kinase (CK), lactate dehydrogenase (LDH), and aspartate aminotransferase (GOT) were measured. Performances were similar in HbAS and HbAA subjects in both the predominantly anaerobic and aerobic exercise series. There were no observable differences in work, power, or heart rate in the two groups both during peak exercise or recovery periods. A significant hemoconcentration was observed during P, with hematocrit increasing in HbAS from 46.4 +/- 0.7% to 48.3 +/- 0.4% at the end of the last recovery period. Similar changes were seen in HbAA. Significantly greater fluid losses were found during A (1.3 +/- 0.2 l in A and 0.6 +/- 0.1 l in P for HbAS; P0.001), but fluid losses were similar in each type of recovery in the two groups. Despite similar performance, significantly lower blood lactate concentrations were consistently found in HbAS in each of the three exercise series (P0.001). Lower lactate levels in HbAS were observed only at exercise loads above the lactate threshold during the incremental test (P0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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

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.

In exercise stress testing the quantification of effort on which the value and significance of the test depend is based on two simple and practical criteria: theoretical maximal heart rate for age (MHR) and serum lactic acid levels 3 minutes after exercise. Usually only MHR is used, 85% of MHR being the common cut-off point between "interpretable" maximal or "inframaximal" effort and useless effort. Our study was based on 1 000 exercise stress tests performed over a two year period with the same protocol and equipment. Initially, we determined our values of MHR and serum lactic acid in undoubted maximal effort stress tests, as shown by a levelling out of the heart rate during the last load increments, the last stage of exercise being sustained for at least 1.5 minute. The application of both criteria to all the investigations showed significant differences in the evaluation of the exercise obtained when the maximal measured heart rate was between 85 and 95% of MHR. This was also true, to a lesser extent, in patients over 60 years of age or under 30 years of age with maximal measured heart rate of 85% or less than MHR. A discussion of the theoretical basis of the two criteria helps explain this divergence, attributing it to the inaccuracy and unreliability of the MHR. The only obstacle to the use of serum lactate as the preferential indicator of maximal effort is the need for laboratory facilities and the delay in obtaining the result.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Eleven young students were tested to determine the relationship between the improvement of mental performances observed under prolonged submaximal work and central or peripheral catecholamine changes. The subjects pedaled a bicycle ergometer for 1 h at a work load individually calculated to approximate 75% of maximal oxygen uptake. The mental test, consisting of 1-h sessions of time-limited word tests and arithmetical calculations, required a high degree of concentration (vigilance and short-term memory). Catecholamines [epinephrine (E), norepinephrine (NE), dopamine (DA)], metanephrine (MN), normetanephrine (NMN) and the glucuronide conjugate of 3-methoxy 4-hydroxyphenylglycol (MHPG) were assayed in urine to assess peripheral activity: E and MN as indexes of adrenomedullary secretion, NE, NMN and MHPG glucuronide as markers of NE metabolism in sympathetic nerves. Urinary MHPG sulfate was determined as a possible marker of central noradrenergic metabolism. When compared to the effect of single tests, the combination of prolonged submaximal work and mental task induced significant increases in MHPG sulfate and E + MN excretions. Both these increases were correlated each to one another and also correlated to the number of discriminated words. Altogether, the present data show that prolonged submaximal work under mental load activates catecholamine systems and suggest that a relationship exists between adrenomedullary activation and the improvement of mental performance. Based on literature data, the possible modulatory role of peripheral E on mental processes and central noradrenergic activity is discussed.

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.