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Most of increases in energy metabolism are induced by exercise. They are related with power and efficiency. In cycle ergometer exercise efficiency is positively correlated with exercise power and negatively correlated with pedaling rate. Ramp exercises are associated with an apparent increase in efficiency. Movements of daily life activity are too complex to make evaluation of power or efficiency possible. Energy expenditure assessment is based on direct measurement of the energy metabolism increase. The energy cost of movement or economy is calculated. Daily activity recording provides an assessment of the energy metabolism ability of patients. Muscle contractile activity is linked with ATP splitting. The pathways to resynthesize ATP include anaerobic glycogenolysis and the aerobic breakdown of substrates. Type I fibres have a higher oxidative capacity than type II fibres. Type II fibres demonstrate a higher glycolytic capacity, contract faster, and are more fatigable. Information relative to energy expenditure during daily life activity allows clinicians to better assess the clinical implications of the stress tests results.

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.

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 (p < 0.02), due primarily to an increase in Stage 4 (p < 0.01). Stage 2 sleep decreased (p < 0.01). 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 (p < 0.001), 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.

A simple device for three-dimensional recording of human movement was developed. It consisted of four rigid bars linked together by three joints. At each joint an optical transducer, connected to a PC computer via an electronic interface, measured the joint angle, rendering it possible to compute the displacement of one end (measuring end) relative to the other (reference end). This kinematic arm was validated (i) in static conditions; (ii) in dynamic conditions; and (iii) during human jumping. The measured error was 0·4%±0·5% (mean±s.d.) on distance measurements in static conditions, 0·l%± 1·6% on 0·57 m.s−1 rotation velocity measurements and 3·2% ±3·3% on 3·56 m.s−2 rotation acceleration measurements, and l·6%±20·7% on force measurements during human jumping. These error values are equivalent to or lower than errors linked to tracking systems or to film or video analysis. Therefore, if the movement is not disturbed by the spatial limitation due to the mechanical link with the measuring end, the kinemati...

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.

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.

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).

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.

Using the new method of sample preparation developed by the manufacturer in 1979, the lactate analyser LA 640 now provides reliable measurements of blood lactic acid from blood micro-samples of 20 microliters within 2 min. Reproducibility is comparable to that obtained by spectrophotometric assay with +/- 0.2 mmol . l-1 for 95% confidence limits. High accuracy was also obtained with 95% linked confidence limits within +/- 0.19 mmol . l-1 and +/- 0.46 mmol . l-1 for blood lactate concentrations of from 2-4 and 7-9 mmol . l-1 respectively. Due to a lactate concentration increase of 0.5 mmol . l-1 . h-1 in whole blood kept at 20 degrees C, the blood must be immediately diluted in the buffer haemolysing solution after withdrawal. This diluted sample can then be stored at room temperature without alteration, provided the concentration in the dilution is lower than 0.8 mmol . l-1. For serial successive measurements, a new sample can be tested before the electrode current reaches its background value.

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)

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 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.