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Summary. The purpose of this study was to investigate the effects of a 8-week of swim training on total plasma homocysteine and cysteine levels in 16 male Sprague-Dawley rats aged 17 weeks. We also evaluated the activity of hepatic cystathionine ß-synthase (CBS), an enzyme involved in the metabolism of Hcy, the concentration of plasma glutathione, taurine, and a fraction of vitamin B6: the pyridoxal 5-phosphate (PLP). After one week of acclimatization, rats were randomly divided into two groups: 8 non-trained (NTR) and 8 trained rats (TR). Following the training period, body weight gain was lower in TR than in NTR. Plasma homocysteine did not differ among groups while significantly lower plasma cysteine and taurine levels were found in TR (157.83±8.6?µmol/L; 133.01±9.32?µmol/L; P<0.05) compared with data of NTR (176.19±4.9?µmol/L; 162.57±8.16?µmol/L; P<0.05). No significant changes in hepatic CBS activity were observed in TR compared with NTR. Moreover, values for plasma glutathione and PLP concentrations were not affected by training.

The purpose of the study was to compare the cardiovascular, respiratory and metabolic responses to exercise of highly endurance trained subjects after 3 different nights i.e. a baseline night, a partial sleep deprivation of 3 h in the middle of the night and a 0.25-mg triazolam-induced sleep. Sleep-waking chronobiology and endurance performance capacity were taken into account in the choice of the subjects. Seven subjects exercised on a cycle ergometer for a 10-min warmup, then for 20 min at a steady exercise intensity (equal to the intensity corresponding to 75% of the predetermined maximal oxygen consumption) followed by an increased intensity until exhaustion. The night with 3 h sleep loss was accompanied by a greater number of periods of wakefulness (P<0.01) and fewer periods of stage 2 sleep (P<0.05) compared with the results recorded during the baseline night. Triazolam-induced sleep led to an increase in stage 2 sleep (P<0.05), a decrease in wakefulness (P<0.05) and in stage 3 sleep (P<0.05) After partial sleep deprivation, there were statistically significant increases in heart rate (P<0.05) and ventilation (P<0.05) at submaximal exercise compared with results obtained after the baseline night. Both variables were also significantly enhanced at maximal exercise, while the peak oxygen consumption (VO2) dropped (P<0.05) even though the maximal sustained exercise intensity was not different. Lactate accumulation was altered by sleep loss, undergoing an upward drift from the 9th min of steady power output [4.92 (SEM 0.44) mmol·1-1 vs control (CT) 3.91 (SEM 0.27) mmol·1-1, P<0.05] until maximal effort [10.92 (SEM 0.83) mmol·1-1 vs CT 9.26 (SEM 0.79) mmol·1-1, P<0.05]. After triazolam-induced sleep, heart rate, ventilation, (VO2) and blood lactates were not significantly different during steady power output from the values observed after the baseline night. However the maximal sustained exercise intensity was greater [380 (SEM 13.1) W vs CT 361.4 (SEM 13) W, P<0.01], which led to an increase in ventilation (P<0.01) without any change in heart rate, (VO2) or lactate concentration. These results suggested that partial sleep loss may have contributed to the change in athletic performance and that triazolam did not impair the physiological responses to exercise during the following afternoon.

The aim of the present study was to investigate the effects of a delayed bedtime (3 a.m.), an advanced rising (3 a.m.), a sleep under placebo and under a hypnotic compound, i.e. 10 mg of Zolpidem (Stilnox®) on sleep structure and on the adaptations to a subsequent exercise in 8 male athletes. The chronology of these nights was randomized and each treatment administered in a double blind fashion. During each experimental night, subjects were monitored with conventional EEG/EOG/EMG polygraphic recordings. The next day, athletic performance was tested using a bicycle ergometer. A codified exercise was performed and consisted to a 10 min warm up followed by a 30 min steady state cycling corresponding to 75% of predetermined V˙O2 max. Then the work load increased progressively by steps of 10 W every minute until exhaustion. The recovery lasted 30 min. Heart rate, ventilation, V˙O2, ERO2 were monitored during all exercise and recovery. Plasma lactates and catecholamines were also measured at the same time. The data concerning sleep recordings showed that both nights with partial sleep deprivation resulted in a drop of time spent in slow wave sleep II (decrease of 55%) and in rapid eye movement sleep (decrease of 45%) while the amount of slow wave sleep III and IV were identical to that observed after the reference night. The sleep onset latency and the amount of sleep in stage I was reduced only after the delayed bedtime. Sleep data under Zolpidem did not show any significantly difference in the amount of different sleep stages. At subsequent exercise conducted after both reduced-sleep nights, lactate levels and minute ventilation were significantly higher during the constant load cycling whereas heart rate, V˙O2 and catecholamines were not altered. At maximal exercise, neither lactate nor V˙E were impaired while peak V˙O2 decreased and the V˙E/V˙O2 increased. The other parameters were not modified. The maximal sustained work load had a tendency to be lower after the late bedtime (294 ± 31 W) and after the early rising (292 ± 37 W) compared to control (308 ± 28.9 W). At recovery, no difference was observed in the studied parameters. After nights induced by Zolpidem or placebo, no alteration in cardiorespiratory and metabolic values was noted. These findings show that physiological adaptations and the ability to perform maximal exercise are affected by a partial sleep loss but not by a single ingestion of Zolpidem prior to sleep.

The present study compared the effects of partial sleep deprivation and the effects of an intake of a hypnotic compound (zolpidem) prior to bedtime, on sleep and on hormonal and metabolic adaptations to subsequent exercise. Sleep deprivation consisted of a delayed bedtime and an early getting-up time. Eight young subjects, who slept well and were highly trained athletes, were enrolled in this study. Sleep was recorded polygraphically and the following afternoon exercise was performed on a cycle ergometer for 30 min at 75% of maximal oxygen consumption (VO2max) after a 10-min warm up. Met-enkephalin, ß-endorphin, cortisol, and lactate concentrations were measured at rest and during exercise. The data obtained after experimental sleep, with and without medication were compared with those obtained in the reference condition with normal sleep. Both types of sleep reduction decreased the total sleep time, stage 2 sleep, and rapid eye movement sleep, whereas zolpidem administration did not modify either the duration of sleep or the sleep stages. After the reference night, plasma met-enkephalin did not show any significant change at the end of the submaximal exercise, whereas ß-endorphin, cortisol, and lactic acid concentrations increased significantly in all subjects. The changes in concentration in ß-endorphin were significantly related to the changes in cortisol (r=0.78;P<0.01) and to the changes in plasma lactic acid (r=0.58;P<0.05). Cortisol concentrations were also related to lactic acid values (r=0.94;P<0.01). Partial sleep loss altered lactate concentrations during submaximal exercise but did not affect the hormonal levels of met-enkephalin, ß-endorphin and cortisol in the blood. Zolpidem administration failed to change lactate and hormone concentrations. These results suggested that partial sleep deprivation may have contributed to the changes in metabolic responses without significantly altering the hormonal response to exercise. Zolpidem intake did not impair the response of different variables to exercise the following day.

The changes in circulating concentrations of insulin-like growth factors during exercise have to date remained incomplete in their documentation. Therefore, we examined in 25 healthy athletes the effects of three different durations of three types of exercise – incremental ergometer cycling exercise (ICE), long-distance Nordic ski race (NSR) and a treadmill-simulated soccer game (TSG) lasting 20 min, 3 h, and 2 × 45 min separated by a 15-min half-time rest respectively, on plasma concentrations of growth hormone ([GH]), insulin-like growth factor-1 ([IGF-I]) and its binding proteins 1 and 3 ([IGFBP-1], [IGFBP-3]). Compared to baseline, serum [GH] increased by 15.2-fold after ICE ( P < 0.001), 2.9-fold after NSR ( P < 0.01) and 4.6-fold after TSG. Serum [IGF-I] rose by 11.9% after ICE ( P < 0.001), while it decreased by -14.6% after NSR ( P < 0.001) and was unchanged after TSG. Serum [IGFBP-1] was slightly increased (1.7-fold) after ICE ( P < 0.01), but increased markedly (11.8-fold) after NSR ( P < 0.001) and by 6.3-fold after the second session of TSG ( P < 0.01) (it remained unchanged at the end of the first period of TSG, i.e. after 45-min exercise). The [IGFBP-3] increased by 14.7% after ICE ( P < 0.001) and by 6% after TSG ( P < 0.05) while it did not change after NSR. From our results it would appear that [IGFBP-1] increase to bind free IGF and hinder their insulin-like action during long-term exercise (lasting beyond 45 min). It is suggested that IGFBP-1 might thus contribute both to preventing hypoglycaemic action of IGF and to facilitating glucose uptake by muscle cells when muscle glycogen stores become deplete.

Évaluer chez des adolescents obèses la relation entre inflammation et SAOS et de déterminer les facteurs expliquant une baisse de l’inflammation à l’issue d’une prise en charge (PEC) pluridisciplinaire de 9 mois.

L’objectif de cette étude a été de déterminer l’impact de la sévérité du syndrome d’apnée obstructive du sommeil (SAOS) et du niveau d’endurance cardiovasculaire sur les paramètres anthropométriques et métaboliques de jeunes obèses.