Search PubMed⌕ Search

Biomedical subjects

D Davenne

Publications and source records attributed to D Davenne.

10 recordsLinked to original sources
PubMed1992

Met-enkephalin, beta-endorphin and cortisol responses to sub-maximal exercise after sleep disturbances.

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, beta-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 beta-endorphin, cortisol, and lactic acid concentrations increased significantly in all subjects. The changes in concentration in beta-endorphin were significantly related to the changes in cortisol (r = 0.78; P less than 0.01) and to the changes in plasma lactic acid (r = 0.58; P less than 0.05). Cortisol concentrations were also related to lactic acid values (r = 0.94; P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Effects of sleep disturbances on subsequent physical performance.

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 warm-up, 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 less than 0.01) and fewer periods of stage 2 sleep (P less than 0.05) compared with the results recorded during the baseline night. Triazolam-induced sleep led to an increase in stage 2 sleep (P less than 0.05), a decrease in wakefulness (P less than 0.05) and in stage 3 sleep (P less than 0.05). After partial sleep deprivation, there were statistically significant increases in heart rate (P less than 0.05) and ventilation (P less than 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 less than 0.05) even though the maximal sustained exercise intensity was not different.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Regulation of noradrenergic coerulean neuronal firing mediated by 5-HT2 receptors: involvement of the prepositus hypoglossal nucleus.

Previous studies have indicated a 5-HT2-mediated inhibitory influence on unit activity in the locus coeruleus. In the present work, attempts were made to determine which area(s) of the brain is (are) involved in this effect: (1) Microiontophoretic application of serotoninergic compounds (quipazine, ketanserin, RU 24969 (Roussel Uclaf), 8-hydroxy-2(di-n-propylamino) tetralin (8-OH-DPAT), metergoline, serotonin) in the locus coeruleus, did not alter the coerulean discharge. Local microinjection of quipazine or ketanserin in the area of the locus coeruleus, as well as in one of its major afferents, the prepositus hypoglossi, had no effect on the unit activity in the locus coeruleus. (2) Section of the forebrain, caudal to the frontal cortex (rich in 5-HT2 receptors), did not modify the effects of coerulean activity of quipazine-ketanserin injected systemically: quipazine induced an inhibition which was reversed by ketanserin. In contrast, these effects were significantly reduced after the bilateral or contralateral lesion of the prepositus hypoglossi. It is concluded that the prepositus hypoglossal nucleus is part of the network responsible for the 5-HT2-mediated control of unit activity in the locus coeruleus.

Animals↗
PubMed1989

Lesion of the PGO pathways in the kitten. II. Impairment of physiological and morphological maturation of the lateral geniculate nucleus.

Suppression of the geniculate ponto-geniculo-occipital (PGO) waves by bilateral lesions of PGO pathways at the mesencephalic level in 15-day-old kittens has been shown to induce a significant reduction of the mean discharge frequency recorded in the lateral geniculate nucleus (LGN) during paradoxical sleep. The present paper reports that one month after the bilateral lesion (i.e., 6-7 weeks of age) important deficits in the maturation of the LGN were observed: (1) electrophysiologically, the latencies of the LGN cellular responses to stimulation of the optic chiasm were significantly longer than those of age-paired controls or of unilaterally lesioned animals, and the proportion of visual cells characterized as type X by stimulation of the visual field was smaller; and (2) morphologically, the volume of the LGN and the size of its neuronal somata were smaller than those in control. These data suggest that bilateral suppression of extraretinal PGO afferents to the LGN in the kitten induces a significant delay in the development of this nucleus.

Action Potentials↗
PubMed1989

[Current physiologic data on sleep].

Sleep is organized as a succession of different physiological states. Despite the fact that the mechanisms which regulate these states has been located in the central nervous system, our knowledge of these regulations is very poor. In this paper, different hypothesis implying brain locations, neurotransmitters, and neuroimmunomodulators are shortly described.

Age Factors↗
PubMed1989

[Disturbance of sports performance after partial sleep deprivation].

The changes in cardiac and ventilatory responses were measured in 7 endurance athletes during physical exercise on a bicycle ergometer, taking place after a control night and after a night with partial sleep deprivation in the middle of the night. The results show that, despite the maximal work load was not modified with control, heart rate, ventilation and VE/VO2 ratio (ERO2) were greater at the submaximal (75% of the VO2 max) and maximal work load and oxygen consumption decreased at maximal work, after the night of partial sleep deprivation as compared to the control. These findings suggest that acute sleep loss may contribute to alter the endurance performance by impairment of aerobic pathways.

Adult↗
PubMed1987

Bacterial peptidoglycans as modulators of sleep. I. Anhydro forms of muramyl peptides enhance somnogenic potency.

Chemically defined muramyl peptides (MPs), derived primarily from enzymatic digests of Neisseria gonorrhoeae peptidoglycan, were used to define the structural determinants of MP-mediated somnogenic activity. One of these, i.e. N-acetylglucosaminyl-N-acetyl-1,6-anhydro-N-acetylmuramyl-alanyl-glutamy l- diaminopimelyl-alanine, was structurally identical to the major naturally occurring MP previously detected in mammalian brain and urine. The somnogenic potency of this MP was similar to that of the corresponding disaccharide pentapeptide containing an additional alanine at the C-terminus and the analogous anhydro-muramic acid-containing monosaccharide tetrapeptide lacking the glucosamine moiety. Infusion of as little as 1 pmol of these highly active MPs increased significantly the percentage of slow-wave sleep in experimental animals. In fact, each of 5 anhydro-muramyl disaccharide peptides tested was somnogenic at a dose of 10 pmol or less and, as far as tested, the activity was affected only slightly by the length or composition of the peptide side chain. However, none of a matched set of analogous MPs, differing only in replacement of the anhydro-muramyl end by a hydrated muramic acid residue, was somnogenic at this dose. A modified form of the hydrated muramyl tripeptide containing a free amide on the diaminopimelic acid residue was completely inactive in amounts up to 1000 pmol. Together, the current data suggested: that the anhydro-muramic acid end (but not the glucosamine moiety) is essential for maximal somnogenic potency; and that amidation of carboxyl groups on the peptide-side chain may block MP-mediated somnogenic activity.

Anhydrides↗
PubMed1987

Bacterial peptidoglycans as modulators of sleep. II. Effects of muramyl peptides on the structure of rabbit sleep.

Sleep-promoting substances derived from human urine and rabbit brain were identified as muramyl peptides (MPs). We report in the accompanying paper that in the molecular structure of MPs, the 1,6-anhydro muramic acid moiety of MPs is important for enhancement of slow-wave sleep (SWS) in rabbits. Here, we document more extensively the effects of one MP: 1,6-anhydro-muramyl-alanyl-glutamyl-diaminopimelyl-alanine (AMTP for anhydro-muramyl tetrapeptide) on sleep structure of rabbits. AMTP significantly increased percent of time spent in SWS but its effects on rapid eye movement (REM) sleep were dose-dependent. Brain temperatures were significantly elevated but continued to fluctuate with sleep and wake state transitions indistinguishably from control. Sleep was episodic and animals could be easily aroused. AMTP increased number of SWS episodes and decreased number of REM episodes. There was a shift in the distribution of sleep-wake episode durations: longer waking and REM episodes were decreased, thus increased the proportion of shorter episodes. Increased duration of SWS resulted from a larger number of SWS episodes longer than 8 min. We conclude that AMTP amplifies the SWS compenent of physiological sleep.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMedDate not supplied

[Tolerance to exertion after sleep reduction and after taking a hypnotic: zolpidem].

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 VO2 max. Then the work load increased progressively by steps of 10 W every minute until exhaustion. The recovery lasted 30 min. Heart rate, ventilation, VO2, 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.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗