Interindividual variability of surface EMG changes during cycling exercise in healthy humans.

We studied surface electromyogram (SEMG) changes during 1-h endurance cycling in 12 healthy subjects of whom five were involved in mountain bike training programme. The work load was set at 50% of the predicted maximal heart rate. The surface EMG and the compound evoked muscle action potential (M-wave) from the vastus lateralis muscle were recorded at rest, during the 1-h cycling period, and the 20-min recovery period. The root mean square (RMS) and the median frequency (MF) of SEMG power spectrum were computed. In all subjects, there was no shift in the median frequency throughout the cycling period and the increase in RMS remained stable. In subjects untrained to endurance cyclism, the M-wave duration increased at the end of the cycling period and these changes persisted for a consecutive 15-min period during recovery of exercise. By contrast, in trained mountain bikers the M-wave duration decreased after 2 min of exercise--the effect persisting for 2 min during recovery. These data suggest that the interpretation of M-wave changes during cycling must take into consideration the sport practices of the subjects and also that SEMG power spectrum and M-wave explore different electrophysiological events.

Twenty-four-hour time course of intraocular pressure in healthy and glaucomatous Africans: relation to sleep patterns.

OBJECTIVE: The study was performed in early middle-aged African natives with primary open-angle glaucoma to compare the 24-hour intraocular pressure (IOP) variations in healthy versus young glaucoma patients, because IOP follows a circadian (24-hour) oscillation in healthy Caucasians. DESIGN: Case-control study. PARTICIPANTS: Sixteen healthy African volunteers (age 24.5 +/- 1 years, mean +/- standard error of the mean) and 11 open-angle glaucoma African patients (age 36.2 +/- 3.3 years). METHODS: IOP was measured hourly during 24 hours with a Modular One pneumatonometer (Modular One, Digilab, Cambridge, MA), which allows measures in supine subjects. To allow the IOP measurement at night, subjects were awakened under polysomnography (electroencephalogram, electromyogram, electro-oculogram) recorded at night and during a 90-minute afternoon nap. MAIN OUTCOME MEASURES: Hourly IOP values were analyzed for circadian rhythmicity with the Cosinor technique and in relation to the state of wakefulness, light sleep (stages 1 and 2), slow-wave sleep (stages 3 and 4), and rapid eye movement (REM) sleep upon awakening. RESULTS: Sleep patterns did not differ between patients and healthy volunteers. As expected, in the healthy subjects, IOP followed a 24-hour rhythm with a nocturnal peak value (acrophase), and the variations in IOP during sleep were related to sleep structure, being lowest during REM sleep and highest during slow-wave sleep. In the glaucoma patients, however, the 24-hour rhythm of IOP was reversed, with an afternoon acrophase and an early morning trough. CONCLUSIONS: These data suggest a circadian phase shift in IOP in glaucoma patients, with maintained relation to sleep structure.

[Action duality of nitrogen oxide (NO) in experimental African trypanosomiasis]. / Dualité d'action du monoxyde d'azote (NO) dans la trypanosomose africaine expérimentale.

Patients with human African trypanosomiasis present a major dysruption of the circadian rhythmicity of the sleep-wake cycle, which was also found in rats infected with Trypanosoma brucei brucei (T.b.b.). The alterations in the immune function and nervous system in African trypsanosomiasis led us to investigate the involvement of nitric oxide (NO), a key molecule in immune and neurophysiological mechanisms, in experimental trypanosomiasis. NO was measured in 35 Sprague Dawley rats using differential impulsional voltammetry with a carbon fiber coated with porphyrin-nickel and nafion, ex vivo in the blood and in vivo in the brain. The rats were anaesthetized with sodium chlorate. Infection was performed intraperitoneally (i.p.) with 0.2 ml of a T.b.b. cryostabilate (clone AnTat 1.1E). Blood was collected by an intracardiac puncture with immediate replacement of blood volume (1 ml) in 7 control rats and 8 rats infected since 15 days, before and after i.p. administration of L-ANA (L-arginine-p-nitro-anilide, 100 mg.kg-1, an inhibitor of NO synthase). Brain measures were done in 20 rats (8 controls, and 12 rats infected since 15 or 21 days), in the cortex (H, -0.5 mm; AP, -0.8 mm; L, 1.2 mm) and the lateral ventricle (H,-3.2 mm). In infected rats, blood NO was at 70% of control values (p < 0.001), and L-ANA suppressed the NO signal in all animals (p < 0.0001), demonstrating that the signal originated from NO. Cortical NO was higher than in the ventricle in both control (p < 0.0001) and infected rats (p < 0.001). NO was more elevated in both structures in 15-day-infected rats than in control rats (p < 0.0001), the difference being enhanced in 21-day-infected rats (p < 0.001). L-ANA suppressed the NO signal in 30 to 60 min. These data suggest that NO intervenes in the development of trypanosomiasis in different manners. It is increased in the brain, which remains unexplained, where it may be involved in blood-brain barrier permeation. Conversely, it is decreased in the blood, may be because of macrophage function impairment, which would explain why trypanosomes can multiply in the host.

Modafinil, d-amphetamine and placebo during 64 hours of sustained mental work. II. Effects on two nights of recovery sleep.

Polysomnograms were obtained from 37 volunteers, before (baseline) and after (two consecutive recovery nights) a 64-h sleep deprivation, with (d-amphetamine or modafinil) or without (placebo) alerting substances. The drugs were administered at 23.00 hours during the first sleep deprivation night (after 17.5 h of wakefulness), to determine whether decrements in cognitive performance would be prevented; at 05.30 hours during the second night of sleep deprivation (after 47.5 h of wakefulness), to see whether performance would be restored; and at 15.30 hours during the third day of continuous work, to study effects on recovery sleep. The second recovery night served to verify whether drug-induced sleep disturbances on the first recovery night would carry over to a second night of sleep. Recovery sleep for the placebo group was as expected: the debt in slow-wave sleep (SWS) and REM sleep was paid back during the first recovery night, the rebound in SWS occurring mainly during the first half of the night, and that of REM sleep being distributed evenly across REM sleep episodes. Recovery sleep for the amphetamine group was also consistent with previously published work: increased sleep latency and intrasleep wakefulness, decreased total sleep time and sleep efficiency, alterations in stage shifts, Stage 1, Stage 2 and SWS, and decreased REM sleep with a longer REM sleep latency. For this group, REM sleep rebound was observed only during the second recovery night. Results for the modafinil group exhibited decreased time in bed and sleep period time, suggesting a reduced requirement for recovery sleep than for the other two groups. This group showed fewer disturbances during the first recovery night than the amphetamine group. In particular, there was no REM sleep deficit, with longer REM sleep episodes and a shorter REM latency, and the REM sleep rebound was limited to the first REM sleep episode. The difference with the amphetamine group was also marked by less NREM sleep and Stage 2 and more SWS episodes. No REM sleep rebound occurred during the second recovery night, which barely differed from placebo. Hence, modafinil allowed for sleep to occur, displayed sleep patterns close to that of the placebo group, and decreased the need for a long recovery sleep usually taken to compensate for the lost sleep due to total sleep deprivation.

Twenty-four-hour plasma cortisol and prolactin in human African trypanosomiasis patients and healthy African controls.

We have previously demonstrated that human African trypanosomiasis (sleeping sickness) at the stage of meningoencephalitis results in a major disruption of the circadian rhythmicity of sleep and wakefulness that is proportional to the severity of the disease. This paper examines the corresponding 24-hourly secretion in cortisol and prolactin and compares it with the hourly distribution of sleep composition in infected patients and healthy African subjects. The secretion of cortisol in humans follows a circadian rhythm relatively independent of the sleep-wake cycle, whereas that of prolactin exhibits fluctuations over the 24-hr day that are strongly related to the sleep-wake cycle. After the clinical classification of the patients according to the severity of the disease, hourly blood samples were taken over 24 hr via an indwelling catheter. Plasma cortisol and prolactin were analyzed by radioimmunoassay, and the variations in the hourly concentrations were analyzed for the presence of a potential 24-hr rhythm (circadian). All of the healthy African subjects showed significant circadian rhythms in both cortisol and prolactin secretion, similar to data on humans from temperate regions, and a sleep-related anamnestic afternoon peak of prolactin. Major disruptions in the circadian rhythms of plasma cortisol and prolactin were found in the three patients with the most severe illness, in contrast to the four who were less severely ill and the healthy controls. Thus, it appears that as the disease progresses in severity, major disruptions begin to occur in body circadian rhythms, not only in the sleep-wake cycle as reported elsewhere, but also in cortisol and prolactin secretion, suggesting that sleeping sickness affects the circadian timing system.

Twenty-four-hour profiles and sleep-related variations of cortisol, thyrotropin and plasma renin activity in healthy African melanoids.

The 24-h hormone profiles have been well documented in caucasians living in a temperate climate, but they have never been examined in melanoid subjects under equatorial conditions, with a 12-h light-dark cycle in a hot climate. To establish normal data for this population, blood samples were taken at 10-min intervals over 24 h in five healthy young melanoids living in Abidjan (Ivory Coast). Cortisol and thyroid stimulating hormone (TSH) concentrations and plasma renin activity (PRA) were determined by radio-immunoassay and sleep was registered using polysomnography. Data were compared with results obtained in Strasbourg (France) from six healthy aged-matched caucasians. The 24-h profile of cortisol concentration was similar in both groups, with a 2-h phase advance in the melanoids. Nocturnal fluctuations of PRA, strongly linked to the rapid eye movement-non rapid eye movement (REM-NREM) sleep cycles, occurred in both groups, with higher levels in the caucasians in the last 2 h of sleep along with greater amounts of NREM sleep. After an evening increase in TSH, the sleep onset-related decrease seen in the caucasians was not observed in the melanoids. In both groups, increasing concentrations of TSH and cortisol occurred with awakening, decreasing concentrations being observed during slow-wave sleep. As in the caucasians studied in the temperate climates, the melanoid subjects living at the equator showed the same temporal organization of hormone rhythms within the 24-h period and the same relationships between the pulses and specific sleep stages.(ABSTRACT TRUNCATED AT 250 WORDS)

Time-related changes in the sleep-wake cycle of rats infected with Trypanosoma brucei brucei.

Patients with human African trypanosomiasis, sleeping sickness, show a major disturbance in the circadian distribution of sleeping and waking, with sleep and wake episodes equally distributed throughout the nycthemeron. In order to develop an animal model, polysomnography was taken continuously in 8 male OFA rats in a 12:12 h light-dark cycle, during 1 baseline week and for 2 weeks after infection with Trypanosoma brucei brucei. Considerable sleep fragmentation was observed in the infected rats, with numerous sleep-wake stage changes and an increased number of wakefulness and slow-wave sleep phases. Although the infection produced a progressive disruption of the sleep-wake cycle, the extensive disturbances of the circadian rhythm of the sleep-wake cycle observed in humans with sleeping sickness was not attained in the rats.

Exercise and sleep in four African sportsmen living in the Sahel. A pilot study.

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.

[The sleep-wake cycle during Trypanosoma brucei rhodesiense human African trypanosomiasis in 2 French parachutists]. / Cycle veille-sommeil au décours d'une trypanosomose humaine africaine à Trypanosoma brucei rhodesiense chez deux parachutistes français.

Polysomnography was performed in two military personnel who contracted human African trypanosomiasis (HAT) in Rwanda. They were evacuated to France and gramined during the fourth, sixth and eleventh months of evolution. Patient A presented a meningoencephalitis with Trypanosoma brucei rhodesiense (T. b. r.) in the cerebrospinal fluid. Between the second and third treatments with melarsoprol, the patient presented an acute encephalitic attack with pyramidal and cerebellar symptoms, which were improved by corticotherapy and disappeared progressively in 6 months. Patient B presented a major inflammatory syndrome with T. b. r. in the blood and the medulla. Cerebrospinal fluid and serology remained normal. The patient received only one session of melarsoprol treatment. Polysomnography recordings were continuously taken on an ambulatory Oxford Medilog system during 48 hours. The different stages of vigilance were scored according to the classical Rechtschaffen and Kales criteria. During the fourth month, both subjects presented several long diurnal naps, with the presence of rapid-eye-movement sleep at the end of the sleep episodes. These abnormalities disappeared progressively during the following recordings. Electroencephalographic abnormalities were observed in patient A, particularly during the eleventh month. They consisted in transitory arousal phases concomitant with myoclonic jerks and with the persistence of slow waves during slow-wave sleep. The various anomalies noted in the two patients allow us to recommend the supervision of the evolution of HAT by polysomnographic recording in a sleep laboratory.

[The nyctohemeral rhythm of melatonin is preserved in human African trypanosomiasis]. / Le rythme nycthéméral de la mélatonine (MLT) est conservé dans la trypanosomose humaine africaine.

We studied plasma melatonin profiles by radioimmunoassay in nine patients suffering from human african trypanosomiasis and six healthy controls matched according to the age and the photoperiodic conditions. The circadian periodicity of the sleep-wake cycle was disturbed proportionally to the degree of severity of the disease. On the contrary, the patients' plasma melatonin profile was similar to the controls' one. These results suggest that, beside the master clock generating the main circadian rhythms (sleep-wake, melatonin and core temperature rhythms), an additional regulating system of the melatonin rhythm could be involved.

[Maintenance of the relation between the pulsed secretion of hormones and the internal sleep structure in human African trypanosomiasis]. / Maintien des relations entre la sécrétion pulsatile des hormones et la structure interne du sommeil dans la trypanosomiase humaine africaine.

In order to determine whether sleep disturbances would affect the hormonal patterns and the normal relationships between hormone pulses and sleep stages, the 24-hour profiles of cortisol, prolactin and plasma renin activity (PRA) were analysed in 6 sleeping sickness patients studied at Brazzaville and in 5 healthy African controls studied in Abidjan. Polysomnographic recordings were done continuously and blood was taken every 10 minutes throughout the 24-hour period. Plasma was analyzed for cortisol, prolactin and PRA. The circadian rhythm of cortisol, considered as an example of an endogenous rhythm was attenuated in all the patients but one, but as in normal subjects, slow wave sleep (SWS) remained associated with the declining phases of the secretory episodes. Prolactin and PRA profiles, which are strongly influenced by the sleep-wake cycle did not show the increase normally associated with long sleep periods and reflected the spreading of sleep and wakefulness throughout the 24-hour period. However, rapid-eye movement (REM) sleep began in sleeping sickness patients, as in normal subjects, during the descending phases of prolactin pulses. In both groups, PRA reflected the sleep stage distribution with non rapid-eye movement (NREM) sleep occurring during the ascending phases and REM sleep during the descending phases of the oscillations. However, in sleeping sickness patients, the marked sleep fragmentation often did not allow sufficient time for PRA to increase significantly, as observed with regular NREM-REM sleep cycles. These results demonstrate that, together with the disruption of the sleep-wake cycle, there are profound differences in the temporal organization of the 24 hour hormone profiles in human African trypanosomiasis.(ABSTRACT TRUNCATED AT 250 WORDS)

Sleep patterns of European expatriates in a dry tropical climate.

Night sleep in sedentary African subjects living in the sahelian zone lasts from 7 h to 8 h, with high amounts of slow-wave sleep (SWS) and paradoxical sleep (PS), SWS being present in each sleep cycle. We report here on sleep patterns in 6 healthy male European expatriates (aged 32-39 years) living in the same tropical climate. Polysomnography was taken for 3 consecutive nights in February (mean ambient temperature, Ta: 29.5 degrees C), March (Ta: 31.6 degrees C) and May (Ta: 33.3 degrees C). Comparisons between seasons were made with an analysis of variance, with P >/= 0.05. Because of a first night effect, the first nocturnal recording was discarded. Total sleep time (TST) increased in May vs February and March (P < 0.05). Stage 2 was shorter in March than in February (P < 0.001) and its proportion decreased from February to March (P < 0.02) and from March to May (P < 0.05). Conversely, SWS increased from February to March and March to May (duration, P < 0.001; proportion, P < 0.05), due to an augmentation in stage 4 with more numerous and longer stage 4 phases. Stage 3 was also increased in May vs March. The latency to SWS was shorter in March. SWS was present in each sleep cycle. PS was high, but did not vary. The sleep pattern changes were directly correlated with Ta. In conclusion, Caucasians living in the tropics slept similarly to Africans. The seasonal sleep variations favour the hypothesis that SWS is increased when thermoregulatory processes are triggered, either through passive climatic heating or exercise-induced hyperthermia.