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.

We compared the changes in compound muscle mass action potential (M-wave) recorded in vastus lateralis in response to hyperbaric hyperoxia (HBO) in nine combat divers who dived daily while breathing 100% O2 or O2-enriched mixture (O2 divers) to those measured in eight recreational divers who dived occasionally using compressed air/21% O2 (air divers). The O2 divers completed a 6-h HBO exposure in which the inspired oxygen pressure (PiO2) varied from 1.15 to 2.7 absolute atmospheres (ATA), PiO2 being maintained at 1.15 ATA throughout the first 2-h period, whereas the air divers only completed a 2-h HBO exposure with PiO2 constant at 1.15 ATA. Before HBO exposure, there were no intergroup differences between baseline M-wave characteristics (amplitude and duration), but the conduction time was significantly shorter in O2 divers compared with air divers. After 90 min of HBO (1.15 ATA) the air divers demonstrated neuromuscular hyperexcitability, as evidenced by an increased M-wave amplitude (13%, P<0.01 versus baseline), shortened M-wave duration (5%, P<0.05 versus baseline), and reduced conduction time (5%, P<0.01 versus baseline). In O2 divers, similar HBO-induced M-wave changes were only observed when PiO2 was greater than 1.50 ATA. We conclude that HBO elicites neuromuscular hyperexcitability, attenuated in elite O2 divers.

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SUMMARY  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°C), March (Ta: 31.6°C) and May (Ta: 33.3°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.