SUMMARY Sleep is the most important period for recovery from daily load. Regular physical activity enhances overall sleep quality, but the effects of acute exercise on sleep are not well defined. In sleep hygiene recommendations, intensive exercising is not suggested within the last 3 h before bed time, but this recommendation has not been adequately tested experimentally. Therefore, the effects of vigorous late-night exercise on sleep were examined by measuring polysomnographic, actigraphic and subjective sleep quality, as well as cardiac autonomic activity. Eleven (seven men, four women) physically fit young adults (VO 2max 54 ± 8 mLAEkg )1 AEmin )1 , age 26 ± 3 years) were monitored in a sleep laboratory twice in a counterbalanced order: (1) after vigorous late-night exercise; and (2) after a control day without exercise. The incremental cycle ergometer exercise until voluntary exhaustion started at 21:00 ± 00:28 hours, lasted for 35 ± 3 min, and ended 2:13 ± 00:19 hours before bed time. The proportion of non-rapid eye movement sleep was greater after the exercise day than the control day (P < 0.01), while no differences were seen in actigraphic or subjective sleep quality. During the whole sleep, no differences were found in heart rate (HR) variability, whereas HR was higher after the exercise day than the control day (54 ± 7 versus 51 ± 7, P < 0.01), and especially during the first three sleeping hours. The results indicate that vigorous late-night exercise does not disturb sleep quality. However, it may have effects on cardiac autonomic control of heart during the first sleeping hours.k e y w o r d s actigraphy, heart rate variability, polysomnography, recovery, subjective sleep quality

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Heart rate variability (HRV) has been widely used as a measure of vagal activation in physiological, psychological, and clinical examinations. We studied the within-subject quantitative relationship between HRV and vagal effects on the heart in different body postures during a gradually decreasing vagal blockade. Electrocardiogram and respiratory frequency were measured in subjects (8 endurance athletes and 10 participants of nonendurance sports) in supine, sitting, and standing postures before the blockade, under vagal blockade (atropine sulfate, 0.04 mg/kg), and four times during a 150-min recovery from the blockade. Fast Fourier transform was used to calculate low-frequency power (LFP, 0.04-0.15 Hz), high-frequency power (HFP, 0.15-0.40 Hz), and total power (TP, 0.04-0.40 Hz). A within-subject linear regression analysis of recovery time on each HRV index was conducted. Complete vagal blockade decreased all HRV significantly, particularly HFP (P < 0.001). A linear fit explained a large portion of the within-subject variance between recovery time and natural log-transformed (ln) HRV indexes in every posture, with coefficients of determination (R2) in the supine posture [means (SD)]: 98 (SD 2)% for mean R-R interval, 87 (SD 10)% for lnLFP, 87 (SD 13)% for lnHFP, and 91 (SD 10)% for lnTP. Neither body posture nor endurance-training background had an impact on R2 values. There was marked between-subject variation in the R2 values, slopes, and intercepts. In conclusion, all HRV, particularly HFP, is predominantly under vagal control. Within subjects, lnLFP, lnHFP, and lnTP increased linearly with the gradually decreasing vagal blockade in all postures.

Methodological problems have limited the number of studies on heart rate variability (HRV) dynamics immediately after exercise. We used the short-time Fourier transform method to study immediate (5 min) and slow (30 min) recovery of HRV after different high-intensity exercise interventions. Eight male athletes performed two interval interventions at 85% and 93% (IV(85) and IV(93)) and two continuous interventions at 80% and 85% (CO(80) and CO(85)) of the velocity at VO2max (vVO2max). We found no increase in high frequency power (HFP), but low frequency (LFP) and total power (TP) increased (P<0.05) during the first 5 min of the recovery after each intervention. During the 30-min recovery, HFP, LFP and TP (1) increased slowly toward resting values, but HFP remained lower (P<0.01) than at rest, (2) were lower (P<0.05) after IV(93) and CO(85) when compared with IV(85) and CO(80), respectively and (3) were lower (P<0.01) after CO(85) when compared with IV(85). HRV recovery was detected during the immediate recovery after interventions. Increased exercise intensity resulted in lower HRV both in interval and in continuous interventions. In addition, when interval and continuous interventions were performed at a similar workload, HRV was lower after continuous intervention.

High intensity cycling training increases oxidative capacity in skeletal muscles and improves insulin sensitivity. The present study compared the effect of eight weeks of sprint interval running (SIT) and continuous running at moderate intensity (CT) on insulin sensitivity and cholesterol profile in young healthy subjects (age 25.2 ± 0.7; VO(2max) 49.3 ± 1.2 ml·kg(-1)·min(-1)). SIT and CT increased maximal oxygen uptake by 5.3 ± 1.8 and 3.8 ± 1.6%, respectively (p < 0.05 for both). Oral glucose tolerance test (OGTT) was performed before and 60 h after the last training session. SIT, but not CT, reduced glucose area under curve and improved HOMA β-cell index (p < 0.05). Insulin area under curve did not decrease significantly in any group. SIT, but not CT, reduced LDL and total cholesterol. In conclusion, sprint interval running improves insulin sensitivity and cholesterol profile in healthy subjects, and sprint interval running may be more effective to improve insulin sensitivity than continuous running at moderate intensity.