Effects of Short-Term Acclimatization at the Summit of Mt. Fuji (3776 m) on Sleep Efficacy, Cardiovascular Responses, and Ventilatory Responses.

Horiuchi, Masahiro, Shiro Oda, Tadashi Uno, Junko Endo, Yoko Handa, and Yoshiyuki Fukuoka. Effects of short-term acclimatization at the summit of Mt. Fuji (3776 m) on sleep efficacy, cardiovascular responses, and ventilatory responses. High Alt Med Biol. 18:171-178, 2017.-We investigated the effects of a short period of acclimatization, at 3776 m on Mt. Fuji, on sleep parameters and related physiological responses. Physiological responses were assessed in seven healthy lowlander men during both daytime and sleep while at sea level (SL), as well as for three consecutive nights at high altitude (HA; 3776 m, day 1 [D1], D2, D3, and morning only of D4). Blood pressure variables, heart rate (HR), pulmonary ventilation (VE), and breathing frequency (Bf) progressively increased each day, with significant differences between SL and HA (p < 0.05, respectively). In contrast, end-tidal PCO2 (PETCO2) progressively decreased each day with statistical differences between SL and D3 at HA (p < 0.05). During sleep at HA, mean arterial pressure (MAP) was stable, whereas it decreased during sleep at SL. Sleep efficacy, which was assessed by actigraphy, was linearly impaired with statistical differences between SL and D3 (p < 0.05). These impairments in sleep efficacy at HA were associated with higher MAP and HR, as well as lower Bf and PETCO2 during the daytime (pooled data, p < 0.05, respectively). These results suggest that hypoxia-induced cardiovascular and ventilatory responses may be crucial contributors to changes in sleep efficacy at HA.

Inverse Relationship between Sleep Duration and Cardio-Ankle Vascular Index in Children.

AIM: Poor sleep has been shown to be associated with the development of cardiovascular risk factors, such as obesity, in both adults and children. This study aimed to investigate the relationship between sleep duration and arterial stiffness indices in Japanese children and early adolescents. METHODS: The data on 102 students (56 males, 46 females; mean age, 11.9±1.8 years) were analyzed. As non-invasive arterial stiffness parameters, the cardio-ankle vascular index (CAVI) and heart-ankle pulse wave velocity (haPWV) were evaluated. Their students' sleep habits (bedtime and wake times on a usual weekday) were investigated using questionnaires, and based on these, their sleep durations were calculated. RESULTS: The CAVI values in the males and females were 4.8±0.9 and 4.7±0.9 (arbitrary unit), respectively. haPWV values in the males and females were 5.5±0.6 and 5.4±0.6 m/s, respectively. Sleep duration in the males, but not in the females, was negatively correlated with CAVI (r=－0.356) and haPWV (r=－0.356), suggesting that students with short sleep duration could have increased arterial stiffness. After adjusting for confounders, such as age, sex, systolic blood pressure, heart rate, adiposity, and physical fitness, the correlation of sleep duration with CAVI, but not with haPWV, was still significant (partial r=－0.253, p＜0.05). CONCLUSION: Our findings suggest that shorter sleep duration influences arterial stiffening even in childhood.

Sleep onset is disrupted following pre-sleep exercise that causes large physiological excitement at bedtime.

PURPOSE: Many studies have failed to show that pre-sleep exercise has a negative effect on sleep onset. However, since only a moderate level of physiological excitement was observed at bedtime in these studies, it remains unclear whether a larger magnitude of physiologic excitement present at bedtime would disrupt sleep onset. This study compared the effects of pre-sleep exercise, which led to different levels of physiologic excitement at bedtime (moderate and heavy), on sleep onset. METHODS: Twelve active young men underwent non-exercise, moderate-intensity exercise, and high-intensity exercise conditions. The subjects maintained a sedentary condition on a reclining seat throughout the day. On the non-exercise day, the subjects remained seated at rest until going to bed. On the moderate- and high-intensity exercise days, the subject exercised for 40 min (21:20-22:00) at 60 and 80% heart rate reserve, respectively. Sleep polysomnography, core body and skin temperatures, heart rate (HR), and heart rate variability (HRV) were recorded. RESULTS: We observed a delay in sleep onset (+14.0 min, P < 0.05), a marked physiological excitement at bedtime as reflected by an increased HR (+25.7 bpm, P < 0.01), and a lower high-frequency power of HRV (-590 ms(2), P < 0.01) only on the high-intensity exercise day. CONCLUSIONS: These results indicate that pre-sleep vigorous exercise, which causes a large physiologic excitement at bedtime, might disrupt the onset of sleep.