This article reviews evidence supporting the hypothesis that suicide rates in Japan could be reduced by elevating serotonin levels via increasing the average duration of sleep. Seven major relevant findings were apparent in the literature: 1) Sleep loss is associated with suicide, but the direction of causality is equivocal. 2) Decreased serotonergic activity may be involved in suicidal behavior. 3) Sleep debt may decrease serotonergic activity. 4) The suicide rate in Japan has remained at a heightened level for the past 12 years. 5) The average sleep duration in Japan has decreased over the past 40 years. 6) The average sleep duration in Japan is among the lowest in the world. 7) The average sleep duration in Japan plateaued in 1995 and has been relatively stable since. From the research reviewed, two major problematic issues were apparent: 1) Most people in Japan receive inadequate sleep. 2) Individuals whose sleep is inadequate are unlikely to be sufficiently physically active to stimulate serotonergic systems to a desirable level. I propose that public health initiatives encouraging a longer duration of sleep may provide a relatively simple way of addressing the disturbing current trend in Japan. The combination of actigraph and brain serotonin level measurement could allow large population-based cohort studies to be designed, to elucidate the causal links between sleep duration, serotonin levels, and suicide rates.

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In recent years, parametric speakers have been used in various circumstances. However, nothing has yet been demonstrated about the safety of parametric speakers for the human body. Therefore, we studied their effects on physiological functions. Nine male subjects participated in this study. They completed three consecutive sessions: a 20-min quiet period as a baseline, a 45-min mental task period with a general speaker or a parametric speaker, and a 20-min recovery period. We measured electrocardiogram (ECG), photoplethysmogram (PTG), electroencephalogram (EEG), blood pressure (BP), and baroreflex sensitivity (BRS). Two experiments, one with a general speaker (the general condition), the other with a parametric speaker (the parametric condition), were conducted at the same time of day on separate days. To examine the effects of the parametric speaker, a two-way repeated measures ANOVA (speaker factor and time factor) was conducted. We found that sympathetic nervous activity and second derivative of PTG in task period and recovery period during the parametric condition were significantly lower than those indications during the general condition. Furthermore, Δ parasympathetic nervous activity during the parametric condition in task period and recovery period tended to be smaller than that during the general condition. The results suggested that the burden of the parametric speaker is lower than that of the general speaker for physiological functions, especially those of the cardiovascular system. Furthermore, we verified that the reaction time with the parametric speaker is shorter than that with the general speaker.

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The aim of this cross-sectional study was to examine the factors which may be associated with the metabolic syndrome by exploring the relationship between psychosocial stress, age, body mass index (BMI), C-reactive protein (CRP), lifestyle factors, and the components of the metabolic syndrome, such as glycated hemoglobin (HbA1c), fasting blood sugar (FBS), body fat percentage, and triglyceride concentration, among apparently healthy subjects. Psychosocial stress was measured by the use of the inventory to measure psychosocial stress (IMPS). One thousand four hundred and ninety-nine people out of 1,941 public school workers admitted to a hospital for a medical check-up responded to the IMPS, yielding a response rate of 77.2%. A total of 1,201 workers excluding 298 who were taking medication for various diseases were analyzed with the use of hierarchical multiple regression models. It was found that IMPS-measured stress score, age, BMI, and smoking habit were associated with an increase in glycated hemoglobin among men, while alcohol consumption was associated with a decrease in glycated hemoglobin. Stress score, age, BMI, and alcohol consumption were found to be associated with an increase in FBS among men, while smoking and exercise habits were associated with a decrease in FBS. CRP was found to be associated with an increase in body fat percentage among men, though stress score was not associated with an increase in body fat percentage. Stress score, age, and BMI were associated with an increase in triglyceride concentration among women. The findings of the present study seem to be in line with the hypothesis that psychosocial stress plays an important role in developing the metabolic syndrome, which may be associated with inflammatory processes in the vascular wall, resulting in atherosclerosis and cardiovascular disease.

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After 6-h low-intensity swimming exercise (LIE), peroxisome proliferator-activated receptor γ coactivator -1α (PGC-1α) in whole and nuclear fractions in rat skeletal muscle was higher than the control rats' muscles up to 18 h after LIE. However, no study has reported change in PGC-1α content after that. Therefore, we measured PGC-1α in whole and nuclear fractions in rat skeletal muscle up to 24 h after LIE. Furthermore, we evaluated change in the mRNA of δ-aminolevulinate synthase (ALAS), a mitochondrial protein, to clarify in which fraction of PGC-1α has a physiological role as a transcriptional coactivator for enhancing the mitochondrial oxidative enzymes after exercise. We measured PGC-1α protein content in whole and nuclear fractions in the epitrochlearis (EPI) muscle of male Sprague-Dawley rats (age: 6 w; body weight: 180–200 g) after LIE by Western-blot analysis. The ALAS mRNA content was quantified by RT-PCR. The PGC-1α contents in whole fractions in the rat EPI muscle were 73% and 75% higher than that of the control rats' muscle, 18 h and 24 h after LIE, respectively. The PGC-1α content in nuclear fractions in the muscle and ALAS mRNA was higher than that of the control rats' muscle by 58% and 25%, respectively, while they returned to the control level 24 h after LIE. The present investigation demonstrated that the time-course of PGC-1α content in nuclear fractions in the EPI muscle was the same as the ALAS mRNA, suggesting that PGC-1α in the nucleus may have a physiological function as a transcriptional coactivator for enhancing mitochondrial protein expression after exercise.

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We investigated whether intense interval training on a cycle ergometer would prevent loss of muscle strength and atrophy in the human calf during unilateral lower limb suspension (ULLS). The present study involved 11 healthy men. We defined unloading leg and contralateral leg as ULLS-leg and CONT-leg, respectively. The subjects were divided into 2 groups: one with single-leg cycling training (Tr-UL, n=6); the other as a control (UL, n=5). The Tr-UL group performed an intense 25-min interval cycling training up to 80% of peak oxygen uptake on alternate days during 20-d ULLS. It was found that: 1) in maximal voluntary contraction (MVC) and the cross-sectional area of the planter flexor, there was a significant time- (pre-ULLS and post-ULLS) by-leg (ULLS-leg and CONT-leg) interaction; 2) in voluntary activation during MVC evaluated by the twitch interpolation technique, no significant time-by-leg interaction was detected but the trend of change from before to after ULLS tended to be different between ULLS-leg and CONT-leg; and 3) regarding ULLS-leg, the change in any parameters was not significantly different between the Tr-UL and UL groups. These results suggest that unloading induces dysfunction and atrophy in the human calf and that high-intensity interval training on a cycle ergometer cannot significantly prevent unloading-induced deconditioning in the human calf.

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