Prevalence of Poor Sleep Quality and its Association with Lifestyle Habits, Competition-Based Activities, and Psychological Distress in Japanese Student-Athletes During the COVID-19 Pandemic.

Objectives The present study clarified the prevalence of poor sleep quality and its relation to lifestyle habits, competitive-based activities, and psychological distress among Japanese student-athletes in the initial pandemic period (2020) and 1 year later (2021). Methods In the present study, student-athletes were defined as individuals belonging to university athletic clubs. The data of two cross-sectional surveys (2020: n = 961 and 2021: n = 711) were collected from student-athletes in 6 universities in Japan. First, the prevalence of poor sleep quality (Pittsburgh sleep quality index score > 5) was investigated. Relationships between poor sleep quality and lifestyle habits, competition-based activities, and psychological distress were then explored using multivariate logistic regression analysis adjusted for age, sex, and body mass index. Results The prevalence of poor sleep quality was 33.6% in 2020 and 36.6% in 2021. Poor sleep quality in 2020 was related to late bedtime, taking supplements before bed, part-time job (no late night), stressors of expectations and pressure from others, and psychological distress, whereas that in 2021 was related to early wake-up time, skipping breakfast, taking caffeinated drinks before bed, use of smartphone/cellphone after lights out, stressors of motivation loss, and psychological distress. Conclusions In both 2020 and 2021, one-third of student-athletes had poor sleep quality and psychological distress was its common risk factor. Lifestyle habits and competition stressors associated with poor sleep quality were pandemic-specific in 2020, but similar to the prepandemic period in 2021.

Water balance in Japanese male kendo college athletes during training: a pilot study assessing seasonal differences with adjusted energy expenditure.

BACKGROUND: Due to various factors, water balance may vary across seasons. These effects may be particularly prominent in athletes and dependent upon energy expenditure during training. METHODS: Japanese male kendo college athletes participated in this study during their training sessions. The participants were observed for three days each season, i.e., in spring, summer, and winter. The energy expenditure of the participants during training was monitored using the heart rate method. Data regarding the total amount of sweating, rate of sweating, amount of water intake, and rate of water intake were collected for each season and the differences were assessed using analysis of covariance, with energy expenditure as the covariate. RESULTS: The water balance parameter values observed during a kendo training session in summer were the highest, whereas these values were significantly reduced in winter. Energy expenditure was the highest in spring. The amount of sweating per energy expenditure varied seasonally, reaching as high as 2.14 g/kcal in summer. After adjusting for the influence of energy expenditure, the amount of sweating, amount of water intake, and water intake rate varied significantly by seasons, with the highest values in summer (P<0.001). The sweating rate was high in all the seasons, but the highest rate was observed in summer, followed by spring and then winter. There was a significant difference in the sweating rate in each season (P<0.001). The rehydration rate was 28% in spring, 39% in summer, and 22% in winter. CONCLUSIONS: After adjusting for the influence of energy expenditure, seasonal differences in water balance were observed in Japanese male kendo college athletes during training. These results suggest that water intake is essential after training in any season to maintain the water balance of the body.

Sleep disorder risk factors among student athletes.

OBJECTIVE: To clarify sleep disorder risk factors among student athletes, this study examined the relationship between lifestyle habits, competition activities, psychological distress, and sleep disorders. METHODS: Student athletes (N = 906; male: 70.1%; average age: 19.1 ± 0.8 years) in five university sports departments from four Japanese regions were targeted for analysis. Survey items were attributes (age, gender, and body mass index), sleep disorders (recorded through the Pittsburgh Sleep Quality Index), lifestyle habits (bedtime, wake-up time, smoking, drinking alcohol, meals, part-time jobs, and use of electronics after lights out), competition activities (activity contents and competition stressors), and psychological distress (recorded through the K6 scale). The relation between lifestyle habits, competition activities, psychological distress, and sleep disorders was explored using logistic regression analysis. RESULTS: Results of multivariate logistic regression analysis with attributes as adjustment variables showed that "bedtime," "wake-up time," "psychological distress," "part-time jobs," "smartphone/cellphone use after lights out," "morning practices," and "motivation loss stressors," were risk factors that were independently related to sleep disorders. CONCLUSIONS: Sleep disorders among student athletes are related to lifestyle habits such as late bedtime, early wake-up time, late night part-time jobs, and use of smartphones/cellphones after lights out; psychological distress; and competition activities such as morning practices and motivation loss stressors related to competition. Therefore, this study suggests the importance of improving these lifestyle habits, mental health, and competition activities.

CD56(dim)CD16(high) and CD56(bright)CD16(-) cell percentages associated with maximum knee extensor strength and incidence of death in elderly.

Physical fitness is an indicator of systemic well-being in humans. Little is known about the role of physical fitness for maintaining systemic health in the elderly. Here, we study elderly subjects to determine the relationships between physical fitness and CD56 and CD16 surface NK cell markers on peripheral blood lymphocytes, as well as to analyze the relationship between the surface markers and incidence of death. We selected 253 independent elderly subjects (122 female; 131 male) who were 79-80 years old. Subjects having a higher proportion of CD56(dim)CD16(high) within CD56(+)CD16(+) cells, or ration of CD56(dim)CD16(high) and CD56(dim)CD16(-) cells had a significant positive correlation with maximum bilateral knee extensor strength/weight (kg) (r = 0.425; P < 0.0001 or r = 0.323; P < 0.0001). In contrast, an increased proportion of CD56(bright)CD16(-) cells within lymphocyte significantly negatively correlated with the maximum bilateral knee extensor strength/weight (kg) (r = -0.290; P = 0.0004); and these subjects had a significantly lower mortality during the 5 years following measurement of death. Therefore, we found that a synergistic effect of the right and left leg muscle strength was associated with proportion of matured NK and NKT cells and induced a low proportion of CD56(bright)CD16(-) cells within lymphocyte. Moreover, the low proportion of CD56(bright)CD16(-) cells was associated with incidence of death. In conclusion, measurements of physical fitness, the proportion of CD56(dim)CD16(high) within CD56(+)CD16(+) cells, the ratio of CD56(dim)CD56(high) and CD56(dim)CD16(-) cells, and the proportion of CD56(bright)C16(-) cells in lymphocytes are important indicators to check elderly health.

[Experimental Approach to Analysis of the Relationship between Food Environments and Lifestyle-Related Diseases, Including Cardiac Hypertrophy, Fatty Liver, and Fatigue Symptoms].

The food habit is involved in the onset and development of lifestyle-related diseases. In this review I would like to describe a historical case of vitamin B1 deficiency, as well as our case study of fatty acid metabolism abnormality due to carnitine deficiency. In history, the army and navy personnel in Japan at the end of the 19th century received food rations based on a high-carbohydrate diet including white rice, resulting in the onset of beriberi. An epidemiological study by Kenkan Takaki revealed the relationship between the onset of beriberi and rice intake. Then, Takaki was successful in preventing the onset of beriberi by changing the diet. However, the primary cause had yet to be elucidated. Finally, Christian Eijkman established an animal model of beriberi (chickens) showing peripheral neuropathy, and he identified the existence of an anti-beriberi substance, vitamin B1. This is an example of the successful control of a disease by integrating the results of epidemiological and experimental studies. In our study using a murine model of fatty acid metabolism abnormality caused by carnitine deficiency, cardiac abnormality and fatty liver developed depending on the amount of dietary fat. In addition, the mice showed disturbance of orexin neuron activity related to the sleep-arousal system, which is involved in fatigue symptoms under fasting condition, one of the states showing enhanced fatty acid metabolism. These findings suggest that fatty acid toxicity is enhanced when the mice are more dependent on fatty acid metabolism. Almost simultaneously, a human epidemiological study showed that narcolepsy, which is caused by orexin system abnormality, is associated with the polymorphism of the gene coding for carnitine palmitoyltransferase 1B, which is involved in carnitine metabolism. To understand the pathological mechanism of fatty acid toxicity, not only an experimental approach using animal models, but also an epidemiological approach is necessary. The results will be applied to preventing and treating lifestyle-related diseases associated with fatty acid metabolism abnormality.

Failure of the feeding response to fasting in carnitine-deficient juvenile visceral steatosis (JVS) mice: involvement of defective acyl-ghrelin secretion and enhanced corticotropin-releasing factor signaling in the hypothalamus.

Carnitine-deficient juvenile visceral steatosis (JVS) mice, suffering from fatty acid metabolism abnormalities, have reduced locomotor activity after fasting. We examined whether JVS mice exhibit specific defect in the feeding response to fasting, a key process of anti-famine homeostatic mechanism. Carnitine-deficient JVS mice showed grossly defective feeding response to 24 h-fasting, with almost no food intake in the first 4 h, in marked contrast to control animals. JVS mice also showed defective acyl-ghrelin response to fasting, less suppressed leptin, and seemingly normal corticotropin-releasing factor (CRF) expression in the hypothalamus despite markedly increased plasma corticosterone. The anorectic response was ameliorated by intraperitoneal administration of carnitine or acyl-ghrelin, with decreased CRF expression. Intracerebroventricular treatment of CRF type 2 receptor antagonist, anti-sauvagine-30, recovered the defective feeding response of 24 h-fasted JVS mice. The defective feeding response to fasting in carnitine-deficient JVS mice is due to the defective acyl-ghrelin and enhanced CRF signaling in the hypothalamus through fatty acid metabolism abnormalities. In this animal model, carnitine normalizes the feeding response through an inhibition of CRF.

Prolonged effect of single carnitine administration on fasted carnitine-deficient JVS mice regarding their locomotor activity and energy expenditure.

Carnitine is an essential cofactor for the oxidation of fatty acid in the mitochondria and an efficient therapeutics for primary carnitine deficiency. We herein analyzed the prolonged effects of carnitine on the reduced locomotor activity and energy metabolism of fasted carnitine-deficient juvenile visceral steatosis (jvs(-/-)) mice. We found that a single carnitine administration to 24-h fasted jvs(-/-) mice in the morning increased both the locomotor activity and oxygen consumption at night not only on the same day, but also on the next day, when the carnitine levels in the blood and tissues were already as low as at the original carnitine-deficient state. We also found that fat utilization for energy production significantly increased under fasting even in jvs(-/-) mice and was stimulated in the carnitine-administrated fasted jvs(-/-) mice at night, in comparison to that observed in the saline-administered jvs(-/-) mice, at least for 2 days even under the low plasma and tissue carnitine levels. These results suggest that the low tissue carnitine levels are therefore not the sole rate-limiting factor of general fatty acid oxidation in carnitine-deficient jvs(-/-) mice.

Fasting-induced reduction in locomotor activity and reduced response of orexin neurons in carnitine-deficient mice.

We found reduced locomotor activity (LA) under fasting in systemic carnitine-deficient juvenile visceral steatosis (jvs(-/-)) mice. When food was withdrawn at 8:00 a.m. (lights-off at 7:00 p.m., 12h/cycle), the nocturnal LA of jvs(-/-) mice was much less than the control (jvs(+/+) and jvs(+/-)) mice. LA recovered under carnitine or sucrose administration, but not under medium-chain triglyceride. In addition, fasted jvs(-/-) mice, without any energy supply, were activated by modafinil, a stimulator of the dopamine pathway. These results suggest that the reduced LA is not adequately explained by energy deficit. As the fasted jvs(-/-) mice showed lower body core temperature (BT), we examined the central nervous system regulating LA and BT. We found lower percentage of c-Fos positive orexin neurons in the lateral hypothalamus and reduced orexin-A concentration in the cerebrospinal fluid of fasted jvs(-/-) mice. Sleep analysis revealed that fasted jvs(-/-) mice had disruption of prolonged wakefulness, with a higher frequency of brief episodes of non-REM sleep during the dark period than fasted jvs(+/+) mice. These results strongly suggest that the reduced LA in fasted jvs(-/-) mice is related to the inhibition of orexin neuronal activity.

Hyperammonemia in carnitine-deficient adult JVS mice used by starvation.

Juvenile visceral steatosis (JVS) mouse is an animal model of human primary carnitine deficiency caused by a mutation of the gene encoding carnitine transporter, and suffers from various symptoms, such as fatty liver, growth retardation, hyperammonemia, hypoglycemia, and cardiac hypertrophy. We have shown that hyperammonemia during the weaning period (15-26 days of age) is caused by suppression of urea cycle enzyme gene expression. The suppression resulted from activation of a transcription factor, AP-1. We have found that a cis-element for AP-1 binding is present in the enhancer region of the carbamoylphosphate synthetase (CPS) gene, and that the AP-1 binding site is involved in the suppression of CPS induction by dexamethasone in cultured hepatocytes and in the suppression of CPS expression in the liver of JVS mice. The blood ammonia levels in JVS mice increased during the weaning period, and then decreased to almost control levels after 30 days of age. In this paper, we report that in adult JVS mice, ammonia levels again increased after starvation for at least 24 hr and this effect was suppressed by carnitine treatment. Starvation for 48 hr did not significantly suppress CPS activity in the liver and did not cause any change in hepatic ornithine concentration. The concentration of N-acetylglutamate in the liver of starved JVS mice was not significantly different from that of JVS mice treated with carnitine. These results indicate that the hyperammonemia in carnitine-deficient adult JVS mice during starvation and the suppression by carnitine treatment differ from those found during the weaning period, and thus the cause of hyperammonemia and the mechanism of suppression remain to be solved.