The aim of the study was to investigate the psychological features, sleep quality and daytime sleepiness of different chronotypes in healthy young participants. Seventy-nine female and 63 male medical students aged between 17 and 23 years (mean age: 19.8 ± 1.3 years) participated voluntarily in this study. They completed the Morningness-Eveningness Questionnaire, self-reported symptom inventory SCL-90-R, the Pittsburgh Sleep Quality Index and the Epworth Sleepiness Scale. Psychological symptoms and sleep features of morning types, evening types and intermediate types were compared with each other. Out of 141 subjects, 30 were evening types (21%), 34 were morning types (24%) and 77 were intermediate types (55%). Positive-symptom total scores of SCL-90-R were higher in the evening types than the morning and intermediate types. There were significant differences in the psychological symptoms of anxiety, obsessive-compulsiveness, hostility and phobia among these groups (p < 0.05). Total sleep quality was poorer and daytime sleepiness was significantly higher in the evening types than the morning and intermediate types (p < 0.05). Our findings suggest that evening chronotypes suffer from more anxiety, obsessive-compulsiveness, hostility and phobia symptoms, sleep problems and daytime sleepiness than the other chronotypes.

The aim of this study was to investigate the plasma adipokine responses to high-intensity interval training (HIT) in overweight/obese women. Twelve women (age 21.7 ± 3.8 years) completed a 19 days of HIT comprising six session of 4–6 repeats of a Wingate test (0.065 kg load/kg). Plasma adipokine levels were measured before exercise, and at 5 and 90 min after exercise on the first and the last training days. Adiponectin was higher at 5 min than 90 min post-exercise (11.7 ± 7.3 and 10.5 ± 5.8 ng/ml; p = .01) in the first exercise day. Leptin decreased 5 min after exercise (23.6 ± 13.2 vs. baseline 27.8 ± 14.4 ng/ml; p < .01) and remained depressed following 90 min (p < .01). The changes in adiponectin and leptin concentrations were similar on the first and last exercise days. No consistent effect was found on resistin concentration. Future studies are required to disclose the functional consequences of these alterations in plasma adipokine levels.

Athletes misuse recombinant human growth hormone (r‑hGH) to enhance their performance. Although r‑hGH is known to increase cardiac hypertrophy, the underlying molecular mechanism remains unclear. The aim of the present study was to investigate the role of r‑hGH in cardiac intracellular signaling pathways and of miR‑21 and miR‑133 expression in rat hearts during exercise. A total of 36 adult male Sprague‑Dawley rats were divided into sedentary control (SC, n=9), swimming exercise (SE, n=8), r‑hGH (GH, n=10) and swimming exercise plus r‑hGH (SE‑GH, n=9) groups. The exercise groups completed a 1‑h swimming exercise 5 times a week for 8 weeks. Subcutaneous r‑hGH was administered as 0.3 mg/kg/day. Phosphoinositide‑3‑kinase (PI3K), serine/threonine protein kinase 1 (AKT1), extracellular signal‑regulated kinase (ERK), microRNA (miR)‑21 and miR‑133 expression was evaluated in ventricular muscle by real‑time quantitative polymerase chain reaction. Protein expression of PI3K, AKT1, ERK and mechanistic target of rapamycin (mTOR) was also assessed by immunohistochemistry. Statistical differences were analyzed by two‑way ANOVA. PI3K and AKT1 expression and the gene and protein levels was notably increased in the SE‑GH group compared with in SC ventricular tissues (P<0.05). mTOR protein expression was higher in the GH, SE and SE‑GH groups compared with in the SC group (P<0.05, <0.05 and <0.001, respectively). ERK gene/protein expression was similar across all groups. miR‑21 and miR‑133 levels in ventricular muscle were higher in the SE and GH groups than those in the SC group. In summary, growth hormone application coupled with swimming exercise appeared to affect the PI3K/AKT/mTOR signaling pathway in the left ventricular tissue of rats; however, ERK signaling pathway appeared inactive in physiological left ventricular hypertrophy caused by swimming and GH administration over 8 weeks. Furthermore, GH treatment resulted in increased miR‑21 and miR‑133 expression. Future study by our group will aim to assess the effects of higher dose GH treatment.