These findings demonstrate that the application of a 12-wk strength and aerobic interval training program reduced the oxygen cost of arm cranking, improved aerobic capacity, and improved gross motor function in children and adolescents with CP.
Exercise is important in the prevention and treatment of the metabolic syndrome (MetS), a cluster of risk factors that raises morbidity. Metabolomics can facilitate the optimization of exercise prescription. This study aimed to investigate whether the response of the human urinary metabolic fingerprint to exercise depends on the presence of MetS or exercise mode. Twenty-three sedentary men (MetS, n = 9, and Healthy, n = 14) completed four trials: resting, high-intensity interval exercise (HIIE), continuous moderate-intensity exercise (CME), and resistance exercise (RE). Urine samples were collected pre-exercise and at 2, 4, and 24 h for targeted analysis by liquid chromatography-mass spectrometry. Time exerted the strongest differentiating effect, followed by exercise mode and health status. The greatest changes were observed in the first post-exercise samples, with a gradual return to baseline at 24 h. RE caused the greatest responses overall, followed by HIIE, while CME had minimal effect. The metabolic fingerprints of the two groups were separated at 2 h, after HIIE and RE; and at 4 h, after HIIE, with evidence of blunted response to exercise in MetS. Our findings show diverse responses of the urinary metabolic fingerprint to different exercise modes in men with and without metabolic syndrome.
It seems likely that the neuropeptide Y (NPY)-leptin axis is involved in the regulation of energy expenditure in man. The purpose of this study was to observe the effect of a model of intense prolonged exercise-mediated energy expenditure (25 km swim race in 6.9-10.5 hours) on leptin and NPY concentrations in male long-distance swimmers. Sixteen long-distance swimmers (mean age 25, range 18-45 years) who took part in a 25 km sea swimming competition (Toroneos golf, Chalkidiki, Greece) participated in the study. Mean competition time was 8.5 hours (range 6.5-10.5). The participants were allowed food and beverage intake ad libitum before and throughout the 25 km race. Venous blood samples were taken prior and immediately after the race for the measurement of serum leptin and plasma NPY. Non-esterified free fatty acids (NEFFA) and glycerol levels were determined as indicators of adipose tissue lipids mobilization. Results showed that leptin levels after marathon swimming were significantly reduced (p<0.001) in all athletes. There was a statistically significant negative correlation (r=-0.812, p<0.01) between the values of leptin and glycerol just after the termination of swimming. Blood serum glycerol and free fatty acid levels were significantly increased (p<0.001) in all swimmers. Plasma NPY levels were also increased (p<0.01) in 81.2% of the swimmers. Linear regression analysis revealed a significant negative correlation between the values of leptin and NPY (r=-0.789, p<0.01). In conclusion, these data support our initial hypothesis that appropriate changes in leptin and NPY take place during marathon swimming to compensate for the negative energy balance produced due to this prolonged effort. This indicates the NPY-leptin axis involvement in the regulation of energy expenditure in man.
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