Melatonin administration does not alter muscle glycogen concentration during recovery from exhaustive exercise in rats

Abstract

The purpose of this study was to investigate the effect of melatonin administration on muscle glycogen concentration during recovery after exhaustive swimming exercise in sedentary and trained rats. Male Wistar rats were assigned to one of four groups: sedentary control (C), sedentary melatonin-injected (M), exercise-trained (T), and trained and melatonin-injected (MT) groups. Exercise-trained groups were subjected to six weeks of swimming exercise. All rats completed an exhaustive swimming exercise. Two daily subcutaneous injections of melatonin at a dose of 3 mg·kg^?1 were given to the rats in the M and MT groups immediately after the exhaustive exercise. Plasma melatonin, glucose and lactate concentrations, and glycogen concentrations of the soleus and epitrochlearis muscle tissues were measured after exhaustive exercise. Plasma lactate concentration was significantly lower in the T and MT groups than in the C group. Plasma melatonin concentration was higher in the supplemented groups than in the C group. Plasma glucose concentration was significantly higher in the T and MT groups than in the C group. Both epitrochlearis and soleus muscle glycogen concentrations were higher in the trained groups than in the C group. In conclusion, although exercise training results in improvement in muscle glycogen, exogenous melatonin administration after exhaustive exercise did not restore the glycogen concentrations in fast- or slow-twitch muscle tissues.     

Identification of critical intensity from a single lactate measure during a 3-min,submaximal cycle-ergometer test

We tested the hypothesis that critical intensity in cycling can be determined from a single delta blood lactate in the third minute of a submaximal cycle ergometer trial. Fourteen healthy young men performed four to six constant-power-output trials on a cycle ergometer to the limit of tolerance. Critical intensity was calculated via a linear model and subsequently validated. Lactate was measured at baseline and at 3 min from exercise onset. Delta lactate was the difference between these measures. Based on individual trials, we obtained the delta lactate–% validated critical intensity relationship and thereafter an estimate of critical intensity was computed. Validated and estimated critical intensity were compared by effects sizes, paired-sample t-test and Bland–Altman analysis. Delta lactate was a linear function of the intensity of exercise, expressed as % validated critical intensity (R² = 0.89). Estimated critical intensity was not different from (d = 0.03, P = 0.98) and highly correlated with (R² = 0.88) validated critical intensity. The bias between measures was 0.03 W (≠0) with a precision of 7 W. The results suggest that critical intensity in cycling can be accurately and precisely determined from delta lactate during a sub-maximal trial and so provides a practical and valid alternative to direct determination.