Effects of physical training on the metabolic profile of rats exposed to chronic restraint stress

体育锻炼对长期受束缚应激大鼠代谢特征的影响

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Abstract

INTRODUCTION: Despite strong evidences supporting the protective role of exercise against stress-induced repercussions, the literature remains inconclusive regarding metabolic aspects. Therefore, this study aimed to evaluate the effect of Physical Training (PT) by swimming on the metabolic parameters of rats subjected to restraint stress. METHODS: Wistar rats (n = 40) were divided into four groups: Control (C), Trained (T), Stressed (S), and Trained/Stressed (TS). The restraint stress protocol involved confining the animals in PVC pipes for 60 minutes/day for 12 weeks. Concurrently, the swimming PT protocol was performed without additional load in entailed sessions of 60 minutes conducted five days a week for the same duration. The following parameters were analyzed: fitness progression assessed by the physical capacity test, body mass, serum level of glucose, triglyceride, cholesterol and corticosterone, as well as glycemic tolerance test, evaluated after glucose administration (2 g/kg, i.p.). RESULTS: Trained groups (T and TS) exhibited enhanced physical capacity (169 ± 21 and 162 ± 22% increase, respectively) compared to untrained groups (C: 9 ± 5 and S: 11 ± 13% increase). Corticosterone levels were significantly higher in the S group (335 ± 9 nmoL/L) compared to C (141 ± 3 nmoL/L), T (174 ± 3 nmoL/L) and TS (231 ± 7 nmoL/L), which did not differ from each other. There were no significant changes in serum glucose, cholesterol, and triglyceride levels among the groups. However, the glycemic curve after glucose loading revealed increased glycemia in the S group (area under curve 913 ± 30 AU) but the TS group exhibited values (673 ± 12 AU) similar to the groups C (644 ± 10 AU) and T (649 ± 9 AU). CONCLUSION: Swimming-based training attenuated stress-induced corticosterone release and prevented glucose intolerance in rats, reinforcing the importance of exercise as a potential strategy to mitigate the pathophysiological effects of stress.

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