Effect Of Intermittent Heat Stress After Muscle Damage On Signaling Pathway In Rat Skeletal Muscle

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PURPOSE: It is suggested that intermittent heat stress after muscle damage facilitate recovery from muscle damage. However, the mechanism is not clear, especially about the response of protein synthesis signaling pathways. The aim of this study was to examine the effect of intermittent heat stress after muscle damage on protein synthesis signaling pathways. METHODS: Male Wistar rats (14-wk-old, n=12) were assigned to a control (n=6) or a muscle damage (n=6) group, and then one leg of both groups was served as heat stress leg; control (C), muscle damage (D), heat stress (H) or muscle damage + heat stress (DH) legs. To induce skeletal muscle damage, 0.5ml of 0.5% bupivacaine was injected into the tibialis anterior (TA) muscle of D and DH rats. One leg of H and DH rats were heated for 30 min in hot water (43°C) on day 2, day 4 and day 6 after bupivacaine injection. The rats were fasted over 18 hours before the last heat stress to avoid the response of protein synthesis signaling pathways by nutrition. Immediately after the last heat stress, the rats were anesthetized and TA muscles were removed. Total protein content, phosphorylation of Akt and mTOR, 4E-BP1 and p70s6k were analyzed. RESULTS: Total protein content was significantly decreased by bupivacaine injection (p < 0.01), however, heat stress did not affect the total protein content. Phosphorylation of Akt, mTOR and p70s6k in H and DH groups were significantly elevated compared to C and D legs (p < 0.01), although there was no significant difference in phosphorylation of 4E-BP1 between groups. CONCLUSIONS: These results suggested that intermittent heat stress after muscle damage could stimulate phosphorylation of Akt, mTOR and p70s6k although total protein content was not increased during a short recovery period.