Objective: 

Hypoxia can lead oxidative damage in tissues. Increase in the heat shock 72 protein level, mainly formed with heat, is involved in the protection of cells from different types of stresses including oxidative stress. The aim of this investigation is to determine that whether heat stress is effective for preventing rat skeletal muscle from hypoxia inducible oxidative protein damage.

Methods: 

Thirty-five Wistar Albino male rats randomly assigned to one of the four groups: Hypoxia (HN=9), hypoxia with heat stress (HS=10), normoxia (NN=8) and normoxia with heat stress (NS=8). The hypoxia groups were kept in simulated altitude of 6000m (%9.7 O2, 90.3 N2) for up to 15 days. For heat treatment, animals were retained at 41 0 C environment for 60 minutes. Total of three heat sessions, two consecutive days just before the and at the 8th day of experiment were applied. At the end of the 15th day, all rats were anesthetized with sodium pentobarbutirate (50 mg/kg) and then were killed via servical dislocation. Plantaris (PLA) and Extensor digitorum longus (EDL) muscles were used for analyzing protein carbonyl (PCO), advanced oxidation protein products (AOPP) and protein thiol (P-SH). One Way ANOVA and Post Hoc Tukey tests were used for statistical analysis.

Results: 

Fifteen days of hypoxia resulted in increase in PCO and AOPP and decrease in P-SH levels in both PLA and EDL muscles only in HN group (p<0.05). There were no differences among experimental groups in variables investigated.

Conclusions: 

In conclusion, heat stress provided protection against hypoxia-induced oxidative protein damage in rat skeletal muscles.