Abstract

It's generally believed that delayed onset muscle soreness (DOMS) induced by unaccustomed exercise session causes myofibrillar damage. In recent years, the use of cold water immersion (CWI) following heavy training sessions has become common among athletes aiming to reduce soreness, although there isn't any strong scientific rational behind this method. The question is raised in this regard that if this method really accelerates recovery. PURPOSE: HSP25 as one of the stress proteins that have been shown to play an important role after damage and following remodeling process in skeletal muscle have been discussed in this study. The purpose of this study was to investigate the expression of HSP25 after damaging exercise followed by cold water immersion in different recovery time courses. METHODS: male Wistar rats (n=96; W= 280±10gr) were divided into two groups of exercise (Ex) and exercise followed by cold water immersion (Ex+CWI). Each group divided to seven subgroups for seven time-courses (0, 0.5, 24, 48, 72, and 168 h after exercise). The time points were chosen to reflex the early events (0.5 and 24 h) and the delayed response (48-168 h) to damaging exercise. The exercise protocol was consisted of 40 minutes of downhill running (20m/min, -16°) on animal treadmill. Following exercise protocol, animals of Ex+CWI group were immersed in cold water (10 degree of centigrade) for 10 minutes up to their shoulder. At the predetermined time points, the rats were euthanized with an overdose of Ketamine-xylazine (IP) and the soleus muscles were removed. Muscle samples obtained from rats were used to measure protein content of HSP25. To analyze significant changes in HSP25 expression, the repeated measure ANOVA test was performed with a P value of ≤0.05 for establishing statistical significance. RESULTS: we observed that the level of HSP25 in exercised muscles was increased significantly in all time courses except 168 hour after exercise (p<0.05). The increment pattern was the same in both groups: a gradual significant increase during the time points, reaching to peak level at late recovery periods, and returning to near basal level after one week. In Ex group, HSP25 level reach to its peak level 48 hours post exercise, while the peak time course for Ex+CWI group was 72 hours post exercise. CONCLUSION: the most important finding of this study is that using CWI after exercise session causes delay in expression of HSP25 in recovery period. Also, the level of expression after CWI is higher. These findings indirectly indicate that using cold water immersion after exercise session may increase the response of muscle to exercise-induced muscle damage and delay the recovery period.

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