Abstract

PURPOSE: Apoptosis is a process of programmed cell death that occurs in different stress factors in the body. One of these stresses is exercise, exercise is a strong physiological stimulus which can influence a number of intracellular and extracellular signaling pathways. Till now, few researches shows the effect of sprint interval training and eccentric training on caspase3, bcl2 and bax gene expression changes. This study is exploring the effect of nine weeks of sprint interval training and eccentric training on caspase3, bcl2 and bax expression in soleus and SVL muscles METHODS: twenty four male Sprague Dawley rats purchased from Razi Institute were divided into three groups: control (n=8), sprint interval training (n=8) and eccentric training (n=8). Sprint interval training was included of one minute sprinting on animal treadmill with 2-4 minutes rest, 6-10 sets per session on 5-6 days a week, and eccentric downhill running was included running on -16° slope with 16 m/min for 90 minutes which in both the intensity of the trainings during the nine weeks gradually increased. The evaluation of gene expression was done by Real time PCR method RESULTS: Considering the low number of samples (n=8) and the normality of data rejected by Shapiro-Wilk test, Mann Whitney teat for differential between training and control groups were used. Also, caspase3 expression increased in all groups. All of these differences were not significant except for soleus muscle of eccentric training group. Also Bax/bcl-2 ratio increased in all groups and All of these differences were not significant. CONCLUSIONS: we conclude that nine weeks of Sprint interval training could lead to a small increase in caspase3 expression, Bax/bcl-2 ratio as the influential factor of apoptosis in all groups, except a large increase in caspase3 expression and ultimately strong apoptosis for soleus muscle in eccentric training group. Furthermore, it should be mentioned that the type of training and muscle could influenced the amount of gene expression levels of caspase3, bax/bcl2.

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