The Effect of a Detraining After Resistance Training on the Histochemical Expression of Potassium Channels and Mitochondrial Biogenesis of Heart Tissue in Male Rats

• Main Authors: Fatemeh Ahmadi, Marefat Siahkouhian, Shadmehr Mirdar, Leily Tapak
• Format: Article
• Language: English
• Published: Gonabad University of Medical Sciences (GMU) 2021-03-01
• Series: Ufuq-i Dānish
• Subjects: resistance training; detraining; potassium channels; mitochondrial biogenesis
• Online Access: http://hms.gmu.ac.ir/article-1-3501-en.html

Aims: Detraining may affect cardiovascular adaptations. The present study aimed to investigate the effect of a detraining period followed by resistance training on immunohistochemical expression of ATP-sensitive potassium channels and mitochondrial biogenesis of heart tissue in male rats. Methods & Materials: The present study was experimental. Thirty male Wistar rats were randomly divided into four groups (control, control-detraining, resistance training, and resistance-detraining training). The control group was sacrificed at the beginning of the study, and the control-detraining group did not exercise for 11 weeks. The resistance training group performed eight weeks of training. The resistance-detraining group did not train for three weeks after training. One-way analysis of variance and Tukey’s post hoc test were used for statistical analysis. Findings: The expression of KIR6.2, SUR2a, PGC1α, and TFAM in the heart tissue of the control-detraining group was significantly lower than those in the resistance training group (P=0.001). Also, they were significantly higher in the resistance training group compared to those in the resistance-detraining group (P=0.001). PGC1α expression in the resistance-detraining group was higher than in the control-detraining group (P=0.001). Conclusion: Resistance training increases PGC1α and TFAM in the heart tissue of rats by increasing the expression of KIR6.2 and SUR2a. But lack of exercise reduces the expression of potassium channels and factors that increase mitochondrial biogenesis.