Introduction and purpose: Skeletal muscle immobility distorts cardiac adaptations by reducing hemodynamic pressure and causes decrease in cardiac function by increasing oxidative pressure. The aim of was to investigate the expression-changes of mitochondrial regulatory genes, AMPK, PGC-1α, SIRT-1,2 and NRF-1 as cardiac atrophy effective factors following a period of inactivity in trained/ not-trained rats.
Material and methods: 18male rats were divided into three random groups (exercise, exercise+inactivity, control+inactivity). The training group ran on the treadmill for six weeks, five sessions/week, 15-60 minutes, from 17.5 m/min in the first week to 30 m/min in the last. The trained rats' lower limb was immobilized by molding 48 hours after the last training session, for seven days. The cardiac muscle was extracted, weighed, and the expression level of the mentioned genes was measured (RT-PCR). One-way ANOVA and Tukey's post-hoc test were used (significant level (α<0.05)).
Results: In the exercise group compared to exercise+inactivity and control+inactivity, the expression of genes (F=24.38, P<0.01) SIRT-1, SIRT-6 (F=23.07, P<0.01) 0.01), AMPK (F=4.03, P<0.05), (F=32.46, P<0.01) PGC1-α and (F=35.10, P<0.01) NRF-1 was significantly higher, but heartweight/bodyweight was significantly higher in exercise+inactivity group (F=74.47, P<0.01).
Discussion and Conclusion: The immobility of the organs causes mitochondrial dysfunction by reducing the hemodynamic pressure of the heart and increasing the oxidative pressure, and causes cardiac atrophy by decreased regulation of genes. Aerobic activities have protective effect in cells by stimulating AMPK, but don't prevent changes in the period of inactivity.
Key words: Aerobic training, Cardiac atrophy, Oxidative stress, PGC-1, Mitochondria, Immobilization.