Abstract
Introduction: Mitochondria are essential in regulating healthy skeletal muscle metabolism, cellular respiration, oxidative stress, and calcium and energy homeostasis. Also, they perform various functions, including reactive oxygen species signaling, apoptosis, and immune signaling. It has been shown that High-Fat diet (HFD) consumption can decrease gene expression and protein levels of PGC1-α and disrupt mitochondrial biogenesis in humans and rodents. Studies have shown the positive effects of various exercise training, such as resistance and endurance training on mitochondrial biogenesis. Also, High-intensity interval training (HIIT) can induce mitochondrial biogenesis. Few studies have examined the effects of HIIT in reducing and managing the negative effects of HFD consumption, and their results have been contradictory. The aim of the present study was to investigate the effect of HIIT training with and without HFD consumption on PGC1-α gene expression in the soleus muscle of male Wistar rats.

Methodology: Thirty-two healthy 6-week-old male Wistar rats were randomly divided into four groups: 1) Control (Standard diet), 2) Control+HIIT, 3) HFD, and 4) HFD+HIIT. HIIT training consisted of 8 bouts of 2.5 minutes of running with an intensity of 90% of Maximum Running capacity (MRC) and 2.5 minutes of active rest with an intensity of 50% of MRC, three sessions per week. Also, HFD interventions were applied simultaneously in the form of free access for 10 weeks. RT-PCR was used to investigate gene expression. Two-way ANOVA and LSD post hoc test were used to investigate the differences between groups.

Results: HFD decreased the expression of PGC1-α gene (P<0.001). Results further showed that HIIT training increased the expression of PGC1-α gene (P=0.005).

Conclusion: The consumption of HFD leads to disruption in the biogenesis and ultimately reduces mitochondrial function. HIIT training moderates the negative effects of HFD consumption and improves mitochondrial biogenesis.