Exercise Physiology
faeghe ghasemi; Hamid Mohebbi
Abstract
Background and Purpose: Consuming a high-fat diet leads to disruption of liver mitochondrial biogenesis. Training exercise and hypoxia, which are new preventive or therapeutic strategies for obesity-induced NAFLD, may improve the impaired mitochondrial function. The aim of this study was to determine ...
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Background and Purpose: Consuming a high-fat diet leads to disruption of liver mitochondrial biogenesis. Training exercise and hypoxia, which are new preventive or therapeutic strategies for obesity-induced NAFLD, may improve the impaired mitochondrial function. The aim of this study was to determine the effect of nutrition, training and hypoxia on liver mitochondrial biogenesis in male Wistar rats. Methods: Thirty-two male rats (age: 6 weeks old; average weight: 167.25 grams) were randomly divided into four groups of eight including normal diet (ND), high-fat diet (HFD), high-fat diet and training in normoxia (HFD-HIIT) and high-fat diet and training in hypoxia (HFD-HHIIT). After determining the maximum aerobic velocity (MAV) in normoxia and hypoxia-hypobaric, the HIIT protocol was performed for 12 weeks and three sessions per week, which included 3 to 8 bouts 4-minute activity with an intensity of 80 to 93 percent of MAV and 2-minute active rest periods with an intensity of 50 percent of MAV. At the end, the levels of PGC-1α and Tfam genes were measured through RT-PCR. Results: Both HFD-HIIT and HFD-HHIIT groups showed a significant increase in the expression of PGC-1α and Tfam genes and a significant decrease in liver fat content compared to the HFD group (p<0.05). While, there was no significant difference in the expression of these genes between the two training groups. Conclusions: It seems that HIIT training has been able to increase mitochondrial biogenesis and reduce liver fat content independently of hypoxia conditions.
