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.
B Mirzaei; A barjaste; F Rahmani-nia
Abstract
Aim: This study aimed to examine the effect of aerobic exercise with and without BFR on blood lactate, cortisol and PGC-1α response in human skeletal muscle.
Method: On two different occasions, five healthy untrained male subjects (mean±SE; age: 33.4±1.02 years, height: 173.9±4.02 ...
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Aim: This study aimed to examine the effect of aerobic exercise with and without BFR on blood lactate, cortisol and PGC-1α response in human skeletal muscle.
Method: On two different occasions, five healthy untrained male subjects (mean±SE; age: 33.4±1.02 years, height: 173.9±4.02 cm, body mass: 79.64±4.69 kg), were required to perform (i) a BFR aerobic exercise at an exercise intensity of 40 % of VO2max; and (ii) similar exercise bouts without BFR (Ctrl). For each condition, baseline and 3 h post-exercise muscle biopsy samples (vastus lateralis) were performed for PGC-1α protein expression analysis. Venous blood samples were also collected at pre-exercise, immediately and 2 h post-exercise to measure changes in blood lactate and serum cortisol.
Results: PGC-1α protein content was significantly higher (P < 0.05) at 3-h post-exercise with BFR compared with Ctrl. Blood lactate and serum cortisol did not significantly change from baseline to immediately after exercise and at 2-h post exercise.
Conclusion: Metabolic stimuli are not a mechanism to mediate cell signaling network responsible for mitochondrial biogenesis. However, the addition of blood flow restriction during aerobic exercise induces an increase in PGC-1α to regulate mitochondrial biogenesis.
