High-intensity endurance exercise inhibits mitochondrial biogenesis in the skeletal muscle
10.3969/j.issn.2095-4344.2015.46.008
- VernacularTitle:大强度耐力运动抑制骨骼肌线粒体的生物合成
- Author:
Guohua ZHANG
;
Shuzhuang CHEN
;
Suping LI
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2015;(46):7419-7424
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:There are many reports on the effects of low-to-moderate intensity endurance exercise on mitochondrial biogenesis in the skeletal muscle, but there is no understanding about the high-intensity endurance exercise. It has not been reported whether the high-intensity endurance exercise influence the mitochondrial biogenesis in the skeletal muscle through 5′-adenosine monophosphate-activated protein kinase (AMPK)/silent information regulator factor 2 related enzyme 1 (SIRT1) signal molecules. OBJECTIVE: To investigate the effect of AMPK/SIRT1 signaling cascade on the mitochondrial biogenesis in the skeletal muscle during different intensities of endurance exercises. METHODS:Forty-two male Sprague-Dawley rats were randomly divided into sedentary group, moderate-intensity exercise group and high-intensity exercise group. Moderate-intensity exercise load was 28 m/min, 60 min/d;high-intensity exercise load was 38 m/min, 60 min/d. In both exercise groups, the rats had 5 days of exercise and 2 days of rest within 1 week, and the exercise lasted for totaly 7 weeks. The animals of exercise groups were kiled immediately, 6 hours and 24 hours after exercise. Quantitative PCR was used to detect peroxisome proliferators γ activated receptor coativator-1α (PGC-1α) and SIRT1 gene expression, and western blot to detect phosphorylated-AMPK (P-AMPK) and SIRT1 protein expression. RESULTS AND CONCLUSION:(1) Immediately, 6 hours, 24 hours after moderate-intensity exercise, PGC-1α mRNA expression in the skeletal muscle was 362% (P < 0.01), 675% (P < 0.01) and 116% of that in the sedentary group, P-AMPK protein expression was 112%, 165% (P < 0.05), 129% (P < 0.05) of that in the sedentary group, the expressions of SIRT1 protein and mRNA were 55% (P < 0.05), 86%, 103% and 109% (P < 0.05), 155%, 132% (P < 0.05) of those in the the sedentary group, respectively. (2) Immediately, 6 hours, 24 hours after high-intensity exercise, PGC-1α mRNA expression in the skeletal muscle was 274% (P < 0.01), 130% (P < 0.05), 68% (P < 0.05) of that in the sedentary group, the expression of P-AMPK protein was 235% (P < 0.01), 166% (P < 0.05), 160% (P < 0.05) of that in the sedentary group, the expressions of SIRT1 protein and mRNA were 199% (P < 0.01), 166% (P < 0.05), 164% (P < 0.05) and 255% (P < 0.01), 292% (P < 0.01), 122% of those in the sedentary group, respectively. These findings indicate that (1) 7 weeks of moderate-intensity endurance exercise significantly increased PGC-1α gene expression in the skeletal muscle, and its mechanism may involve AMPK/SIRT1 signaling cascade; (2) 7 weeks of high-intensity endurance exercise significantly inhibited PGC-1α gene expression at 24 hours after exercise,and this process was carried out in an AMPK/SIRT1 signal cascade independent manner.