Integrative effects of resistance training and endurance training on mitochondrial remodeling in skeletal muscle

被引:0
作者
Zhao, Yong-Cai [1 ]
Gao, Bing-hong [2 ]
机构
[1] Tianjin Univ Sport, Coll Exercise & Hlth, 16 Donghai Rd, Tianjin 301617, Peoples R China
[2] Shanghai Univ Sport, Sch Athlet Performance, 399 Changhai Rd, Shanghai 200438, Peoples R China
关键词
Concurrent training; Mitochondrial biogenesis; Skeletal muscle; AEROBIC EXERCISE; MOLECULAR-MECHANISMS; SIGNALING RESPONSES; OXIDATIVE FUNCTION; PROTEIN-SYNTHESIS; MAMMALIAN TARGET; ACTIVATION; STRENGTH; HYPERTROPHY; MTORC1;
D O I
10.1007/s00421-024-05549-5
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Resistance training activates mammalian target of rapamycin (mTOR) pathway of hypertrophy for strength gain, while endurance training increases peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1 alpha) pathway of mitochondrial biogenesis benefiting oxidative phosphorylation. The conventional view suggests that resistance training-induced hypertrophy signaling interferes with endurance training-induced mitochondrial remodeling. However, this idea has been challenged because acute leg press and knee extension in humans enhance both muscle hypertrophy and mitochondrial remodeling signals. Thus, we first examined the muscle mitochondrial remodeling and hypertrophy signals with endurance training and resistance training, respectively. In addition, we discussed the influence of resistance training on muscle mitochondria, demonstrating that the PGC-1 alpha-mediated muscle mitochondrial adaptation and hypertrophy occur simultaneously. The second aim was to discuss the integrative effects of concurrent training, which consists of endurance and resistance training sessions on mitochondrial remodeling. The study found that the resistance training component does not reduce muscle mitochondrial remodeling signals in concurrent training. On the contrary, concurrent training has the potential to amplify skeletal muscle mitochondrial biogenesis compared to a single exercise model. Concurrent training involving differential sequences of resistance and endurance training may result in varied mitochondrial biogenesis signals, which should be linked to the pre-activation of mTOR or PGC-1 alpha signaling. Our review proposed a mechanism for mTOR signaling that promotes PGC-1 alpha signaling through unidentified pathways. This mechanism may be account for the superior muscle mitochondrial remodeling change following the concurrent training. Our review suggested an interaction between resistance training and endurance training in skeletal muscle mitochondrial adaptation.
引用
收藏
页码:2851 / 2865
页数:15
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