Advances in mitochondrial mechanisms of skeletal muscle for exercise intolerance in heart failure patients
10.3760/cma.j.cn114798-20240204-00086
- VernacularTitle:心力衰竭患者运动不耐受的骨骼肌线粒体机制研究进展
- Author:
Qingxuan YANG
1
;
Yuqin SHEN
Author Information
1. 同济大学医学院 同济大学附属同济医院心脏康复科，上海 200331
- Keywords:
Heart failure;
Skeletal muscle;
Mitochondria;
Sports therapy
- From:
Chinese Journal of General Practitioners
2024;23(9):998-1003
- CountryChina
- Language:Chinese
-
Abstract:
Severe exercise intolerance is one of the main clinical manifestations in heart failure (HF) patients, which seriously affects patients′ quality of life. Recent studies have demonstrated that peripheral dysfunction, especially the skeletal muscle dysfunction, is a fundamental cause of exercise intolerance, rather than conventionally perceived cardiac factors. Notably, the alternation of mitochondrial function and structure dominate skeletal muscle dysfunction, and aerobic exercise is the only basic treatment for HF patients with the highest level of evidence-based medicine. This article reviews research advances on the mechanisms of skeletal muscle dysfunction and exercise intolerance in HF patients, focusing on the biogenesis, fusion, fission and autophagy of mitochondria, and further discusses the possibility of exercise training for enhancing exercise tolerance through improving mitochondrial function in HF patients.
