Markers of Human Skeletal Muscle Mitochondrial Biogenesis and Quality Control: Effects of Age and Aerobic Exercise Training

被引：151

作者：

Konopka, Adam R. ^{[1
]}

Suer, Miranda K. ^{[1
]}

Wolff, Christopher A. ^{[1
]}

Harber, Matthew P. ^{[1
]}

机构：

[1] Ball State Univ, Human Performance Lab, Muncie, IN 47306 USA

来源：

JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES | 2014年 / 69卷 / 04期

关键词：

Mitofusin; FIS1; Mitochondrial dynamics; PGC-1; alpha; Sarcopenia; Hypertrophy; CROSS-SECTIONAL AREA; OLDER MEN; ENDURANCE EXERCISE; COMBINED RESISTANCE; OXIDATIVE CAPACITY; PROTEIN-METABOLISM; GENE-EXPRESSION; FUSION; WOMEN; ADAPTATIONS;

D O I：

10.1093/gerona/glt107

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

Perturbations in mitochondrial health may foster age-related losses of aerobic capacity (VO2peak) and skeletal muscle size. However, limited data exist regarding mitochondrial dynamics in aging human skeletal muscle and the influence of exercise. The purpose of this study was to examine proteins regulating mitochondrial biogenesis and dynamics, VO2peak, and skeletal muscle size before and after aerobic exercise training in young men (20 +/- 1 y) and older men (74 +/- 3 y). Exercise-induced skeletal muscle hypertrophy occurred independent of age, whereas the improvement in VO2peak was more pronounced in young men. Aerobic exercise training increased proteins involved with mitochondrial biogenesis, fusion, and fission, independent of age. This is the first study to examine pathways of mitochondrial quality control in aging human skeletal muscle with aerobic exercise training. These data indicate normal aging does not influence proteins associated with mitochondrial health or the ability to respond to aerobic exercise training at the mitochondrial and skeletal muscle levels.

引用

页码：371 / 378

页数：8

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