期刊
FASEB JOURNAL
卷 30, 期 2, 页码 959-970出版社
FEDERATION AMER SOC EXP BIOL
DOI: 10.1096/fj.15-276907
关键词
mitochondrial biogenesis; exercise; PHF20; TFAM; mitochondrial remodeling
资金
- ANZ-MASON foundation
- Natural Sciences and Engineering Research Council of Canada [RGPIN 435807-13]
Exercise training has been associated with increased mitochondrial content and respiration. However, no study to date has compared in parallel how training at different intensities affects mitochondrial respiration and markers of mitochondrial biogenesis. Twenty-nine healthy men performed 4 wk (12 cycling sessions) of either sprint interval training [SIT; 4-10 x 30-s all-out bouts at similar to 200% of peak power output (W-Peak)], high-intensity interval training (HIIT; 4-7 x 4-min intervals at similar to 90% W-Peak), or sublactate threshold continuous training (STCT; 20-36 min at similar to 65% W-Peak). The STCT and HIIT groups were matched for total work. Resting biopsy samples (vastus lateralis) were obtained before and after training. The maximal mitochondrial respiration in permeabilized muscle fibers increased significantly only after SIT (25%). Similarly, the protein content of peroxisome proliferator-activated receptor gamma coactivator (PGC)-1 alpha, p53, and plant homeodomain finger-containing protein 20 (PHF20) increased only after SIT (60-90%). Conversely, citrate synthase activity, and the protein content of TFAM and subunits of the electron transport system complexes remained unchanged throughout. Our findings suggest that training intensity is an important factor that regulates training-induced changes in mitochondrial respiration and that there is an apparent dissociation between training-induced changes in mitochondrial respiration and mitochondrial content. Moreover, changes in the protein content of PGC-1 alpha, p53, and PHF20 are more strongly associated with training-induced changes in mitochondrial respiration than mitochondrial content.
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