TY - JOUR
T1 - Training intensity modulates changes in PGC-1α and p53 protein content and mitochondrial respiration, but not markers of mitochondrial content in human skeletal muscle
AU - Granata, Cesare
AU - Oliveira, Rodrigo S F
AU - Little, Jonathan P.
AU - Renner, Kathrin
AU - Bishop, David J.
PY - 2016/2/1
Y1 - 2016/2/1
N2 - 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 × 30-s all-out bouts at~200% of peak power output (WPeak)], high-intensity interval training (HIIT; 4-7 × 4-min intervals at ~90% WPeak), or sublactate threshold continuous training (STCT; 20-36 min at ~65% WPeak). The STCT and HIIT groups werematched for total work.Resting biopsy samples (vastus lateralis) were obtained before and after training. The maximal mitochondrial respiration in permeabilizedmuscle fibers increased significantly only after SIT (25%). Similarly, the protein content of peroxisome proliferator-activated receptor g coactivator (PGC)-1a, 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 systemcomplexes 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-1a, p53, and PHF20 are more strongly associated with training-induced changes in mitochondrial respiration than mitochondrial content.¡ Granata,C., Oliveira, R. S. F.,Little, J.P., Renner,K., Bishop, D. J. Training intensity modulates changes in PGC-1a and p53 protein content and mitochondrial respiration, but not markers of mitochondrial content in human skeletal muscle.
AB - 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 × 30-s all-out bouts at~200% of peak power output (WPeak)], high-intensity interval training (HIIT; 4-7 × 4-min intervals at ~90% WPeak), or sublactate threshold continuous training (STCT; 20-36 min at ~65% WPeak). The STCT and HIIT groups werematched for total work.Resting biopsy samples (vastus lateralis) were obtained before and after training. The maximal mitochondrial respiration in permeabilizedmuscle fibers increased significantly only after SIT (25%). Similarly, the protein content of peroxisome proliferator-activated receptor g coactivator (PGC)-1a, 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 systemcomplexes 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-1a, p53, and PHF20 are more strongly associated with training-induced changes in mitochondrial respiration than mitochondrial content.¡ Granata,C., Oliveira, R. S. F.,Little, J.P., Renner,K., Bishop, D. J. Training intensity modulates changes in PGC-1a and p53 protein content and mitochondrial respiration, but not markers of mitochondrial content in human skeletal muscle.
KW - Exercise
KW - Mitochondrial biogenesis
KW - Mitochondrial remodeling
KW - PHF20
KW - TFAM
UR - http://www.scopus.com/inward/record.url?scp=84959010491&partnerID=8YFLogxK
U2 - 10.1096/fj.15-276907
DO - 10.1096/fj.15-276907
M3 - Article
C2 - 26572168
AN - SCOPUS:84959010491
SN - 0892-6638
VL - 30
SP - 959
EP - 970
JO - The FASEB Journal
JF - The FASEB Journal
IS - 2
ER -