4.6 Article

Repeated Sprints Alter Signaling Related to Mitochondrial Biogenesis in Humans

Journal

MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
Volume 44, Issue 5, Pages 827-834

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1249/MSS.0b013e318240067e

Keywords

HIGH-INTENSITY INTERMITTENT TRAINING; PROTEIN SIGNALING; MITOCHONDRIAL BIOGENESIS; PGC-1 alpha

Categories

Funding

  1. Department of Education, Employment and Workplace Relations, Australia [407_2008]
  2. National Health and Medical Research Council [606553]

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SERPIELLO, F. R., M. J. MCKENNA, D. J. BISHOP, R. J. AUGHEY, M. K. CALDOW, D. CAMERON-SMITH, and N. K. STEPTO. Repeated Sprints Alter Signaling Related to Mitochondrial Biogenesis in Humans. Med. Sci. Sports Exerc., Vol. 44, No. 5, pp. 827-834, 2012. Purpose: We investigated the effects of acute and chronic repeated-sprint exercise (RSE) on the skeletal muscle messenger RNA (mRNA) expression and protein abundance/phosphorylation associated with mitochondrial biogenesis. Methods: Ten healthy young adults (seven males, three females) performed the RSE trial, comprising three sets of 5 x 4-s maximal sprints on a nonmotorized treadmill, with a 20-s recovery between sprints and 4.5 min between sets. After 4 wk of repeated-sprint training, three times per week, participants repeated the RSE. A vastus lateralis muscle biopsy was obtained at rest, immediately after, and 1 and 4 h after RSE, before and after training. Venous blood lactate and glucose were measured at rest and during recovery. Real-time reverse transcriptase polymerase chain reaction and Western blot techniques were used to measure mRNA expression and protein abundance, respectively. Results: Acute RSE increased the phosphorylation of acetyl-CoA carboxylase (86%, effect size (ES) = 1.4 +/- 0.8, P < 0.001) and Ca2+ calmodulin-dependent protein kinase II (69%, ES = 0.7 +/- 0.6). Peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1 alpha; 208%, ES = 1.5 +/- 0.7, P < 0.001) and nuclear respiratory factor 1 (92%, ES = 0.7 +/- 0.8) mRNA expression was increased after RSE. Four weeks of training increased the abundance of PGC-1 alpha protein at rest (33%, ES = 0.9 +/- 0.7). Conclusions: Both acute and chronic RSE, despite only 60 s and 12 min of exercise, respectively, altered the molecular signaling associated with mitochondrial adaptations and PGC-1 alpha mRNA expression in skeletal muscle. However, the small-to-moderate changes in resting PGC-1 alpha protein abundance after training, together with the absence of changes in aerobic fitness, require further research to understand the functional significance of PGC-1 alpha in response to RSE.

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