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Similar Expression of Oxidative Genes after Interval and Continuous Exercise

WANG, LI1,3; PSILANDER, NIKLAS1,2; TONKONOGI, MICHAIL1,4; DING, SHUZHE3; SAHLIN, KENT1,2,5

Medicine & Science in Sports & Exercise: December 2009 - Volume 41 - Issue 12 - p 2136-2144
doi: 10.1249/MSS.0b013e3181abc1ec
Basic Sciences

Purpose: There is a debate whether interval or traditional endurance training is the most effective stimulus of mitochondrial biogenesis. Here, we compared the effects of acute interval exercise (IE) or continuous exercise (CE) on the muscle messenger RNA (mRNA) content for several genes involved in mitochondrial biogenesis and lipid metabolism.

Methods: Nine sedentary subjects cycled for 90 min with two protocols: CE (at 67% V˙O2max) and IE (12 s at 120% and 18 s at 20% of V˙O2max). The duration of exercise and work performed with CE and IE was identical. Muscle biopsies were taken before and 3 h after exercise.

Results: There were no significant differences between the two exercise protocols in the increases in V˙O2 and HR, the reduction in muscle glycogen (35%-40% with both protocols) or the changes in blood metabolites (lactate, glucose, and fatty acids). The mRNA content for major regulators of mitochondrial biogenesis [peroxisome proliferator-activated receptor (PPAR) γ coactivator 1α (PGC-1α), PGC-1-related coactivator, PPAR/δ] and of lipid metabolism [pyruvate dehydrogenase kinase isozyme 4 (PDK4)] increased after exercise, but there was no significant difference between IE and CE. However, the mRNA content for several downstream targets of PGC-1α increased significantly only after CE, and mRNA content for nuclear respiratory factor 2 was significantly higher after CE (P < 0.025 vs IE).

Conclusions: The present findings demonstrate that, when the duration of exercise and work performed is the same, IE and CE influence the transcription of genes involved in oxidative metabolism in a similar manner.

1GIH, the Swedish School of Sport and Health Sciences, Åstrands Laboratory, Stockholm, SWEDEN; 2Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, SWEDEN; 3Institute of Physical Education and Health, East China Normal University, Shanghai, CHINA; 4LIVI, Dalarna University, Falun, SWEDEN; and 5Institute of Sport Sciences and Clinical Biomechanics, University of Southern Denmark, Odense, DENMARK

Address for correspondence: Kent Sahlin, GIH, The Swedish School of Sport and Health Sciences, Box 5626, SE-114 86 Stockholm, Sweden; E-mail: kent.sahlin@gih.se.

Submitted for publication January 2009.

Accepted for publication April 2009.

©2009The American College of Sports Medicine