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J Appl Physiol 100: 1679-1687, 2006. First published December 29, 2005; doi:10.1152/japplphysiol.00421.2005
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Vitamin E isoform-specific inhibition of the exercise-induced heat shock protein 72 expression in humans

Christian P. Fischer,1 Natalie J. Hiscock,2 Samar Basu,3 Bengt Vessby,3 Anders Kallner,4 Lars-Börje Sjöberg,5 Mark A. Febbraio,2 and Bente K. Pedersen1

1Centre of Inflammation and Metabolism, The Department of Infectious Diseases and The Copenhagen Muscle Research Centre, Rigshospitalet and The Faculty of Health Sciences, University of Copenhagen, Denmark; 2Skeletal Muscle Research Laboratory, School of Medical Sciences, Royal Melbourne Institute of Technology University, Victoria, Australia; 3Clinical Nutrition Research, Department of Public Health and Caring Sciences/Geriatrics, University of Uppsala; 4Division of Clinical Chemistry, Karolinska University Hospital, Stockholm; and 5Research and Quality Department, Semper Foods, Stockholm, Sweden

Submitted 14 April 2005 ; accepted in final form 26 December 2005

ABSTRACT

Increased levels of reactive oxygen and nitrogen species, as seen in response to exercise, challenge the cellular integrity. Important protective adaptive changes include induction of heat shock proteins (HSPs). We hypothesized that supplementation with antioxidant vitamins C (ascorbic acid) and E (tocopherol) would attenuate the exercise-induced increase of HSP72 in the skeletal muscle and in the circulation. Using randomization, we allocated 21 young men into three groups receiving one of the following oral supplementations: RRR-{alpha}-tocopherol 400 IU/day + ascorbic acid (AA) 500 mg/day (CE{alpha}), RRR-{alpha}-tocopherol 290 IU/day + RRR-{gamma}-tocopherol 130 IU/day + AA 500 mg/day (CE{alpha}{gamma}), or placebo (Control). After 28 days of supplementation, the subjects performed 3 h of knee extensor exercise at 50% of the maximal power output. HSP72 mRNA and protein content was determined in muscle biopsies obtained from vastus lateralis at rest (0 h), postexercise (3 h), and after a 3-h recovery (6 h). In addition, blood was sampled for measurements of HSP72, {alpha}-tocopherol, {gamma}-tocopherol, AA, and 8-iso-prostaglandin-F2{alpha} (8-PGF2{alpha}). Postsupplementation, the groups differed with respect to plasma vitamin levels. The marker of lipid peroxidation, 8-iso-PGF2{alpha}, increased from 0 h to 3 h in all groups, however, markedly less (P < 0.05) in CE{alpha}. In Control, skeletal muscle HSP72 mRNA content increased 2.5-fold (P < 0.05) and serum HSP72 protein increased 4-fold (P < 0.05) in response to exercise, whereas a significant increase of skeletal muscle HSP72 protein content was not observed (P = 0.07). In CE{alpha}, skeletal muscle HSP72 mRNA, HSP72 protein, and serum HSP72 were not different from Control in response to exercise. In contrast, the effect of exercise on skeletal muscle HSP72 mRNA and protein, as well as circulating HSP72, was completely blunted in CE{alpha}{gamma}. The results indicate that {gamma}-tocopherol comprises a potent inhibitor of the exercise-induced increase of HSP72 in skeletal muscle as well as in the circulation.

{alpha}-tocopherol; ascorbic acid; {gamma}-tocopherol; serum; skeletal muscle


Address for reprint requests and other correspondence: C. P. Fischer, Dept. of Infectious Diseases, Rigshospitalet Univ. Hospital of Copenhagen, Blegdamsvej 9, section M7641, DK-2100 Copenhagen, Denmark (e-mail: cfischer{at}dadlnet.dk)




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