HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 292/3/E748    most recent 00311.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Adhihetty, P. J. Articles by Hood, D. A. Search for Related Content PubMed PubMed Citation Articles by Adhihetty, P. J. Articles by Hood, D. A.

Effect of chronic contractile activity on SS and IMF mitochondrial apoptotic susceptibility in skeletal muscle

¹Department of Biology and ²School of Kinesiology and Health Science, York University, Toronto, Ontario, Canada

Submitted 28 June 2006 ; accepted in final form 31 October 2006

Chronic contractile activity of skeletal muscle induces an increase in mitochondria located in proximity to the sarcolemma [subsarcolemmal (SS)] and in mitochondria interspersed between the myofibrils [intermyofibrillar (IMF)]. These are energetically favorable metabolic adaptations, but because mitochondria are also involved in apoptosis, we investigated the effect of chronic contractile activity on mitochondrially mediated apoptotic signaling in muscle. We hypothesized that chronic contractile activity would provide protection against mitochondrially mediated apoptosis despite an elevation in the expression of proapoptotic proteins. To induce mitochondrial biogenesis, we chronically stimulated (10 Hz; 3 h/day) rat muscle for 7 days. Chronic contractile activity did not alter the Bax/Bcl-2 ratio, an index of apoptotic susceptibility, and did not affect manganese superoxide dismutase levels. However, contractile activity increased antiapoptotic 70-kDa heat shock protein and apoptosis repressor with a caspase recruitment domain by 1.3- and 1.4-fold (P < 0.05), respectively. Contractile activity elevated SS mitochondrial reactive oxygen species (ROS) production 1.4- and 1.9-fold (P < 0.05) during states IV and III respiration, respectively, whereas IMF mitochondrial state IV ROS production was suppressed by 28% (P < 0.05) and was unaffected during state III respiration. Following stimulation, exogenous ROS treatment produced less cytochrome c release (25–40%) from SS and IMF mitochondria, and also reduced apoptosis-inducing factor release (30%) from IMF mitochondria, despite higher inherent cytochrome c and apoptosis-inducing factor expression. Chronic contractile activity did not alter mitochondrial permeability transition pore (mtPTP) components in either subfraction. However, SS mitochondria exhibited a significant increase in the time to V_max of mtPTP opening. Thus, chronic contractile activity induces predominantly antiapoptotic adaptations in both mitochondrial subfractions. Our data suggest the possibility that chronic contractile activity can exert a protective effect on mitochondrially mediated apoptosis in muscle.

exercise; respiration; reactive oxygen species; apoptosis; mitochondrial permeability transaction pore

This article has been cited by other articles:

				M. F. N. O'Leary and D. A. Hood Effect of prior chronic contractile activity on mitochondrial function and apoptotic protein expression in denervated muscle J Appl Physiol, July 1, 2008; 105(1): 114 - 120. [Abstract] [Full Text] [PDF]

				V. Ljubicic and D. A. Hood Kinase-specific responsiveness to incremental contractile activity in skeletal muscle with low and high mitochondrial content Am J Physiol Endocrinol Metab, July 1, 2008; 295(1): E195 - E204. [Abstract] [Full Text] [PDF]

				A. N. Kavazis, J. M. McClung, D. A. Hood, and S. K. Powers Exercise induces a cardiac mitochondrial phenotype that resists apoptotic stimuli Am J Physiol Heart Circ Physiol, February 1, 2008; 294(2): H928 - H935. [Abstract] [Full Text] [PDF]