Coronary smooth muscle adaptation to exercise: does it play a role in cardioprotection?
Article first published online: 23 MAY 2003
Acta Physiologica Scandinavica
Volume 178, Issue 2, pages 117–121, June 2003
How to Cite
Bowles, D. K. and Wamhoff, B. R. (2003), Coronary smooth muscle adaptation to exercise: does it play a role in cardioprotection?. Acta Physiologica Scandinavica, 178: 117–121. doi: 10.1046/j.1365-201X.2003.01130.x
- Issue published online: 23 MAY 2003
- Article first published online: 23 MAY 2003
- Received 31 December 2002, accepted 21 January 2003
- calcium channels;
- phenotypic modulation;
- potassium channels;
- vascular smooth muscle
Substantial evidence exists supporting the role of chronic exercise in reducing the incidence and severity of coronary vascular disease. Physical inactivity is an independent risk factor for coronary heart disease suggesting that the cardioprotective effect of exercise is due, in part, to an intrinsic adaptation within the coronary vasculature. Surprisingly, a paucity of information exists regarding the intrinsic cellular changes within the coronary vasculature associated with exercise training and even less is known regarding the effect of physical activity on long-term phenotypic modulation of coronary smooth muscle (CSM). The purpose of this symposium is to provide a concise update on the current knowledge regarding CSM adaptation to exercise training and the potential for these adaptations to contribute to exercise-induced cardioprotection. The potential role of CSM in exercise-induced cardioprotection will be approached from two perspectives. First, endurance exercise training effects on the regulation of coronary vasomotor tone via changes in CSM calcium regulation will be reviewed, i.e. short-term functional adaptation. Secondly, we will discuss potential long-term consequences of this altered calcium regulation, i.e. exercise-induced phenotypic modulation of CSM. We propose that exercise training alters CSM intracellular calcium regulation to reduce Ca2+-dependent activation of the contractile apparatus and Ca2+-dependent gene transcription and increase activation of sarcolemmal potassium channels. The overall effect is to increase the gain of the vasomotor system and maintain a stable, contractile CSM phenotype.