| 研究実績の概要 |
Exercise is a powerful intervention to increase health span in humans and widely advocated to prevent the functional decline occurring in old age. Exercise builds muscle mass, which prevents frailty, increases mobility, as a consequence, quality of life. Oxidative stress has long been seen as a negative consequence of exercise, but recent results suggest that reducing oxidative stress can prevent the beneficial effects of exercise. Using transgenic mice expressing a ratiometric redox-sensitive fluorescent protein (roGFP1) in mitochondrial or cytosol, we recorded the cellular redox state in skeletal muscle of live animals using in vivo confocal imaging.
Activation of intact muscle alone did not cause any changes in the redox state of cytosol or mitochondria of muscle, but in a serendipitous discovery, electrical stimulation did induce oxidative stress in muscle fibers surrounding a single injured muscle fiber. Muscle fiber injury is a common occurrence in exercise, and seen as negative consequence of strenuous muscle activation. Our results indicate that muscle fiber injury probably plays an important role in mediating the redox signaling necessary for the beneficial effects of exercise. We tentatively conclude that danger associated molecular patterns (DAMPs) released by injured muscle fibers cause, together with muscle activation, the observed redox transients in adjacent tissue muscle fibers. Our findings resolve many conflicting observations concerning the role of oxidative stress and muscle injury in the benefits of exercise.
|
