Effects of Aging and Exercise on Mitochondrial Physiology

Abstract

Mitochondria are organelles which main function is to generate energy in the form of ATP, although they are involved in a myriad of cellular processes. Mitochondria form a dynamic network that responds to the energetic demands of the cell, and that undergoes constant remodeling through biogenesis, fusion, fission, and mitophagy. Proper mitochondrial function is essential for the maintenance of health, and their (dys)function is involved in aging and in the development of several pathologies. Physical exercise is one of the best non-pharmacological interventions to improve mitochondrial function. Chapter 1 reviews the skeletal muscle ribosome and mitochondrial biogenesis in response to different exercise training modalities. Previous work has suggested a possible competition between both processes. However, the available literature suggests that untrained individuals present a generic response to exercise, with either resistance training (RT) or endurance (ET) training stimulating both ribosome and mitochondrial biogenesis. As the individual becomes trained in a particular modality, mitochondrial biogenesis is prioritized with endurance training, while ribosome biogenesis is prioritized with resistance training. Chapter 2 investigated the effects of aging and long-term physical activity on mitochondrial physiology and redox state of the cortex and cerebellum of female rats. There were minimal changes in several markers of mitochondrial content, function, and dynamics in the cortex and cerebellum in response to both aging and long-term physical activity. Furthermore, the redox status of the tissues investigated remained overall unaltered. The results suggest that the brain mitochondrial physiology and redox homeostasis of females may be more resilient to the aging process than initially thought. Chapter 3 investigated the acute and chronic effects of RT on skeletal muscle markers of mitochondrial remodeling in older adults. Ten weeks 3 of RT increased mitochondrial protein content and markers of mitochondrial dynamics, although no changes in these markers were detected following the first training bout. Importantly, the results show that besides the known improvements in muscle mass and strength, RT could be a viable approach to improve mitochondrial health in older adults. Chapter 4 investigated the effects of RT on the redox status of skeletal muscle in older adults. Six weeks of RT significantly decreased oxidative damage to lipids and increased the activity of different antioxidant enzymes. Therefore, RT may be a viable approach to counteract a possible age-related disruption of skeletal muscle redox homeostasis in older adults. Lastly, chapter 5 investigated the effects of prior RT on the molecular and performance adaptations to subsequent ET in humans. The results showed that prior RT had no additional benefits on adaptations to ET. Even though both groups had similar endurance performance improvements, most mitochondrial adaptations to ET were blunted in the RT+ET group, but such impairments seem to be related to the cessation of RT.