Granata, Cesare (2015) Effects of different exercise intensity and volume on markers of mitochondrial biogenesis in human skeletal muscle. PhD thesis, Victoria University.

Abstract

Mitochondria are key components of skeletal muscles as they provide the energy required for almost all cellular activities, and play an important role in ageing and cell pathology. Different forms of exercise training have been associated with mitochondrial adaptations, such as increased mitochondrial content and function, and enhanced mitochondrial biogenesis, as well as improved endurance performance. However, the role of training intensity and training volume, in determining these changes remains elusive. Therefore, the aim of this thesis was to investigate the role of training intensity and volume on changes in mitochondrial content and function (as measured by mitochondrial respiration in permeabilised muscle fibres), in the skeletal muscle of healthy humans, and to study the molecular mechanisms underlying these changes. It was demonstrated that training intensity is a key factor regulating changes in mitochondrial respiration, but not mitochondrial content, and that an apparent dissociation exists between changes in these two parameters. Training consisting of repeated 30-s “all-out” sprints lead to improved mitochondrial (mt)-specific respiration (indicative of improved mitochondrial quality). Conversely, training volume was shown to be a key factor regulating mitochondrial content, with the associated increase in mitochondrial respiration being likely driven by the increase in mitochondrial content (i.e., unchanged mt-specific respiration). A training volume reduction resulted in a rapid decrease in most mitochondrial parameters, underlining the importance of maintaining the training stimulus to preserve training-induced mitochondrial adaptations. The protein content of PGC-1α, p53 and PHF20 was shown to be regulated in a training intensity-dependent manner, and was more strongly associated with changes in mitochondrial respiration rather than content, whereas changes in the protein content of TFAM were primarily associated with changes in mitochondrial content. Moreover, it was demonstrated that exercise intensity induced an increase in nuclear PGC-1α protein content and nuclear p53 phosphorylation, two events that may represent the initial phase of different pathways of the exercise-induced adaptive response. Collectively, this research provides novel information regarding mitochondrial adaptations to different training stimuli, and could have important implications for the design of exercise programs in conditions of compromised mitochondrial function.

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