Exercise training leads to substantial remodelling of the protein composition in skeletal muscle. The main factors that determines training-induced adaptations are training intensity and training volume. Intense interval training has gained considerable attention due to its effectiveness in promoting training-induced adaptations with noticeable upregulation of mitochondrial proteins and respiratory function in the skeletal muscle. However, it remains elusive how differences in intense interval training intensity affect mitochondrial adaptations in human skeletal muscle. Therefore, the overall aim of this PhD thesis was to examine how intense interval training with different exercise intensities
affected mitochondrial adaptations in human skeletal muscle.
To address this, three studies were conducted using different exercise training intensities: paper I ~75%, paper II ~100%, and paper III ~225% of incremental peak power output (iPPO). To assess the role of training intensity on adaptations in the skeletal muscle, advancements in mass spectrometrybased proteomic technology were utilized to explore global changes in protein composition of the
exercised muscle (paper I and paper II). Mitochondrial respiration was measured in permeabilized muscle fibres using high-resolution respirometry to determine the respiratory capacity of specific complexes of the electron transport chain (paper I-III). In addition, training-induced adaptations in mitochondrial respiration were investigated together with exercise-related metabolic and ionic
perturbations in relation to exercise performance (paper III).

Leveraging advances in the proteomic field extensive depth was achieved with 3168 quantified proteins in paper I and 2525 proteins in paper II. Training led to robust remodelling of the proteome with marked enrichment of mitochondrial-related proteins in paper I and paper II. Further exploration of mitochondrial proteins revealed that paper I appeared to increase complex I, II, and IV of the
electron transport chain to a greater extent than paper II. In contrast, complex II abundance seemed to increase more robustly in paper II and paper III compared with paper I. Similar trends were observed in the mitochondrial respiratory measurements where training-induced increases in complex I-coupled respiration were greatest in paper I despite comparable improvements in complex I+IIcoupled respiration between paper I-III. In paper III, training-induced increases in mitochondrial respiration were associated with postponed exercise-related metabolic and ionic perturbation, which may have contributed to the enhanced exercise performance.

In conclusion, the findings in this PhD thesis demonstrate that intense interval training induces marked upregulation of mitochondrial proteins, including the complexes that constitute the electron transport chain, regardless of exercise intensity. These training-induced adaptations may promote mitochondrial respiratory function in a complex-specific manner, depending on distinct changes of the subunits that constitute the electron transport chain. Lastly, increments in mitochondrial respiratory capacity may participate in enhancing exercise capacity by delaying the anaerobic energy contribution during incremental exercise thereby postponing metabolic and ionic perturbations that
contribute to the development of muscle fatigue.