Muscle fatigue development during intense exercise in humans : the mitigating role of high-intensity intermittent training

This thesis adds to the knowledge of potential factors causing muscle fatigue during high-intensity exercise lasting few minutes and provides a new insight on how manipulation of exercise training may affect the regulation of some key transport proteins involved in fatigue development, and how these adaptations are related to changes in exercise performance. Study I showed that performance during an intense exercise bout corresponding to ~130% of V&O2-max was more depressed when preceded by previous fatiguing exercise lasting ~3 min or ~2 h compared to previous exhaustive exercise lasting ~30 s. These results suggest that muscle fatigue during intense dynamic exercise can occur for different reasons and that muscle CP is not likely to be a critical factor. Muscle pH may play a contributing role, but it does not seem to cause fatigue, whereas muscle glycogen could be of importance if it is low. Contraction-induced loss of cellular K+ could be a major cause of muscle fatigue during intense exercise lasting ~2 min in duration. However, it appears not to be the K+ ion that causes fatigue, but more likely the concurrent depolarization of the membrane potential. In Study II it was demonstrated that an alteration from regular endurance training to intense intermittent training in humans resulted in improved performance during short-duration exhaustive and repeated intense exercise. These improvements were associated with higher expression of muscle Na+,K+ pump α1 subunit and NHE1, as well as elevated capillary density and relative number of FTx fibres. After the intense training period there was a lowered venous K+ accumulation during and in recovery from intense exercise, whereas the amount of some subunits of the Na+,K+ pump were related to performance variables. Together, these findings support a role for the Na+,K+pump in the control of K+ homeostasis and in the development of fatigue during repeated intense exercise. Furthermore V&O2-max, endurance performance and oxidative enzyme activity remained unaltered despite the dramatic reduction in training volume, suggesting that very intense exercise training also in fit subjects is a powerful stimulus for the maintenance of oxidative capacity.