Metabolic adaptation to high-intensity exercise

Metabolic adaptation to high-intensity exercise: manipulation of training stimulus and nutritional support

This thesis investigated the acute and chronic responses of human skeletal muscle to high-intensity exercise, with a particular focus on markers of mitochondrial content, and the potential for nutrition to manipulate the adaptive response in recreationally active individuals. The acute response was primarily assessed via measurement of signalling proteins and mRNA species linked to exercise-induced mitochondrial biogenesis. The chronic response was determined via changes in the protein content or maximal activities of mitochondrial enzymes after training. Study 1 examined whether the manner in which a given amount of high-intensity cycling work was performed (i.e., in an intermittent or continuous fashion) altered the acute metabolic response to exercise, and whether the acute response was indicative of longer-term adaptations. Despite the similar acute activation of signalling proteins after the intermittent and continuous matched-work exercise protocols, 6 wk of training with the continuous protocol did not increase mitochondrial content, contrary to what we have previously shown after 6 wk training with the intermittent protocol. This suggests that the intermittent application of a low-volume, high-intensity stimulus is important to elicit training-induced increases in mitochondrial content. Furthermore, Study 1 showed that acute changes in specific signalling proteins did not necessarily predict chronic adaptations. Studies 2 and 3 examined whether specific nutritional interventions, previously shown to modulate acute exercise capacity or metabolic response, altered the mitochondrial adaptive response to several weeks of HIT. Neither manipulating carbohydrate availability between twice daily training sessions, or chronic ingestion of β-alanine, augmented skeletal muscle adaptations in response to 2-6 wk of HIT. It is possible that small influences of nutrition were overwhelmed by the potency of HIT, which stimulated marked increases in mitochondrial content in this population. Overall this thesis advances our basic understanding of the skeletal muscle adaptive response to HIT and the influence of nutrition.

So, endurance training caused NO increase in mitochondrial biogenesis, while a work-matched high intensity interval protocol did. The lesson seems to be that to obtain all the benefits of exercise, workouts must be of sufficient intensity. If they don’t leave you gasping for breath, they are not.

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