Cardiovascular adaptations to exercise, heat and dehydration

Abstract

Exercise incurs multiple forms of strain and in several physiological systems. The nature of exercise dictates the profile of strain and thus the adaptive stimulus. Exercise intensity is a key parameter, and much interest has recently centred on the effects of high-intensity interval exercise (HIIT) for eliciting short- and longer- term cardiovascular adaptations. Heat strain is incurred by exercise and exacerbated by the environment, and is important for stimulating cardiovascular and haematological adaptation. The role of dehydration is less clear. Accordingly, this thesis examined the independent and interactive roles of exercise intensity, heat, and dehydration as acute, short-, and long-term stimuli for cardiovascular adaptation.

Study one was informed by a comprehensive pilot study, and designed to delineate the additive roles of muscular activity, heat stress, and dehydration on acute (24-h) cardiovascular, haematological and fluid regulatory outcomes. A low- intensity, orthostatically stressful exercise (i.e., callisthenics) was used to separate the independent effects of each stressor, but also as a novel viable conditioning method per se. Based on the outcomes, study two examined the cardiovascular strain of HIIT with and without exogenous heat stress, in eliciting short-term (8- wk) cardiovascular and haematological adaptation. One key purpose was to explore the role of hypervolaemia in mediating short-term integrative cardiovascular adaptation. The final study was conducted concurrently to determine the extent to which these short-term adaptations resembled a long- term exercise-adapted phenotype. Specifically, to what extent does short-term conditioning bridge the gap between the disparate resting cardiovascular function in chronically-trained athletes and untrained individuals, and the contributing role of hypervolaemia.

Callisthenics, heat and dehydration contributed additively to thermal and cardiovascular strain and produced an effective stimulus for meaningful cardiovascular and haematological outcomes (Chapters Three and Four). Specifically, post-exercise hypotension (PEH) and plasma volume expansion at 24 h were strongly interrelated and associated with the magnitude of preceding cardiovascular and thermal strain. But, additive stimuli (HIIT and heat) did not enhance short-term (8-wk) adaptations (Chapter Four) above those from HIIT alone; i.e., they elicited similar increases in aerobic power and cardiac volumes, and reductions in blood pressure and resting HR, but no consistent changes to blood volume, systemic vascular, or cerebrovascular function. In contrast to the acute 24-h response (Chapter Three), adaptive responses were associated with maintenance of strain over the 8-wk period rather than simply the largest overall. Despite substantial developments following short-term training, these responses were still dissimilar to a long-term adapted phenotype, and were not meaningfully influenced by blood volume differences (Chapter Five).

To conclude, independent stressors may be combined to exacerbate the strain incurred by a conditioning bout and the subsequent stimulus for cardiovascular and haematological outcomes. However, this may not be the case when repetitively applied, and more extensive or varied training develops the long-term adapted phenotype. These findings provide important information pertaining to the development of integrative cardiovascular adaptation, and the role of exercise characteristics in stimulating these responses. The findings are of particular importance in conceiving conditioning strategies to target health- and exercise performance-related cardiovascular outcomes.