Individual differences in the mechanisms governing oxygen delivery - Implications for exercise performance and tolerance

Abstract

Oxygen delivery (O2D) is an important factor for maintaining intracellular homeostasis during exercise. Disruptions in intracellular homeostasis increase fatigue progression and the perception of exercise. The presence of inter-individual differences in the mechanisms governing O2D : demand matching during small and large muscle exercise remains unknown. Preliminary evidence from our laboratory, as well as investigations from decades ago that received surprisingly little attention, suggest these differences are of particular importance. Purpose: 1) To identify and characterize cardiovascular response phenotypes during perfusion pressure induced compromises to exercising forearm skeletal muscle perfusion and establish an intervention to mitigate the adverse effects associated with non-compensation. 2) To determine the effects of differences in cardiac output (CO) on submaximal exercise tolerance and explore the efficacy of sprint interval training in augmenting the submaximal cardiac response. Methods: Cardiovascular response phenotypes were assessed in healthy, young, recreationally active male participants during moderate intensity forearm exercise with a sudden perfusion pressure induced compromise to skeletal muscle perfusion. Those who responded without compensatory vasodilation completed the same experimental protocol after nitrate rich and nitrate depleted beetroot juice in an effort to restore compensation. In a similar group of individuals, CO, perceived exertion and skeletal muscle properties were assessed during progressive cycling. The same test was completed after 4 weeks of training to determine if submaximal cardiac responses are augmented following exercise training. Results: 1) Individuals presented either with (n = 13) or without (n = 8) compensatory vasodilation. 2) Non-compensation compromised O2D and exercise performance. 3) Nitrate rich beetroot juice restored compensatory vasodilation in previously identified non-compensators (n=6), which abolished perfusion pressure induced reductions in O2D and exercise performance. 5). Cardiac responses differed by up to five liters per minute and were not explained by arterial oxygen content or skeletal muscle properties. 6) Submaximal CO did not predict exercise tolerance, but was increased following training in low, but not high cardiac responders. Conclusion: Differences in the mechanisms governing O2D : demand matching are present within a healthy, young, otherwise similar group of individuals. These differences have real and functional impacts on O2D and exercise performance.