Adaptions of exercise energetics and performance to high altitude

• Main Author: Levett, D. Z. H.
• Published: University College London (University of London) 2014
• Subjects: 610
• Online Access: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.634617

There is wide inter-individual variability in the reduction of exercise capacity at altitude, and the factors underlying this remain obscure. In this thesis, I used well-validated cardiopulmonary exercise testing paradigms in a large healthy volunteer cohort to interrogate exercise intolerance from an integrative physiological systems perspective. I focused on the mechanisms that contribute to human endurance performance at altitude, including oxygen transport, the efficiency of oxygen utilization, ventilatory control and cerebral oxygenation. I found that the lactate threshold (LaT) and thus sustainable exercise is relatively preserved at altitude in comparison with peak exercise (V ̇O_2 peak) and furthermore that there is some recovery of the LaT with prolonged altitude exposure (whilst V ̇O_2 peak remains depressed). A greater reduction in exercise capacity at altitude was predicted by higher sea level V ̇O_2 peak, lower peak ventilation at altitude, lower maximum heart rate at altitude and lower [haemoglobin] at altitude. After prolonged altitude exposure and at extreme altitude normalisation of oxygen content did not restore performance suggesting that some or all of systemic flow (reduced cardiac output), regional flow (pulmonary steal) or microcirculatory function and tissue diffusion limitation contribute to exercise limitation. At 7950m, flattening of the oxygen pulse suggests either limitation of stroke volume and/or a-v oxygen extraction. I found neither evidence of mechanical ventilatory limitation at V ̇O_2 peak nor of any association between cerebral oxygenation and V ̇O_2 peak. I found a subtle increase in gross efficiency (GE) on short-term exposure to 5300m, the physiological significance of which is uncertain. At extreme altitude (6400m) and after sustained exposure to 5300m, I found significant increases in GE that may be explained by changes in mitochondrial efficiency or may relate to weight loss. Future work should focus on the role of regional and microcirculatory flow in exercise limitation and mitochondrial function in exercise efficiency.