Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCA189

Poster Communications

Systemic molecular adaptations to intermittent hypoxia: impact on microvascular oxygenation and hypoxic exercise performance.

J. D. Woodside2,1, T. A. Calverley2, J. McEneny3, I. Young3, D. M. Bailey2

1. Vascular Physiology Unit, Institute of Cardiovascular Science, University College London, London, United Kingdom. 2. Neurovascular Research Laboratory, Faculty of Life Sciences and Education, University Of South Wales, Pontypridd, United Kingdom. 3. Centre for Public Health, Nutrition and Metabolism Group, Queen's University Belfast, Belfast, United Kingdom.


Intermittent hypoxia (IH) presents a less arduous training tool than chronic exposure for athletes seeking to improve cardiorespiratory fitness. While the sea-level (normoxic) performance benefits of IH remain equivocal (1, 2), less is known regarding its impact on hypoxic performance. Therefore, we examined if IH had the capacity to improve cardiorespiratory fitness in hypoxia and if so, identify the haemodynamic and molecular responses driving this adaptation. Eighteen healthy human male participants (22 ± 4 years) were randomly assigned single-blind to an intermittent normoxia (IN; 21% O2, n = 9) or IH (10% O2, n = 9) group. They completed ten sessions in a normobaric environmental chamber, each of which incorporated nine exposure periods (in normoxia or hypoxia depending on group). Each period was 5-minutes in length and separated by 5-minutes of exposure to normal ambient air (21% O2). Peak oxygen uptake (VO2peak) was assessed in hypoxia (10% O2) via online respiratory gas analysis during an incremental cycling test to exhaustion prior to and following the IH/IN programme. Continuous wave near-infrared spectroscopy was employed before and during exercise to monitor concentration changes in cerebral and muscular (vastus lateralis) oxy- and deoxyhaemoglobin (O2Hb and HHb), which also served as an index of regional changes in blood volume (O2Hb + HHb). Antecubital blood samples obtained at rest and VO2peak were analysed to assess oxidative (ascorbate radical (A●-) by electron paramagnetic resonance spectroscopy), nitrosative (nitric oxide metabolites by ozone-based chemiluminescence) and inflammatory (sVCAM-1 and sICAM-1 by enzyme-linked immunosorbent assay) stress. Data were analysed using a three-way repeated measures ANOVA. VO2peak increased by 2.3% following IH, whereas no changes were observed following IN. Furthermore, submaximal VO2 at a workload of 60 watts decreased by 4.5% following IH, compared to a decrease of 1.6% following IN. Notably, improvements in exercise performance subsequent to IH were accompanied by significant increases in nitric oxide at rest and VO2peak (P < 0.05), and augmented levels of sVCAM-1 and sICAM-1 at VO2peak (P < 0.05). Moreover, A●- accumulation was attenuated at VO2peak succeeding IH, however this difference was non-significant (P = 0.10). Additionally, significant increases in cerebral oxygenation at rest and VO2peak (P < 0.05), and elevated blood flow at the muscle site during exercise (P < 0.05) were observed following IH. This is paramount given that hypoxic exercise performance is limited by cerebral and muscular deoxygenation (3). Collectively, these findings indicate that enhanced hypoxic exercise performance subsequent to IH may be due to attenuated oxidative-nitrosative-inflammatory stress and consequential improvements in microvascular oxygenation.

Where applicable, experiments conform with Society ethical requirements