1Department of Internal Medicine & Cardiology, Heart Center, Leipzig University, Leipzig, Germany2School of Biomedical Sciences, University of Leeds, Leeds, UK3Rehabilitation Clinical Trials Center, Division of Respiratory & Critical Care Physiology & Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA, USA4Laboratory for Applied Human Physiology, Graduate School of Human Development and Environment, Kobe University, Kobe, Japan5School of Kinesiology6Department of Physiology and Pharmacology, The University of Western Ontario, London, Ontario, Canada7Applied Physiology Laboratory, Kobe Design University, Kobe, Japan
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New findingsWhat is the central question of the study?Does a transient overshoot in skeletal muscle deoxygenation (reflecting a kinetic mismatch of microvascular O2 delivery to consumption) and/or its spatial distribution slow the adjustment of oxidative energy provision at the onset of exercise?What is the main finding and its importance?Slowed oxidative energy provision at the onset of exercise was correlated with the transient skeletal muscle deoxygenation peak and the reduced spatial distribution, measured by quantitative near-infrared spectroscopy. It was not correlated with a microvascular O2 delivery-to-consumption mismatch per se. This suggests that an absolute, rather than kinetic, mismatch of microvascular O2 delivery and consumption limits the kinetics of muscular oxidative energy provision, but only when muscle deoxygenation reaches some ‘critical’ level.It remains unclear whether an overshoot in skeletal muscle deoxygenation (HHb; reflecting a microvascular kinetic mismatch of O2 delivery to consumption) contributes to the slowed adjustment of oxidative energy provision at the onset of exercise. We progressively reduced the fractional inspired O2 concentration (Symbol) to investigate the relationship between slowed pulmonary O2 uptake (Symbol) kinetics and the dynamics and spatial distribution of absolute [HHb]. Seven healthy men performed 8 min cycling transitions during normoxia (Symbol), moderate hypoxia (Symbol) and severe hypoxia (Symbol). Symbol uptake was measured using a flowmeter and gas analyser system. Absolute [HHb] was quantified by multichannel, time-resolved near-infrared spectroscopy from the rectus femoris and vastus lateralis (proximal and distal regions), and corrected for adipose tissue thickness. The phase II Symbol time constant was slowed (P < 0.05) as Symbol decreased (normoxia, 17 ± 3 s; moderate hypoxia, 22 ± 4 s; and severe hypoxia, 29 ± 9 s). The [HHb] overshoot was unaffected by hypoxia, but the transient peak [HHb] increased with the reduction in Symbol (P < 0.05). Slowed Symbol kinetics in hypoxia were positively correlated with increased peak [HHb] in the transient (r2= 0.45; P < 0.05), but poorly related to the [HHb] overshoot. A reduction of spatial heterogeneity in peak [HHb] was inversely correlated with slowed Symbol kinetics (r2= 0.49; P < 0.05). These data suggest that aerobic energy provision at the onset of exercise may be limited by the following factors: (i) the absolute ratio (i.e. peak [HHb]) rather than the kinetic ratio (i.e. [HHb] overshoot) of microvascular O2 delivery to consumption; and (ii) a reduced spatial distribution in the ratio of microvascular O2 delivery to consumption across the muscle.