Abstract
The time constant of the primary phase of pulmonary V˙O2 on‐kinetics (τ p), which reflects muscle V˙O2 kinetics during moderate‐intensity exercise, is about 30 s in young healthy untrained individuals, while it can be as low as 8 s in endurance‐trained athletes. We aimed to determine the intramuscular factors that enable very low values of t 0.63 to be achieved (analogous to τ p, t 0.63 is the time to reach 63% of the V˙O2 amplitude). A computer model of oxidative phosphorylation (OXPHOS) in skeletal muscle was used. Muscle t0.63 was near‐linearly proportional to the difference in phosphocreatine (PCr) concentration between rest and work (ΔPCr). Of the two main factors that determine t0.63, a huge increase in either OXPHOS activity (six‐ to eightfold) or each‐step activation (ESA) of OXPHOS intensity (>3‐fold) was needed to reduce muscle t 0.63 from the reference value of 29 s (selected to represent young untrained subjects) to below 10 s (observed in athletes) when altered separately. On the other hand, the effect of a simultaneous increase of both OXPHOS activity and ESA intensity required only a twofold elevation of each to decrease t 0.63 below 10 s. Of note, the dependence of t 0.63 on OXPHOS activity and ESA intensity is hyperbolic, meaning that in trained individuals a large increase in OXPHOS activity and ESA intensity are required to elicit a small reduction in τ p. In summary, we postulate that the synergistic action of elevated OXPHOS activity and ESA intensity is responsible for extremely low τ p (t 0.63) observed in highly endurance‐trained athletes.
Highlights
The exponential time constant s of phase 2 of oxygen consumption (V O2) on-kinetics in skeletal muscle is the fundamental parameter characterizing the muscle bioenergetic system (Grassi et al 1996; Whipp and Rossiter 2005; Zoladz et al 2014)
This relationship was independent of whether difference between resting and exercising PCr concentration (DPCr) was changed through a change in the resting oxidative phosphorylation (OXPHOS) activity, that is, without each-step activation (ESA), or through a change in ESA intensity (AOX)
When the resting OXPHOS activity and ESA intensity were modified separately, a huge increase in these parameter values was necessary in order to diminish muscle t0.63 significantly from the reference state value of 29.2 s
Summary
The exponential time constant s of phase 2 of oxygen consumption (V O2) on-kinetics in skeletal muscle (i.e., the time to reach 63% of the V O2 amplitude, termed sp or t0.63) is the fundamental parameter characterizing the muscle bioenergetic system (Grassi et al 1996; Whipp and Rossiter 2005; Zoladz et al 2014). During moderateintensity (i.e., below the lactate threshold) whole-body exercise such as cycling, muscle V O2 on-kinetics is well reflected by the time constant of phase 2 pulmonary V O2 on-kinetics (sp) (Grassi et al 1996). Pulmonary phase 2 V O2 kinetics is slow in mitochondrial diseases and McArdle’s disease (Grassi et al 2009), where oxidative phosphorylation (OXPHOS) activity is compromised
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