Abstract

The fundamental pulmonary O2 uptake (o2) response to moderate, constant-load exercise can be characterized as (do2/dt)(τ) + Δo2 (t) = Δo2SS where Δo2SS is the steady-state response, and τ is the time constant, with the o2 kinetics reflecting intramuscular O2 uptake (o2) kinetics, to within 10%. The role of phosphocreatine (FCr) turnover in o2 control can be explored using 31P-MR spectroscopy, simultaneously with o2. Although τo2 and τPCr vary widely among subjects (approx. 20–65 s), they are not significantly different from each other, either at the on- or off-transient. A caveat to interpreting the ‘well-fit’ exponential is that numerous units of similar Δo2SS but with a wide τ distribution can also yield a o2 response with an apparent single τ. This τ is, significantly, inversely correlated with lactate threshold and o2max (but is poorly predictive; a frail stamen, therefore), consistent with τ not characterizing a compartment with uniform kinetics. At higher intensities, the fundamental kinetics become supplemented with a slowly-developing phase, setting o2 on a trajectory towards maximum o2. This slow component is also demonstrable in Δ[PCr]: the decreased efficiency thereby reflecting a predominantly high phosphate-cost of force production rather than a high O2-cost of phosphate production. We also propose that the O2-deficit for the slow-component is more likely to reflect shifting Δo2SS rather than a single one with a single τ.

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