The fundamental pulmonary O-2 uptake ((V) over dot O-2) response to moderate, constant-load exercise can be characterized. as (d(V) over dot O-2/dt)(tau)+Delta(V) over dot O-2 (t) = Delta(V) over dot O-2SS where Delta(V) over dot O-2SS is the steady-state response, and tau is the time constant, with the (V) over dot O-2 kinetics reflecting intramuscular O-2 uptake ((Q) over dot O-2) kinetics, to within 10%. The role of phosphocreatine (PCr) turnover in (Q) over dot O-2 control can be explored using P-31-MR spectroscopy, simultaneously with (V) over dot O-2. Although tau(V) over dot O-2 and tauPCr 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 Delta(V) over dot O-2SS but with a wide tau distribution can also yield a (V) over dot O-2 response with an apparent single tau. This tau is, significantly, inversely correlated with lactate threshold and (V) over dot O-2max (but is poorly predictive; a frail stamen, therefore), consistent with tau not characterizing a compartment with uniform kinetics. At higher intensities, the fundamental kinetics become supplemented with a slowly-developing phase, setting (V) over dot O-2 on a trajectory towards maximum (V) over dot O-2. This slow component is also demonstrable in Delta[PCr]: the decreased efficiency thereby reflecting a predominantly high phosphate-cost of force production rather than a high O-2-cost of phosphate production. We also propose that the O-2-deficit for the slow-component is more likely to reflect shifting Delta(V) over dot O-2SS rather than a single one with a single tau.