Pulmonary O2 uptake during exercise:: Conflating muscular and cardiovascular responses

For moderate-intensity exercise (below lactate threshold, theta(L)), muscle O-2 consumption (QO(2)) kinetics are expressed in a first-order phase 2 (or fundamental) pulmonary O-2 uptake (VO2) response: dVO(2)/dt (.) tau + Delta VO2(c) = Delta VO2(ss); where Delta VO2(ss) is the steady-state VO2 increment, and tau the VO2 time constant (which is within approximately 10% of tau QO(2)). A likely source of QO(2) control in this intensity domain is ADP-mediated, for which intramuscular phosphocreatine (PCr) may serve as a proxy variable. Whether, in reality, this behavior reflects the operation of a single homogeneous compartment is unclear, however; a multicompartment structure comprised of units having a similar Delta VO2(ss) but with widely varying T can also yield a well-fit exponential response with an apparent single T. In support of this is the inverse (although poorly predictive) correlation between tau and both theta(L) and VO2max. Above theta(L) the fundamental VO2 kinetics are supplemented with a delayed, slowly developing component that can Set VO2 on a trajectory towards VO2max, and that has complex temporal- and intensity-related kinetics. This VO2 slow component is also demonstrable in [PCr], suggesting that the decreased efficiency above theta(L) predominantly reflects a high phosphate cost of force production rather than a high O-2 cost of phosphate production. In addition, the oxygen deficit for the slow component is more likely to reflect a progressive shifting of Delta VO2(ss) rather than a single Delta VO2(ss) having a single tau.