MODULATION OF MUSCLE AND PULMONARY O-2 UPTAKES BY CIRCULATORY DYNAMICS DURING EXERCISE

The effect of cardiovascular adjustments on the coupling of cellular to pulmonary gas exchange during unsteady states of exercise remains controversial. Computer simulations were performed to assess these influences on O2 delivery and pulmonary O2 uptake (pV̇O2). Algorithms were developed representing muscle and 'rest-of-body' compartments, connected in parallel by arterial and venous circulations to a pump-and-lungs compartment. Exercise-induced increases in V̇O2 and cardiac output went to the muscle compartment. Model parameters [e.g., time constants for blood flow and muscle O2 uptake (mV̇O2)] could be varied independently. Simulation results demonstrated that 1) the rise in pV̇O2 during exercise contains three phases; 2) the contribution f changes in venous O2 stores to pV̇O2 kinetics and the O2 deficit occur almost entirely in phase 1; 3) under a wide variety of manipulations, the kinetics of pV̇O2 in phase 2 were within a couple of seconds of that assigned to mV̇O2 (i.e., there is not an obligatory slowing of V̇O2 kinetics at the lungs relative to those at the muscles; 4) by use of available estimates of blood flow adjustment, O2 delivery would not limit mV̇O2 after exercise onset; and 5) blood flow could limit O2 delivery in recovery, if blood flow returned to base-line levels at rates similar to those during the on-transient phase.