Oxygen uptake kinetics at work onset: role of cardiac output and of phosphocreatine breakdown

The hypothesis that variability in individual's cardiac output response affects the kinetics of pulmonary O2 uptake (V̇O2) was tested by investigating the time constants of cardiac output (Q̇) adjustment (τQ), of PCr splitting (τPCr), and of phase II pulmonary O2 uptake (τVO2) in eight volunteers. V̇O2, Q̇, and gastrocnemius [PCr] (by 31P-MRS) were measured at rest and during low intensity two-legged exercise. Steady state V̇O2 and Q̇ increased (ΔV̇O2s=182±58 mL min-1; ΔQ̇=1.3±0.4 L min-1), whereas [PCr] decreased significantly (21±8%). τVO2, τPCr and τQ were significantly different from each other (38.3±4.0, 23.9±2.5, 11.6±4.6s, respectively; p<0.001). τPCr assumed to be equal to the time constant of V̇O2 at the muscle level (τmVO2), was not related to τQ, whereas τVO2 and τQ were significantly related (p<0.05) as were τVO2 and τPCr (p<0.05). Venous blood O2 stores changes, as determined from arterio-to-mixed-venous O2 content, were essentially equal to those estimated as (τVO2-τPCr)ΔV̇O2s. This suggests that cardiac output responses affect O2 stores utilization and hence τVO2: thus τVO2 is not necessarily a good estimate of τmVO2.