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 (V˙O2) was tested by investigating the time constants of cardiac output (Q˙) adjustment (τQ), of PCr splitting (τPCr), and of phase II pulmonary O2 uptake (τVO2τVO2) in eight volunteers. V˙O2, Q˙, and gastrocnemius [PCr] (by 31P-MRS) were measured at rest and during low intensity two-legged exercise. Steady state V˙O2 and Q˙ increased (ΔV˙O2s=182±58 mL min−1; ΔQ˙=1.3±0.4 L min−1), whereas [PCr] decreased significantly (21 ± 8%). τVO2τVO2, τPCr and τQ were significantly different from each other (38.3 ± 4.0, 23.9 ± 2.5, 11.6 ± 4.6 s, respectively; p < 0.001). τPCr assumed to be equal to the time constant of V˙O2 at the muscle level (τmVO2τmVO2), was not related to τQ, whereas τVO2τVO2 and τQ were significantly related (p < 0.05) as were τVO2τVO2 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–τPCrτVO2–τPCr)ΔV˙O2s. This suggests that cardiac output responses affect O2 stores utilization and hence τVO2τVO2: thus τVO2τVO2 is not necessarily a good estimate of τmVO2τmVO2.