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 (VO₂) was tested by investigating the time constants of cardiac output (Q) adjustment (τ(Q)), of PCr splitting (τ(PCr)), and of phase II pulmonary O₂ uptake (τ(VO₂)) in eight volunteers. VO₂, Q, and gastrocnemius [PCr] (by (31)P-MRS) were measured at rest and during low intensity two-legged exercise. Steady state VO₂ and Q increased (ΔVO₂(s) = 182 ± 58 mL min⁻¹; ΔQ = 1.3 ± 0.4 L min⁻¹), whereas [PCr] decreased significantly (21 ± 8%). τ(VO₂), τ(PCr) and τ(Q) were significantly different from each other (38.3 ± 4.0, 23.9 ± 2.5, 11.6 ± 4.6 s, respectively; p<0.001). τ(PCr) assumed to be equal to the time constant of VO₂ at the muscle level (τ(mVO₂)), was not related to τ(Q), whereas τ(VO₂) and τ(Q) were significantly related (p<0.05) as were τ(VO₂) and τ(PCr) (p<0.05). Venous blood O₂ stores changes, as determined from arterio-to-mixed-venous O₂ content, were essentially equal to those estimated as (τ(VO₂)-τ(PCr))·ΔVO₂(s). This suggests that cardiac output responses affect O₂ stores utilization and hence τ(VO₂) : thus τ(VO₂) is not necessarily a good estimate of τ(mVO₂).