Skeletal muscle VO₂ kinetics from cardio-pulmonary measurements: assessing distortions through O₂ transport by means of stochastic work-rate signals and circulatory modelling.

During non-steady-state exercise, dynamic changes in pulmonary oxygen uptake (VO₂pulm) are dissociated from skeletal muscle VO₂ (VO₂musc) by changes in lung and venous O₂ concentrations (CvO₂), and the dynamics and distribution of cardiac output (CO) between active muscle and remaining tissues (Qrem). Algorithms can compensate for fluctuations in lung O₂ stores, but the influences of CO and CvO₂ kinetics complicate estimation of VO₂musc from cardio-pulmonary measurements. We developed an algorithm to estimate VO₂musc kinetics from VO₂pulm and heart rate (HR) during exercise. 17 healthy volunteers (28 ± 7 years; 71 ± 12 kg; 7 females) performed incremental exercise using recumbent cycle ergometry (VO₂peak 52 ± 8 ml min(-1) kg(-1)). Participants completed a pseudo-random binary sequence (PRBS) test between 30 and 80 W. VO₂pulm and HR were measured, and CO was estimated from HR changes and steady-state stroke volume. VO₂musc was derived from a circulatory model and time series analyses, by solving for the unique combination of venous volume and the perfusion of non-exercising tissues that provided close to mono-exponential VO₂musc kinetics. Independent simulations showed that this approach recovered the VO₂musc time constant (τ) to within 7% (R(2) = 0.976). Estimates during PRBS were venous volume 2.96 ± 0.54 L; Qrem 3.63 ± 1.61 L min(-1); τHR 27 ± 11 s; τVO₂musc 33 ± 8 s; τVO₂pulm 43 ± 14 s; VO₂pulm time delay 19 ± 8 s. The combination of stochastic test signals, time series analyses, and a circulatory model permitted non-invasive estimates of VO₂musc kinetics. Large kinetic dissociations exist between muscular and pulmonary VO₂ during rapid exercise transients.