Cardiac output, oxygen consumption and arteriovenous oxygen difference following a sudden rise in exercise level in humans.

1. To investigate the relative contributions of increases in cardiac output and arteriovenous oxygen difference to the increase in oxygen consumption during exercise, the ventilatory and cardiovascular responses to a sudden transition from unloaded cycling to 70 or 80 W were measured in six normal healthy subjects. 2. Oxygen consumption (VO2) was measured breath-by-breath and corrected for changes in lung gas stores. Cardiac output (Q) was measured beat-by-beat using pulsed Doppler ultrasound, and blood pressure was measured beat-by-beat using a non-invasive finger cuff (Finapres). All data were calculated off-line, second-by-second. 3. Arteriovenous oxygen difference (A-VO2) was calculated from Q and VO2 using the Fick Principle. Left ventricular afterload was calculated by dividing Q by mean blood pressure. 4. The data for Q and VO2 were closely fitted by single exponential curves (mean r2 0.84 and 0.90 respectively; r is the correlation coefficient). These curves yielded mean time constants for the increases in Q and VO2 of 28 and 55 s respectively following the increase in exercise level. In each individual subject, the time course of adjustment of Q was faster than that of VO2. There was a mean lag of 15 s from the start of the new exercise level before the derived A-V O2 began to increase; the mean time constant for A-V O2 was 57 s. 5. If A-V O2 had remained constant, the observed rise in Q alone would have resulted in an average of 87% of the increase in VO2 which was observed after 5 s. If Q had remained constant, the observed increase in A-V O2 would have led to only 8% of the actual increase in VO2 after 5 s. 6. Mean and systolic blood pressure rose and afterload fell immediately after the onset of the increased workload. The time constants of the systolic blood pressure and afterload responses to exercise varied widely and ranged from 37 to 81 and 10 to 26 s respectively (n = 4). 7. We conclude that Q is responsible for most of the early increase in VO2 following a sudden increase in exercise workload. Blood pressure responses to exercise are slower than Q and VO2 responses, probably due to the rapid decrease in afterload. 8. The dominant contribution of Q to adaptation to changing workload may be physiologically important particularly in heart disease, where decreased ability to increase cardiac output may limit the capacity to cope with changing metabolic needs during everyday activities.