A Comparison Of Critical Power And Respiratory Compensation Point In COPD: Coincidence Or Equivalence?

Abstract

Power output at the respiratory compensation point (RCP), measured as the breakpoint in the linear ventilation-carbon dioxide output (V̇E-V̇CO2) relationship during ramp-incremental exercise, is proposed to be equivalent to critical power (CP): the asymptote of the hyperbolic power-duration relationship (P-tLIM). For RCP to be used as a valid index of CP, their values should remain equivalent, even under pulmonary mechanical constraint (e.g., in patients with chronic obstructive pulmonary disease [COPD]). PURPOSE: To determine power output (W) and oxygen uptake (V̇O2) at RCP and CP measured using gold-standard protocols in patients with COPD. METHODS: Ten COPD patients (4 female) volunteered (FEV1 = 41 ± 16% predicted). Power output and V̇O2 at gas exchange threshold (GET) and RCP were measured during ramp-incremental cycle ergometry (5-10 W/min). Critical power was estimated from the asymptote of the hyperbolic P-tLIM relationship from 3-4 constant power exercise tests. Oxygen uptake was measured at 15 and 20 min of a constant power ride at CP. RESULTS: Gas exchange threshold was observed in 9/10 patients and occurred at a V̇O2 of 0.91 ± 0.19 L/min (71 ± 28% V̇O2peak). Respiratory compensation point was identified in 1/10 patients and occurred at a V̇O2 of 1.57 L/min (87% V̇O2peak) versus 1.45 L/min at CP (90 W vs. 67 W, respectively). At intolerance, group mean V̇O2peak was 1.15 ± 0.34 L/min and V̇Epeak was 42.7 ± 20.0 L/min (90 ± 15% of estimated MVV). Ramp-incremental V̇O2peak was not different to that obtained in the 3-4 tests used to characterize the P-tLIM relationship (p = 0.419) and with no differences among tests (p = 0.102; mean V̇O2peak = 1.17 ± 0.32 L/min). Critical power was 37 ± 17 W. In the 9/10 patients who completed the 20 min CP validation ride, V̇O2 reached a steady-state (no difference in values at 15 vs. 20 min; p = 0.47) and was calculated as 1.02 ± 0.27 L/min (90 ± 7 % of ramp-incremental V̇O2peak). CONCLUSIONS: CP was identified in all COPD patients, and the steady-state V̇O2 at CP was sub-maximal. The absence of RCP in 9/10 patients, despite exercise gas-exchange responses consistent with a metabolic acidosis, shows that RCP and CP do not occur at equivalent power output or V̇O2 under conditions of abnormal metabolic, respiratory, and/or ventilatory function. RCP should not be used as a valid surrogate for CP.