Pulmonary O2uptake kinetics as a determinant of high-intensity exercise tolerance in humans

Abstract

Tolerance to high-intensity constant-power (P) exercise is well described by a hyperbola with two parameters: a curvature constant (W′) and power asymptote termed “critical power” (CP). Since the ability to sustain exercise is closely related to the ability to meet the ATP demand in a steady state, we reasoned that pulmonary O 2 uptake (V̇o 2) kinetics would relate to the P-tolerable duration (t lim) parameters. We hypothesized that 1) the fundamental time constant (τV̇o 2) would relate inversely to CP; and 2) the slow-component magnitude (ΔV̇o 2sc) would relate directly to W′. Fourteen healthy men performed cycle ergometry protocols to the limit of tolerance: 1) an incremental ramp test; 2) a series of constant-P tests to determine V̇o 2max, CP, and W′; and 3) repeated constant-P tests (WR 6) normalized to a 6 min t lim for τV̇o 2 and ΔV̇o 2sc estimation. The WR 6 t lim averaged 365 ± 16 s, and V̇o 2max(4.18 ± 0.49 l/min) was achieved in every case. CP (range: 171–294 W) was inversely correlated with τV̇o 2(18–38 s; R 2= 0.90), and W′ (12.8–29.9 kJ) was directly correlated with ΔV̇o 2sc(0.42–0.96 l/min; R 2= 0.76). These findings support the notions that 1) rapid V̇o 2 adaptation at exercise onset allows a steady state to be achieved at higher work rates compared with when V̇o 2 kinetics are slower; and 2) exercise exceeding this limit initiates a “fatigue cascade” linking W′ to a progressive increase in the O 2 cost of power production (V̇o 2sc), which, if continued, results in attainment of V̇o 2max and exercise intolerance. Collectively, these data implicate V̇o 2 kinetics as a key determinant of high-intensity exercise tolerance in humans.