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The mechanism for slow pulmonary O2uptake (V̇o2) kinetics in patients with chronic heart failure (CHF) is unclear but may be due to limitations in the intramuscular control of O2utilization or O2delivery. Recent evidence of a transient overshoot in microvascular deoxygenation supports the latter. Prior (or warm-up) exercise can increase O2delivery in healthy individuals. We therefore aimed to determine whether prior exercise could increase muscle oxygenation and speed V̇o2kinetics during exercise in CHF. Fifteen men with CHF (New York Heart Association I–III) due to left ventricular systolic dysfunction performed two 6-min moderate-intensity exercise transitions ( bouts 1 and 2, separated by 6 min of rest) from rest to 90% of lactate threshold on a cycle ergometer. V̇o2was measured using a turbine and a mass spectrometer, and muscle tissue oxygenation index (TOI) was determined by near-infrared spectroscopy. Prior exercise increased resting TOI by 5.3 ± 2.4% ( P = 0.001), attenuated the deoxygenation overshoot (−3.9 ± 3.6 vs. −2.0 ± 1.4%, P = 0.011), and speeded the V̇o2time constant (τV̇o2; 49 ± 19 vs. 41 ± 16 s, P = 0.003). Resting TOI was correlated to τV̇o2before ( R2= 0.51, P = 0.014) and after ( R2= 0.36, P = 0.051) warm-up exercise. However, the mean response time of TOI was speeded between bouts in half of the patients (26 ± 8 vs. 20 ± 8 s) and slowed in the remainder (32 ± 11 vs. 44 ± 16 s), the latter group having worse New York Heart Association scores ( P = 0.042) and slower V̇o2kinetics ( P = 0.001). These data indicate that prior moderate-intensity exercise improves muscle oxygenation and speeds V̇o2kinetics in CHF. The most severely limited patients, however, appear to have an intramuscular pathology that limits V̇o2kinetics during moderate exercise.

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 O2 uptake (V̇o2) kinetics would relate to the P-tolerable duration (tlim) parameters. We hypothesized that 1) the fundamental time constant (τV̇o2) would relate inversely to CP; and 2) the slow-component magnitude (ΔV̇o2sc) 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 V̇o2max, CP, and W′; and 3) repeated constant-P tests (WR6) normalized to a 6 min tlim for τV̇o2 and ΔV̇o2sc estimation. The WR6 tlim averaged 365 ± 16 s, and V̇o2max (4.18 ± 0.49 l/min) was achieved in every case. CP (range: 171–294 W) was inversely correlated with τV̇o2 (18–38 s; R2 = 0.90), and W′ (12.8–29.9 kJ) was directly correlated with ΔV̇o2sc (0.42–0.96 l/min; R2 = 0.76). These findings support the notions that 1) rapid V̇o2 adaptation at exercise onset allows a steady state to be achieved at higher work rates compared with when V̇o2 kinetics are slower; and 2) exercise exceeding this limit initiates a “fatigue cascade” linking W′ to a progressive increase in the O2 cost of power production (V̇o2sc), which, if continued, results in attainment of V̇o2max and exercise intolerance. Collectively, these data implicate V̇o2 kinetics as a key determinant of high-intensity exercise tolerance in humans.

to the editor: We thank Dr. Francescato and colleagues for their interest in our study ([1][1]) and for their letter ([3][2]). The authors requested clarification of why we concluded that 1-s interpolation of breath-by-breath pulmonary oxygen uptake (Vo2P) data resulted in the most accurate and