The intramuscular contribution to the slow oxygen uptake kinetics during exercise in chronic heart failure is related to the severity of the condition
The mechanism for slow pulmonary O2 uptake (V̇o2) kinetics in patients with chronic heart failure (CHF) is unclear but may be due to limitations in the intramuscular control of O2 utilization or O2 delivery. Recent evidence of a transient overshoot in microvascular deoxygenation supports the latter. Prior (or warm-up) exercise can increase O2 delivery in healthy individuals. We therefore aimed to determine whether prior exercise could increase muscle oxygenation and speed V̇o2 kinetics 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. V̇o2 was 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 V̇o2 time constant (τV̇o2; 49 ± 19 vs. 41 ± 16 s, P = 0.003). Resting TOI was correlated to τV̇o2 before ( 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 V̇o2 kinetics ( P = 0.001). These data indicate that prior moderate-intensity exercise improves muscle oxygenation and speeds V̇o2 kinetics in CHF. The most severely limited patients, however, appear to have an intramuscular pathology that limits V̇o2 kinetics during moderate exercise.