The intramuscular contribution to the slow oxygen uptake kinetics during exercise in chronic heart failure is related to the severity of the condition

Bowen TS, Cannon DT, Murgatroyd SR, Birch KM, Witte KK, Rossiter HB. The intramuscular contribution to the slow oxygen uptake kinetics during exercise in chronic heart failure is related to the severity of the condition. J Appl Physiol 112: 378-387, 2012. First published October 27, 2011; doi: 10.1152/japplphysiol.00779.2011.-The mechanism for slow pulmonary O-2 uptake ((V) over dotO(2)) kinetics in patients with chronic heart failure (CHF) is unclear but may be due to limitations in the intramuscular control of O-2 utilization or O-2 delivery. Recent evidence of a transient overshoot in microvascular deoxygenation supports the latter. Prior (or warm-up) exercise can increase O-2 delivery in healthy individuals. We therefore aimed to determine whether prior exercise could increase muscle oxygenation and speed (V) over dotO(2) 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. (V) over dotO(2) 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 (V) over dotO(2) time constant (tau(V) over dotO(2); 49 +/- 19 vs. 41 +/- 16 s, P = 0.003). Resting TOI was correlated to tau(V) over dotO(2) before (R-2 = 0.51, P = 0.014) and after (R-2 = 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 (V) over dotO(2) kinetics (P = 0.001). These data indicate that prior moderate-intensity exercise improves muscle oxygenation and speeds (V) over dotO(2) kinetics in CHF. The most severely limited patients, however, appear to have an intramuscular pathology that limits (V) over dotO(2) kinetics during moderate exercise.