Oxygen uptake (V̇o2) kinetics are prolonged in patients with chronic heart failure (CHF). This may be caused by impaired oxygen delivery or skeletal muscle derangements. We investigated whether impaired cardiac output (Q̇) kinetics limit skeletal muscle oxygen delivery relative to the metabolic demands at submaximal exercise in CHF patients by evaluating the relation between Q̇ kinetics and skeletal muscle deoxygenation. Forty-three CHF patients, NYHA II-III, performed a constant-load exercise test at 80% of the ventilatory aerobic threshold (VAT) to assess V̇o2 kinetics (τV̇o2). Q̇ kinetics (τQ̇) were assessed by a radial artery pulse contour analysis method. Skeletal muscle deoxygenation was assessed by near infrared spectroscopy at the m. vastus lateralis, using the minimal value of the tissue saturation index during onset of exercise (TSImin). Patients were categorized in slow and normal Q̇ responders relative to metabolic demands (τQ̇/V̇o2 ≥1 and τQ̇/V̇o2 <1, respectively), τQ̇ (62 ± 29 s), and τV̇o2 (60 ± 21 s) were significantly related (r = 0.66, P = 0.001). There was a significant correlation between τQ̇ and TSImin in the slow Q̇ responders [rs= −0.57, P = 0.005, n = 22 (51%)]. In conclusion, in moderately impaired CHF patients with relatively slow Q̇ kinetics, central hemodynamics may limit skeletal muscle oxygenation during moderate-intensity exercise.
- chronic heart failure
- oxygen uptake kinetics
- cardiac output kinetics
- skeletal muscle oxygenation
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