The relation between cardiac output kinetics and skeletal muscle oxygenation during moderate exercise in moderately impaired patients with chronic heart failure

Oxygen uptake (VO₂) 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 (Q) kinetics limit skeletal muscle oxygen delivery relative to the metabolic demands at submaximal exercise in CHF patients by evaluating the relation between Q kinetics and skeletal muscle deoxygenation. Forty-three CHF patients, NYHA II-III, performed a constant-load exercise test at 80% of the VAT to assess VO₂ kinetics (VO₂). Q kinetics (Q) 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 Q responders relative to metabolic demands (Q/ VO₂ ≥ 1 and Q/ VO₂ < 1, respectively) Q (62 +/- 29s) and VO₂ (60+/-21s) were significantly related (r=0.66, p= 0.001). There was a significant correlation between Q and TSImin in the slow Q responders (r_s= -0.57, p=0.005, n=22 (51%)) In conclusion, in moderately impaired CHF patients with relatively slow Q kinetics, central hemodynamics may limit skeletal muscle oxygenation during moderate-intensity exercise.

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