The Relation Between Cardiac Output Kinetics And Skeletal Muscle Oxygenation During Moderate Exercise In Moderately Impaired Patients With Chronic Heart Failure

Oxygen uptake ((V)over dot(O2)) 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)over dot) kinetics limit skeletal muscle oxygen delivery relative to the metabolic demands at submaximal exercise in CHF patients by evaluating the relation between (Q)over dot 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 (V)over dot(O2) kinetics tau(V)over dot(O2)). tau(Q)over dot kinetics ((Q)over dot) 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)over dot responders relative to metabolic demands (tau(Q)over dot/(V)over dotO(2) >= 1 and tau(Q)over dot /(V)over dot(O2) < 1, respectively), tau(V)over dot (62 +/- 29 s), and tau(V)over dot(O2) (60 +/- 21 s) were significantly related (r = 0.66, P = 0.001). There was a significant correlation between tau(Q)over dot and TSImin in the slow (Q)over dot responders [r(s) = -0.57, P = 0.005, n = 22 (51%)]. In conclusion, in moderately impaired CHF patients with relatively slow (Q)over dot kinetics, central hemodynamics may limit skeletal muscle oxygenation during moderate-intensity exercise.