Abstract
Background: VO2 kinetics, or mean response time (MRT), quantifies oxygen uptake at the onset of exercise reflecting the rapidity with which the cardiovascular system can match the metabolic demands of skeletal muscle. Slowed kinetics leads to myofibril oxygen deficit which must be buffered by increased glycolysis and depletion of high energy phosphate stores. To date no studies have assessed changes in VO2 kinetics in HFpEF but growing evidence suggests peripheral abnormalities in oxygen utilization play an important role in exertional intolerance. We hypothesized HFpEF patients would have prolonged MRT during exercise compared to healthy senior controls reflecting abnormalities in skeletal muscle oxygen utilization. Methods: Eight senior control and 13 carefully screened HFpEF subjects underwent cardiopulmonary exercise testing. AV nodal blocking agents were held 5 half-lives and subjects performed submaximal exercise at 30% of VO2max for 5 minutes. VO2 and cardiac output (Qc; acetylene rebreathe) were collected at rest and during exercise. MRT and O2 deficit were calculated from VO2 response curves plotted on a breath by breath basis. Results: HFpEF patients had lower peak VO2 compared to seniors (13.2 ± 3.1 vs 20.3 ± 3.5 ml/min/kg; p<0.001). During fixed submaximal exercise, Qc, HR and VO2 were similar between groups. (Table) HFpEF patients had significantly prolonged MRT (69 v. 49s) compared to controls despite similar aerobic power and central cardiovascular and hemodynamic response. HFpEF patients also had a trend towards larger oxygen deficit (p=0.16) suggesting increased reliance on glycolytic metabolism during early exercise. Conclusions: HFpEF patients have slowed VO2 kinetics and an exaggerated O2 deficit during submaximal exercise. These findings establish abnormalities in muscle tissue oxygen utilization in HFpEF patients and suggest defects in oxygen metabolism are important contributors to exercise intolerance.
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