Introduction: Obesity is a known risk factor for HFpEF. This connection is thought to be driven by concentric ventricular remodeling, diastolic dysfunction, and low fitness. We investigated whether the mechanisms for low fitness were similar between “at risk” middle age obese subjects and HFpEF patients. We hypothesized obese subjects would have similar impairments in cardiovascular response to exercise as HFpEF.
Methods: Cardiopulmonary exercise testing was performed on 49 middle aged, obese subjects (33% men; age 49 ± 6 yrs; BMI 38.8 kg/m2) who were deemed at risk for HFpEF by elevated cardiac biomarkers (NT-proBNP > 40 pg/ml; hs-cTnT > 3 pg/ml) and increased visceral adiposity (> 2.5 kg). Sixty one middle aged, healthy, non-obese (CON) subjects 48% men; age: 52 ± 5 yrs; BMI 26.0 kg/m2) and 25 HFpEF patients (38% men; age: 71 ± 7 yrs; BMI 34.4 kg/m2) were used as references for exercise performance. Peak VO2 (Douglas bags) and cardiac output (Qc; acetylene rebreather) were measured at rest, sub-max, and max exercise. AVO2 difference was calculated from VO2 and Qc. Stroke volume (SV) reserve was defined as change in SV from rest to sub-max exercise.
Results: Peak VO2 was significantly different between all three groups (HFpEF: 13.1 OB: 17.2 CON: 29.3 ml/kg/min; p<0.05). OB subjects had peak Qc and AVO2 difference that were lower than CON but higher than HFpEF. (Figure) SV reserve, the ability to augment SV from rest to exercise was lower than both CON and HFpEF (CON 83%; OB 39%; HFpEF 58%; p <0.001).
Conclusions: Mechanisms for low fitness are similar, albeit to a lesser degree, between “at risk” obese subjects and HFpEF despite a difference in age of two decades. An inability to augment stroke volume or peripheral extraction, characteristic features of HFpEF, contribute to poor exercise performance in obesity. Further sedentary aging and development of comorbid conditions may amplify these impairments leading to HFpEF.