Abstract 16602: Pulmonary Vascular Response to Metaboreflex Stimulation During Submaximal Exercise in Heart Failure
Introduction: Neural feedback from skeletal muscle during exercise contributes to changes in pulmonary pressures in healthy individuals. Heart failure patients (HF) often develop pulmonary hypertension; however, the relationship between muscle afferent feedback and the pulmonary vasculature in HF remains unclear.
Hypothesis: We examined the influence of metaboreceptor stimulation on pulmonary vascular capacitance using a validated non-invasive gas exchange equivalent (GXCAP) in HF.
Methods: Eleven HF patients (age 51±5 yrs; EF, 32±3%; NYHA class, 1.6±0.2) and 11 controls (CTL; age 43±3 yrs) completed 3 cycling session (4-min at 60% of peak oxygen consumption, VO2). Session one: baseline control trial. Sessions 2 and 3: bilateral upper-thigh tourniquets inflated suprasystolic for 2 min at end-exercise (regional circulatory occlusion, RCO) with or without addition of inspired CO2 to maintain end-exercise end-tidal CO2 (PETCO2) (RCO+CO2) (randomized). Rest, exercise, and recovery heart rate (HR), PETCO2, and VO2 were measured. O2 pulse (VO2/HR) and GXCAP (O2 pulseхPETCO2) were calculated.
Results: During all conditions at end-exercise, HF demonstrated significantly lower GXCAP compared to CTL (p<0.01). Percent change in GXCAP from end-exercise to 2 min post-exercise was attenuated in HF compared to CTL (41±5% vs 64±1%, respectively, p<0.01) during the baseline trial. During RCO, HF had a 55±6% reduction in GXCAP from end-exercise compared to 77±2% in CTL (p<0.01). During RCO+CO2, HF had a 49±4% reduction in GXCAP from end-exercise compared to 69±2% in CTL (p<0.01). GXCAP was similar between sessions within HF. The CTL group demonstrated an attenuated return of GXCAP during RCO compared to both baseline and RCO+CO2 (p<0.01) with no difference between baseline and RCO+CO2.
Conclusion: These data suggest the exercise mediated rise and post-exercise recovery of pulmonary vascular capacitance are attenuated in HF during constant-load submaximal exercise compared to CTL. Additionally, our data confirm previous reports that locomotor muscle afferent feedback influences pulmonary vascular capacitance in CTL; however, this model of locomotor muscle metaboreflex stimulation appears to a differential response in HF compared to CTL.
Author Disclosures: E.H. VanIterson: None. E.M. Snyder: None. B.D. Johnson: None. T.P. Olson: Research Grant; Significant; AHA - 12GRNT11630027.
This research has received full or partial funding support from the American Heart Association.
- © 2014 by American Heart Association, Inc.