Abstract 16786: Influence of Locomotor Muscle Afferent Feedback Inhibition on Pulmonary Vascular Conductance During Submaximal Exercise in Heart Failure
Introduction: Afferent feedback from skeletal muscle contributes to changes in pulmonary vascular pressures in healthy humans.
Hypothesis: We examined the effect of skeletal muscle afferent feedback inhibition on pulmonary vascular capacitance using a validated non-invasive gas exchange equivalent (GXCAP) during exercise in HF.
Methods: In a randomized, controlled design, 9 HF (age 60±2 yrs; EF, 27±2%; NYHA class, 2±1) and 9 controls (CTL; age 63±2 yrs) completed 5 min of constant-load submaximal cycling (65% peak power) with lumbar intrathecal fentanyl (FNL; inhibiting cephalad projection of opioid receptor sensitive afferents) or sham. Heart rate (HR), partial pressure of end-tidal CO2 (PETCO2) and VO2 were measured at rest, during exercise, and recovery. Calculations include O2 pulse (VO2/HR) and GXCAP (O2 pulse x PETCO2). Cephalad migration of FNL was assessed by hypercapnic ventilatory response with no differences within or between groups.
Results: At rest with sham, there was no difference in GXCAP between HF and CTL (192±16 vs 171±14, p=0.34). With FNL, HF had significantly higher GXCAP compared to CTL (216±12 vs 165±15, p<0.05). During exercise with sham, there was no difference in GXCAP between HF and CTL (549±38 vs 474±49, p=0.22). With FNL, HF demonstrated a trend towards higher GXCAP compared to CTL (691±59 vs 536±59, p=0.08). During exercise with FNL, HF demonstrated a significant increase in GXCAP compared to sham (549±38 vs 691±59, p<0.05) with no difference between FNL and sham in CTL (474±49 vs 536±59, p=0.41). The change in GXCAP from rest to exercise was significantly greater in the FNL condition compared to sham in HF (474±49 vs 357±30, p<0.05) whereas there was no difference in CTL (371±47 vs 304±32, p=0.25). However, there was no difference comparing the change from rest to exercise in HF vs CTL for FNL (475±49 vs 371±47, p=0.15) or sham (357±30 vs 304±32, p=0.24).
Conclusion: These data suggest that inhibiting locomotor muscle afferent feedback improves resting pulmonary vascular capacitance in HF. Further, inhibiting this afferent feedback results in an increase in pulmonary vascular capacitance during exercise in HF suggesting locomotor muscle afferent feedback plays a role in pulmonary vascular hemodynamics in HF.
Author Disclosures: E.H. VanIterson: None. E.M. Snyder: None. M.J. Joyner: 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.