Erik H Van Iterson1, Eric M Snyder, Bruce D Johnson, Thomas P Olson. 1. 1Department of Kinesiology, University of Minnesota, Minneapolis, MN; 2Cardiovascular Medicine Division, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA; and 3Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN.
Abstract
PURPOSE: An impaired metaboreflex is associated with abnormal ventilatory and peripheral vascular function in heart failure (HF), whereas its influence on cardiac function or pulmonary vascular pressure remains unclear. We aimed to assess whether metabolite-sensitive neural feedback (metaboreflex) from locomotor muscles via postexercise regional circulatory occlusion (RCO) attenuates pulmonary vascular capacitance (GXCAP) and/or circulatory power (CircP) in patients with HF. METHODS:Eleven patients with HF (NYHA class, I/II; ages, 51± 15 yr; ejection fraction, 32% ± 9%) and 11 age- and gender-matched controls (ages, 43 ± 9 yr) completed three cycling sessions (4 min, 60% peak oxygen uptake (V˙O2)). Session 1 was a control trial including normal recovery (NR). Session 2 or 3 included bilateral upper thigh pressure tourniquets inflated suprasystolic at end of exercise (RCO) for 2-min recovery with or without inspired CO2 (RCO + CO2) (randomized). Mean arterial pressure, HR, and V˙O2 were continuously measured. Estimates of central hemodynamics; CircP = (V˙O2 × mean arterial pressure)/weight; oxygen pulse index (O2pulseI = (V˙O2/HR)/body surface area); and GXCAP = O2pulseI × end-tidal partial pressure CO2 were calculated. RESULTS: At rest and end of exercise, CircP and GXCAP were lower in HF versus those in controls (P < 0.05), with no differences between transients (P > 0.05). At 2-min recovery, GXCAP was lower during RCO versus that during NR in both groups (72 ± 23 vs 98 ± 20 and 73 ± 34 vs 114 ± 35 mL·beat·mm Hg·m, respectively; P < 0.05), whereas CircP did not differ between transients (P > 0.05). Differences (% and Δ) between baseline and 2-min recovery among transients suggest that metaboreflex attenuates GXCAP in HF. Differences (% and Δ) between baseline and 2-min recovery among transients suggest that metaboreflex may attenuate CircP in controls. CONCLUSIONS: The present observations suggest that locomotor muscle metaboreflex activation may influence CircP in controls but not in HF. However, metaboreflex activation may evoke decreases in GXCAP (increased pulmonary vascular pressures) in HF and controls.
RCT Entities:
PURPOSE: An impaired metaboreflex is associated with abnormal ventilatory and peripheral vascular function in heart failure (HF), whereas its influence on cardiac function or pulmonary vascular pressure remains unclear. We aimed to assess whether metabolite-sensitive neural feedback (metaboreflex) from locomotor muscles via postexercise regional circulatory occlusion (RCO) attenuates pulmonary vascular capacitance (GXCAP) and/or circulatory power (CircP) in patients with HF. METHODS: Eleven patients with HF (NYHA class, I/II; ages, 51 ± 15 yr; ejection fraction, 32% ± 9%) and 11 age- and gender-matched controls (ages, 43 ± 9 yr) completed three cycling sessions (4 min, 60% peak oxygen uptake (V˙O2)). Session 1 was a control trial including normal recovery (NR). Session 2 or 3 included bilateral upper thigh pressure tourniquets inflated suprasystolic at end of exercise (RCO) for 2-min recovery with or without inspired CO2 (RCO + CO2) (randomized). Mean arterial pressure, HR, and V˙O2 were continuously measured. Estimates of central hemodynamics; CircP = (V˙O2 × mean arterial pressure)/weight; oxygen pulse index (O2pulseI = (V˙O2/HR)/body surface area); and GXCAP = O2pulseI × end-tidal partial pressure CO2 were calculated. RESULTS: At rest and end of exercise, CircP and GXCAP were lower in HF versus those in controls (P < 0.05), with no differences between transients (P > 0.05). At 2-min recovery, GXCAP was lower during RCO versus that during NR in both groups (72 ± 23 vs 98 ± 20 and 73 ± 34 vs 114 ± 35 mL·beat·mm Hg·m, respectively; P < 0.05), whereas CircP did not differ between transients (P > 0.05). Differences (% and Δ) between baseline and 2-min recovery among transients suggest that metaboreflex attenuates GXCAP in HF. Differences (% and Δ) between baseline and 2-min recovery among transients suggest that metaboreflex may attenuate CircP in controls. CONCLUSIONS: The present observations suggest that locomotor muscle metaboreflex activation may influence CircP in controls but not in HF. However, metaboreflex activation may evoke decreases in GXCAP (increased pulmonary vascular pressures) in HF and controls.
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