Influence of the Metaboreflex on Pulmonary Vascular Capacitance in Heart Failure

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.

Figure 1

Differences in circulatory power (CircP) or pulmonary vascular capacitance (GX_CAP) between end-exercise and 2 min post-exercise. Data presented as means±SD. (A) CircP, absolute change (Δ). (B) CircP, percentage (%) change. (C) GX_CAP, absolute Δ. (D) GX_CAP, % change. ^†NR vs. RCO or RCO+CO₂ in controls (P<0.05). *Heart failure vs. control (P<0.05).

Figure 2

Differences in circulatory power (CircP) or pulmonary vascular capacitance (GX_CAP) between baseline and 2 min post-exercise. Data presented as means±SD. (A) CircP, absolute change (Δ). (B) CircP, percentage (%) change. (C) GX_CAP, absolute Δ. (D) GX_CAP, % change. †NR vs RCO in controls, (P<0.05); ΔDifferent between RCO and RCO+CO₂ in controls, (P<0.05); ‡Different between NR and RCO in heart failure and controls, (P<0.05); ♦Different between NR and RCO in heart failure, and RCO+CO₂ vs NR or RCO in controls, (P<0.05); *Heart failure vs. controls (P<0.05).

Figure 3

Schematic representation of the linked pathways between locomotor muscle metaboreflex afferent signaling and adjustments in circulatory power (CircP) or pulmonary vascular capacitance (GX_CAP) in heart failure patients. Heightened afferent signaling associated with metaboreflex activation of locomotor muscles contributes to efferent signaling toward the pulmonary system causing decreases in GX_CAP and, hence, pulmonary vasoconstriction and elevations in pulmonary pressures. In contrast, efferent signaling toward the myocardium contributes little to increases in CircP (cardiac pumping capacity), and that increases in peripheral pressures are not likely contributed to by increasing cardiac hemodynamics, but more likely due to robust peripheral vasoconstriction in heart failure patients.