Group III/IV Mediated Muscle Reflexes Restrain Vascular Conductance During Exercise In Patients With Hypertension

Abstract

PURPOSE: We investigated the role of group III/IV-mediated muscle reflexes (i.e. the exercise pressor reflex) in determining the circulatory response to physical activity in patients with essential hypertension. METHODS: Five patients with stage 1–2 hypertension (HT; systolic: 155 ± 5 mmHg; diastolic: 90 ± 2 mmHg; 64 ± 3 years) and eight age-matched normotensive control subjects (NT; systolic: 120 ± 6 mmHg; diastolic: 80 ± 6 mmHg) performed single-leg knee extensor exercise (7, 15, 20 and 30 W) under control conditions and with lumbar intrathecal fentanyl impairing feedback from μ-opioid receptor-sensitive lower limb muscle afferents. Cardiac output (Q; photoplethysmography), leg perfusion pressure (PP = arterial pressure - venous pressure; femoral arterial and venous catheters), and femoral blood flow (QL; Doppler ultrasound) were measured continuously during exercise. Leg vascular conductance (LVC) was calculated as QL/PP. RESULTS: Hypertension had a significant main effect on PP (∼22% higher in HT vs. NT), LVC (∼30% lower in HT vs. NT), and QL (∼13% lower in HT vs. NT) during exercise in control conditions (P < 0.05). Following fentanyl blockade, which had no measurable effects at rest, Q during exercise in HT was, secondary to a small reduction in heart rate (P = 0.08) and a significant decrease in stroke volume, about ∼20% lower compared to control conditions (P < 0.05). In contrast, fentanyl blockade had no effect on Q during exercise in NT (P = 0.4). Additionally, in the face of a similar 8-10% reduction in PP during exercise with fentanyl blockade in NT and HT, there was ∼20% increase in QL during exercise with fentanyl blockade in patients with HT (P < 0.05), contrasting with the unaltered QL response in NT individuals. The net outcome of these changes was a significantly elevated LVC in both groups, but the increase was nearly three-fold greater in HT compared to NT (26 ± 3% vs. 10 ± 2%; P < 0.05). CONCLUSION: Although the exercise pressor reflex plays a critical role in facilitating central hemodynamics (i.e. Q) in HT, it also impairs QL and LVC in these patients. The excessive muscle reflex-mediated sympatho-excitation in HT contributed to the deficit in QL and LVC during exercise under normal conditions and might therefore be a substantial contributor to the exercise intolerance which characterizes this population.