Abstract

Chronic heart failure (CHF) causes deficiencies in skeletal muscle blood flow resulting in compromised skeletal muscle capillary red blood cell (RBC) distribution and hemodynamics. These impairments are thought to be due, in part, to reductions in nitric oxide (NO) bioavailability within skeletal muscle. In healthy animals, nitrate (NO3‐) supplementation via beetroot juice (BR) elevates skeletal muscle blood flow and raises the pressure head for capillary‐myocyte O2 flux during exercise presumably following a stepwise reduction to NO in vivo. We tested the hypothesis that BR supplementation would increase the % of capillaries supporting RBC flow at rest and during contractions in CHF rats. CHF was induced in young adult male Sprague‐Dawley rats via myocardial infarction (MI). Following a 5‐week recovery period rats were given BR ([NO3‐] 1 mmol/kg/day, CHF+BR) or water (CHF) for 5 days. MI size was not different between groups (CHF: 28 ± 5, CHF+BR: 28 ± 6 %). Intravital microscopy was used to study the in vivo spinotrapezius muscle microcirculation at rest and during 180 s 1Hz twitch contractions (6‐8 V). The percentage of capillaries supporting continuous RBC flow was elevated in CHF+BR rats at rest (CHF: 65 ± 6, CHF+BR: 76 ± 2 %, P蠄0.05) and during contractions (CHF: 78 ± 6, CHF+BR 82: ± 2 %, P<0.05). The improvements seen herein are likely due to enhanced arteriolar vasodilation mediated, in part, by elevated NO bioavailability. These results have important implications and suggest that NO3‐ supplementation via BR may constitute a viable therapeutic modality that improves muscle vascular and potentially metabolic function in CHF.Grant Funding Source: Supported by NIH‐HL108328

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