Creatine monohydrate supplementation and NOX impact skeletal muscle microvascular blood flow: a pilot study.

Abstract

Impaired blood flow and elevated reactive oxygen species (ROS) concentrations, generated primarily from NADPH oxidase (NOX), indicate risk for cardiovascular disease (CVD). Creatine monohydrate (CM) may reduce CVD risk by lowering ROS concentrations and increasing skeletal muscle microvascular blood flow (SMBF). To determine if NOX-derived ROS impairs SMBF and whether five days of CM supplementation reduces in-vivo ROS concentrations and improves SMBF. Seven individuals had two microdialysis probes placed (control (CON) and apocynin (APO): NOX inhibitor) in skeletal muscle to measure in-vivo ROS (Hydrogen Peroxide (H₂O₂)) concentrations and SMBF (ethanol outflow/inflow ratio, inversely related to blood flow) at rest and four hours post-meal consumption. Procedures were performed before (PRE) and after (POST) five days of CM supplementation (20 g/day). Dialysate H₂O₂ concentrations were lower in the APO probe compared to CON from 120-140 min (APO: 1.19 ± 0.39 µM; CON: 2.04 ± 0.95 µM, p = 0.039), 140-160 min (APO: 1.17 ± 0.37 µM; CON: 2.06 ± 0.98 µM, p = 0.034) and 160-180 min post meal ingestion (p ≤ 0.05). APO perfusion increased SMBF at 20-40 min, 120-140 min (APO: 0.61 ± 0.13; CON: 0.75 ± 0.09 µM, p = 0.048), 140-160 min (APO: 0.61 ± 0.12 µM; CON: 0.76 ± 0.14 µM, p = 0.046), 160-180 min, and 180-200 min post meal (p ≤ 0.05). Ethanol outflow/inflow ratio was lower (higher SMBF) POST CM supplementation compared to PRE CM supplementation at 0-20 min (p = 0.036) and 20-40 min (p = 0.049) following HC/HF meal consumption. Inhibition of NOX-derived ROS increased SMBF, suggesting that NOX activity may impair blood flow regulation over the duration of baseline and post-prandial time points. Further, CM supplementation could be an effective strategy for enhancing postprandial blood flow.