Racial Differences in Hemodynamic Responses to Lower Body Negative Pressure: The Effects of Capsaicin

Abstract

Previous work in vitro suggests that capsaicin, the spicy ingredient in peppers, attenuates the vascular response to sympathetic activity (“sympatholysis”), likely mediated through vascular transient receptor potential vanilloid type 1 (TRPV1), and was associated with improved vascular function, though translational studies are needed. Further, given racial disparities in vascular function, and reported racial differences in sensory TRPV1 activity, exploring the potential TRPV1-related mechanisms underpinning these vascular differences is warranted. Purpose To determine if racial differences existed in the central hemodynamic responses to sympathetic stimuli, via lower body negative pressure (LBNP) at rest and during exercise. Second, using an acute dose of oral capsaicin, we sought to determine the potential role of TRPV1 receptors in mediating any racial differences in sympatholysis or vascular function. Methods In a blinded placebo-controlled crossover design, 23 young healthy black (BM, n=13, 23±5 yrs) and white males (WM, n=10, 19±1 yrs) were given capsules containing either placebo (800mg fiber) or capsaicin (780 mg Chile pepper extract, 2.4±0.04 mg capsaicin, 0.5±0.04 mg dihydrocapsaicin). To assess microvascular responses, frequency-domain, multi-distance, near infrared spectroscopy (NIRS) was placed over the muscular medial forearm (i.e. flexor digitorum profundus) providing measure of oxyhemoglobin (HbO, in μM). Central hemodynamics, namely stroke volume (SV), cardiac output (CO), mean arterial pressure (MAP), and heart rate (HR), were measured continuously using a Finometer. To assess hemodynamic responses and potential differences in sympatholysis, these measures performed at rest, during LBNP (-20 mmHg), handgrip (HG) exercise (30% MVC), and HG+LBNP. Results Under placebo conditions, at rest HR, SV, CO, and MAP were not different between BM and WM (p>0.05), and groups were unaffected by capsaicin (p>0.05). The LBNP-induced changes at rest appeared larger for black males (SV -18±4ml vs. -8±11ml and MAP 4.6±6 vs. 1.3± 5mmHg, BM vs. WM), which were seemingly reversed with acute capsaicin (SV -11±13 vs. -9±16ml and MAP -2±9 vs. 1.2± 8mmHg, BM vs. WM). At rest, with placebo, the LBNP-induced ΔHbO, was similar between groups (-2±6 vs. -2±2μM, BM vs WM), and relatively unaffected by capsaicin (-3±6 vs. -1±2 μM, BM vs WM). During HG exercise, the LBNP-induced ΔHbO was disparate between groups (-5±7 vs. 1±3 μM, BM vs WM), and this difference was ablated by the capsaicin (1±6 vs. 2±2 μM, BM vs WM). Conclusion There were racial differences in the central and peripheral hemodynamic response to LBNP at rest and during exercise, suggesting impaired sympatholysis or altered autonomic regulation. Capsaicin, and assumed activation of TRPV1 receptors, seems to affect the hemodynamic response to LBNP, in a relatively race-specific manner at rest and during exercise, potentially mitigating race-related differences. Further work is needed to determine whether such differences may be due to altered TRPV1 expression between groups.