Abstract
Our group has recently identified that African‐American (AA) men have attenuated hyperemic responses to moderate and high‐intensity rhythmic handgrip exercise, compared to Caucasian‐American (CA) men. The mechanisms leading to this lower blood flow response to exercise are unknown. It has been demonstrated that, in comparison with CA, AA individuals present augmented vasoconstriction after intra‐arterial infusion of phenylephrine (α1‐adrenergic receptor agonist), as well as in response to spontaneous bursts of muscle sympathetic nerve activity at rest. These findings suggest that AA individuals have augmented sympathetic vasoconstriction. It is important to note that, during exercise, sympathetic vasoconstriction is normally attenuated in the active muscles (i.e., functional sympatholysis), which facilitates increases in blood flow to exercising muscles. Whether functional sympatholysis is impaired in AA remains unknown. Hence, we tested the hypothesis that, compared to CA men, AA men have impaired functional sympatholysis, which manifests as greater reductions in forearm vascular conductance (FVC) following sympathetic activation during rhythmic handgrip exercise. Healthy young CA [n = 8, 20 ± 1 years (mean ± SEM)] and AA (n = 7, 20 ± 1 years) men were studied. Beat‐to‐beat forearm blood flow (FBF, duplex Doppler ultrasound), and mean arterial pressure (MAP, Finometer) were measured, and FVC was calculated as FBF/MAP. Sympathetic activation was induced via lower body negative pressure (LBNP) applied at −20 Torr for 2 min, both at rest, and from the 3rd to the 5th min of a 6‐min rhythmic handgrip trial at 30% maximal voluntary contraction (MVC), with a duty cycle of 1‐s contraction/ 2‐s relaxation. Sympathetic vasoconstriction was assessed as the percent reduction in FVC during LBNP. The groups presented similar resting FVC (CA: 106 ± 20 vs. AA: 88 ± 16 mL min−1 100 mmHg−1; P = 0.499), FBF (CA: 93 ± 18 vs. AA: 76 ± 13 mL min−1; P = 0.469), and MAP (CA: 89 ± 2 vs. AA: 90 ± 2 mmHg; P = 0.685). LBNP at rest induced similar reductions in FVC between the groups [CA: −42.9 ± 3.7, AA: −36.3 ± 4.0%; Group difference P = 0.244, LBNP effect P < 0.001 for both groups), indicating reflex‐induced sympathetic vasoconstriction. In contrast, there were minimal to no reductions in FVC with LBNP applied during handgrip exercise in either group (CA: +1.2 ± 2.7, AA: +5.4 ± 6.1%; Group difference P = 0.517, LBNP effect P = 0.681 for CA, and P = 0.410 for AA), indicating functional sympatholysis in both groups. Of note, the interpretation of results was the same when FBF responses were analyzed. The groups had similar MVC (CA: 53 ± 2 vs. AA: 54 ± 2 kg, P = 0.744), and reported similar ratings of perceived exertion during handgrip trials (CA: 11 ± 1 vs. AA: 11 ± 1, P = 0.574). These preliminary findings indicate that functional sympatholysis is preserved in healthy young AA men, and an exaggerated sympathetic vasoconstriction in AA likely does not play a major role in the attenuated hyperemic response to moderate‐intensity rhythmic handgrip exercise.Support or Funding InformationNational Heart, Lung, and Blood Institute HL‐130906This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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