Mechanisms Underlying Exaggerated Metaboreflex Activation in Prehypertensive Men

Previously, we found that the pressor response to muscle metaboreflex activation is enhanced in prehypertension and associated with peripheral vasoconstriction. However, mechanisms underlying this exaggerated response are not clear. Therefore, we tested the hypothesis that activation of this reflex is augmented owing to increased production of muscle metabolites (i.e., lactate, K, and H).

Twenty-two men (11 normotensive and 11 prehypertensive) were studied. Changes in cardiac output (Q˙), mean arterial pressure (MAP), and total peripheral resistance (TPR) were compared between the two groups during static exercise (SE) and postexercise muscular ischemia (PEMI). Subjects completed 2 min of SE at 50% of maximal voluntary contraction (MVC) followed by 2 min of PEMI. Venous blood samples for determination of metabolites and hormones (catecholamines, vasopressin, and plasma renin activity) were taken from the exercising and nonexercising arm, respectively.

Mean arterial pressure responses to SE (39 ± 3 vs 31 ± 2 mm Hg) and PEMI (24 ± 3 vs 19 ± 3 mm Hg) were significantly higher in the prehypertensive group. Increases in lactate and decreases in pH during PEMI were seen in both groups. However, changes in these variables were greater in the prehypertensive group (lactate, 50.1 ± 6.2 vs 32.8 ± 7.6 mg·dL; pH, -0.06 ± 0.02 vs -0.01 ± 0.01) (P < 0.05). Postexercise muscular ischemia did not evoke increases in hormones in either group.

Compared to the normotensive group, the augmented pressor response to the metaboreflex in the prehypertensive group was associated with greater production of muscle metabolites that activate its afferent arm. The augmented response was not associated with activation of the vasopressin and renin-angiotensin systems and greater activation of the sympathetic nervous system was not apparent. Consequently, additional factors specific to prehypertension, such as arterial stiffness, may have been involved.