Augmentation of the exercise pressor reflex in prehypertension: roles of the muscle metaboreflex and mechanoreflex

Abstract

This study investigated the hemodynamic mechanisms underlying the exaggerated blood pressure response to muscle contraction in prehypertensive humans and the potential role of skeletal muscle metabo- and mechanoreceptors in this response. To accomplish this, changes in peak mean arterial blood pressure (ΔMAP), cardiac output, and total peripheral resistance (ΔTPR) were compared between prehypertensive (n = 23) and normotensive (n = 19) male subjects during 2 min of static contraction (at 50% of maximal tension), 2 min of postexercise muscle ischemia (metaboreflex), and 1 min of passive dorsiflexion of the foot (tendon stretch, mechanoreceptor reflex). These variables were assessed before and during the interventions. Percentage increases from baseline in MAP and TPR in response to the exercise pressor reflex were augmented in the prehypertensives, compared with the normotensives (44% ± 5% vs. 33% ± 4% and 34% ± 15% vs. 2% ± 8%, respectively) (p < 0.05). Metaboreflex-induced increases in MAP and TPR were also augmented in the prehypertensives (28% ± 5% vs. 14% ± 4% and 36% ± 12% vs. 14% ± 9%, respectively) (p < 0.05). In response to the mechanoreflex, no differences in the percentage increase in MAP or TPR were seen between groups. The results indicate that the reflex pressor response to static contraction is augmented in prehypertension and suggest that this phenomenon is due, at least in part, to enhanced activation of metaboreceptors.

Attenuated muscle metaboreflex-induced pressor response during postexercise muscle ischemia in renovascular hypertension

“…Farquhar and colleagues (20,25) recently demonstrated in elderly hypertensive humans that the pressor response to static handgrip exercise (30 -40% MVC) is exaggerated in HTN and sustained during PEMI. Similar findings have been reported in prehypertensive humans performing static handgrip exercise (11,31). However, in a previous study from Farquhar and colleagues (53), the pressor response to rhythmic handgrip exercise (60% MVC) was not exaggerated in HTN, yet MAP was sustained during PEMI.…”

“…Recently, we reported that metaboreflex-induced increases cardiac function and arterial pressure are markedly attenuated in HTN when the reflex is activated during dynamic exercise (51). In contrast, several investigators have concluded that the metaboreflex is exaggerated in prehypertension and HTN in both humans (11,20,25,31) and spontaneously hypertensive rats (34,41,59). In the present study, metaboreflex-induced CO and HR responses were markedly attenuated, and the mechanisms sustaining the pressor response during PEMI were altered as CO and HR fell to normal recovery levels.…”

Why Not to Use the Handgrip Test in the Assessment of Cardiovascular Autonomic Neuropathy Among Patients with Diabetes Mellitus?

“…Patients with hypertension were shown to produce exaggerated BP elevation and enhanced muscle sympathetic nerve activation during isometric handgrip exercise compared with age-related healthy controls [23,24]. Increased muscle metaboreflex activation leading to augmented pressor responses was demonstrated in older moderately hypertensive adults [25] and in pre-hypertensive state [26]. The exercise pressor reflex might occur promptly: BP elevation and heart rate increased within 30-60 sec during static contraction in an experimental study [27].…”

Differences in hemodynamic response to metaboreflex activation between obese patients with metabolic syndrome and healthy subjects with obese phenotype

“…In this case, the blood pressure response is achieved mainly by a SVR-mediated mechanism rather than by a flow-mediated mechanism (11,42). This scenario has been proposed especially for heart failure, and hypertension and it has been ascribed to excessive sympathetic activation with exaggerated vasoconstriction (7,11,16,22,46,47), although this is not a universal finding (37,50). Results of the present investigation suggest that a similar phenomenon occurs during the metaboreflex in subjects with OMS, with a functional shift from a flow-mediated mechanism to a vasoconstrict-mediated mechanism through which the target blood pressure level is reached.…”

“…This response is achieved as the result of an elevation in sympathetic tone, which produces arteriolar constriction and enhancement in myocardial performance and in cardiac preload (18,35,39). Differently, in several cardiovascular diseases, such as chronic heart failure and hypertension, although not universally reported (37,50), it has been demonstrated that excessive sympathetic activity can occur during the metaboreflex (7,11,16,41,42). This fact leads to detrimental effects, such as elevated SVR, which in turn causes excessive vasoconstriction and elevated blood pressure (46,47).…”