Effects of Alpha‐adrenergic Receptors Blockade on Cardiovascular Responses to Acute Exercise and Isolated Metaboreflex in Postmenopausal Women

Abstract

Postmenopausal women (PMW) have higher cardiovascular risk when compared to younger women (YM). Nevertheless, acute response to exercise may characterize an additional risk to PMW. One possible mechanism for an increased cardiovascular risk could be the constrictor effect of the alpha-adrenergic receptors (α-AR). Thus, we aimed to test the hypothesis that the contribution of the α-AR in the cardiovascular responses to exercise is greater in PMW when compared to YW. We measured heart rate (HR), mean arterial pressure (MAP), cardiac output (CO), and total vascular resistance (TVR) in 7 YW (24±5 years;24±2kg∙m-2) and 7 PMW (59±4 years;25±3kg∙m-2), during three-minutes bouts of rest, hand grip exercise, isolated metaboreflex and recovery, respectively, in a control session and after α-AR blockade by oral administration of prazosin. HR increased during exercise in both groups but was blunted in PMW (YW: Δ28±15bpm; PMW: Δ15±7bpm; p<0.05). The α-AR blockade increased HR throughout the protocol (p<0.01), and the response to exercise was similar to the control condition (YW: Δ34±14bpm; PMW: Δ13±9bpm; p<0.05). During metaboreflex activation, HR was similar to resting values in both groups, in the control session (YW: Δ4±5bpm; PMW: Δ2±2bpm; p=0.11) and after the α-AR blockade (YW: Δ7±7bpm; PMW: Δ0±4bpm; p<0.05). MAP increased during exercise in both groups (YW: Δ33±10mmHg; PMW: Δ35±12mmHg; p=0.65). The α-AR blockade decreased MAP throughout the protocol (p<0.05) and the response to exercise was similar to the control session (YW: Δ22±16mmHg; PMW: Δ28±12mmHg; p=0.65). The metaboreflex activation kept the MAP elevated in both groups, in the control session (YW: Δ24±10mmHg; PMW: Δ26±7mmHg; p=0.65), while after the blockade, the increase was blunted when compared to the control session (YW: Δ6±20mmHg; PMW: Δ19±13mmHg; p=0.65). Exercise increased CO only in YW (YW: Δ2.3±1.6 l∙min-1; PMW: Δ0.9±1.4 l∙min-1; p<0.05). The α-AR blockade did not change CO throughout the protocol (p=0.21), with the response to exercise similar to the control condition (YW: Δ2.8±1.0 l∙min-1; PMW: Δ1.0±1.3 l∙min-1; p<0.05). During metaboreflex activation, CO increased only in PMW in the control session (YW: Δ1.1±0.8 l∙min-1; PMW: Δ0.4±0.6 l∙min-1; p<0.05), and after the α-AR blockade (YW: Δ0.4±2.6 l∙min-1; PMW: Δ-0.3±1.7 l∙min-1; p<0.05). Exercise increased TVR only in PMW (YW: Δ0±5mmHg∙l∙min-1; PMW: Δ4±4mmHg∙l∙min-1; p <0.05). The α-AR blockade decreased TVR throughout the protocol (p<0.05), but the response to exercise was similar to the control condition (YW: Δ-2±1mmHg∙l∙min-1; PMW: Δ3±3mmHg∙l∙min-1; p<0.05). The metaboreflex activation increased TVR only in PMW, in the control session, (YW: Δ1±3mmHg∙l∙min-1; PMW: Δ5±3mmHg∙l∙min-1; p<0.05), and after the α-AR blockade (YW: Δ-3±5mmHg∙l∙min-1; PMW: 1±8mmHg∙l∙min-1; p<0.05). We observed that PMW presents a peripheral vasoconstrictor response to exercise and metaboreflex activation when compared to YW, which seemed not to be driven by the α-AR vasoconstriction. Additionally, the adjustments in blood pressure were due to CO in YW and relied on TVR in PMW.