We sought to investigate the role of βand α-adrenergic receptors in coronary circulation during static handgrip exercise and isolated muscle metaboreflex activation in humans. Seventeen healthy young men underwent two experimental sessions, consisting of 3 min of static handgrip exercise at a target force of 40% maximum voluntary force (not achieved for the full 3 min), and 3 min of metaboreflex activation (post-exercise ischaemia) in two conditions: (1) control and β-blockade (oral propranolol), and (2) control and α-blockade (oral prazosin). In both sessions, coronary blood velocity (CBV, echocardiography) was increased during handgrip (Δ8.0 ± 7.4 cm s -1 ) but unchanged with metaboreflex activation (Δ2.5 ± 3.2 cm s -1 ) under control conditions. β-Blockade abolished the increase in CBV during handgrip, while CBV was unchanged from control with α-blockade. Cardiac work, estimated from rate pressure product (RPP; systolic blood pressure multiplied by heart rate), increased during handgrip and metaboreflex in control conditions in both sessions. β-Blockade reduced RPP responses to handgrip and metaboreflex, whereas α-blockade increased RPP, but the responses to handgrip and metaboreflex were unchanged. CBV and RPP were only significantly correlated during handgrip under control (r = 0.71, P < 0.01) and β-blockade (r = 0.54, P = 0.03) conditions, and the slope of this relationship was unaltered with β-blockade. Collectively, these findings indicate that β-adrenergic receptors play the primary role to the increase of coronary circulation during handgrip exercise, but CBV is unchanged with metaboreflex activation, while α-adrenergic receptor stimulation seems to exert no effect in the control of the coronary circulation during handgrip exercise and isolated muscle metaboreflex activation in humans.
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 press...
Coronary circulation is tightly regulated by several redundant mechanisms matched to the myocardial metabolic demand, which is directly related to myocardial mechanical work. However, our knowledge about the integrated autonomic control of coronary circulation during stress in humans is incomplete. The cold pressor test (CPT) has been used to evaluate the effect of centrally mediated increases in sympathetic activation. This noxious reflex evokes the increase of vascular resistance (VR), blood pressure (BP) and cardiac work. However, the effect of the sympathetic control on coronary circulation during a sympathetic mediated reflex is unknown. Therefore, we aimed to test the effect of the β‐adrenergic receptor (AR) and α‐AR on coronary circulation in humans during CPT. In 19 men (27±1 years; 23±1 kg‧m‐2; mean±SE) and 13 women (24±1 years; 24±1 kg‧m‐2; mean±SE), we measured heart rate (HR), BP, cardiac output (CO), total (TVR) and coronary blood peak velocity (CBV). Coronary conductance index (CCI: CBV/diastolic BP) and the estimated myocardial oxygen consumption (MVO2: 7.2 × 10‐4 (Systolic BP × HR) + 1.43)were calculated; at rest and during CPT, before and after an oral administration a β‐AR blocker (propranolol; men: 1.6±0.1mg‧kg‐1 and women: 1.7±0.1mg‧kg‐1), and a α‐AR blocker (prazosin; men: 0.038±0 mg‧kg‐1 and women: 0.039±0 mg‧kg‐1), in two laboratory visits. On the control session, CPT did not change HR, increased mean arterial pressure (MAP), CO and TVR only in men. Also, CPT increased the MVO2, CBV and decreased CCI. The β‐AR blockade decreased HR and did not change BP at rest. CPT did not change HR (men: ‐1±2 bpm; women:1±1 bpm), and increased MAP (men: 26±10 mmHg; women: 21±11 mmHg). CO decreased at rest after the β‐AR blockade while maintaining the response to CPT (men: 0.4±0.2 l‧min‐1; women: 1.0±0.1 l‧min‐1). The β‐AR blockade increased TVR at rest, but did not change the response to CPT (men: 3±1 mmHg‧l‧min‐1; women: ‐1±0.4 mmHg‧l‧min‐1). The β‐AR blockade reduced MVO2 and blunted its response to CPT (men: 2.3±0.3 a.u.; women: 2.1±0.3 a.u.); however abolishing the increase of CBV, then not changing the CCI response to CPT (men: ‐0.15±0.02 cm‧s‐1‧mmHg‐1; women: ‐0.13±0.02 cm‧s‐1‧mmHg‐1). The α‐AR blockade increased HR at rest, not changing the response to CPT (men: 3±3bpm; women: 4±3 bpm). There was no effect of the α‐AR blockade on BP at rest; however, blunted its response to CPT (MAP ‐ men: 20±4 mmHg; women: 8±3 mmHg). The α‐AR blockade did not change CO, which increased during CPT (men: 0.66 ±0.21 l‧min‐1; women: 1.10±0.21 l‧min‐1). The α‐AR blockade did not change TVR, and prevented its increase during CPT. The estimated MVO2 did not change after the α‐AR blockade, and increased during CPT (men: 2.0±0.4 a.u.; women: 1.4±0.5 a.u.). The α‐AR blockade did not change CBVat rest or the response to CPT (men: 3.1±1.4 cm‧s‐1; women: 5.4± 3.6 cm‧s‐1), as well as, did not change the CCI at rest or the response to CPT. Ultimately, no sex differences were observed. The β‐AR vasodilation plays a key role to th...
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