Key result
Alpha-1 adrenergic receptor blockade during static handgrip exercise resulted in similar increases in contra- and ipsilateral internal carotid artery blood flow, indicating sympathetic modulation.
Why the study?
Does α1-adrenergic receptor blockade alter the regional distribution of cerebral blood flow during static handgrip exercise in healthy men?
Does α1-adrenergic receptor blockade alter the regional distribution of cerebral blood flow during static handgrip exercise in healthy men?
Sympathetic nerve activity plays a role in regulating the regional distribution of cerebral blood flow during static handgrip exercise.
No immediate clinical implications for cerebral perfusion; hypothesis-generating for sympathetic regulation in patients.
Handgrip-induced increases in blood flow through the contralateral artery that supplies the cortical representation of the arm have been hypothesized as a consequence of neurovascular coupling and a resultant metabolic attenuation of sympathetic cerebral vasoconstriction. In contrast, sympathetic restraint, in theory, inhibits changes in perfusion of the cerebral ipsilateral blood vessels. To confirm whether sympathetic nerve activity modulates cerebral blood flow distribution during static handgrip (SHG) exercise, beat-to-beat contra- and ipsilateral internal carotid artery blood flow (ICA; Doppler) and mean arterial pressure (MAP; Finometer) were simultaneously assessed in nine healthy men (27 ± 5 yr), both at rest and during a 2-min SHG bout (30% maximal voluntary contraction), under two experimental conditions: 1) control and 2) α1-adrenergic receptor blockade. End-tidal carbon dioxide (rebreathing system) was clamped throughout the study. SHG induced increases in MAP (+31.4 ± 10.7 mmHg, P < 0.05) and contralateral ICA blood flow (+80.9 ± 62.5 ml/min, P < 0.05), while no changes were observed in the ipsilateral vessel (-9.8 ± 39.3 ml/min, P > 0.05). The reduction in ipsilateral ICA vascular conductance (VC) was greater compared with contralateral ICA (contralateral: -0.8 ± 0.8 vs. ipsilateral: -2.6 ± 1.3 ml·min(-1)·mmHg(-1), P < 0.05). Prazosin was effective to induce α1-blockade since phenylephrine-induced increases in MAP were greatly reduced (P < 0.05). Under α1-adrenergic receptor blockade, SHG evoked smaller MAP responses (+19.4 ± 9.2, P < 0.05) but similar increases in ICAs blood flow (contralateral: +58.4 ± 21.5 vs. ipsilateral: +54.3 ± 46.2 ml/min, P > 0.05) and decreases in VC (contralateral: -0.4 ± 0.7 vs. ipsilateral: -0.4 ± 1.0 ml·min(-1)·mmHg(-1), P > 0.05). These findings indicate a role of sympathetic nerve activity in the regulation of cerebral blood flow distribution during SHG.
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Fernandes et al. (2016) studied Healthy (n=9). α1-adrenergic receptor blockade (Prazosin) vs. Control was evaluated on Contra- and ipsilateral internal carotid artery blood flow and mean arterial pressure. Alpha-1 adrenergic receptor blockade during static handgrip exercise resulted in similar increases in contra- and ipsilateral internal carotid artery blood flow, indicating sympathetic modulation.
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