Key result
Beta-adrenergic receptor blockade abolished the increase in coronary blood velocity during handgrip exercise, while alpha-blockade had no effect.
Why the study?
The role of beta- and alpha-adrenergic receptors in coronary circulation control during static handgrip exercise and isolated muscle metaboreflex activation in humans was unclear.
Does beta- or alpha-adrenergic blockade alter coronary blood velocity during handgrip exercise and isolated muscle metaboreflex activation in healthy young men?
Does beta- or alpha-adrenergic blockade alter coronary blood velocity during handgrip exercise and isolated muscle metaboreflex activation in healthy young men?
β-adrenergic receptors, but not α-adrenergic receptors, play a primary role in increasing coronary circulation during handgrip exercise in humans.
β-blockade may blunt coronary velocity responses to handgrip in healthy men; extends adrenergic control mechanisms but leaves open relevance to patients.
New Findings What is the central question of this study? What is the role of β‐ and α‐adrenergic receptors in the control of the coronary circulation during handgrip exercise and isolated muscle metaboreflex activation in humans? What is the main finding and its importance? β‐Adrenergic receptor, but not α‐adrenergic receptor, blockade significantly blunted the increases in coronary blood velocity observed during handgrip. Coronary blood velocity was unchanged from baseline during isolated muscle metaboreflex activation. This highlights the important role of β‐adrenergic receptors in the coronary circulation during handgrip in humans, and the more limited involvement of the α‐adrenergic receptors. Abstract We sought to investigate the role of β‐ and 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.
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A 2021 study studied Healthy (n=17). Beta-blockade (oral propranolol) and alpha-blockade (oral prazosin) vs. Control was evaluated on Coronary blood velocity (CBV). Beta-adrenergic receptor blockade abolished the increase in coronary blood velocity during handgrip exercise, while alpha-blockade had no effect.
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