Abstract
We previously demonstrated that acute hypoperfusion in exercising human muscle causes an immediate increase in vascular resistance that is followed by a partial restoration (less than 100% recovery) of flow. In the current study we examined the contribution of α-adrenergic vasoconstriction in the initial changes in vascular resistance at the onset of hypoperfusion as well as in the recovery of flow over time. Nine healthy male subjects (29 ± 2) performed rhythmic forearm exercise (20% of maximum) during hypoperfusion evoked by intra-arterial balloon inflation. Each trial included; baseline, exercise prior to inflation, exercise with inflation, and exercise after deflation (3 min each). Forearm blood flow (FBF; ultrasound), local (brachial artery), and systemic arterial pressure (MAP; Finometer) were measured. The trial was repeated during phentolamine infusion (α-adrenergic receptor blockade). Forearm vascular conductance (FVC; ml min−1 100 mmHg−1) and resistance (mmHg ml min−1) was calculated from BF (ml min−1) and local MAP (mmHg). Recovery of FBF and FVC (steady state inflation plus exercise value − nadir)/[steady state exercise (control) value − nadir] with phentolamine was enhanced compared with the respective control (no drug) trial (FBF = 97 ± 5% vs. 81 ± 6%, P < 0.05; FVC = 126 ± 9% vs. 91 ± 5%, P < 0.01). However, the absolute (0.05 ± 0.01 vs. 0.06 ± 0.01 mmHg ml min−1; P = 0.17) and relative (35 ± 5% vs. 31 ± 2%; P = 0.41) increase in vascular resistance at the onset of balloon inflation was not different between the α-adrenergic receptor inhibition and control (no drug) trials. Therefore, our data indicate that α-adrenergic mediated vasoconstriction restricts compensatory vasodilation during forearm exercise with hypoperfusion, but is not responsible for the initial increase in vascular resistance at the onset of hypoperfusion.
Highlights
We previously demonstrated that acute hypoperfusion in exercising human muscle causes an immediate increase in vascular resistance that is followed by a partial restoration of flow
Forearm blood flow (FBF) and Forearm vascular conductance (FVC) at the end of inflation were partially restored to exercise levels, which were substantially higher than their respective nadir values (P < 0.001)
The findings of the present study suggest that an enhanced α-adrenergic vasoconstriction at the onset of balloon inflation does not explain the initial increase in vascular resistance
Summary
In animals, when blood flow is restricted and/or perfusion pressure is reduced, the active muscle is capable of autoregulating its blood flow (Stainsby, 1962; Jones and Berne, 1964; Britton et al, 1985; Metting et al, 1986) via intrinsic control mechanisms (Jones and Berne, 1964; Britton et al, 1985). Using a novel balloon catheter model in the brachial artery to reduce blood flow to contracting forearm muscles, we previously demonstrated that local vasodilator and/or myogenic mechanisms, rather than a pressor response, are responsible for a substantial portion of the restoration of flow to hypoperfused exercising human muscle (Casey and Joyner, 2009b). Our series of studies (Casey and Joyner, 2009a,b, 2011a,c) demonstrated that there is only partial compensation of flow (
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