Variable effects of β‐adrenoceptor blockade on muscle blood flow during exercise

Abstract

The role of beta-adrenoceptors in exercise-induced muscle hyperaemia was investigated. Exercise was performed with a small and a large muscle mass: knee extension (KE) and bicycle exercise (BE). Seven healthy subjects performed light and maximal KE and eight subjects performed stepwise dynamic BE to exhaustion before and after acute i.v. administration of propranolol (0.15 mg kg-1). Leg blood flow was measured by a bolus dye dilution technique. During KE at low and high power leg blood flow was reduced by 8.7 and 10.5% after propranolol was administered, mean arterial blood pressure (MAP) was reduced at low, but not at high power resulting in increased leg vascular resistance (LVR) during high intensity. During BE propranolol reduced leg blood flow and increased LVR at low power, but not at high power. At high BE intensity LVR did not change with increasing power and was slightly decreased after propranolol was administered. In this situation oxygen uptake was close to maximum and the concentration of catecholamines was 3-5 times higher compared with KE. There was no significant effect of propranolol on lactate release or arterial-femoral venous (a-fv) differences for adrenaline or noradrenaline. We conclude that beta-adrenoceptors modulate local vasodilation in skeletal muscles during exercise independently of local muscle energy demand, but that the effect is highly dependent on active muscle mass since alpha-adrenergic activity during maximal BE seemed to disguise any effect of propranolol on LVR.

Local and systemic effects on blood lactate concentration during exercise with small and large muscle groups

“…Glycogen breakdown was unchanged by β-blockade [18]. This is in line with authors who were also unable to show any differences in muscle lactate-release pattern and systemic lactate concentrations during moderate exercise intensity after β-blockade [16,21]. Our findings seem to be in contrast to others [25,45].…”

“…This indicates that high [lac] can be reached without high [EPI]. The consequence is that, during exercise of moderate intensity, epinephrine is not the main factor for an elevated lactate release [16,21].…”

“…On the other hand, results from studies with β-blockade are inconsistent [6,16,21,23]. In some studies, there was no effect on lactate release [16,21], and in others, lactate release was reduced [6]. But it is clear from studies of isolated muscles that [lac] can increase without the presence of epinephrine [9].…”

“…Those findings suggest the possibility of a causal relationship between the increase of plasma catecholamines and [lac]. On the other hand, results from studies with β-blockade are inconsistent [6,16,21,23]. In some studies, there was no effect on lactate release [16,21], and in others, lactate release was reduced [6].…”

Middle cerebral artery blood velocity is reduced with hyperthermia during prolonged exercise in humans

“…However, even within the autoregulatory range a small influence of reduced MAP on the cerebral circulation cannot be excluded (Heistad & Kontos, 1983). That blood flow to various tissue compartments can be reduced as a result of insufficient cardiac output is supported by the observations that reductions in cardiac output are accompanied by reduced leg blood flow both in dehydrated athletes (González-Alonso et al 1998) and in patients with b-adrenergic blockade (Pawelczyk et al 1992;Gullestad et al 1993). Furthermore, patients with heart failure who are not able to increase cardiac output sufficiently have a lower MCA V mean during dynamic exercise (Ide et al 1999).…”