Middle cerebral artery blood velocity during exercise with β-1 adrenergic and unilateral stellate ganglion blockade in humans
A reduced ability to increase cardiac output (CO) during exercise limits blood flow by vasoconstriction even in active skeletal muscle. Such a flow limitation may also take place in the brain as an increase in the transcranial Doppler determined middle cerebral artery blood velocity (MCA Vmean) is attenuated during cycling with β-1 adrenergic blockade and in patients with heart insufficiency. We studied whether sympathetic blockade at the level of the neck (0.1% lidocain; 8 mL; n=8) affects the attenuated exercise – MCA Vmean following cardio-selective β-1 adrenergic blockade (0.15 mg kg−1 metoprolol i.v.) during cycling. Cardiac output determined by indocyanine green dye dilution, heart rate (HR), mean arterial pressure (MAP) and MCA Vmean were obtained during moderate intensity cycling before and after pharmacological intervention. During control cycling the right and left MCA Vmean increased to the same extent (11.4 ± 1.9 vs. 11.1 ± 1.9 cm s−1). With the pharmacological intervention the exercise CO (10 ± 1 vs. 12 ± 1 L min−1; n=5), HR (115 ± 4 vs. 134 ± 4 beats min−1) and ΔMCA Vmean (8.7 ± 2.2 vs. 11.4 ± 1.9 cm s−1) were reduced, and MAP was increased (100 ± 5 vs. 86 ± 2 mmHg; P < 0.05). However, sympathetic blockade at the level of the neck eliminated the β-1 blockade induced attenuation in ΔMCA Vmean (10.2 ± 2.5 cm s−1). These results indicate that a reduced ability to increase CO during exercise limits blood flow to a vital organ like the brain and that this flow limitation is likely to be by way of the sympathetic nervous system.
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