The effect of augmented sympathetic outflow on forearm vascular conductance after single handgrip contractions of graded intensity was examined to determine whether sympatholysis occurs early in exercise (n ϭ 7). While supine, subjects performed contractions that were 1 s in duration and 15, 30, and 60% of maximal voluntary contraction (MVC) in intensity. The contractions were repeated during control and lower body negative pressure (LBNP) (Ϫ40 mmHg) sessions. Forearm blood flow (FBF; Doppler ultrasound) and mean arterial pressure were measured continuously for 30 s before and 60 s after the single contractions. Vascular conductance (VC) was calculated. Total postcontraction blood flow increased in an exercise intensity-dependent manner. Compared with control, LBNP caused a reduction in baseline and postexercise FBF (P Ͻ 0.05), VC (P Ͻ 0.01), as well as total excess flow (P Ͻ 0.01). Specifically, during LBNP, baseline FBF and VC were reduced by 29 and 34% of control, respectively (P Ͻ 0.05). After the 15% MVC contraction, peak VC during LBNP was reduced by a magnitude similar to that during baseline (i.e., ϳ30%), but it was only reduced by 15% during both the 30 and 60% MVC trials (P Ͻ 0.01). It was concluded that the stimuli for exercise hyperemia during moderate and heavy, but not mild, handgrip exercise intensities, diminish the vasoconstrictor effects of LBNP. Furthermore, these data demonstrate that this sympatholysis occurs early in exercise. Doppler ultrasound; forearm blood flow; vascular conductance; lower body negative pressure; sympathetic nervous system DESPITE CONSIDERABLE RESEARCH, the mechanisms responsible for the control of muscle blood flow at the onset of exercise remain elusive. Vascular tone at rest and during exercise is determined by the ability of vascular smooth muscle to integrate competing vasodilatory and vasoconstrictor signals from endothelial, metabolic, and neurogenic sources. At the onset of exercise, the early increase in muscle blood flow has been attributed to the muscle pump and an early rapid vasodilation (8,28,33). However, attempts to identify the substance(s) responsible for this early vasodilation have not been successful (34), and thus the search for an alternative explanation is warranted. The ability of the sympathetic nervous system to restrain blood flow to active skeletal muscle has been an active area of investigation. Several studies have demonstrated that there is sympathetic vasoconstriction in active skeletal muscle (4,14,21,22,27), and OЈLeary et al. (21) have argued that sympathetic activity directed to active skeletal muscle increases as exercise intensity increases.Conversely, other investigations have demonstrated an attenuation of vasoconstriction in active skeletal muscle during exercise (5, 24). This diminished vascular responsiveness to sympathetic stimulation was termed "sympatholysis" by Remensnyder et al. (24). Prejunctional inhibition of neurotransmitter release from the nerve terminal or an attenuation of postjunctional adrenergic-receptor respon...
During Valsalva manoeuvers the Millar and Colin tonometers similarly tracked PP over a wide range of rapidly changing pressures. This observation provided confidence for the further use of the hand-held device for central measurements during changes in posture. The results from Protocol B indicate that peripheral PP measurements are not suitable surrogates for carotid pulse pressures during HUT.
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