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Tschakovsky, M E.1; Sujirattanawimol, K1; Ruble, S B.1; Valic, Z1; Joyner, M J.1
1Mayo Clinic, Rochester, Minnesota
The need for local exercising muscle perfusion to meet metabolic demand may be opposed by the need for sympathetic restraint of muscle perfusion to regulate blood pressure. Thus, understanding the nature of the interaction(s) between local vasodilator influences and sympathetic neural vasoconstrictor influences in muscle is fundamental for understanding vascular control and blood pressure regulation in exercise.
Data are presented from a recent study designed to test the hypothesis that local factors in exercising muscle blunt vessel responsiveness to sympathetic vasoconstriction in humans.
Selective infusion of three doses of tyramine into the brachial artery (n = 8) were used to evoke endogenous release of norepinephrine at rest and during moderate (MEx) and heavy (HEx) rhythmic handgrip exercise. In separate experiments, tyramine was administered during two doses of adenosine infusion (n = 7) and two doses of sodium nitroprusside infusion (n = 8). Vasoconstrictor effectiveness across conditions was assessed as the percentage reduction in forearm vascular resistance (%rFVC), calculated from invasive blood pressure and non-invasive Doppler ultrasound blood flow measurements at the brachial artery.
All values mean ± SE. Tyramine evoked a similar dose-dependent vasoconstriction at rest in all three groups, with the highest dose resulting in a 42–46% reduction in FVC. This vasoconstriction was blunted with increasing exercise intensity (e.g. tyramine high dose %rFVC; rest −43 ± 3.7%, MEx −27.5 ± 2.3%, HEx −16.7 ± 3.6% P < 0.05). In contrast, tyramine infusion during vasodilator-induced elevations in forearm blood flow resulted in a greater percentage reduction in FVC vs. rest.
These observations support the concept of exercise intensity-dependent functional sympatholysis. A schema of cardiovascular control is presented in which functional sympatholysis permits appropriate blood pressure control while minimizing the potentially deleterious effects of sympathetic restraint of muscle perfusion in active muscle. Supported by NIH Grant #HL46493;NSERC Canada
©2003The American College of Sports Medicine
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