Is rapid rise in vascular conductance at onset of dynamic exercise due to muscle pump?
| Autor: | Allen M. Scher, Loring B. Rowell, D. D. Sheriff |
|---|---|
| Rok vydání: | 1993 |
| Předmět: |
Male
medicine.medical_specialty Cardiac output Central Venous Pressure Physiology Physical Exertion Hemodynamics Vasodilation Blood Pressure chemistry.chemical_compound Dogs Reference Values Physiology (medical) Internal medicine Medicine Animals Cardiac Output business.industry Muscles Central venous pressure Anatomy Hindlimb medicine.anatomical_structure chemistry Regional Blood Flow Circulatory system Blood Circulation Cardiology Hexamethonium Female Vascular Resistance medicine.symptom Cardiology and Cardiovascular Medicine business Blood vessel Muscle contraction Autonomic Nerve Block |
| Zdroj: | The American journal of physiology. 265(4 Pt 2) |
| ISSN: | 0002-9513 |
| Popis: | We tested the hypothesis that rapid increases in muscle blood flow and vascular conductance (C) at onset of dynamic exercise are caused by the muscle pump. We measured arterial (AP) and central venous pressure (CVP) in nine awake dogs, eight with atrioventricular block, pacemakers, and ascending aortic flow probes for control of cardiac output (CO) (2 also had terminal aortic flow probes). One dog had only an iliac artery probe. At exercise onset (0 and 10% grade, 4 mph) C and CVP rose to early plateaus, and AP reached a nadir, all in 2-5 s. At 20% grade and 4 mph, C increased continuously after its initial sudden rise. Timing and magnitude of initial change in conductance (delta C) were independent of CO, AP, work rate (change in grade at constant speed), or autonomic function (blocked by hexamethonium). Speed of initial delta C and its independence from work rate and blood flow ruled out metabolic vasodilation as its cause; insensitivity to AP and autonomic blockade ruled out myogenic relaxation and sympathetic vasodilation as causes of sudden delta C. Sensitivity to contraction frequency (not work per se) implicates the muscle pump. When reflexes were blocked, a large secondary rise in C, presumably caused by metabolic vasodilation, began after 10 s of mild exercise. When reflexes were intact in mild exercise, C was lowered below its initial plateau by sympathetic vasoconstriction, which partially raised AP from its nadir toward its preexercise level. Our conclusion is that dynamic exercise has a large rapid effect on C that is not explained by known neural, metabolic, myogenic, or hydrostatic influences.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Databáze: | OpenAIRE |
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