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1 Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, Davis 95616 - 8634; and 2 Department of Medicine, University of California, Irvine, Irvine, California 92888
We tested the hypothesis that static
contraction causes greater reflex cardiovascular responses than dynamic
contraction at equivalent workloads [i.e., same tension-time index
(TTI), holding either contraction time or peak tension constant] in
chloralose-anesthetized cats. When time was held constant and tension
was allowed to vary, dynamic contraction of the hindlimb muscles evoked
greater increases (means ± SE) in mean arterial pressure (MAP;
50 ± 7 vs. 30 ± 5 mmHg), popliteal blood velocity (15 ± 3 vs. 5 ± 1 cm/s), popliteal venous
PCO2 (15 ± 3 vs. 3 ± 1 mmHg), and a
greater decrease in popliteal venous pH (0.07 ± 0.01 vs.
0.03 ± 0.01), suggesting greater metabolic stimulation during
dynamic contraction. Similarly, when peak tension was held constant and
time was allowed to vary, dynamic contraction evoked a greater increase
in blood velocity (13 ± 1 vs.
1 ± 1 cm/s) without causing
any differences in other variables. To investigate the reflex
contribution of mechanoreceptors, we stretched the hindlimb dynamically
and statically at the same TTI. A larger reflex increase in MAP during
dynamic stretch (32 ± 8 vs. 24 ± 6 mmHg) was observed when
time was held constant, indicating greater mechanoreceptor stimulation.
However, when peak tension was held constant, there were no differences
in the reflex cardiovascular response to static and dynamic stretch. In
conclusion, at comparable TTI, when peak tension is variable, dynamic
muscle contraction causes larger cardiovascular responses than static
contraction because of greater chemical and mechanical stimulation.
However, when peak tensions are equivalent, static and dynamic
contraction or stretch produce similar cardiovascular responses.
static and dynamic muscle stretch; skeletal muscle blood flow; exercise; kao stimulator
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