Nonhypotensive lower body negative pressure (LBNP) from -5 to -15 mmHg increased total muscle sympathetic nerve activity by up to 149% compared to control (P<0.05).
Does nonhypotensive lower body negative pressure increase sympathetic discharge to leg muscles in conscious humans?
Nonhypotensive lower body negative pressure triggers a mass sympathetic discharge to skeletal muscles in the leg, demonstrating the role of the cardiac baroreflex during orthostatic stress.
p-value: p=<0.05
Recent studies indicate that nonhypotensive orthostatic stress in humans causes reflex vasoconstriction in the forearm but not in the calf. We used microelectrode recordings of muscle sympathetic nerve activity (MSNA) from the peroneal nerve in conscious humans to determine if unloading of cardiac baroreceptors during nonhypotensive lower body negative pressure (LBNP) increases sympathetic discharge to the leg muscles. LBNP from -5 to -15 mmHg had no effect on arterial pressure or heart rate but caused graded decreases in central venous pressure and corresponding large increases in peroneal MSNA. Total MSNA (burst frequency X mean burst amplitude) increased by 61 +/- 22% (P less than 0.05 vs. control) during LBNP at only -5 mmHg and rose progressively to a value that was 149 +/- 29% greater than control during LBNP at -15 mmHg (P less than 0.05). The major new conclusion is that nonhypotensive LBNP is a potent stimulus to muscle sympathetic outflow in the leg as well as the arm. During orthostatic stress in humans, the cardiac baroreflex appears to trigger a mass sympathetic discharge to the skeletal muscles in all of the extremities.
Victor et al. (Tue,) reported a other. Lower body negative pressure (LBNP) vs. control was evaluated on Total muscle sympathetic nerve activity (MSNA) (p=<0.05). Nonhypotensive lower body negative pressure (LBNP) from -5 to -15 mmHg increased total muscle sympathetic nerve activity by up to 149% compared to control (P<0.05).
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