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Muscle sympathetic outflow during horizontal linear acceleration in humans
1Department of Autonomic Neuroscience, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan.
Summary
Linear acceleration significantly reduces muscle sympathetic nerve activity (MSNA) in humans. This vestibular system stimulation may inhibit MSNA to aid blood redistribution during passive movements.
Area of Science:
- Physiology
- Neuroscience
- Cardiovascular Research
Background:
- Muscle sympathetic nerve activity (MSNA) is crucial for regulating cardiovascular function and blood pressure.
- The vestibular system's role in sympathetic regulation is not fully understood, particularly its response to dynamic linear acceleration.
Purpose of the Study:
- To investigate the impact of linear acceleration on MSNA in healthy human subjects.
- To determine if vestibular stimulation via linear acceleration influences sympathetic nerve outflow.
Main Methods:
- Sixteen healthy men underwent testing in a linear accelerator, experiencing sinusoidal linear acceleration.
- Measurements included MSNA, electrocardiogram, blood pressure, and thoracic impedance.
- Acceleration was applied in anteroposterior (Gx) and lateral (Gy) directions at peak values of +/-0.10, +/-0.15, and +/-0.20 G.
Main Results:
- A significant decrease in both total activity and burst rate of MSNA was observed during forward, backward, left, and right linear accelerations.
- At peak +/-0.20 G acceleration, MSNA total activity reduced to approximately 50-70% of baseline levels across directions.
- The inhibition of MSNA was evident across all tested directions and magnitudes of linear acceleration.
Conclusions:
- Dynamic stimulation of otolith organs by linear acceleration in horizontal directions inhibits MSNA in humans.
- This inhibition likely facilitates rapid blood redistribution to muscles during passive postural reflexes.
- The findings support a significant role for the vestibular system in the sympathetic regulation of cardiovascular function.