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Related Concept Videos

Autonomic Nervous System01:22

Autonomic Nervous System

The autonomic nervous system (ANS) is a critical component of the peripheral nervous system, primarily responsible for regulating involuntary bodily functions and maintaining homeostasis. It functions in tandem with the central nervous system (CNS) to seamlessly coordinate various physiological processes without the need for conscious control.
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The regulation of heart rate is a complex process controlled by the autonomic nervous system (ANS), hormonal influences, and intrinsic cardiac mechanisms. The ANS has two main components: the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS).
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Nondepolarizing neuromuscular blockers prevent the membrane depolarization of muscle cells and inhibit muscle contraction. These are usually administered with anesthetics to achieve complete muscle relaxation. Upon administration, these drugs first block the small, rapidly contracting muscles of the face and hands, followed by the larger muscles of the trunk and the intercostal muscles. The diaphragm is the last muscle to be affected.
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The parasympathetic division of the autonomic nervous system (ANS) regulates rest and digestion functions in the body. It works in opposition to the sympathetic division, promoting relaxation, conservation of energy, and digestion. The parasympathetic division consists of preganglionic fibers originating from specific cranial nerves (III, VII, IX, X) and the sacral spinal nerves (S2-S4). These fibers synapse with postganglionic neurons in the terminal ganglia, innervating various organs and...
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Central command does not decrease cardiac parasympathetic efferent nerve activity during spontaneous fictive motor

Akito Kadowaki1, Kanji Matsukawa, Rie Wakasugi

  • 1Department of Physiology, Graduate School of Health Sciences, Hiroshima University, Japan.

American Journal of Physiology. Heart and Circulatory Physiology
|February 8, 2011
PubMed
Summary

Central command activates cardiac sympathetic nerves but does not withdraw parasympathetic activity at exercise onset. This study reveals that increased sympathetic nerve activity, not vagal withdrawal, drives initial exercise tachycardia.

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Area of Science:

  • Cardiovascular Physiology
  • Neuroscience
  • Exercise Physiology

Background:

  • The initiation of exercise involves complex neural control of the cardiovascular system.
  • It remains debated whether tachycardia at exercise onset is primarily driven by withdrawal of cardiac vagal efferent nerve activity (CVNA) or activation of cardiac sympathetic efferent nerve activity (CSNA).

Purpose of the Study:

  • To investigate the roles of CVNA and CSNA in controlling heart rate at the onset of exercise.
  • To determine whether central command or reflex mechanisms are responsible for these autonomic changes during motor activity.

Main Methods:

  • Direct assessment of CVNA and CSNA during spontaneous fictive motor activity in unanesthetized, decerebrate cats.
  • Utilized partial sinoaortic denervation (SAD) to attenuate baroreceptor and muscle receptor afferent inputs, isolating central command effects.

Main Results:

  • CSNA abruptly increased at motor activity onset, preceding and correlating with a modest heart rate increase.
  • CVNA increased throughout motor activity, alongside a rise in mean arterial blood pressure (MAP).
  • Partial SAD abolished the CVNA increase during motor activity, while CSNA remained elevated, suggesting central command drives sympathetic activation without parasympathetic withdrawal.

Conclusions:

  • Central command, the neural drive to active muscles, primarily activates cardiac sympathetic outflow at exercise onset.
  • Withdrawal of cardiac parasympathetic outflow is not the primary mechanism for tachycardia at the start of exercise.
  • These findings clarify the neural control of the heart during the transition to physical activity.