Abstract
It has long been established that neural activity generated wholly within the central nervous system can affect cardiovascular control. Even during complete paralysis the central cycling of respiratory neurones can impose respiratory rhythmicity on heart rate and vasomotion, and alter the effectiveness of purely cardiovascular reflexes. During muscular exercise centrally-generated voluntary motor command signals contribute to the stimulation of heart rate and the rise in blood pressure. This is seen, for example, when muscular weakness is induced by partial curarization, by fatigue, or by other means, so that a given level of muscular contraction is achieved only with an increased motor command, or 'effort'. Such command-related stimuli are essentially without cardiovascular feedback and are likely at most to provide coarse adjustments upon which finer controls are superimposed by well-known reflex mechanisms.
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