The relevance of central command for the neural cardiovascular control of exercise

University of Texas Southwestern Medical Center, Department of Health Care Sciences, 5323 Harry Hines Boulevard, Dallas, TX 75390-9082, USA.
Experimental physiology (Impact Factor: 2.67). 11/2010; 95(11):1043-8. DOI: 10.1113/expphysiol.2009.051870
Source: PubMed


This paper briefly reviews the role of central command in the neural control of the circulation during exercise. While defined as a feedforward component of the cardiovascular control system, central command is also associated with perception of effort or effort sense. The specific factors influencing perception of effort and their effect on autonomic regulation of cardiovascular function during exercise can vary according to condition. Centrally mediated integration of multiple signals occurring during exercise certainly involves feedback mechanisms, but it is unclear whether or how these signals modify central command via their influence on perception of effort. As our understanding of central neural control systems continues to develop, it will be important to examine more closely how multiple sensory signals are prioritized and processed centrally to modulate cardiovascular responses during exercise. The purpose of this article is briefly to review the concepts underlying central command and its assessment via perception of effort, and to identify potential areas for future studies towards determining the role and relevance of central command for neural control of exercise.

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Available from: Jon W Williamson
    • "In the transition from rest to exercise, the cardiovascular response includes an immediate increase in heart rate (HR; Krogh & Lindhard, 1913; Fagraeus & Linnarsson, 1976; Williamson et al. 1995) that is influenced by 'central command' , i.e. the CNS (Williamson, 2010). The influence of the 'exercise pressor reflex' (mechanoreflex DOI: 10.1113/expphysiol.2014.083857 "
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    ABSTRACT: New findings: What is the central question of this study? Neural feedback from group III/IV muscle afferents has a key role in regulation of cardiovascular responses to exercise. Blood pressure oscillates in the first seconds of dynamic exercise, but the contribution of muscle afferent feedback to this pattern is unclear. What is the main finding and its importance? We demonstrate that attenuation of group III/IV muscle afferent feedback by spinal fentanyl impairs the pressor response after 10 s of moderate leg cycling exercise, but this afferent feedback does not appear to be necessary for induction of the oscillatory pattern of blood pressure at the onset of exercise. We investigated whether attenuation of the central projections of group III/IV skeletal muscle afferents via lumbar intrathecal administration of the μ-opioid receptor agonist fentanyl affects the oscillatory blood pressure (BP) response to the onset of dynamic exercise. Eight healthy, recreationally active men (28 ± 3 years old) performed 40 s of cycling at 80 W (60 r.p.m.) before (control) and after fentanyl administration, while heart rate, stroke volume, cardiac output, systolic, mean and diastolic BP and total vascular conductance were continuously monitored. Sytolic and mean BP responses to cycling included an initial increase (from 0 to 3 s), followed by a transient decrease below resting levels (from 3 to 10 s) and then a sustained increase (>10 s). In the presence of fentanyl, systolic and mean BP responses closely matched those in control conditions in the first 10 s, but were blunted thereafter (P < 0.05). In contrast, fentanyl did not modify the heart rate, stroke volume, cardiac output, diastolic BP or total vascular conductance responses to 40 s of cycling (P > 0.05). These findings suggest that during moderate leg cycling exercise the muscle afferents contribute to the BP response after ∼10 s, but that they do not appear to be implicated in the oscillation of BP at the onset of exercise.
    No preview · Article · Jan 2015 · Experimental physiology
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    • "There is ample evidence for anticipatory response patterning in the central autonomic network. For example, heart rate and blood pressure can increase just before the onset of physical activity—a phenomenon called " central command " (Williamson 2010). Expectation-induced increases of heart rate and blood pressure may thus be explained by the activation of " central command " circuits. "
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    ABSTRACT: It is widely acknowledged that placebo responses are accompanied by physiological changes in the central nervous system, but little is known about placebo responses on end organ functions. The present chapter aims to fill this gap by reviewing the literature on peripheral placebo responses. Overall, there is a wide range of placebo and nocebo responses on various organ functions of the cardiovascular, the gastrointestinal system, and the respiratory system. Most of these studies used expectation paradigms to elicit placebo and nocebo responses. Expectations can affect heart rate, blood pressure, coronary diameter, gastric motility, bowel motility, and lung function. Classical conditioning can induce placebo respiratory depression after prior exposure to opioid drugs, and habitual coffee drinkers show physiological arousal in response to coffee-associated stimuli. Similar to findings in placebo pain research, peripheral placebo responses can be target specific. The autonomic nervous system is a likely candidate to mediate peripheral placebo responses. Further studies are necessary to identify the brain mechanisms and pathways involved in peripheral placebo responses.
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    • "The nervous centres and relationships between them that are involved in the processing of stress stimuli within the CNS are not well known. However, several hypotheses exist with respect to the role of the CC in fatigue [31], and different parts of the CNS (cortex, hippocampus, brainstem, encephalon, hypothalamus and amygdala) have been related directly or indirectly with the physiological response to stress [32]. The amygdala, which forms part of the limbic system, appears to have an important role in the latter. "
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    ABSTRACT: The anaerobic threshold (AT) has been one of the most studied of all physiological variables. Many authors have proposed the use of several markers to determine the moment at with the AT is reached. The present work discusses the physiological responses made to exercise - the measurement of which indicates the point at which the AT is reached - and how these responses might be controlled by the central nervous system. The detection of the AT having been reached is a sign for the central nervous system (CNS) to respond via an increase in efferent activity via the peripheral nervous system (PNS). An increase in CNS and PNS activities are related to changes in ventilation, cardiovascular function, and gland and muscle function. The directing action of the central command (CC) allows for the coordination of the autonomous and motor systems, suggesting that the AT can be identified in the many ways: changes in lactate, ventilation, plasma catecholamines, heart rate (HR), salivary amylase and muscular electrical activity. This change in response could be indicative that the organism would face failure if the exercise load continued to increase. To avoid this, the CC manages the efferent signals that show the organism that it is running out of homeostatic potential.
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