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Abstract
Mechanisms underlying the development of chronic muscle pain in humans remain unknown. Our current understanding is principally based on experimentation in animals, which has resulted in the formulation of a multitude of theories and physiological models to postulate these mechanisms in humans. The vicious cycle theory – a popularised but unsupported theory in humans – suggests that muscle metabolites produced by static muscle contractions stimulate group III and IV muscle nociceptors leading to an excitation of gamma-motoneurones through a reflex mechanism. Increased gamma-motor drive causes intrafusal fibres to contract increasing muscle spindle afferent firing. This activity in turn will raise the likelihood of activation in the pool of alpha-motorneurones projecting to the primary muscle increasing resting muscle tonus.
Muscle spindle afferents and postganglionic sympathetic outflow to skin and muscle were recorded from healthy subjects using the technique of microneurography. Cardiorespiratory function (blood pressure, heart rate, and respiration) was measured non-invasively. Muscle pain was induced using a solution of hypertonic saline tonically infused via indwelling cannulae delivered by an infusion pump. The rate of infusion was controlled to ensure subjects experienced mild to moderate pain.
Muscle spindle afferents fail to show any change in spontaneous discharge rate in response to tonic muscle pain contradicting the observations and conclusions from animal studies. Sympathetic outflow to skin demonstrated a transient increase followed by a sustained decrease during infusion of hypertonic saline. Sympathetic outflow to muscle demonstrated a dichotomy of responses during muscle pain: half of the subjects showing increasing sympathetic activity, blood pressure, and heart rate; whilst the others showed decreasing sympathetic activity, blood pressure, and heart rate. Consistent responses were seen in the same individuals when the study was reproduced in a second recording.
This investigation advances our understanding of the physiological consequences tonic pain has on sympathetic outflow and muscle spindle afferents in the context of developing chronic muscle pain. After undertaking experimentation in awake human subjects there is no apparent evidence to suggest that tonic pain increases the discharge rate of spontaneously active muscle spindle afferents to result in increased muscle tone as proposed by the “vicious cycle” theory. There is, however, evidence of sustained changes in sympathetic outflow to muscle and skin in response to tonic pain that may contribute to the development of chronic pain.