Key result
Arterial pulsations significantly modulated the discharge rate in 53% of spontaneously active human muscle spindle afferents, an effect that remained robust and relatively insensitive to fluctuations in blood pressure during apnoea and acute pain.
Observational (n=40)
No
Arterial pulsations modulate human muscle spindle discharge, acting as a robust endogenous noise source that is relatively insensitive to fluctuations in blood pressure.
Hypothesis-generating for vascular modulation of proprioception; leaves open relevance to sensorimotor function in cardiovascular or pain states.
Arterial pulsations are known to modulate muscle spindle firing; however, the physiological significance of such synchronised modulation has not been investigated. Unitary recordings were made from 75 human muscle spindle afferents innervating the pretibial muscles. The modulation of muscle spindle discharge by arterial pulsations was evaluated by R-wave triggered averaging and power spectral analysis. We describe various effects arterial pulsations may have on muscle spindle afferent discharge. Afferents could be "driven" by arterial pulsations, e.g., showing no other spontaneous activity than spikes generated with cardiac rhythmicity. Among afferents showing ongoing discharge that was not primarily related to cardiac rhythmicity we illustrate several mechanisms by which individual spikes may become phase-locked. However, in the majority of afferents the discharge rate was modulated by the pulse wave without spikes being phase locked. Then we assessed whether these influences changed in two physiological conditions in which a sustained increase in muscle sympathetic nerve activity was observed without activation of fusimotor neurones: a maximal inspiratory breath-hold, which causes a fall in systolic pressure, and acute muscle pain, which causes an increase in systolic pressure. The majority of primary muscle spindle afferents displayed pulse-wave modulation, but neither apnoea nor pain had any significant effect on the strength of this modulation, suggesting that the physiological noise injected by the arterial pulsations is robust and relatively insensitive to fluctuations in blood pressure. Within the afferent population there was a similar number of muscle spindles that were inhibited and that were excited by the arterial pulse wave, indicating that after signal integration at the population level, arterial pulsations of opposite polarity would cancel each other out. We speculate that with close-to-threshold stimuli the arterial pulsations may serve as an endogenous noise source that may synchronise the sporadic discharge within the afferent population and thus facilitate the detection of weak stimuli.
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Birznieks et al. (2012) conducted an observational in Healthy (n=40). Arterial pulsations and physiological challenges (apnoea, acute pain) vs. Baseline/rest was evaluated on Modulation of muscle spindle discharge by arterial pulsations (variance explained). Arterial pulsations significantly modulated the discharge rate in 53% of spontaneously active human muscle spindle afferents, an effect that remained robust and relatively insensitive to fluctuations in blood pressure during apnoea and acute pain.
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