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J Physiol Volume 586, Number 11, 2713-2723, June 1, 2008 DOI: 10.1113/jphysiol.2008.151746
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NEUROSCIENCE

The effects of experimental muscle and skin pain on the static stretch sensitivity of human muscle spindles in relaxed leg muscles

 Ingvars Birznieks1, Alexander R. Burton1 and Vaughan G. Macefield1,2

1 Prince of Wales Medical Research Institute and University of New South Wales, Sydney, NSW 2031, Australia
2 School of Medicine, University of Western Sydney, NSW 1797, Australia

Animal studies have shown that noxious inputs onto {gamma}-motoneurons can cause an increase in the activity of muscle spindles, and it has been proposed that this causes a fusimotor-driven increase in muscle stiffness that is believed to underlie many chronic pain syndromes. To test whether experimental pain also acts on the fusimotor system in humans, unitary recordings were made from 19 spindle afferents (12 Ia, 7 II) located in the ankle and toe extensors or peronei muscles of awake human subjects. Muscle pain was induced by bolus intramuscular injection of 0.5 ml 5% hypertonic saline into tibialis anterior (TA); skin pain was induced by 0.2 ml injection into the overlying skin. Changes in fusimotor drive to the muscle spindles were inferred from changes in the mean discharge frequency and discharge variability of spindle endings in relaxed muscle. During muscle pain no afferents increased their discharge activity: seven afferents (5 Ia, 2 II) showed a decrease and six (4 Ia, 2 II) afferents were not affected. During skin pain of 13 afferents discharge rate increased in one (Ia) and decreased in two (1 Ia, 1 II). On average, the overall discharge rate decreased during muscle pain by 6.1% (P < 0.05; Wilcoxon), but remained essentially the same during skin pain. There was no detectable correlation between subjective pain level and the small change in discharge rate of muscle spindles. Irrespective of the type of pain, discharge variability parameters were not influenced (P > 0.05; Wilcoxon). We conclude that, contrary to the ‘vicious cycle’ hypothesis, acute activation of muscle or skin nociceptors does not cause a reflex increase in fusimotor drive in humans. Rather, our results are more aligned with the pain adaptation model, based on clinical studies predicting pain-induced reductions of agonist muscle activity.

(Received 28 January 2008; accepted after revision 3 April 2008; first published online 10 April 2008)
Corresponding author I. Birznieks: Prince of Wales Medical Research Institute, Barker Street, Randwick, NSW 2031, Sydney, Australia. Email: ingvars.birznieks{at}unsw.edu.au






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