**10. Fasciculations as a sign of muscle injury after exercise**

We studied the appearance of muscle fasciculations after exercise with stretch-shortening cycle (SSC), with partly eccentric contractions. Nine healthy men, aged 25–50 years, were recruited for the study. Spontaneous fasciculations of the soleus muscle were recorded immediately before and at 11 min after 100 jumps with the ball of the right foot with extended knee joint. Fasciculation potentials were recorded with two concentric needle electrodes (diameter 0.3 mm), interelectrode distance 10 mm. The recording was performed before exercise, and 1–2, 4–5, 6–7 and 10–11 min after exercise with Dantec Keypoint EMG machine and Sony DAT recorder. The needles were removed temporarily, and were not used during the exercise. There was a significant increase of the number of fasciculations, beginning at 4–5 min after the 100 jumps and increasing thereafter (**Table 1**). Statistical analyses were performed using IBM SPSS Statistics for Windows (Version 24.0, IBM Corp., Armonk, NY). The differences between the number of fasciculations before and after the 100 jumps (i.e. 1–2, 4–5, 6–7 and 10–11 min after the jumps) were normally distributed, as assessed by the Shapiro-Wilk test (*p* > 0.05). Therefore, a paired-samples t-test was used to determine whether there was a statistically significant difference in the mean number of fasciculations before and after the 100 jumps; the test was repeated for the four conditions corresponding to 1–2, 4–5, 6–7 and 10–11 min after the jumps. The level of significance was set at *α* = 0.05.


**11. Final comments**

**Acknowledgements**

guage corrections.

**Author details**

Juhani V. Partanen

**References**

of Helsinki, Helsinki, Finland

1970;**33**:519-523

Address all correspondence to: junipartanen@gmail.com

cle. Journal of Neurophysiology. 1949;**12**:231-244

Neurosurgery, and Psychiatry. 1949;**12**:268-273

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The aim of this chapter is to emphasise the major role of muscle spindles in muscle pain. Inflammatory muscle diseases with major histopathological changes are usually not associated with muscle pain. On the other hand, another disease with minor histopathological changes, the myofascial syndrome, may have severe muscle pain and local tenderness to pressure in TrPs. This fact can be explained by inflammation and pain elicited in the muscle spindles. Painful spots in needle EMG may simply be muscle spindles with nociception. Polymyalgia rheumatica may be associated with interstitial muscle pain. It remains to be studied whether there is also pain caused by inflammation of the muscle spindle capsules. DOMS may express

Muscle Pain and Muscle Spindles

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http://dx.doi.org/10.5772/intechopen.72223

The author is grateful to Hanna-Reetta Lajunen, MD, Jukka Vanhanen, MD and Kaarina Partanen, MD for their invaluable comments for the manuscript, and to Sara Liljander, MSc, who performed the statistical analyses. Thanks are due to Juha Heiskala, MD, for the lan-

Clinical Neurosciences, Clinical Neurophysiology, Helsinki University Hospital, University

[1] Meadows JC. Observations of muscle pain in man, with particular reference to pain during needle electromyography. Journal of Neurology, Neurosurgery, and Psychiatry.

[2] Jasper H, Ballem G. Unipolar electromyograms of normal and denervated human mus-

[3] Snodgrass JM, Sperry RW. Mammalian muscle action potentials of less than a millisec-

[4] Kugelberg E, Petersen I. "Insertion activity" in electromyography. Journal of Neurology,

both interstitial pain and muscle spindle pain with mild intrafusal inflammation.

**Table 1.** Number of fasciculations before and after 100 jumps with the ball of foot.

There was no statistically significant difference in the mean number of fasciculations between the measurements before the jumps (*M* = 3.56, *SD* = 4.58) and 1–2 min after the 100 jumps (*M* = 3.00, *SD* = 3.94), *t*(8) = −1.17, *p* = 0.28, *r* = 0.38. However, the number of fasciculations was, on average, significantly greater for 4–5 min after the jumps (*M* = 20.9, *SD* = 18.3) in comparison to the number before the jumps, *t*(8) = 3.58, *p* = 0.007, *r* = 0.78. The increase in the number of fasciculations was further enhanced 6–7 min after the jumps (*M* = 34.1, *SD* = 24.7), *t*(8) = 4.08, *p* = 0.004, *r* = 0.82, and even more so for 10–11 min after the jumps (*M* = 38.4, *SD* = 24.4), *t*(8) = 4.69, *p* = 0.002, *r* = 0.86.

We conjectured that the eccentric phase of SSC contractions with minor injury [57] caused some biochemical substances, such as cytokines, creatine kinase and [K<sup>+</sup> ], to be released. Increased extracellular concentration of these substances, especially [K<sup>+</sup> ] [58], may elicit spontaneous ectopic potentials in intramuscular motor nerve twigs or nerve terminals, spreading to the corresponding motor units and recorded as fasciculation potentials in needle EMG (author's presentation in Single Fibre and Quantitative EMG Meeting, Nijmegen, The Netherlands, June 6–10, 2004). In this case, fasciculations reflect slight damage of muscle fibres caused by the exercise.

Both low-volume high-intensity interval exercise and continuous exercise cause DOMS. Pressure-pain threshold, pressure-pain tolerance and perceived pain intensity were changed in 24 h after exercise [59]. Tenderness to palpation is unevenly distributed in muscles with DOMS. There are regions that are tender to pressure and some regions that are not. Trigger points, referred pain or taut bands, are not observed (author's unpublished observations). Thus, DOMS may reflect both interstitial muscle pain and painful muscle spindles. A question remains: why is there a 24 h delay before the appearance of soreness? It may take time until the extracellular concentration of K<sup>+</sup> , caused by the leakage through muscle membranes with minor injuries, is sufficient to increase the firing of interstitial C nerve axons. On the other hand, exercise is associated with overload of muscle and increased fusimotor activity, which increases the concentration of contraction metabolites in the periaxial space of muscle spindles. Accumulated contraction metabolites may induce increase of inflammation metabolites, cytocines and finally pain metabolites intrafusally. Intrafusal pain C-fibres are sensitised by increased periaxial concentration of [K<sup>+</sup> ] [60]. Thus, there may be a slight inflammation of muscle spindles, and consequently increased pressure sensitivity and pain generated by the intrafusal C-fibres. The development of pain in this way apparently needs some time.
