**Acknowledgements**

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,

**N = 9 Mean min max SD** Before 3.6 0 15 4.6 1–2 min after jumps 3.0 0 13 4.0 4–5 min after jumps 20.9\* 1 55 18.3 6–7 min after jumps 34.1\* 3 87 24.7 10–11 min after jumps 38.4\* 4 88 24.4

We conjectured that the eccentric phase of SSC contractions with minor injury [57] caused some

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 Trigger points, referred pain or taut bands, are not observed (author's unpublished observations).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

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

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.

], to be released. Increased

] [58], may elicit spontaneous

, caused by the leakage through muscle membranes

] [60]. Thus, there may be a slight inflammation of

biochemical substances, such as cytokines, creatine kinase and [K<sup>+</sup>

*p* < 0.01 (compared to the number of fasciculations before jumps, paired-samples t-test).

10 Anatomy, Posture, Prevalence, Pain, Treatment and Interventions of Musculoskeletal Disorders

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

extracellular concentration of these substances, especially [K<sup>+</sup>

*SD* = 24.4), *t*(8) = 4.69, *p* = 0.002, *r* = 0.86.

\*

until the extracellular concentration of K<sup>+</sup>

by increased periaxial concentration of [K<sup>+</sup>

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 language corrections.
