Preservation of shortening velocity and power output in single muscle fibres from patients with idiopathic inflammatory myopathies

Abstract

Idiopathic inflammatory myopathies (IIMs) are autoimmune disorders of skeletal muscle causing weakness and disability. Utilizing single fibre contractility studies, we have previously shown that contractility is affected in muscle fibres from individuals with IIMs. For the current study, we hypothesized that a compensatory increase in shortening velocity occurs in muscle fibres from individuals with IIMs in an effort to maintain power output. We performed in vitro single fibre contractility studies to assess force-velocity relationships and maximum shortening velocity (V max ) of muscle fibres from individuals with IIMs (25 type I and 58 type IIA) and healthy controls (66 type I and 27 type IIA) and calculated maximum power output (W max ) for each fibre. We found significantly higher V max (mean ± SEM) of fibres from individuals with IIMs, for both type I (1.40 ± 0.31 fibre lengths/s, n = vs. 0.63 ± 0.13 fibre lengths/s; p = 0.0019) and type IIA fibres (2.00 ± 0.17 fibre lengths/s vs 0.77 ± 0.10 fibre lengths/s; p < 0.0001). Furthermore, W max (mean ± SEM) was maintained compared to fibres from healthy controls, again for both type I and type IIA fibres (4.10 ± 1.00 kN/m 2 •fibre lengths/s vs. 2.00 ± 0.16 kN/m 2 •fibre lengths/s; p = ns and 9.00 ± 0.64 kN/m 2 •fibre lengths/s vs. 6.00 ± 0.67 kN/m 2 •fibre lengths/s; p = ns respectively). In addition, type I muscle fibres from individuals with IIMs was able to develop maximum power output at lower relative force. The findings of this study suggest that compensatory responses to maintain power output, including increased maximum shortening velocity and improved efficiency, may occur in muscle of individuals with IIMs. The mechanism underlying this response is unclear, and different hypotheses are discussed.

Electromyographic signature of isometric squat in the highest refuge in Europe

“…In this regard, it should be of interest to evaluate the force-velocity relationship in response to hypoxia and physical exertion, since shortening velocity adaptations have been suggested as compensatory mechanisms to support power production in inflammatory myopathies. 27 It should be kept in mind that the hypoxia-related cascade is one of the main non-immune pathological mechanisms in inflammatory myopathies. 28 As an issue limiting the generation of novel insights, despite the use of hd-sEMG matrices, the signals did not allow adequate estimation of single MU contributions.…”