Abstract
Trapezius myalgia is the most common type of chronic neck pain. While physical exercise reduces pain and improves muscle function, the underlying mechanisms remain unclear. Nitric oxide (NO) signaling is important in modulating cellular function, and a dysfunctional neuronal NO synthase (nNOS) may contribute to an ineffective muscle function. This study investigated nNOS expression and localization in chronically painful muscle. Forty-one women clinically diagnosed with trapezius myalgia (MYA) and 18 healthy controls (CON) were included in the case-control study. Subsequently, MYA were randomly assigned to either 10 weeks of specific strength training (SST, n = 18), general fitness training (GFT, n = 15), or health information (REF, n = 8). Distribution of fiber type, cross-sectional area, and sarcolemmal nNOS expression did not differ between MYA and CON. However, MYA showed increased sarcoplasmic nNOS localization (18.8 ± 12 versus 12.8 ± 8%, P = 0.049) compared with CON. SST resulted in a decrease of sarcoplasm-localized nNOS following training (before 18.1 ± 12 versus after 12.0 ± 12%; P = 0,027). We demonstrate that myalgic muscle displays altered nNOS localization and that 10 weeks of strength training normalize these disruptions, which supports previous findings of impaired muscle oxygenation during work tasks and reduced pain following exercise.
Highlights
Musculoskeletal disorders are among the most frequent and costly health care problems in North America and Europe [1]
Women suffering from trapezius myalgia show more frequent localization of neuronal NO synthase (nNOS) to the sarcoplasm compared to healthy controls and this sarcoplasmic localization can be reversed by specific strengthening exercises
We showed that sarcolemmal nNOS expression is irregular and absent from selected fibers in the trapezius muscle
Summary
Musculoskeletal disorders are among the most frequent and costly health care problems in North America and Europe [1]. Numerous studies have shown that trapezius myalgia is accompanied by poor oxygenation, focal cell death, and disrupted metabolic homeostasis [8] Taken together these data have led to the development of the “Cinderella theorem,” which proposes that selected type I fibers are the first to be recruited during repetitive movements at low static tension and, these motor units are constantly activated leading to overload of single muscle fibers [2]. The theory is supported by the finding of an increased proportion of hypertrophied type I mega fibers with poor capillarization [12] and a reduced capillary to fiber area [3] in trapezius myalgia Overall, these intramuscular changes create disturbances in energy homeostasis and cellular hypoperfusion of enlarged type I fibers has been suggested as a major factor in the development of muscle pain [13, 14]
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