Pathophysiology of upper extremity muscle disorders

Journal of Electromyography and Kinesiology, 2006

A review of the literature on the pathophysiology of upper extremity muscle disorders (UEMDs) was performed. An overview is given of clinical findings and hypotheses on the pathogenesis of UEMDs. The literature indicates that disorders of muscle cells and limitations of the local circulation underlie UEMDs. However, these disorders identified do not necessarily lead to symptoms. The following mechanisms have been proposed in the literature: (1) selective recruitment and overloading of type I (Cinderella) motor units; (2) intra-cellular Ca 2+ accumulation; (3) impaired blood flow; (3b) reperfusion injury; (3.3c) blood vessel-nociceptor interaction; (4a) myofascial force transmission; (4b) intramuscular shear forces; (5) trigger points; (6) impaired heat shock response. The results of the review indicate that there are multiple possible mechanisms, but none of the hypotheses forms a complete explanation and is sufficiently supported by empirical data. Overall, the literature indicates that: (1) sustained muscle activity, especially of type I motor units, may be a primary cause of UEMDs; (2) in UEMDs skeletal muscle may show changes in morphology, blood flow, and muscle activity; (3) accumulation of Ca 2+ in the sarcoplasm may be the cause of muscle cell damage; (4) it seems plausible that suboptimal blood flow plays a role in pathogenesis of UEMDs; (5) since the presence of fiber disorders is not a sufficient condition for the development of UEMSDs additional mechanisms, such as sensitization, are assumed to play a role.

PLoS ONE, 2014

Unilateral strength training can cause cross-transfer strength effects to the homologous contralateral muscles. However, the impact of the cross-over effects on the muscle tissue is unclear. To test the hypothesis that unilateral muscle overuse causes bilateral alterations in muscle fiber composition and vascular supply, we have used an experimental rabbit model with unilateral unloaded overstrain exercise via electrical muscle stimulation (E/EMS). The soleus (SOL) and gastrocnemius (GA) muscles of both exercised (E) and contralateral nonexercised (NE) legs (n524) were morphologically analyzed after 1w, 3w and 6w of EMS. Non-exercised rabbits served as controls (n56). After unilateral intervention the muscles of both E and NE legs showed myositis and structural and molecular tissue changes that to various degrees mirrored each other. The fiber area was bilaterally smaller than in controls after 3w of E/EMS in both SOL (E 4420 and NE 4333 mm 2 vs. 5183 mm 2 , p,0.05) and GA (E 3572 and NE 2983 mm 2 vs. 4697 mm 2 , p,0.02) muscles. After 6w of E/EMS, the percentage of slow MyHCI fibers was lower than in controls in the NE legs of SOL (88.1% vs. 98.1%, p,0.009), while the percentage of fast MyHCIIa fibers was higher in the NE legs of GA (25.7% vs. 15.8%, p50.02). The number of capillaries around fibers in the E and NE legs was lower (SOL 13% and 15%, respectively, GA 25% and 23%, respectively, p,0.05) than in controls. The overall alterations were more marked in the fast GA muscle than in the slow SOL muscle, which on the other hand showed more histopathological muscle changes. We conclude that unilateral repetitive unloaded overuse exercise via EMS causes myositis and muscle changes in fiber type proportions, fiber area and fiber capillarization not only in the exercised leg, but also in the homologous muscles in the non-exercised leg.

Journal of Rehabilitation Medicine, 2011

Acta Physiologica Scandinavica, 1994

and swelling for the exercise-induced sore vastus lateralis muscle. Acra Physiol Scand 152, 265-277. This study investigated changes in intramuscular fluid pressure (IMP), torque and swelling related to delayed onset muscle soreness (DOMS) of the vastus lateralis muscle. IMP was measured via catheterization in the unstretched (0", full extension) and stretched (90" of knee flexion) muscle at rest; then IMP and knee extension torque were determined during maximal contractions pre and 2 d after (post) repetitive eccentric activity in one leg for eight male subjects. DOMS of the vastus lateralis muscle was associated with a significant elevation in IMP at rest as indicated by pre (0": 5.4 mmHg, 90":80 mmHg) and post (0":8.4 mmHg, 90": 13.2 mmHg) comparisons ( P = 0.02). Soreness symptoms were aggravated when the muscle was stretched and this was accompanied by a significantly higher post IMP at 90" vs. 0" ( P = 0.01). During maximal contractions, peak torque declined by 1596 relative to pre and peak IMP declined by 26%; DOMS symptoms, however, were most severe during this manoeuvre. Biopsies from the sore vastus lateralis muscle revealed significantly larger fibre areas for all fibre types as compared with contralateral controls ( P < 0.01); however, no differences were detected for extracellular volume percent comparisons. This study shows that DOMS of the vastus lateralis muscle is associated with extensive intracellular swelling and with elevated IMP. In line with previous studies, fibre swelling may be a common subsequence to repetitive eccentric activity; the ability of IMP measurements to detect this swelling at rest and during various manoeuvres for other muscles may depend on compartmental compliance.

Internal Medicine Journal, 2013

Patients with muscle disorders can present a diagnostic challenge to physicians because of the different ways they can present and the large number of different underlying causes. Recognition of the 'myopathic phenotype' coupled with investigations usually including electrodiagnostic and histological investigations have been essential for diagnosing the underlying cause of a myopathy. Despite these standard investigations, some patients can remain undiagnosed. New tests including more specific antibody tests for immune-mediated myopathies and the introduction of next-generation sequencing promise to revolutionise diagnostic approaches for immune and inherited myopathies, but clinical expertise remains essential to choose the most appropriate tests and interpret the results. The aim of this review is to provide an overview of the different presentations to the neuromuscular clinic and the latest investigations that can be helpful in the diagnosis of muscle disorders.

Medicine & Science in Sports & Exercise, 2001

Purpose: There have been conflicting reports of muscle fiber type changes in patients with peripheral arterial disease (PAD). The purpose of this study was to examine the myosin heavy chain (MHC) expression as well as histochemical changes in the gastrocnemius muscle in patients with symptomatic PAD. Methods: Needle biopsy specimens were obtained from the medial gastrocnemius of 14 subjects with PAD (mean age (Ϯ SD), 69.7 Ϯ 4.8 yr) and eight activity-matched control subjects (mean age, 65.1 Ϯ 6.6 yr). Ankle-brachial index was assessed using Doppler ultrasound to determine the hemodynamic status of the patients, and maximal walking performance was determined during a graded treadmill test. Expression of MHC isoforms was determined by SDS-PAGE. Results: The proportion of MHC I was significantly smaller in PAD than in the controls (45.6 Ϯ 9.1% vs 58.8 Ϯ 15.0%). The proportion of MHC IIx was also larger in the subjects with PAD compared with the controls (22.9 Ϯ 9.1% vs 16.0 Ϯ 11.3%). In addition, there was a significant decrease in the cross-sectional area of the type I and type IIA fibers in the subjects with PAD as well as enhanced capillary density. Conclusion: This study showed a significant modification in the expression of MHC isoforms and muscle fiber type in the gastrocnemius in patients with symptomatic PAD. These results suggest that muscle ischemia resulting from PAD is an important factor in causing the adaptations in the contractile apparatus of the muscle.

Revista Brasileira de Fisioterapia, 2008

Muscular strength production may be impaired in myopathic patients. Myopathies represent a heterogeneous group of diseases with distinct clinical and morphological characteristics. It has been hypothesized that functional performance fi ndings may be related to the predominant fi ber type expressed in the muscle analyzed. Objective: To correlate the proportion of type 2 fi bers in the biceps brachii muscles of subjects with a clinical hypothesis of myopathy with their peak isometric and isokinetic torque during elbow fl exion. Method: Seven subjects with a clinical hypothesis of myopathy participated in this study: four females of mean age 37 years (sd = 9), weight 73kg (sd= 26) and height 155cm (sd= 6); and three males of mean age 39 years (sd= 1), weight 88kg (sd= 5) and height 172cm (sd= 4). The muscle fi ber proportion was analyzed using the mATPase technique. One month after taking biopsies, the subjects performed concentric isometric and isokinetic strength tests for elbow fl exion and extension using an isokinetic dynamometer. The isometric and isokinetic peak torques at 90°s-¹ and 180°s-¹ were evaluated and the relative 90° (RT90) and 180° (RT180) torques were calculated. Spearman's correlation (r) was used for statistical analyses. Results: The proportion of type 2 fi bers correlated positively with RT180 (r= 0.89, p= 0.01), and there was a moderate correlation with RT90 (r= 0.75, p= 0.05). Conclusions: The results suggest that the contractile behavior of type 2 fi bers was not modifi ed in these subjects. The isokinetic dynamometer was shown to be an instrument capable of noninvasively evaluating muscle fi ber type predominance.

Journal of Hand Therapy, 1997

Journal of Neurology, Neurosurgery & Psychiatry, 1996

Journal of Applied Physiology, 2008

SP. Evidence of skeletal muscle damage following electrically stimulated isometric muscle contractions in humans. It is unknown whether muscle damage at the level of the sarcomere can be induced without lengthening contractions. To investigate this, we designed a study where seven young, healthy men underwent 30 min of repeated electrical stimulated contraction of m. gastrocnemius medialis, with the ankle and leg locked in a fixed position. Two muscle biopsies were collected 48 h later: one from the stimulated muscle and one from the contralateral leg as a control. The biopsies were analyzed immunohistochemically for inflammatory cell infiltration and intermediate filament disruption. Ultrastructural changes at the level of the z-lines were investigated by transmission electron microscopy. Blood samples were collected for measurement of creatine kinase activity, and muscle soreness was assessed in the days following stimulation. The biopsies from the stimulated muscle revealed macrophage infiltration and desmin-negative staining in a small percentage of myofibers in five and four individuals, respectively. z-Line disruption was evident at varying magnitudes in all subjects and displayed a trend toward a positive correlation (r ϭ 0.73, P ϭ 0.0663) with the force produced by stimulation. Increased muscle soreness in all subjects, combined with a significant increase in creatine kinase activity (P Ͻ 0.05), is indirectly suggestive of muscle damage, and the novel findings of the present study, i.e., 1) macrophages infiltration, 2) lack of desmin staining, and 3) z-line disruption, provide direct evidence of damage at the myofiber and sarcomere levels. These data support the hypothesis that muscle damage at the level of the sarcomere can be induced without lengthening muscle contractions.