Muscle changes in work-related chronic myalgia.

Area of Science:

• Muscle physiology and pathology
• Occupational health
• Biochemistry

Background:

• Chronic myalgia is often linked to repetitive static loading in occupational settings.
• Understanding the underlying muscle pathology is crucial for effective treatment and prevention.

Purpose of the Study:

• To investigate the specific muscle fiber alterations and biochemical changes in individuals with chronic myalgia.
• To differentiate pathological findings between myalgic patients and healthy controls.

Main Methods:

• Muscle biopsies were obtained from the trapezius muscle of healthy subjects and patients with chronic myalgia.
• Histopathological analysis included assessment of fiber atrophy, internal nuclei, fiber splitting, and specific staining for mitochondrial damage (ragged red fibers).
• Biochemical analysis measured levels of adenosine triphosphate (ATP), adenosine diphosphate (ADP), lactate, pyruvate, glycogen, phosphoryl creatine, and total creatine.

Main Results:

• Both groups showed general muscle fiber abnormalities like atrophy and internal nuclei.
• Frequent "moth-eaten" fibers, indicating oxidative enzyme loss, were observed in both healthy and myalgic individuals.
• Pathognomonic "ragged red" fibers, indicative of mitochondrial damage, were predominantly found in myalgia patients (8/10) and confined to Type 1 fibers.
• Type 1 fiber frequency was increased in myalgia patients.
• Reduced levels of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) were noted in myalgia patients, while other metabolites remained normal.

Conclusions:

• Chronic myalgia associated with static load is linked to specific mitochondrial damage in Type 1 muscle fibers.
• Reduced ATP and ADP levels suggest impaired energy metabolism in affected muscles.
• These findings highlight the role of mitochondrial dysfunction in the pathophysiology of occupational myalgia.