Key result
A patient with chronic post-exertional muscle pain exhibited abnormal muscle metabolism during exercise and a ~90% reduction in sarcoplasmic reticulum Ca2+-ATPase activity.
Why the study?
What is the underlying metabolic and enzymatic defect in a patient with verapamil-responsive exertional muscle pain syndrome?
Population
A patient with verapamil-responsive, chronic, progressive post-exertional muscle pain (n=1).
Comparison
31P Magnetic resonance spectroscopy in vivo on… vs Normal physiological responses.
Design
Case_report
Authors
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Hypothesis-generating for Ca2+-ATPase defect in verapamil-responsive myalgia; larger studies needed before clinical adoption.
Case Report (n=1)
What is the underlying metabolic and enzymatic defect in a patient with verapamil-responsive exertional muscle pain syndrome?
A patient with chronic exertional muscle pain syndrome was found to have a ~90% reduction in sarcoplasmic reticulum Ca2+-ATPase activity, suggesting a primary defect in muscle Ca2+ handling.
Taylor et al. (1988) conducted a case report in Verapamil-responsive, chronic, progressive post-exertional muscle pain (n=1). Ca2+-ATPase deficiency vs. Normal rates was evaluated on Muscle metabolism during exercise and recovery, and Ca2+-ATPase activity. A patient with chronic post-exertional muscle pain exhibited abnormal muscle metabolism during exercise and a ~90% reduction in sarcoplasmic reticulum Ca2+-ATPase activity.
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