Ca2+-ATPase deficiency in a patient with an exertional muscle pain syndrome. (original) (raw)

Ca2+-ATPase deficiency in a patient with an exertional muscle pain syndrome.

Loading

  1. D J Taylor,
  2. M J Brosnan,
  3. D L Arnold,
  4. P J Bore,
  5. P Styles,
  6. J Walton,
  7. G K Radda
  8. MRC Biochemical and Clinical Magnetic Resonance Unit, University of Oxford, UK.

Abstract

31P Magnetic resonance spectroscopy studies were carried out in vivo on skeletal muscle of a patient with verapamil-responsive, chronic, progressive post-exertional muscle pain. A sister suffered from a similar complaint. The results showed that the muscle: (1) decreased its high energy phosphate content more rapidly than normal during exercise, indicating either increased utilisation or decreased production of ATP; (2) acidified more rapidly than normal during exercise suggesting an increased glycolytic rate; (3) continued in some studies to acidify markedly during the first minute after exercise, indicating that glycolysis remained active into the recovery period; (4) had phosphocreatine and ADP recovery rates consistent with normal rates of oxidative phosphorylation. On the basis of these results, it was proposed that the patient suffers from a defect in Ca2+ handling in the muscle. Subsequently, direct measurement of Ca2+-ATPase activity in the sarcoplasmic reticulum fraction from a muscle biopsy sample showed that the activity of this enzyme was reduced by about 90%.

Statistics from Altmetric.com

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Read the full text or download the PDF:

Log in using your username and password

Read the full text or download the PDF:

Log in using your username and password