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Postexercise phosphocreatine resynthesis is slowed in multiple sclerosis
J A Kent-Braun1, K R Sharma, R G Miller
1Department of Radiology, University of California, San Francisco.
Muscle & Nerve
|August 1, 1994
Summary
Multiple sclerosis (MS) patients show impaired skeletal muscle oxidative metabolism, evidenced by slower phosphocreatine (PCr) resynthesis after exercise. This suggests deconditioning contributes to muscle dysfunction in MS.
Area of Science:
- Neurology
- Muscle Physiology
- Biochemistry
Background:
- Multiple sclerosis (MS) is a chronic neurological disease.
- Altered skeletal muscle function is reported in MS patients.
- The underlying mechanisms, particularly oxidative metabolism, remain unclear.
Purpose of the Study:
- To investigate skeletal muscle oxidative metabolism in individuals with MS.
- To compare the rate of phosphocreatine (PCr) resynthesis after exercise between MS patients and healthy controls.
Main Methods:
- Utilized phosphorus magnetic resonance spectroscopy (31P-MRS).
- Measured PCr recovery kinetics in dorsiflexor muscles post-exercise.
- Included 13 MS patients and 8 healthy controls.
Main Results:
- No significant differences in PCr or pH decline during exercise between groups.
- Significantly prolonged PCr recovery half-time (T1/2) in MS patients (2.3 min) versus controls (1.2 min).
- Indicates slower intramuscular energy restoration in MS.
Conclusions:
- Skeletal muscle oxidative capacity is impaired in individuals with MS.
- Slowed PCr resynthesis suggests deconditioning contributes to MS-related muscle dysfunction.
- Findings highlight potential therapeutic targets for improving muscle function in MS.