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Muscle wasting in emphysema.

W L Morrison1, J N Gibson, C Scrimgeour

  • 1Department of Physiology, University of Dundee, U.K.

Clinical Science (London, England : 1979)
|October 1, 1988
PubMed
Summary
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Muscle wasting in emphysema is primarily due to decreased muscle protein synthesis, not increased breakdown. Whole-body protein turnover also declines in these patients.

Area of Science:

  • Physiology
  • Metabolic Research
  • Pulmonary Disease

Background:

  • Emphysema is associated with muscle wasting, but the underlying mechanisms are not fully understood.
  • Identifying the specific protein balance alterations in emphysema is crucial for understanding disease progression.

Purpose of the Study:

  • To investigate arteriovenous exchanges of tyrosine and 3-methylhistidine in leg tissue to assess protein balance and myofibrillar protein breakdown in emphysema.
  • To measure whole-body protein turnover using L-[1-13C]leucine in patients with emphysema and healthy controls.

Main Methods:

  • Arteriovenous balance studies of tyrosine and 3-methylhistidine across leg tissue.
  • Measurement of whole-body protein turnover using stable isotope tracers (L-[1-13C]leucine).
  • Comparison between eight emphysema patients and 11 healthy controls in the postabsorptive state.

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Main Results:

  • Leg tyrosine efflux was significantly increased (47%) in emphysema patients compared to controls.
  • Leg 3-methylhistidine efflux, an indicator of myofibrillar protein breakdown, was not significantly altered.
  • Whole-body leucine flux was normal, but leucine oxidation was increased and protein synthesis was depressed in emphysema.

Conclusions:

  • The primary driver of muscle wasting in emphysema is a reduction in muscle protein synthesis.
  • This is accompanied by an overall decrease in whole-body protein turnover, suggesting a complex metabolic derangement.