Skeletal muscle fiber-type specific succinate dehydrogenase activity in cerebral palsy

Andrew M Zogby1, Sudarshan Dayanidhi2,3, Henry G Chambers2,4

  • 1School of Medicine, University of California, San Diego, California, USA.

Muscle & Nerve
|August 13, 2016
PubMed

Insights

Children with cerebral palsy (CP) have similar skeletal muscle mitochondrial oxidative capacity compared to typically developing (TD) children. This indicates that increased energy expenditure in CP is not due to impaired mitochondrial function.

Area of Science:

  • Skeletal muscle physiology
  • Mitochondrial function
  • Cerebral palsy research

Background:

  • Children with cerebral palsy (CP) demonstrate elevated energy expenditure during movement.
  • The underlying cause for this increased energy expenditure, specifically concerning skeletal muscle mitochondrial oxidative capacity, remains unclear.

Purpose of the Study:

  • To investigate and compare fiber-type specific succinate dehydrogenase (SDH) activity in children with CP versus typically developing (TD) children.
  • To determine if decrements in skeletal muscle mitochondrial oxidative capacity contribute to increased energy expenditure in children with CP.

Main Methods:

  • Biopsies of the semitendinosus muscle were obtained from children with CP and TD children (n=5 per group).
  • Succinate dehydrogenase (SDH) activity and myofiber areas were measured for type 1 and type 2A fibers.

Main Results:

  • SDH activity was approximately 35% higher in type 1 fibers compared to type 2A fibers within both groups.
  • No significant differences in SDH activity were found between children with CP and TD children.
  • Average myofiber area was 45% smaller in children with CP compared to TD children, with type 2A fibers being 32% larger than type 1 fibers exclusively in TD children.

Conclusions:

  • Skeletal muscle mitochondrial oxidative capacity, assessed by fiber-type specific SDH activity, is comparable between children with CP and TD children.
  • The findings suggest that the increased energy expenditure observed in children with CP is unlikely to be a result of impaired mitochondrial oxidative capacity.
Abstract

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