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Endurance training attenuates the decrease in skeletal muscle malonyl-CoA with exercise

C A Hutber1, B B Rasmussen, W W Winder

  • 1Zoology Department, Brigham Young University, Provo, Utah 84602, USA.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|February 14, 1998
PubMed
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Endurance training reduces the exercise-induced drop in muscle malonyl-CoA, contrary to expectations. This finding impacts understanding of fatty acid metabolism regulation during prolonged exercise in trained individuals.

Area of Science:

  • Exercise Physiology
  • Biochemistry
  • Metabolic Regulation

Background:

  • Muscle malonyl-CoA is believed to regulate fatty acid metabolism by inhibiting carnitine palmitoyltransferase 1.
  • Endurance training enhances muscle reliance on fatty acids for energy.
  • During exercise, malonyl-CoA levels typically decrease in non-trained muscle.

Purpose of the Study:

  • To investigate if trained muscle exhibits a greater decline in malonyl-CoA during exercise compared to non-trained muscle.
  • To determine the effect of endurance training on malonyl-CoA regulation during prolonged submaximal exercise.
  • To understand the implications for fatty acid oxidation in trained muscle.

Main Methods:

  • Rats underwent 6-10 weeks of endurance training or treadmill habituation.

Related Experiment Videos

  • Animals were exercised at a 15% grade at 21 m/min for 5, 20, or 60 minutes.
  • Muscle malonyl-CoA levels and acetyl-CoA carboxylase regulation were analyzed at rest and during exercise.

    • Main Results:

    • Contrary to hypothesis, endurance training attenuated the exercise-induced decrease in malonyl-CoA.
    • The decline in malonyl-CoA was less pronounced in trained muscle compared to non-trained muscle.
    • Training prevented the exercise-induced increase in the citrate activation constant for acetyl-CoA carboxylase.

    Conclusions:

    • Endurance training alters the regulation of muscle malonyl-CoA during prolonged exercise.
    • The reduced decline in malonyl-CoA in trained muscle may influence fatty acid oxidation regulation.
    • Findings challenge the initial hypothesis regarding malonyl-CoA's role in exercise adaptation.