4.4 Article

Short-term endurance training does not alter the oxidative capacity of human subcutaneous adipose tissue

Journal

EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY
Volume 109, Issue 2, Pages 307-316

Publisher

SPRINGER
DOI: 10.1007/s00421-010-1356-3

Keywords

White adipose; Brown adipose; WAT; BAT; Mitochondrial; Obesity; Adrenergic; UCP1

Funding

  1. RMIT University
  2. National Health and Medical Research Council of Australia

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Endurance training results in adaptations that enhance regulation of energy storage and expenditure at rest and during exercise. While processes involved in skeletal muscle oxidative remodelling are well described, it is unknown whether oxidative capacity of human subcutaneous white adipose tissue (WAT) is modified by endurance training. Since human WAT retains rudimentary characteristics required for upregulation of oxidative function, we hypothesised that 10 days of intense endurance training would promote changes in WAT that favour an increase in oxidative capacity. Eleven untrained males (age 22 +/- A 1 years, body mass 81 +/- A 5 kg, peak oxygen uptake (VO2peak) 3.7 +/- A 0.2 l/min) undertook a 10-day endurance training protocol. Subcutaneous adipose tissue biopsies were taken from the abdomen prior to and 1 day after completion of training and analysed for fatty acid oxidative capacity, citrate synthase activity, and mitochondrial content via electron microscopy and gene expression analyses. There was a reduction in whole-body rates of carbohydrate oxidation, and concomitant increases in fat oxidation rate measured during 20-min of submaximal cycling (70% of pre-training VO2peak) and an increase in basal GLUT4 protein in skeletal muscle. Despite these training-induced adaptations, there were no changes in WAT of ex-vivo fat oxidation rate, maximal citrate synthase activity, mitochondrial volume or in selected genes involved in adipose tissue oxidative capacity. We conclude that 10 days training in previously untrained subjects results in adaptations in skeletal muscle but does not increase the oxidative capacity of WAT.

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