Exercise Training-Enhanced Lipolytic Potency to Catecholamine Depends on the Time of the Day

Int J Mol Sci. 2020 Sep 21;21(18):6920. doi: 10.3390/ijms21186920.

Abstract

Exercise training is well known to enhance adipocyte lipolysis in response to hormone challenge. However, the existence of a relationship between the timing of exercise training and its effect on adipocyte lipolysis is unknown. To clarify this issue, Wistar rats were run on a treadmill for 9 weeks in either the early part (E-EX) or late part of the active phase (L-EX). L-EX rats exhibited greater isoproterenol-stimulated lipolysis expressed as fold induction over basal lipolysis, with greater protein expression levels of hormone-sensitive lipase (HSL) phosphorylated at Ser 660 compared to E-EX rats. Furthermore, we discovered that Brain and muscle Arnt-like (BMAL)1 protein can associate directly with several protein kinase A (PKA) regulatory units (RIα, RIβ, and RIIβ) of protein kinase, its anchoring protein (AKAP)150, and HSL, and that the association of BMAL1 with the regulatory subunits of PKA, AKAP150, and HSL was greater in L-EX than in E-EX rats. In contrast, comparison between E-EX and their counterpart sedentary control rats showed a greater co-immunoprecipitation only between BMAL1 and ATGL. Thus, both E-EX and L-EX showed an enhanced lipolytic response to isoproterenol, but the mechanisms underlying exercise training-enhanced lipolytic response to isoproterenol were different in each group.

Keywords: adipocyte; circadian rhythm; exercise training; lipolysis; timing of exercise.

MeSH terms

  • A Kinase Anchor Proteins / metabolism
  • Animals
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Isoproterenol / pharmacology*
  • Lipolysis / drug effects*
  • Male
  • Phosphorylation / drug effects
  • Physical Conditioning, Animal*
  • Rats
  • Rats, Wistar
  • Sterol Esterase / metabolism*

Substances

  • A Kinase Anchor Proteins
  • Akap5 protein, rat
  • Cyclic AMP-Dependent Protein Kinases
  • Sterol Esterase
  • Isoproterenol