Glycogen depletion increases peroxisome proliferator activated receptor‐δ (PPAR‐δ) activity following acute exercise

Abstract

Performing exercise with low muscle glycogen has profound effects on substrate utilization and gene transcription. The aim of the present study was to examine signaling pathways potentially responsible for modulating gene transcription during exercise in a glycogen-depleted state. Methods Twenty female Wistar rats were randomly assigned to 5 experimental groups: control [CON]; normal glycogen control [NG-C]; normal glycogen exercise [NG-E]; low glycogen control [LG-C]; and low glycogen exercise [LG-E]). Results Exercise reduced muscle glycogen by 47 and 75% post exercise in the NG-E and LG-E groups respectively. The exercise protocol meant that the LG-E group began exercise with a 40% decrease in resting glycogen levels (2.1 ± 0.1 to 1.3 ± 0.3 nmol.mg.wet wt; P<0.05). Exercise in low glycogen increased AMPK α1 activity by 32% (CON 0.04 ± 0.002, LG-E 0.06 ± 0.006 Units mg/AMPK; P<0.05) and AMPK α2 activity by 147% (CON 0.03 ± 0.004, LG-E 0.07 ± 0.005 Units mg/AMPK; P<0.05). In addition to the increase in AMPK activity, ChIP analysis demonstrated increased PPAR-δ binding to the CPT1 promoter in the LG-C, LG-E, and NG-E experimental groups compared to the CON group or the NG-C groups. Discussion Our data suggests that PPAR-δ activation may contribute to the altered gene transcription previously reported during exercise in a glycogen-depleted state.