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Updated: Jan 23, 2026

Muscle Function Obtained with Motion Mode Ultrasound and Surface Electromyography during Core Endurance Exercise
Published on: August 25, 2022
Low pre-exercise muscle glycogen availability offsets the effect of post-exercise cold water immersion in augmenting
Robert Allan1,2, Adam P Sharples1,3, Matthew Cocks1
1Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, UK.
Abstract:
We assessed the effects of post-exercise cold-water immersion (CWI) in modulating PGC-1α mRNA expression in response to exercise commenced with low muscle glycogen availability. In a randomized repeated-measures design, nine recreationally active males completed an acute two-legged high-intensity cycling protocol (8 × 5 min at 82.5% peak power output) followed by 10 min of two-legged post-exercise CWI (8°C) or control conditions (CON). During each trial, one limb commenced exercise with low (LOW: <300 mmol·kg-1 dw) or very low (VLOW: <150 mmol·kg-1 dw) pre-exercise glycogen concentration, achieved via completion of a one-legged glycogen depletion protocol undertaken the evening prior. Exercise increased (P < 0.05) PGC-1α mRNA at 3 h post-exercise. Very low muscle glycogen attenuated the increase in PGC-1α mRNA expression compared with the LOW limbs in both the control (CON VLOW ~3.6-fold vs. CON LOW ~5.6-fold: P = 0.023, ES 1.22 Large) and CWI conditions (CWI VLOW ~2.4-fold vs. CWI LOW ~8.0 fold: P = 0.019, ES 1.43 Large). Furthermore, PGC-1α mRNA expression in the CWI-LOW trial was not significantly different to the CON LOW limb (P = 0.281, ES 0.67 Moderate). Data demonstrate that the previously reported effects of post-exercise CWI on PGC-1α mRNA expression (as regulated systemically via β-adrenergic mediated cell signaling) are offset in those conditions in which local stressors (i.e., high-intensity exercise and low muscle glycogen availability) have already sufficiently activated the AMPK-PGC-1α signaling axis. Additionally, data suggest that commencing exercise with very low muscle glycogen availability attenuates PGC-1α signaling.
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