Low pre-exercise muscle glycogen availability offsets the effect of post-exercise cold water immersion in augmenting PGC-1α gene expression

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.

Keywords: Carbohydrate; cooling; skeletal muscle; training adaptation.

Figure 1

Overview of the experimental protocol used in each trial. HIIT, High‐intensity intermittent exercise; CHO, carbohydrate; PRO, protein; CWI, cold water immersion condition; PPO, peak power output; CON, control condition; LOW, low CHO limb; VLOW, very low CHO limb.

Figure 2

Skeletal muscle glycogen content immediately pre‐ and post‐exercise and after 3 h of recovery. Biopsies were obtained from both limbs in each condition (CON or CWI) with limbs starting the day being low (LOW) or very low (VLOW) in glycogen stores. A main effect for time (P = 0.001) and condition (P = 0.008) was observed. No interaction effects were present (P > 0.05). *Significantly different from PRE. a Significantly lower than contralateral LOW limb (P < 0.05). Data are mean ± SD.

Figure 3

Rectal temperature (°C) (a), thigh skin temperature (°C) (b), and deep muscle temperature (3 cm; °C) (c) during immersion and the 3 h post‐exercise period. *Significantly different from pre‐. ^#Significantly different from CON (n = 9 skin, n = 8 rectal, muscle; mean ± SD). Shaded area represents CWI.

Figure 4

PGC‐1α mRNA 2^−ΔΔCT fold change in expression with the calibrator as preexercise and the reference gene as GAPDH (see methods for details). Values are mean ± SD. A time × condition interaction effect was observed (P = 0.034). * significantly greater than Pre‐ and Post‐Exercise (P < 0.001). ^asignificantly less than CON LOW (P < 0.05), ^bsignificantly greater than CON VLOW (P = 0.05), ^csignificantly less than CWI LOW (P = 0.019).

Figure 5

mRNA 2^−ΔΔCT fold change in expression with the calibrator as pre‐exercise and the reference gene as GAPDH (see methods for details). Values are mean ± SD.