Postexercise cold water immersion modulates skeletal muscle PGC-1α mRNA expression in immersed and nonimmersed limbs: evidence of systemic regulation

Abstract

Mechanisms mediating postexercise cold-induced increases in PGC-1α gene expression in human skeletal muscle are yet to be fully elucidated but may involve local cooling effects on AMPK and p38 MAPK-related signaling and/or increased systemic β-adrenergic stimulation. Therefore, we aimed to examine whether postexercise cold water immersion enhancement of PGC-1α mRNA is mediated through local or systemic mechanisms. Ten subjects completed acute cycling (8 × 5 min at ~80% peak power output) followed by seated-rest (CON) or single-leg cold water immersion (CWI; 10 min, 8°C). Muscle biopsies were obtained preexercise, postexercise, and 3 h postexercise from a single limb in the CON condition but from both limbs in CWI [thereby providing tissue from a CWI and nonimmersed limb (NOT)]. Muscle temperature decreased up to 2 h postexercise following CWI (-5°C) in the immersed limb, with lesser changes observed in CON and NOT (-3°C, < 0.05). No differences between limbs were observed in p38 MAPK phosphorylation at any time point ( < 0.05), whereas a significant interaction effect was present for AMPK phosphorylation ( = 0.031). Exercise (CON) increased gene expression of PGC-1α 3 h postexercise (~5-fold, < 0.001). CWI augmented PGC-1α expression above CON in both the immersed (CWI; ~9-fold, = 0.003) and NOT limbs (~12-fold, = 0.001). Plasma normetanephrine concentration was higher in CWI vs. CON immediately postimmersion (860 vs. 665 pmol/l, = 0.034). We report for the first time that local cooling of the immersed limb evokes transcriptional control of PGC-1α in the nonimmersed limb, suggesting increased systemic β-adrenergic activation of AMPK may mediate, in part, postexercise cold induction of PGC-1α mRNA. We report for the first time that postexercise cold water immersion of one limb also enhances PGC-1α expression in a contralateral, nonimmersed limb. We suggest that increased systemic β-adrenergic stimulation, and not localized cooling per se, exerts regulatory effects on local signaling cascades, thereby modulating PGC-1α expression. Therefore, these data have important implications for research designs that adopt contralateral, nonimmersed limbs as a control condition while also increasing our understanding of the potential mechanisms underpinning cold-mediated PGC-1α responses.

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

“…Further bi‐lateral muscle biopsies occurred immediately after exercise and 3 h post‐exercise in line with previous research (Allan et al. ; Bartlett et al. ; Ihsan et al.…”

“…), an effect that is likely regulated systemically (via β‐adrenergic activation of local cell signaling pathways), as opposed to local cooling effects per se (Allan et al. ). In accordance with the acute effects of CWI, chronic application of the CWI stimulus in response to consecutive training sessions up‐regulates chronic markers of training adaptations such as lipid enzyme activity and oxidative enzyme protein content (Ihsan et al.…”

Cold water immersion: kill or cure?

“…Allan et al . () have presented similar evidence for increased PGC‐1α expression with leg CWI, but also demonstrated increased PGC‐1α in the non‐immersed leg (relative to control conditions), suggesting that this is a systemic response to CWI, possibly as a consequence of β‐adrenergic activation of AMP‐activated protein kinase (AMPK).…”

Postexercise cooling impairs muscle protein synthesis rates in recreational athletes

“…; Allan et al . ). However, it is important to note that not all studies show beneficial effects of CWI on markers of postexercise recovery (Paddon‐Jones & Quigley, ; Goodall & Howatson, ; Versey et al .…”