Despite its widespread use in post-exercise recovery (Broatch et al., 2014), debate currently exists surrounding the merit of cold-water immersion (CWI) in athletic training regimes. Short-term improvements in recovery from exercise may be thwarted by unfavourable long-term skeletal muscle adaptations (Yamane et al., 2006). The aim of this study was to investigate the underlying molecular mechanisms by which CWI may alter the signalling pathways associated with mitochondrial biogenesis following an acute bout of high-intensity interval exercise.
Nineteen males (mean ± SD; age 24 ± 6 y; V̇O2peak 46.5 ± 8.1 mL•kg-1•min-1) performed an acute high-intensity interval training (HIT) bout, comprising 4 × 30s all-out efforts on a cycle ergometer, immediately followed by one of two 15 min recovery conditions: CWI (10.3 ± 0.2°C) or a passive control at ambient room temperature (CON; 23 ± 0.1°C). Muscle biopsies (vastus lateralis) were obtained pre-exercise, post-recovery and 3 h post-recovery to determine the acute molecular signalling response following HIT and CWI. Phosphorylation (p-) of p38 MAPKThr180/182 (3.0 ± 0.9 vs 2.4 ± 0.6), AMPKThr172 (2.7 ± 0.8 vs 5.5 ± 1.6) and p53Ser15 (1.9 ± 0.4 vs 3.6 ± 1.0) increased immediately post-recovery (P < 0.05) in CON and CWI, respectively. p-p38 MAPK returned to basal levels by 3 hours post-recovery, whereas p-AMPK (2.3 ± 0.5 vs 6.5 ± 2.6) and p-p53 (1.6 ± 0.3 vs 4.8 ± 1.5) remained significantly elevated for both conditions (P < 0.05). When compared with CON, CWI resulted in larger increases in p-p53 (ES = 0.92, p = 0.058) and the content of its upstream regulator PHF20 (P < 0.05) immediately post-recovery and 3 h post-recovery (Figure).
Total PHF20 protein and phosphorylation of p53Ser15 immediately pre-exercise (Pre), post-recovery (Post), and 3 h post recovery (3h) for CON (open bars) and CWI (closed bars) conditios. *Significant difference from pre-exercise (P < 0.05). **Significant difference from CON. #Large effect (ES > 0.8) from CON. Data are presented as mean ± S.E.M.
We provide novel data demonstrating that post-exercise CWI alters acute molecular signalling pathways associated with mitochondrial biogenesis. Recently implicated as an important regulator of mitochondrial function (Saleem et al., 2011), p53 activation following CWI may serve as a novel and potent stimulus by which to enhance contraction-induced mitochondrial biogenesis. Our findings are consistent with reports of post-exercise CWI increasing the expression of peroxisome proliferator-activated receptor gamma (PPARγ) coactivator 1-alpha (PGC-1α) (Ihsan et al., 2014). The mechanisms by which increases in PHF20 and p53occur following CWI are currently unknown, but may be related to the cellular stress imposed by a hypothermic shock and subsequent rewarming.
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