Cold-water immersion following sprint interval training does not alter endurance signaling pathways or training adaptations in human skeletal muscle
Broatch JR, Petersen A, Bishop DJ
American journal of physiology. Regulatory, integrative and comparative physiology · 27 citations
How it was studied
- Design
- Randomized controlled trial (indexed by PubMed)
- Studied in
- People
- Main outcome
- Health markers and function
Who paid for it
- Funding
- Independent funding
- Nonprofit
- Exercise and Sports Science Australia
Based on 1 listed funder(s).
Publication
- Published
- 2017-07-05 · Am J Physiol Regul Integr Comp Physiol · vol. 313 · issue 4 · pp. R372–R384
- Publisher
- American Physiological Society
- Cited
- 30 citations · more than 87% of similar papers · 2.1× the field average
- References
- 75 works
- Access
- Free to read
- Research areas
- Adipose Tissue and Metabolism · Cardiovascular and exercise physiology · Exercise and Physiological Responses
- Keywords
- Mitochondrial biogenesis, Sprint, Endurance training, Interval training, AMPK, Internal medicine, Endocrinology, Skeletal muscle, Medicine, High-intensity interval training, VO2 max, TFAM, Chemistry, Biology, Physical therapy, Phosphorylation, Mitochondrion, Protein kinase A, Heart rate, Biochemistry, Blood pressure
- MeSH
- muscle, skeletal, humans, body temperature, immersion, adaptation, physiological, recovery of function, signal transduction, physical endurance, adult, female, male, cold temperature, high-intensity interval training
3 authors
From AU
- James R. Broatch · correspondingVictoria University
- Aaron C. PetersenVictoria University
- David John BishopEdith Cowan University; Victoria University
Abstract
We investigated the underlying molecular mechanisms by which postexercise cold-water immersion (CWI) may alter key markers of mitochondrial biogenesis following both a single session and 6 wk of sprint interval training (SIT). Nineteen men performed a single SIT session, followed by one of two 15-min recovery conditions: cold-water immersion (10°C) or a passive room temperature control (23°C). Sixteen of these participants also completed 6 wk of SIT, each session followed immediately by their designated recovery condition. Four muscle biopsies were obtained in total, three during the single SIT session (preexercise, postrecovery, and 3 h postrecovery) and one 48 h after the last SIT session. After a single SIT session, phosphorylated (p-)AMPK, p-p38 MAPK, p-p53, and peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) mRNA were all increased (P P < 0.05). However, regular CWI had no effect on changes in these markers, consistent with the lack of response in the markers of mitochondrial biogenesis. Although these observations suggest that CWI is not detrimental to endurance adaptations following 6 wk of SIT, they question whether postexercise CWI is an effective strategy to promote mitochondrial biogenesis and improvements in endurance performance.
Abstract via Europe PMC. Copyright remains with the authors or publisher.
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