Postexercise cold water immersion modulates skeletal muscle PGC-1α mRNA expression in immersed and nonimmersed limbs: evidence of systemic regulation
Allan R, Sharples AP, Close GL, Drust B, Shepherd SO, Dutton J, Morton JP, Gregson W
Journal of applied physiology (Bethesda, Md. : 1985) · 32 citas
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- Diseño
- Ensayo controlado aleatorizado (clasificado por nuestro filtro de IA)
- Estudiado en
- Personas
- Resultado principal
- Solo mecanismos
Quién lo pagó
- Financiación
- Financiación independiente
- Universidad u hospital
- Liverpool John Moores University
Según 1 financiador declarado.
Publicación
- Publicado
- 2017-05-25 · J Appl Physiol (1985) · vol. 123 · número 2 · págs. 451–459
- Editorial
- American Physiological Society
- Citado
- 36 citas · más que el 88% de estudios similares · 2.4× el promedio de su campo
- Referencias
- 48 trabajos
- Acceso
- Acceso abierto (copia en repositorio)
- Áreas de investigación
- Adipose Tissue and Metabolism · Exercise and Physiological Responses · Sports Performance and Training
- Palabras clave
- Skeletal muscle, Messenger RNA, Immersion (mathematics), Endocrinology, Internal medicine, Gene expression, Cell biology, Biology, Muscle contraction, Chemistry, Anatomy, Medicine, Gene, Biochemistry
- MeSH
- extremities, muscle, skeletal, humans, water, p38 mitogen-activated protein kinases, rna, messenger, body temperature, exercise, cross-over studies, gene expression regulation, phosphorylation, adult, male, cold temperature, peroxisome proliferator-activated receptor gamma coactivator 1-alpha
8 autores
- Robert Allan🇬🇧 · autor de correspondenciaUniversity of Lancashire; Liverpool John Moores University
- Adam Philip Sharples🇬🇧Liverpool John Moores University
- Graeme Leonard Close🇬🇧Liverpool John Moores University
- Barry Drust🇬🇧Liverpool John Moores University
- Sam O. Shepherd🇬🇧Liverpool John Moores University
- John J Dutton🇬🇧University of East Anglia; Norwich Research Park
- James Peter Morton🇬🇧Liverpool John Moores University
- Warren A. Gregson🇬🇧Liverpool John Moores University
Resumen
El texto original del estudio, en el idioma en que se publicó.
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, P P P = 0.031). Exercise (CON) increased gene expression of PGC-1α 3 h postexercise (~5-fold, P P = 0.003) and NOT limbs (~12-fold, P = 0.001). Plasma normetanephrine concentration was higher in CWI vs. CON immediately postimmersion (860 vs. 665 pmol/l, P = 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.NEW & NOTEWORTHY 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.
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