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 citas
Cómo se estudió
- Diseño
- Ensayo controlado aleatorizado (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Organización sin fines de lucro
- Exercise and Sports Science Australia
Según 1 financiador declarado.
Publicación
- Publicado
- 2017-07-05 · Am J Physiol Regul Integr Comp Physiol · vol. 313 · número 4 · págs. R372–R384
- Editorial
- American Physiological Society
- Citado
- 31 citas · más que el 87% de estudios similares · 3.1× el promedio de su campo
- Referencias
- 75 trabajos
- Acceso
- Lectura gratuita
- Áreas de investigación
- Adipose Tissue and Metabolism · Cardiovascular and exercise physiology · Exercise and Physiological Responses
- Palabras clave
- 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 autores
- James R. Broatch🇦🇺 · autor de correspondenciaVictoria University
- Aaron C. Petersen🇦🇺Victoria University
- David John Bishop🇦🇺Edith Cowan University; Victoria University
Resumen
El texto original del estudio, en el idioma en que se publicó.
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.
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