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Financiado en parte por Gatorade Sports Science Institute

Fish oil supplementation suppresses resistance exercise and feeding-induced increases in anabolic signaling without affecting myofibrillar protein synthesis in young men

McGlory C, Wardle SL, Macnaughton LS, Witard OC, Scott F, Dick J, Bell JG, Phillips SM, Galloway SD, Hamilton DL, Tipton KD

Physiological reports · 74 citas

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Financiado por la industria

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Cómo se estudió

Diseño
Ensayo controlado aleatorizado (indexado por PubMed)
Estudiado en
Personas
Resultado principal
Marcadores de salud y funcionamiento

Quién lo pagó

Financiación
Financiado por la industria
Empresa
Gatorade Sports Science Institute
Sin clasificar
Sporting Chance Initiative

Según 2 financiadores declarados y la declaración de financiación del texto completo.

Publicación

Publicado
2016-03-01 · Physiol Rep · vol. 4 · número 6 · pág. e12715
Editorial
Wiley
Citado
105 citas · más que el 97% de estudios similares · 5.9× el promedio de su campo
Impacto
Entre el 10 % más citado de su campo
Referencias
30 trabajos
Acceso
Acceso abierto (revista) · CC-BY
Áreas de investigación
Muscle metabolism and nutrition · Sports Performance and Training · Cardiovascular and exercise physiology
Palabras clave
Anabolism, Ingestion, Endocrinology, Internal medicine, Medicine, Fish oil, Skeletal muscle, Biology, Fish <Actinopterygii>
MeSH
myofibrils, muscle, skeletal, humans, ribosomal protein s6 kinases, 70-kda, phospholipids, fish oils, muscle proteins, dietary proteins, anabolic agents, biopsy, treatment outcome, signal transduction, protein biosynthesis, phosphorylation, time factors, dietary supplements, scotland, male, proto-oncogene proteins c-akt, resistance training, amp-activated protein kinases, young adult

11 autores

  • Chris McGlory🇬🇧🇨🇦 · autor de correspondenciaUniversity of Stirling; McMaster University
  • Sophie Louise Wardle🇬🇧University of Stirling
  • Lindsay S. Macnaughton🇬🇧University of Stirling
  • Oliver C. Witard🇬🇧University of Stirling
  • Fraser Scott🇬🇧University of Stirling
  • James Dick🇬🇧University of Stirling
  • John Gordon Bell🇬🇧University of Stirling
  • Stuart M. Phillips🇨🇦McMaster University
  • Stuart D. R. Galloway🇬🇧University of Stirling
  • David Lee Hamilton🇬🇧University of Stirling
  • Kevin D. Tipton🇬🇧University of Stirling

Resumen

El texto original del estudio, en el idioma en que se publicó.

Fish oil (FO) supplementation potentiates muscle protein synthesis (MPS) in response to a hyperaminoacidemic-hyperinsulinemic infusion. Whether FO supplementation potentiates MPS in response to protein ingestion or when protein ingestion is combined with resistance exercise (RE) remains unknown. In a randomized, parallel group design, 20 healthy males were randomized to receive 5 g/day of either FO or coconut oil control (CO) for 8 weeks. After supplementation, participants performed a bout of unilateral RE followed by ingestion of 30 g of whey protein. Skeletal muscle biopsies were obtained before and after supplementation for assessment of muscle lipid composition and relevant protein kinase activities. Infusion of L-[ring-(13)C6] phenylalanine was used to measure basal myofibrillar MP Sat rest (REST), in a nonexercised leg following protein ingestion (FED) and following RE and protein ingestion (FEDEX).MPS was significantly elevated above REST during FEDEX in both the FO and CO groups, but there was no effect of supplementation. There was a significant increase in MPS in both groups above REST during FED but no effect of supplementation. Supplementation significantly decreased pan PKB activity at RESTin the FO group but not the CO group. There was a significant increase from REST at post-RE for PKB and AMPKα2 activity in the CO group but not in the FO group. In FEDEX, there was a significant increase in p70S6K1 activity from REST at 3 h in the CO group only. These data highlight that 8 weeks of FO supplementation alters kinase signaling activity in response to RE plus protein ingestion without influencing MPS.

Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).

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