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Ensayo controlado aleatorizado2014Financiación no declaradaSolo mecanismos

Effects of β-hydroxy-β-methylbutyrate free acid and cold water immersion on expression of CR3 and MIP-1β following resistance exercise

Gonzalez AM, Fragala MS, Jajtner AR, Townsend JR, Wells AJ, Beyer KS, Boone CH, Pruna GJ, Mangine GT, Bohner JD, Fukuda DH, Stout JR, Hoffman JR

American journal of physiology. Regulatory, integrative and comparative physiology · 20 citas

Etiquetas de revisión

Financiación no declaradaSolo mecanismos

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Cómo se estudió

Diseño
Ensayo controlado aleatorizado (indexado por PubMed)
Estudiado en
Personas
Resultado principal
Solo mecanismos

Quién lo pagó

Financiación
Financiación no declarada

Publicación

Publicado
2014-02-06 · Am J Physiol Regul Integr Comp Physiol · vol. 306 · número 7 · págs. R483–R489
Editorial
American Physiological Society
Citado
26 citas · más que el 88% de estudios similares · 2.5× el promedio de su campo
Referencias
49 trabajos
Acceso
Acceso abierto (copia en repositorio)
Áreas de investigación
Exercise and Physiological Responses · Muscle metabolism and nutrition · High Altitude and Hypoxia
Palabras clave
Squat, Monocyte, Internal medicine, Chemistry, CD14, Endocrinology, Receptor, Resistance training, Medicine, Andrology, Animal science, Biology, Physiology
MeSH
muscle, skeletal, monocytes, humans, water, valerates, macrophage-1 antigen, double-blind method, immersion, recovery of function, muscle contraction, time factors, adult, florida, male, chemokine ccl4, cold temperature, resistance training, young adult

13 autores

  • Adam M. Gonzalez🇺🇸University of Central Florida
  • Maren Susan Fragala🇺🇸 · autor de correspondenciaUniversity of Central Florida
  • Adam R. Jajtner🇺🇸University of Central Florida
  • Jeremy R. Townsend🇺🇸University of Central Florida
  • Adam J. Wells🇺🇸University of Central Florida
  • Kyle S. Beyer🇺🇸University of Central Florida
  • Carleigh H. Boone🇺🇸University of Central Florida
  • Gabriel J. Pruna🇺🇸University of Central Florida
  • Gerald T. Mangine🇺🇸University of Central Florida
  • Jonathan D. Bohner🇺🇸University of Central Florida
  • David Hideyoshi Fukuda🇺🇸University of Central Florida
  • Jeffrey R. Stout🇺🇸University of Central Florida
  • Jay R. Hoffman🇺🇸University of Central Florida

Resumen

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

The inflammatory response to muscle-damaging exercise requires monocyte mobilization and adhesion. Complement receptor type 3 (CR3) and macrophage inflammatory protein (MIP)-1β enables monocyte recruitment, adhesion, and subsequent infiltration into damaged muscle tissue. The purpose of this study was to examine the effects of cold water immersion (CWI) and/or β-hydroxy-β-methylbutyrate free acid (HMB-FA) on CR3 expression and MIP-1β concentration after four sets of up to 10 repetitions of squat, dead lift, and split squat exercises at 70-80% 1-repetition maximum. Thirty-nine resistance-trained men (22.2 ± 2.5 yr) were randomly divided into four groups: 1) placebo (PL), 2) HMB-FA, 3) HMB-FA-CWI, and 4) PL-CWI. The HMB-FA groups ingested 3 g/day, and CWI groups were submersed into 10-12°C water for 10 min after exercise. Blood was sampled at baseline (PRE), immediately post- (IP), 30 min post- (30P), 24 h post- (24P), and 48 h post (48P)-exercise. Circulating MIP-1β was assayed and CR3 expression on CD14+ monocytes was measured by flow cytometry. Without treatment, CR3 expression significantly elevated at 30P compared with other time points (P = 0.030-0.047). HMB-FA significantly elevated the percentage of monocytes expressing CR3 between IP and 24P (P = 0.046) and between IP and 48P (P = 0.046). No time effect was observed for MIP-1β concentration. The recovery modalities showed to attenuate the rise in CR3 following exercise. Additionally, supplementation with HMB-FA significantly elevated the percentage of monocytes expressing CR3 during recovery. Although the time course that inflammatory responses are most beneficial remains to be determined, recovery modalities may alter immune cell mobilization and adhesion mechanisms during tissue recovery.

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