PMID- 24458747
OWN - NLM
STAT- MEDLINE
DCOM- 20150122
LR  - 20161125
IS  - 1522-1601 (Electronic)
IS  - 0161-7567 (Linking)
VI  - 116
IP  - 11
DP  - 2014 Jun 1
TI  - Influence of divergent exercise contraction mode and whey protein supplementation 
      on atrogin-1, MuRF1, and FOXO1/3A in human skeletal muscle.
PG  - 1491-502
LID - 10.1152/japplphysiol.00136.2013 [doi]
AB  - Knowledge from human exercise studies on regulators of muscle atrophy is lacking, 
      but it is important to understand the underlying mechanisms influencing skeletal 
      muscle protein turnover and net protein gain. This study examined the regulation 
      of muscle atrophy-related factors, including atrogin-1 and MuRF1, their upstream 
      transcription factors FOXO1 and FOXO3A and the atrogin-1 substrate eIF3-f, in 
      response to unilateral isolated eccentric (ECC) vs. concentric (CONC) exercise 
      and training. Exercise was performed with whey protein hydrolysate (WPH) or 
      isocaloric carbohydrate (CHO) supplementation. Twenty-four subjects were divided 
      into WPH and CHO groups and completed both single-bout exercise and 12 wk of 
      training. Single-bout ECC exercise decreased atrogin-1 and FOXO3A mRNA compared 
      with basal and CONC exercise, while MuRF1 mRNA was upregulated compared with 
      basal. ECC exercise downregulated FOXO1 and phospho-FOXO1 protein compared with 
      basal, and phospho-FOXO3A was downregulated compared with CONC. CONC single-bout 
      exercise mediated a greater increase in MuRF1 mRNA and increased FOXO1 mRNA 
      compared with basal and ECC. CONC exercise downregulated FOXO1, FOXO3A, and 
      eIF3-f protein compared with basal. Following training, an increase in basal 
      phospho-FOXO1 was observed. While WPH supplementation with ECC and CONC training 
      further increased muscle hypertrophy, it did not have an additional effect on 
      mRNA or protein levels of the targets measured. In conclusion, atrogin-1, MuRF1, 
      FOXO1/3A, and eIF3-f mRNA, and protein levels, are differentially regulated by 
      exercise contraction mode but not WPH supplementation combined with 
      hypertrophy-inducing training. This highlights the complexity in understanding 
      the differing roles these factors play in healthy muscle adaptation to exercise.
CI  - Copyright (c) 2014 the American Physiological Society.
FAU - Stefanetti, Renae J
AU  - Stefanetti RJ
AD  - Centre for Physical Activity and Nutrition, School of Exercise and Nutrition 
      Sciences, Deakin University, Burwood, Australia;
FAU - Lamon, Severine
AU  - Lamon S
AD  - Centre for Physical Activity and Nutrition, School of Exercise and Nutrition 
      Sciences, Deakin University, Burwood, Australia;
FAU - Rahbek, Stine K
AU  - Rahbek SK
AD  - Section of Sport Science, Department of Public Health, Aarhus University, Aarhus, 
      Denmark; and.
FAU - Farup, Jean
AU  - Farup J
AD  - Section of Sport Science, Department of Public Health, Aarhus University, Aarhus, 
      Denmark; and.
FAU - Zacharewicz, Evelyn
AU  - Zacharewicz E
AD  - Centre for Physical Activity and Nutrition, School of Exercise and Nutrition 
      Sciences, Deakin University, Burwood, Australia;
FAU - Wallace, Marita A
AU  - Wallace MA
AD  - Centre for Physical Activity and Nutrition, School of Exercise and Nutrition 
      Sciences, Deakin University, Burwood, Australia;
FAU - Vendelbo, Mikkel H
AU  - Vendelbo MH
AD  - Department of Internal Medicine and Endocrinology, Aarhus University Hospital, 
      Aarhus, Denmark.
FAU - Russell, Aaron P
AU  - Russell AP
AD  - Centre for Physical Activity and Nutrition, School of Exercise and Nutrition 
      Sciences, Deakin University, Burwood, Australia;
FAU - Vissing, Kristian
AU  - Vissing K
AD  - Section of Sport Science, Department of Public Health, Aarhus University, Aarhus, 
      Denmark; and vissing@sport.au.dk.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140123
PL  - United States
TA  - J Appl Physiol (1985)
JT  - Journal of applied physiology (Bethesda, Md. : 1985)
JID - 8502536
RN  - 0 (FOXO1 protein, human)
RN  - 0 (FOXO3 protein, human)
RN  - 0 (Forkhead Box Protein O1)
RN  - 0 (Forkhead Box Protein O3)
RN  - 0 (Forkhead Transcription Factors)
RN  - 0 (Milk Proteins)
RN  - 0 (Muscle Proteins)
RN  - 0 (Tripartite Motif Proteins)
RN  - 0 (Whey Proteins)
RN  - EC 2.3.2.27 (FBXO32 protein, human)
RN  - EC 2.3.2.27 (SKP Cullin F-Box Protein Ligases)
RN  - EC 2.3.2.27 (TRIM63 protein, human)
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
SB  - IM
MH  - Administration, Oral
MH  - Adult
MH  - Dietary Supplements
MH  - Exercise/*physiology
MH  - Forkhead Box Protein O1
MH  - Forkhead Box Protein O3
MH  - Forkhead Transcription Factors/drug effects/*metabolism
MH  - Humans
MH  - Male
MH  - Milk Proteins/*administration & dosage/pharmacokinetics
MH  - Muscle Contraction/physiology
MH  - Muscle Proteins/drug effects/*metabolism
MH  - Muscle, Skeletal/*physiology
MH  - Physical Conditioning, Human/methods
MH  - SKP Cullin F-Box Protein Ligases/drug effects/*metabolism
MH  - Tripartite Motif Proteins
MH  - Ubiquitin-Protein Ligases/drug effects/*metabolism
MH  - Whey Proteins
OTO - NOTNLM
OT  - atrophy signaling
OT  - exercise mode
OT  - strength training
OT  - whey protein supplementation
EDAT- 2014/01/25 06:00
MHDA- 2015/01/23 06:00
CRDT- 2014/01/25 06:00
PHST- 2014/01/25 06:00 [entrez]
PHST- 2014/01/25 06:00 [pubmed]
PHST- 2015/01/23 06:00 [medline]
AID - japplphysiol.00136.2013 [pii]
AID - 10.1152/japplphysiol.00136.2013 [doi]
PST - ppublish
SO  - J Appl Physiol (1985). 2014 Jun 1;116(11):1491-502. doi: 
      10.1152/japplphysiol.00136.2013. Epub 2014 Jan 23.