Abstract
Muscle disuse is often observed after injury or during periods of illness, resulting in the loss of muscle mass and strength, with sometimes debilitating consequences. Although substantial advancements have been made in determining the mechanisms responsible for the etiology of muscle disuse atrophy in rodents, only in recent years have studies of any significant number focused on reaffirming these findings in humans. In this review, we discuss the processes responsible for disuse atrophy as based on current evidence and highlight where gaps in our knowledge persist. Furthermore, given the emphasis placed on resistance exercise and nutrition as potential therapeutic countermeasures, we consider recent advancements in the study of resistance exercise and nutrition in the stimulation of muscle protein synthesis and the associated implications when devising effective treatment strategies.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 22-28 |
| Number of pages | 7 |
| Journal | Nutrition |
| Volume | 29 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jan 2013 |
| Externally published | Yes |
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Keywords
- Amino acids
- Bedrest
- Immobilization
- Muscle protein synthesis
- Ubiquitin proteasome system
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Nutrition and Dietetics
Cite this
Mechanisms responsible for disuse muscle atrophy : Potential role of protein provision and exercise as countermeasures. / Mallinson, Joanne E.; Murton, Andrew.
In: Nutrition, Vol. 29, No. 1, 01.2013, p. 22-28.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Mechanisms responsible for disuse muscle atrophy
T2 - Potential role of protein provision and exercise as countermeasures
AU - Mallinson, Joanne E.
AU - Murton, Andrew
PY - 2013/1
Y1 - 2013/1
N2 - Muscle disuse is often observed after injury or during periods of illness, resulting in the loss of muscle mass and strength, with sometimes debilitating consequences. Although substantial advancements have been made in determining the mechanisms responsible for the etiology of muscle disuse atrophy in rodents, only in recent years have studies of any significant number focused on reaffirming these findings in humans. In this review, we discuss the processes responsible for disuse atrophy as based on current evidence and highlight where gaps in our knowledge persist. Furthermore, given the emphasis placed on resistance exercise and nutrition as potential therapeutic countermeasures, we consider recent advancements in the study of resistance exercise and nutrition in the stimulation of muscle protein synthesis and the associated implications when devising effective treatment strategies.
AB - Muscle disuse is often observed after injury or during periods of illness, resulting in the loss of muscle mass and strength, with sometimes debilitating consequences. Although substantial advancements have been made in determining the mechanisms responsible for the etiology of muscle disuse atrophy in rodents, only in recent years have studies of any significant number focused on reaffirming these findings in humans. In this review, we discuss the processes responsible for disuse atrophy as based on current evidence and highlight where gaps in our knowledge persist. Furthermore, given the emphasis placed on resistance exercise and nutrition as potential therapeutic countermeasures, we consider recent advancements in the study of resistance exercise and nutrition in the stimulation of muscle protein synthesis and the associated implications when devising effective treatment strategies.
KW - Amino acids
KW - Bedrest
KW - Immobilization
KW - Muscle protein synthesis
KW - Ubiquitin proteasome system
UR - http://www.scopus.com/inward/record.url?scp=84870780979&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84870780979&partnerID=8YFLogxK
U2 - 10.1016/j.nut.2012.04.012
DO - 10.1016/j.nut.2012.04.012
M3 - Review article
C2 - 22951156
AN - SCOPUS:84870780979
VL - 29
SP - 22
EP - 28
JO - Nutrition International
JF - Nutrition International
SN - 0899-9007
IS - 1
ER -