Rebuttal from Michael B. Reid, Andrew R. Judge and Sue C. Bodine.
Rebuttal from Michael B. Reid, Andrew R. Judge and Sue C. Bodine.
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Michael B. Reid、Andrew R. Judge 和 Sue C. Bodine 的反驳。
DOI:
10.1113/jphysiol.2014.284398
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发表时间:
2014
期刊:
影响因子:
--
通讯作者:
Bodine,SueC
中科院分区:
文献类型:
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作者:
Reid,MichaelB;Judge,AndrewR;Bodine,SueC
The arguments put forward by Phillips and McGlory do not take into consideration advances in the field over the past 5 years. These new discoveries have provided critical information on disuse atrophy in both human and rodent muscle. They also call into question key elements of our opponents’ reasoning. The assertion that disuse atrophy largely reflects a decline in protein synthesis is based solely on data from human vastus lateralis muscle. Recent studies demonstrate the limitations of this approach. For example, during cast immobilization, disuse atrophy occurs in a variety of leg muscles at least 2 weeks before significant atrophy is detectable in vastus lateralis (Psatha et al. 2012), suggesting the response of vastus lateralis is delayed relative to other muscles. New data also show that atrophy of vastus lateralis is non-uniform, affecting some regions more than others (Miokovic et al. 2012). Such confounding variables preclude the use of localized measurements in vastus lateralis, indeed any single muscle, as the sole source of information on disuse atrophy.Our opponents argue for limiting research to human vastus lateralis because ‘inherent species-specific differences’ exist between rodent and human muscles. Again, a plethora of recent research has debunked this misconception. As in rodent limb muscle, new data show that human type I fibres undergo greater atrophy than human type II fibres in soleus, gastrocnemius and