Observations that muscle is injured as part of critical illness were made decades ago,1- 3 but the effect of this on the diaphragm4 and long-term functional disability,5 as well as an understanding of its molecular mechanism were not appreciated or research priorities until recently. The mass, strength, and metabolic function of muscle affect its role as a major reservoir of amino acids, driver of metabolic homeostasis, and consumer of energy substrates. In the context of critical illness, muscle atrophy captured by direct or indirect measurements such as frailty6 and reduced body mass index7 have all been linked to poor outcome. Simultaneously, a decrease in muscle strength can occur independently as a result of multifactorial dysregulation in different processes such as myofiber calcium sequestration and homeostasis, and uncoupling of mitochondrial-dependent pathways. Even though there may be significant overlap in molecular biologic networks that regulate both mass and contractility, process-specific pathways that play a role in determining contractility or mass may have significant and independent effects on prognosis and treatment of weakness acquired in the intensive care unit (ICU).
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