1.
[Intensive Care Unit-Acquired Weakness].
Siao, SF, Yen, YH, Yu, YF, Zong, SL, Chen, CC
Hu li za zhi The journal of nursing. 2020;(3):6-13
Abstract
Intensive care unit (ICU)-acquired weakness is a common neuromuscular complication of critical illness that is considered to be associated with prolonged duration on mechanical ventilation and systemic inflammatory response syndrome. In addition, nutrition and metabolic alternations, which are commonly seen in patients in the ICU, may further accelerate muscle wasting and increase the incidence of ICU-acquired weakness. The clinical features of ICU-acquired weakness include acute generalized muscle weakness that develops after the onset of critical illness. Diaphragmatic dysfunction, post-extubation dysphagia, and functional decline also are common in patients with ICU-acquired weakness. As the recovery of these physical functions is lengthy and difficult, a multidisciplinary team management is recommended. This mini-review was conducted to provide a scientific overview for ICU-acquired weakness, including its definition, etiology, diagnosis/screening, impacts, and potential intervention strategies. We hope that increasing the understanding of frontline staff will promote the timely planning and implementation of related screenings and interventions to enhance the functional recovery of patients receiving care in the ICU.
2.
Sarcopenia: characteristics, mechanisms and functional significance.
Narici, MV, Maffulli, N
British medical bulletin. 2010;:139-59
Abstract
Sarcopenia reflects a progressive withdrawal of anabolism and an increased catabolism, along with a reduced muscle regeneration capacity. Muscle force and power decline more than muscle dimensions: older muscle is intrinsically weak. Sarcopenic obesity (SO) among the elderly corroborates to the loss of muscle mass increasing the risk of metabolic syndrome development. Recent studies on the musculoskeletal adaptations with ageing and key papers on the mechanisms of muscle wasting, its functional repercussions and on SO are included. Neuropathic, hormonal, immunological, nutritional and physical activity factors contribute to sarcopenia. Selective fast fibre atrophy, loss of motor units and an increase in hybrid fibres are typical findings of ageing. Satellite cell number decreases reducing muscle regeneration capacity. SO promotes further muscle wasting and increases risk of metabolic syndrome development. The proportion of fast to slow fibres seems maintained in old age. In elderly humans, nuclear domain is maintained constant. Basal protein synthesis and breakdown show little changes in old age. Instead, blunting of the anabolic response to feeding and exercise and of the antiproteolytic effect of insulin is observed. Further understanding of the mechanisms of sarcopenia requires disentangling of the effects of ageing alone from those of disuse and disease. The causes of the greater anabolic resistance to feeding and exercise of elderly women need elucidating. The enhancement of muscle regeneration via satellite cell activation via the MAPK/notch molecular pathways seems particularly promising.