Claassen Wout J, van Ruijven Isabel M, van den Berg Marloes, Baelde Rianne J, Fortes Monteiro Alexcia, Balesar Rajvi M N, Hania Sylvia W, van der Peet Donald L, Weijs Peter J M, Ottenheijm Coen A C, Stapel Sandra N
Department of Physiology, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Center, Vrije Universiteit, Amsterdam, The Netherlands.
Department of Adult Intensive Care Medicine, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Center, Vrije Universiteit, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.
Intensive Care Med Exp. 2025 Jun 3;13(1):57. doi: 10.1186/s40635-025-00755-7.
Loss of muscle mass and strength is provoked by critical illness. Our primary aim was to study the development of muscle atrophy and weakness in vitro in isolated myofibers and in vivo muscle mass and in vitro muscle strength during the first week of critical illness. Furthermore, we explored how in vitro muscle strength compares to healthy controls. Finally, we studied correlations between in vitro muscle mass and strength and in vivo muscle mass in critically ill patients.
We performed a secondary analysis using data from a randomized controlled trial. We studied contractile force of single myofibers isolated from muscle biopsies around admission (day 1-3) and around 1 week after inclusion (day 8-10). Furthermore, we studied myofiber cross-sectional area (CSA), proportion of fast-twitch myofibers, bio-electrical impedance analysis-derived fat-free mass index (FFMI), ultrasound-derived quadriceps muscle layer thickness (QMLT) and diaphragm thickness. In the control group, only contractile force outcomes were available.
In total, ten ICU patients had two muscle biopsies taken. Maximum force of both fast and slow-twitch myofibers was reduced at day 8-10 compared to day 1-3, even though there were no differences in normalized force and calcium sensitivity. FFM and QMLT did not change over time, nor were there differences between groups. Compared to healthy controls, maximum force of myofibers was lower in the ICU group at day 8-10 in both slow and fast-twitch myofibers, while the calcium sensitivity of force was lower in slow-twitch myofibers. We found a significant correlation between myofiber CSA vs. FFMI (r = 0.68) and maximum force of the fast-twitch fibers vs. QMLT (r = 0.72).
During the first week of critical illness, maximum force declined over time, while no other in vitro parameters changed. We found a moderate correlation between myofiber CSA vs. FFMI and maximum force of the fast-twitch fibers vs. QMLT.
危重病会导致肌肉质量和力量的丧失。我们的主要目的是研究危重病第一周内体外分离肌纤维的肌肉萎缩和无力的发展情况,以及体内肌肉质量和体外肌肉力量。此外,我们探讨了体外肌肉力量与健康对照相比的情况。最后,我们研究了危重病患者体外肌肉质量和力量与体内肌肉质量之间的相关性。
我们使用来自一项随机对照试验的数据进行了二次分析。我们研究了入院时(第1 - 3天)和纳入后约1周(第8 - 10天)从肌肉活检中分离出的单个肌纤维的收缩力。此外,我们研究了肌纤维横截面积(CSA)、快肌纤维比例、生物电阻抗分析得出的去脂体重指数(FFMI)、超声测量的股四头肌层厚度(QMLT)和膈肌厚度。在对照组中,仅有收缩力结果可用。
总共10名ICU患者进行了两次肌肉活检。与第1 - 3天相比,第8 - 10天快肌纤维和慢肌纤维的最大力量均降低,尽管标准化力量和钙敏感性没有差异。FFM和QMLT随时间没有变化,组间也没有差异。与健康对照相比,ICU组在第8 - 10天慢肌纤维和快肌纤维的肌纤维最大力量均较低,而慢肌纤维的力量钙敏感性较低。我们发现肌纤维CSA与FFMI之间存在显著相关性(r = 0.68),快肌纤维的最大力量与QMLT之间存在显著相关性(r = 0.72)。
在危重病的第一周内,最大力量随时间下降,而其他体外参数没有变化。我们发现肌纤维CSA与FFMI之间以及快肌纤维的最大力量与QMLT之间存在中度相关性。