Shahrjerdi Samira, Bahrpeyma Farid, C M Savelberg Hans H, Bagherian Seyed Ahmad, Jamshidpour Boshra
Department of Physical Therapy, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Department of Nutrition and Movement Science, Faculty of Health, Medicine and Life Sciences, Maastricht University, Maastricht, The Netherlands.
J Med Signals Sens. 2023 Mar 27;13(1):65-71. doi: 10.4103/jmss.jmss_129_21. eCollection 2023 Jan-Mar.
Type 2 diabetes mellitus (T2DM) is associated with decreased muscle force generation. The disturbed force generation process in T2DM could be attributed to either or both agonist and antagonist muscles activation. The present study aims to assess the effects of T2DM on the interaction of antagonist and agonist muscles in the knee joint.
The peak torque, root mean square (RMS) of the SEMG signals, the ratio of torque/RMS, and the interaction of antagonists and agonist muscles were compared between healthy and T2DM patients. Surface ElectroMyoGraphy (SEMG) of knee flexor and extensor muscles were recorded during concentric contraction with an isokinetic dynamometer at 60°/s in 13 T2DM and 12 healthy subjects. The independent sample -tests were used to compare diabetic and healthy subjects. The significance level was set at 0.05.
The antagonist/agonist interaction during maximal extension ( = 0.010) and flexion ( = 0.022) torques of the knee joint showed significantly lower activation of antagonist muscles in T2DM patients than in healthy subjects. Lower knee flexion (41.3%) and extension torques (49.1%) and RMS of agonist and antagonist muscles were observed in T2DM. The torque/RMS ratio ( > 0.05) showed no significant differences in T2DM and healthy subjects.
The reduced maximal knee flexor and extensor torques in T2DM are accompanied with the decreased myoelectric activity of corresponding muscles. The related mechanism could be attributed to lower values of antagonist/agonist interaction, which may point out some neural compensatory processes to preserve the functional capacity of the neuromuscular system in T2DM.
2型糖尿病(T2DM)与肌肉力量生成减少有关。T2DM中力生成过程的紊乱可能归因于主动肌和拮抗肌的激活异常或两者皆有。本研究旨在评估T2DM对膝关节拮抗肌和主动肌相互作用的影响。
比较健康受试者和T2DM患者之间的峰值扭矩、SEMG信号的均方根(RMS)、扭矩/RMS比值以及拮抗肌和主动肌的相互作用。在13名T2DM患者和12名健康受试者中,使用等速测力计以60°/s的速度进行向心收缩时,记录膝关节屈伸肌的表面肌电图(SEMG)。采用独立样本t检验比较糖尿病患者和健康受试者。显著性水平设定为0.05。
在膝关节最大伸展(P = 0.010)和屈曲(P = 0.022)扭矩时,T2DM患者拮抗肌/主动肌的相互作用显示拮抗肌的激活明显低于健康受试者。T2DM患者的膝关节屈曲(41.3%)和伸展扭矩(49.1%)以及主动肌和拮抗肌的RMS均较低。扭矩/RMS比值(P > 0.05)在T2DM患者和健康受试者之间无显著差异。
T2DM患者膝关节最大屈伸扭矩降低,同时相应肌肉的肌电活动也降低。相关机制可能归因于拮抗肌/主动肌相互作用值较低,这可能指出了一些神经代偿过程,以维持T2DM患者神经肌肉系统的功能能力。