人类发声过程中不对称甲杓肌与环甲肌激活的计算分析

文献信息

中文摘要

背景： 喉内肌的不对称激活在人类发声过程中很常见，但其对声带振动及声学输出的影响仍不清楚。方法：在本研究中，我们采用高保真、解剖学分辨的三维计算框架，探讨甲杓肌（TA）和环甲肌（CT）的不对称激活如何调控声带应变、振动动力学及与气流相关的声学特性。结果：结果表明，TA激活是左右机械不平衡的主要来源。相比之下，由于甲状软骨的双侧解剖约束，CT不对称产生的振动不对称有限。在TA不对称条件下，增加CT激活主要调节纵向应变并增强双侧耦合。在低至中度TA不对称时，声带保持频率锁定，基频由两侧共同调制。当不对称超过临界阈值时，频率优势转向机械上更软的一侧，同步性被破坏，产生双音。增加CT激活通过提高纵向张力、重新分配机械不对称性，并在广泛的TA不对称条件下抑制频率分离，从而稳定系统。气流和声学指标遵循这些耦合驱动的趋势，不稳定的耦合与声学效率降低和气息声增加相关。结论：总之，这些发现阐明了神经肌肉控制与机械耦合如何共同塑造不对称发声。

英文摘要

Asymmetric activation of intrinsic laryngeal muscles is common in human phonation, yet its effects on vocal fold (VF) vibration and acoustic output remain unclear. In this study, we used a high-fidelity, anatomically resolved 3D computational framework to examine how asymmetric thyroarytenoid (TA) and cricothyroid (CT) activation regulates VF strain, vibratory dynamics, and flow-related acoustics. The results show that TA activation is the primary source of left-right mechanical imbalance. In contrast, CT asymmetry produces limited vibratory asymmetry due to the bilateral anatomical constraints of the thyroid cartilage. Under TA asymmetry, increasing CT activation primarily regulates longitudinal strain and strengthens bilateral coupling. With low-moderate TA asymmetry, the VFs remained frequency-locked, with fundamental frequency jointly modulated by both sides. As asymmetry increased beyond a critical threshold, frequency dominance shifted toward the mechanically softer fold and synchronization broke down, producing biphonation. Increasing CT activation stabilized the system by increasing longitudinal tension, redistributing mechanical asymmetry, and suppressing frequency divergence across a wide range of asymmetric TA conditions. Flow and acoustic measures followed these coupling-driven trends, with unstable coupling associated with reduced acoustic efficiency and breathier phonation. Together, these findings clarify how neuromuscular control and mechanical coupling jointly shape asymmetric phonation.