Computational analysis of asymmetric thyroarytenoid and cricothyroid activation in human phonation.

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.