Abstract

It is well known that control of vocal frequency is determined primarily by variation in the mass and stiffness of the vocal folds and by subglottic pressure. In turn, variation in vocal fold mass and stiffness results (in part, at least) from changes in vocal fold length. But how is vocal fold lengthening accomplished physiologically? There is no question but that the major control for this action results from contraction of the cricothyroid muscle—which reduces the CT space and, hence, stretches the vocal folds. However, we are challenging the notion that cricothyroid m. action is the only (major) factor in that regard. In order to do so, the following steps were taken. (1) Mean and maximum variations in vocal fold length were calculated. (2) Estimates were obtained of laryngeal cartilage size. (3) A variety of potential laryngeal cartilage dimensions were calculated. (4) Based on these values, appropriate computer software was developed. (5) By this means, the effect of the CT mechanism on vocal fold length was tested. It was found that CT activity alone could not account for all of the lengthening observed. A complimentary mechanism then was sought. From examination of lateral radiographs, we observed that the shadows of the arytenoid cartilages appear to move posteriorly as a function of increases in f0. This apparent movement was measured on the x rays of a number of subjects. The values obtained appear to account for the balance of vocal fold elongation. The results of some EMG studies support this explanation; others do not. The relationships in question will be discussed.

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