## 1 Introduction
These variables were chosen because they are essential for initiation and self-sustaining vocal fold oscillation at a desired fundamental frequency and intensity. Researchers have made attempts to find these relationships using electromyographic recordings in humans [22; 23; 24; 25; 26], in-vivo canine larynges experiments [27; 28; 29; 30; 31], and computational models [32; 33; 34]. However, majority of these attempts were made to identify the relationship with fundamental frequency only and to a lesser extent with vocal intensity [35; 36]. In this study, we use computational tools to extend to all the four acoustic and two postural features. Additionally, we compare the results from this study with results published in some previous studies. The earlier works of electromyography recordings in humans was done by [PERSON] (1957, 1965) [22; 23], [PERSON] et al. (1969) [24], and [PERSON] et al. (1972) [25]. [PERSON] et al. (1969) recorded the electromyography activity of three intrinsic laryngeal muscles in the regulation of fundamental frequency and vocal intensity in six subjects. The muscles studied were CT, IA, and the vocalis portion of the TA muscles. The results suggested that all three muscles were involved in regulating fundamental frequency and intensity, with \(f_{o}\) and intensity increasing with an increase in CT activation. [PERSON] et al. (1972) also found that CT plays a major role among all the five intrinsic laryngeal muscles in the control of fundamental frequency, and subglottal pressure in the control of intensity. With electromyography conducted on four subjects, [PERSON] et al., (1989) [32] found that \(f_{o}\) can both increase and decrease with increased TA activity, but only increases with CT activity. More recent studies in humans focused on intrinsic laryngeal muscle coordination during normal speech, respiration, and swallowing [37; 38; 39]. [PERSON], (2001) [38] found that TA and LCA activity decreased after initial burst preceding phonation onset, while the IA sustained glottis position during phonation. Animal model studies on muscle activations predominantly focused on amines because their vocal fold physiology is close to that of humans. Earlier in vivo canine model studies used electrical stimulation to study the function of IA [27; 28] and PCA [29] muscles during phonation. The IA was thought to mainly control the amount of subglottic pressure available during phonation. Recent studies using in vivo canine models also used electrical stimulation but with much finer control to investigate the effect of intrinsic laryngeal muscle activation on the fundamental frequency and glottal posture [30], as well as on fundamental frequency and intensity [31]. The muscles were activated independently from threshold to maximal contraction while airflow was increased to phonation onset and beyond. It was observed that onset frequency was primarily affected by CT activation, and TA increased or decreased \(f_{o}\) and sound pressure level (SPL) under other muscle activation conditions. The LCA/IA activity maintained vocal fold adduction at higher subglottic pressure levels. Sound pressure level was highly correlated with subglottal pressure in all conditions. They also found that the same \(f_{o}\) and SPL could be achieved with a variety of muscle activation combinations, as reported earlier in [32]. Computational models have been used to study the effects of intrinsic laryngeal muscle activations on fundamental frequency and intensity. [PERSON] (1996) [33] used a simplified mathematical model of the larynx to find that \(f_{o}\) is simultaneously controlled by TA, cricothyroid pars oblique (CTO), and cricothyroid pars recta (CTR). [PERSON] and [PERSON] (2002) [34] modeled CT, TA, LCA, and PCA muscle activations along with lung pressure to control a three-mass vocal fold model. The results showed that oscillation regions in muscle activation control spaces are similar to those measured in human subjects.