### Voice Onset Time in Vocal Hyperfunction  
Few studies have applied VOT as an acoustic parameter to investigate voicing onset in patients with VH [28; 29; 30; 31]. Three investigated patients with PVH associated with vocal nodules were compared with a control group in [28; 29; 30]. Two studies reported a shortening in VOT, but found no significant relation between PVH and VOT [28; 30]. In opposition, the other of these works found elongated VOT [29].  
Following the perspective that VOT should be shortened in VH, [PERSON] et al. (2020) [31] compared the voiceless stop production of two groups, 32 women with VH (21 with NPVH and 11 with PVH) and 32 vocally healthy women. In their study, VOT did not distinguish between the groups. A significantly shortened VOT was found only in a subset of women with VH who also had moderate perceptual dysphonia. The authors concluded that the increase in laryngeal muscle tension, as supposed in PVH conditions, may not impact VOT in a consistent way.  
A relationship between VOT and VQ was consistently pointed out in two studies [30; 31]. [PERSON] et al. (2022) [30] compared cepstral peak prominence (CPP) and VOT measurements (mean and variability) in stop voiceless production by children with and without vocal fold nodules during the production of Consensus Auditory-Perceptual Evaluation of Voice (CAPE-V) sentences. The authors found a strong positive correlation between CPP and the variability in VOT values for the vocal nodule group and concluded that the more dysphonic voices were, the more variable VOT measurements were.  
It remains unclear how the VH condition influences VOT duration. [PERSON] et al. (2015) [32] described increases in laryngeal muscle tension in both NPVH and PVH, despite their different vocal fold states. In addition, structural laryngeal pathologies may imply differences in vocal fold mass and stiffness, which could impose adaptations in aerodynamic and myoelastic forces and delay voice onset. Findings that VOT decreases as _f_o increases in healthy voices support the argument that VOT should decrease when laryngeal muscle tension rises [10; 33].  
In this context, it is important to highlight that increased vocal amplitude (SPL) has been associated with higher laryngeal muscle tonus. Indeed, SPL has been shown to influence measurable VQ in several aspects, with improved acoustic measurement results for jitter, harmonics-to-noise-ratio (HNR), and cepstral peak prominence (CPPS) in both vocally healthy and disordered individuals [34; 35] in higher speaking voice intensity levels. Even though it is possible that speaking SPL may affect VOT, this relation was not explored in any of the VOT studies addressing individuals with VH.  
In this study, we aim to explore the potential of VOT as an indicator for VH and VQ. Specifically, we investigate whether VH condition and VQ impact the onset of voicing by addressing the followings research questions:  
1. Does the VH condition influence VOT, _f_o, and speaking voice intensity?
2. Is there a relationship between vocal quality, VOT, _f_o, and speaking voice intensity?
3. Does the phonetic environment influence VOT, _f_o, and speaking voice intensity?