The effect of snoring on voice: A controlled study of 30

subjects

Abstract

We conducted a study to determine the prevalence of vocal symptoms in snorers. A total of 30 patients with a
history of snoring were investigated for the presence or absence of three vocal symptoms immediately after they
awoke from sleep: hoarseness, voice weakness, and other changes in voice quality. All patients were also asked
to complete a voice-related quality-of-life (V-RQOL) questionnaire. Findings were compared with those of an
age- and sex-matched control group of 30 nonsnorers. The most common vocal symptom in the snoring group
was hoarseness, which occurred in 11 patients (36.7%); voice weakness and other voice quality changes were
present in 8 snorers each (26.7%). In the control group, the most common vocal symptom was voice weakness,
which was present in 7 subjects (23.3%); 5 controls (16.7%) experienced other changes in voice quality, and 3
controls (10.0%) experienced hoarseness. The difference between the prevalence of hoarseness in the two
groups was statistically significant (p = 0.030), and the differences in voice weakness and other voice quality
changes were not. The mean V-RQOL score was 87.50 ± 26.89 in the snoring group and 96.00 ± 5.82 in the
control group-again, not a statistically significant difference. Finally, we found no association between any of
the three vocal symptoms and the prevalence of mouth breathing, the level of snoring loudness, and the mean
number of snores per minute. We conclude that snorers are more likely to experience hoarseness than are
nonsnorers.

Introduction
Snoring is frequently observed in adults-more often in men, overweight individuals, smokers,
and alcohol drinkers. Although snoring is perceived by many as an obnoxious behavior, it is
also considered a serious medical condition that affects sleep patterns and thus can have an
unfavorable impact on daily activities. For example, patients who snore more often than not
complain of tiredness after sleep and during the day. They may feel sleepy while driving and
experience mood alterations and changes in cognitive behavior. More serious medical
conditions, such as bradyarrhythmia and hypertension, have also been diagnosed in snorers.1,2
The disturbing sound is believed to originate from the vibrations of the soft tissues in the
narrowed upper respiratory passages.1,3 The site of the obstruction varies among individuals,
and some have more than one site. Various methods have been tried in order to identify
differences in the skeletal structures of the upper airway between snorers and normal
controls. These methods have included fluoroscopy, videoendoscopy, nasopharyngoscopy,
cephalometry, magnetic resonance imaging (MRI), and computed tomography.4-7 The most
common narrowing sites reported in the literature are the oropharynx, hypopharynx, and
larynx. Nasal obstruction and an increase in nasal resistance in the recumbent position also
play an important role in snoring, both with and without apnea.
Differences between snorers and nonsnorers in the components of the lateral pharyngeal
walls, in the thickness of the parapharyngeal muscles, and in the narrowing of the
oropharyngeal air column have been reported by Ozturk et al.8 Moreover, anatomic laryngeal
changes, such as an elongated epiglottis and a redundancy in its structure, have been
described by Maurer et al.9

Despite our awareness that known variations in anatomic sites play a critical role in the
modulation of the vocal signal, no study of the prevalence of vocal symptoms in snorers has
been previously published in the literature as far as we know. In this article, we describe our
comparison of the prevalence of hoarseness, voice weakness, and other changes in voice
quality between snorers and a control group of nonsnorers. We also compared voice-related
quality-of-life (V-RQOL) scores, and we looked for associations between each of the three
vocal symptoms and the prevalence of mouth breathing, the level of snoring loudness, and the
number of snores per minute.

Patients and methods

A total of 30 patients who had been admitted to the sleep laboratory at the American
University of Beirut Medical Center for investigation of snoring were invited to participate in
this study. A group of 30 age- and sex-matched nonsnorers was selected to serve as controls.
In addition to demographic data, we obtained information on smoking and mouth breathing.
Information on the level of snoring loudness and the number of snores per minute was
retrieved from sleep laboratory records. The level of snoring loudness for each patient was
classified into one of three categories: extremely loud, moderately loud, or not loud.

In addition, all participants were asked about the presence or absence of three vocal
symptoms immediately after they awoke from sleep: hoarseness, defined as roughness in the
voice; voice weakness, defined as an inability to talk for long or to project the voice; and
other changes in voice quality, such as alterations in pitch or loudness. Finally, all participants
completed the V-RQOL questionnaire. The V-RQOL questionnaire, which was developed by
Hogikyan and Sethuraman10 at the University of Michigan, is a self-administered instrument
that subjectively measures the burden posed by a voice disorder. It is made up of 10 questions
divided to two categories: physical (6 questions) and social-emotional (4 questions). Scores
range from 0 (worst possible V-RQOL) to 100. We considered scores of 75 or more to
be excellent, scores from 50 to 74 as good, scores from 25 to 49 as okay, and scores less than
25 as poor.

Frequencies, means, and standard deviations were used to describe the results. Outliers were
detected by means of a box plot. To assess differences in vocal symptoms, the independent
samples t test and the chi-square test were used for continuous and categorical variables,
respectively. A p value of <0.05 was considered significant. Associations between vocal
symptoms, mouth breathing, snoring loudness, and the number of snores per minute were
computed. All analyses were performed with the Statistical Package for the Social Sciences
software (v. 17; SPSS; Chicago).

Institutional Review Board approval was obtained.

Results

Demographic data. The mean age of the snorers was 50.97 ± 11.27 years, and the male-to-
female ratio was 2:1 (table 1). Eight (26.7%) of the snorers were smokers, and 17 (56.7%)
were mouth breathers. Snoring was classified as extremely loud in 15 snorers (50.0%),
moderately loud in 8 (26.7%), and not loud in 7 (23.3%). The mean number of snores per
minute was 2.30 ± 1.41.

Table 1. Baseline characteristics in the two groups

 Snorers (n = 30) Controls (n = 30)

Mean age (yr) 50.97 ± 11.27 47.33 ± 11.58

Sex, n (%)

Men 20 (66.7) 20 (66.7)

Women 10 (33.3) 10 (33.3)

Smoking, n (%)

Yes 8 (26.7) 14 (46.7)

No 22 (73.3) 16 (53.3)

Mouth breathing, n (%)

Yes 17 (56.7) 2 (6.7)

No 13 (43.3) 28 (93.3)

Loudness level, n (%) N/A

Extremely loud 15 (50.0)

Moderately loud 8 (26.7)

 Snorers (n = 30) Controls (n = 30)

Not loud 7 (23.3)

Mean number of snores per minute 2.30 ± 1.41 N/A

Vocal symptoms. The most common vocal symptom in the snoring group was hoarseness,
which was present in 11 patients (36.7%); voice weakness and other voice quality changes
were present in 8 snorers each (26.7%). In the control group, the most common vocal
symptom was voice weakness, which was present in 7 subjects (23.3%); other changes in
voice quality were present in 5 controls (16.7%), and hoarseness was present in 3 controls
(10%). The only statistically significant difference in vocal symptoms between the two
groups was in the prevalence of hoarseness (p = 0.030) (table 2).

Table 2. Comparisons of vocal symptoms and V-RQOL scores in the two groups

Snorers n (%) Controls n (%) p Value

Hoarseness 0.030

Yes 11 (36.7) 3 (10.0)

No 19 (63.3) 27 (90.0)

Voice weakness >0.999

Yes 8 (26.7) 7 (23.3)

No 22 (73.3) 23 (76.7)

Other changes in voice quality 0.532

 Snorers n (%) Controls n (%) p Value

Yes 8 (26.7) 5 (16.7)

No 22 (73.3) 25 (83.3)

Mean V-RQOL score 87.50 ± 26.89 96.00 ± 5.82 0.096

V-RQOL. The V-RQOL scores were 87.50 ± 26.89 in the snoring group and 96.00 ± 5.82 in
the control group. The difference was not statistically significant (table 2).

Associations between vocal symptoms and mouth breathing, snoring loudness, and the
number of snores per minute. No associations were found between vocal symptoms and the
prevalence of mouth breathing (table 3), the level of snoring loudness (table 4), and the
number of snores per minute (table 5).

Table 3. Association between mouth breathing and vocal symptoms

Mouth breathing present

Yes (n = 17) No n = 13) p Value

Hoarseness, n (%) for all >0.999

Yes 6 (35.3) 5 (38.5)

No 11 (64.7) 8 (61.5)

Voice weakness 0.698

Yes 4 (23.5) 4 (30.8)

 Mouth breathing present

Yes (n = 17) No n = 13) p Value

No 13 (76.5) 9 (69.2)

Other changes in voice quality 0.698

Yes 4 (23.5) 4 (30.8)

No 13 (76.5) 9 (69.2)

Table 4. Association between snoring loudness and vocal symptoms

Level of snoring
loudness

Moderately (n = Not loud (n =

Extremely (n = 15) p Value
8) 7)

Hoarseness, n (%) for

0.785
all

Yes 6 (40.0) 2 (25.0) 3 (42.9)

No 9 (60.0) 6 (75.0) 4 (57.1)

Voice weakness >0.999

Yes 4 (26.7) 2 (25.0) 2 (28.6)

 Level of snoring
loudness

Moderately (n = Not loud (n =

Extremely (n = 15) p Value
8) 7)

No 11 (73.3) 6 (75.0) 5 (71.4)

Other changes in voice

>0.999
quality

Yes 4 (26.7) 2 (25.0) 2 (28.6)

No 11 (73.3) 6 (75.0) 5 (71.4)

Table 5. Association between the mean number of snores per minute and vocal symptoms

Number of snores per

minute

1 (n = 3 (n = 4 (n =
0 (n = 7) 2 (n = 5) pValue
0) 13) 5)

Hoarseness, n (%) for

0.062
all

Yes 4 (57.1) - 2 (40.0) 5 (38.5) 0

No 3 (42.9) - 3 (60.0) 8 (61.5) 5 (100)

Voice weakness 0.080

 Number of snores per
minute

1 (n = 3 (n = 4 (n =
0 (n = 7) 2 (n = 5) pValue
0) 13) 5)

Yes 3 (42.9) - 2 (40.0) 3 (23.1) 0

No 4 (57.1) - 3 (60.0) 10 (76.9) 5 (100)

Other changes in
0.080
voice quality

Yes 3 (42.9) - 2 (40.0) 3 (23.1) 0

No 4 (57.1) - 3 (60.0) 10 (76.9) 5 (100)

Discussion
Snoring arises as a result of vibration of the upper respiratory passages. Many factors are
believed to contribute to an imbalance between the airway aperture and narrowness. These
include the cross-sectional dimension of the airway, the increase in negative airway pressure,
and the nature of the upper respiratory passage dilator muscles.11,12 At the end of expiration,
the low tidal volume and/or increased muscle mass in its inactive phase will lead to a
decrease in positive pressure and a subsequent narrowing of the airway. At the early phase of
inspiration, the delay in achieving an adequate opening of a narrowed or obstructed airway
secondary to the increased negative pressure and/or the prolonged pharyngeal muscle laxity
will result in snoring sounds.13
The various sites of obstruction that have been described in the literature include the
oropharynx, hypopharynx, larynx, and nose. Analysis of snoring sounds has been used as an
acoustic clue to the level of obstruction. Low-frequency snores in the range of 5 to 136 Hz
have been attributed to pharyngeal narrowing, while high-frequency snores in the range of
260 to 330 Hz are more indicative of vocal fold involvement.14 Recent studies have focused
more on the impact of nasal resistance and the effect of pharyngeal soft-tissue components,
namely muscles and fat, on snoring and the apnea-hypopnea index.8,15 Less emphasis has
been devoted to the laryngeal anatomic variations or changes in subjects who snore or who
have sleep disorders.
The nose has always been considered the natural gateway for air despite the fact that the oral
cavity provides less resistance. The respiration of healthy individuals invariably follows the
nasal route during sleep.15 The effects of nasal obstruction and disturbed nasal breathing on
snoring and sleep remain controversial. Some studies have been faulted for heterogeneity in
design, the number of subjects, and the applied methodologies.16-19
Suratt et al observed that nasal obstruction causes only minimal disturbances on the
respiratory system during sleep in subjects with normal oropharyngeal anatomy.16 Moreover,
there seems to be no linear relationship between the degree of nasal resistance and the
severity of sleep apnea. According to Ohki et al, nasal resistance is important only during the
period before the shift to oronasal breathing occurs.17
Hudgel and Robertson reported that despite the fact that assuming the recumbent position
results in vascular engorgement of the nasal mucosa and augments the amplitude of nasal
cycle congestion, total nasal resistance does not seem to change significantly.18 On the other
hand, the same group of researchers demonstrated that transpalatal and hypopharyngeal
resistances increase dramatically during nonrapid eye movement sleep, with the inspiratory
narrowing being located at the palate and hypopharynx rather than the nose.19
The lateral wall of the upper airway is made up of two major components: the parapharyngeal
fat pad and the parapharyngeal wall. The association between fat pad concentration and air
passage dimensions has been substantiated by some researchers and refuted by others. So far,
there is no consensus that an increase in the thickness of the parapharyngeal fat pad leads to
obstruction of the air passage.13,20-24Conversely, there is no question that the thickness of the
parapharyngeal wall can result in constriction of the airway.
Research has shown that the upper respiratory passage expansion is reduced at the end of
expiration partly as a result of an increase in the thickness of the lateral pharyngeal wall.25 On
the other hand, Ozturk et al used MRIs to study the effects of pharyngeal soft-tissue
components on snoring in 56 patients and found no statistically significant difference
between snorers and controls in mean age, pterygoid muscle thickness, or pharyngeal fat pad
thickness.8 However, they did find that body mass index and average pharyngeal wall
thickness were significantly greater in the snorers and that their oropharyngeal air column
area was significantly narrower.
In some cases, an increase in the thickness of the lateral pharyngeal wall is commensurate
with the increase in muscle mass in the hyoglossus, styloglossus, palatoglossus,
palatopharyngeus, and pharyngeal constrictor muscles; these increases are linked to the need
for excessive effort to overcome the increased muscle laxity in snoring or during apnea.26
Irrespective of snoring site and the apnea-hypopnea index, the effect on voice quality of the
vibration of the oropharyngeal walls and the resultant air turbulence projected onto the vocal
folds has not been investigated. Some previous studies have examined the effect of snoring
surgery on voice and speech. For example, Akpinar et al studied 23 men to look at the effects
of a palatal implant on voice and articulation; they found no significant difference in any of
the acoustic variables and formants before and after surgery, although articulation was
affected.27 On the other hand, Mora et al reported an improvement in acoustic parameters,
nasalance scores, and V-RQOL after uvulopalatoplasty performed with the harmonic
scalpel.28

Numerous reports have been published on voice quality and acoustic findings following the
surgical treatment of snoring, but phonatory symptoms and their impact on quality of life in
snorers has not been reported.

Vocal fold oscillation is highly dependent on the rheologic properties of the anatomic
constituents of these folds. It also depends on the adhesive and cohesive forces of the vocal
fold cover while vibrating. The sol layer represents an interface between the vocal fold and
the external environment, an interface that regulates the water influx into and out of the vocal
fold. Various factors such as hydration, relative air humidity, breathing patterns, and
medication intake can affect the sol layer.29-31
Researchers at the University of Pittsburgh showed that exposure to 85 to 100% relative
humidity together with excessive hydration can reduce the phonatory threshold pressure,
especially at high frequencies.32,33 Others have shown that oral breathing for 15 minutes can
induce superficial dehydration of the trachea, bronchial airway, and the vocal folds.34 As a
result, voice changes may be reported by patients or perceived by a treating physician. The
effect is believed to be mediated by thinning of the sol layer, which plays a major role in
reducing the surface adhesiveness of the vocal folds during phonation.
In a study of air inhalation, Hemler et al found that nearly all subjects reported an unpleasant
sensation in the airway and a feeling of impaired voice production after they had inhaled
desiccated air.35 These effects occurred after only 10 minutes of inhaling dry air. The authors
also showed that perturbation parameters increase with desiccation and decrease with
humidification. Along this line of thought, the higher prevalence of vocal symptoms among
the snorers in our study-hoarseness in particular-might have been attributable in part to their
higher prevalence of mouth breathing; more than 50% of the snorers had a history of mouth
breathing, compared with less than 10% of the controls.

Another possible explanation for the significantly higher prevalence of hoarseness among the
snorers is laryngeal behavior. Finally, it is worth mentioning that the prevalence of smoking
in both the snoring and control groups in our study was rather high-26.7 and 46.7%,
respectively. Closer examination of the data reveals that among the 11 snorers with
hoarseness, only 3 (27.3%) were smokers, whereas all 3 controls (100%) with hoarseness
were smokers. This suggests that smoking was a confounding factor in our study, and it
supports the hypothesis that snoring has an adverse effect on voice.

The study by Maurer et al, which was published in 2000, revealed a new inspiratory airway
behavior in snorers.9 Most earlier investigations had focused on the soft palate and the tongue
base as major areas of obstruction, and little attention had been paid to the larynx. Maurer et
al used sleep videoendoscopy to find several laryngeal mechanisms that can be incriminated
in sleep-disordered breathing and that might have contributed to the higher prevalence of
vocal symptoms among the snorers in our study. Two of these mechanisms are epiglottic
collapse secondary to the posterior displacement of the tongue and floppiness of the epiglottic
structure.
Redundancy of the epiglottic structures can result in folding of the epiglottis and possible
irritation of the glottic and supraglottic structures. Another mechanism of laryngeal snoring is
the continuous mechanical irritation of the supraglottic tissue by vibrations of the
laryngopharyngeal tissues. Morphometric analyses by Hamans et al36 and Olofsson et
al37 demonstrated the presence of chronic inflammation of the uvula in patients with sleep-
related breathing disorders. In our study, inflammation of the vocal fold or supraglottic
tissues similar to what has been described for the soft palate is a possible explanation for the
significantly higher prevalence of hoarseness in the snorers.
Another plausible explanation is fluttering of the vocal folds resulting in glottic snoring.
Fluttering is more likely to occur in patients with impaired mobility of the vocal folds.
Fixation of a vocal fold in the median or paramedian position makes it subject to vibration or
fluttering during inspiration and expiration. There have been several reports of snoring as a
symptom in patients with vocal fold paralysis or paresis.38,39

In our study, the vocal symptoms in the snoring group were not associated with mouth
breathing, snoring loudness, or the number of snores per minute. We had anticipated that
mouth breathers would be more likely to have vocal symptoms because of the known drying
effect of mouth breathing on the vocal folds, but they did not. We also anticipated that greater
snoring loudness and a greater number of snores per minute would be associated with vocal
symptoms, but neither was the case.

On the other hand, snorers did have a worse V-RQOL score than the controls, indicating that
snoring had more of an impact on their voices. However, the difference was not statistically
significant and, in fact, the mean V-RQOL score in the snoring group fell well within the
range of excellent scores.

Our study had two limitations of note; one was the small number of subjects, and the other
was the lack of a laryngeal examination to assess the presence or absence of vocal fold
lesions and vocal fold mobility. Nevertheless, our results did clearly indicate that the snorers
had a higher prevalence of vocal symptoms, particularly hoarseness.

Our findings should be substantiated further by a study with a larger number of subjects. The
addition of fiberoptic laryngeal endoscopy during sleep will provide a better understanding of
the concept of laryngeal snoring.

In conclusion, our analysis has shown that subjects who snore are more likely to experience
hoarseness than are nonsnorers, irrespective of whether they are mouth breathers. The
presence of hoarseness, voice weakness, and other changes in voice quality seemed to have a
greater impact on the quality of life of snorers compared with nonsnoring controls. These
vocal symptoms should be addressed in a preventive manner to reduce their prevalence and
clinical implications.

From the Department of Otolaryngology-Head & Neck Surgery (Dr. Hamdan, Dr. Al-Barazi,
Dr. Kanaan, Miss Al-Tamimi, and Mrs. Sinno) and the Department of Internal Medicine (Dr.
Husari), American University of Beirut Medical Center, Beirut, Lebanon. Corresponding
author: Abdul Latif Hamdan, MD, Department of Otolaryngology-Head & Neck Surgery,
American University of Beirut, PO Box 11-0236, Beirut, Lebanon. Email:

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