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Sleep, Body Fatigue, and Voice
Abdul-Latif Hamdan, Robert Thayer Sataloff, and Mary J. Hawkshaw
Vocal fatigue is a broad term commonly used to describe voice impairment that develops with voice use. Kostyk and Rochet have considered vocal fatigue within a spectrum of symptoms that include specific complaints such as loss of voice, and non-specific ones such as running out of breath and throat tightness.1 Professional voice users describe vocal fatigue differently. In a study by Kitch and Oates, actors reported vocal fatigue as “increased difficulty achieving adequate voice production,” whereas singers reported it as “reduction in the pitch and dynamic range.” These descriptions of vocal fatigue, which were retrieved in this study using a questionnaire, highlight the broad nature of this complaint and the multifaceted etiology behind it.2 This chapter provides a brief review of vocal fatigue in the context of sleep deprivation and generalized body fatigue.
Vocal Fatigue Pathophysiology
Vocal fatigue has been associated with various functional and organic voice disorders, with no clear consensus on which comes first. Vocal fatigue can be a symptom of a laryngeal pathology or a prelude to the development of such pathology. Further investigation is needed to understand this problem better. Its presence in patients with normal vocal folds and hyperfunctional supraglottic behavior may be associated with improper technique or repertoire, compensation for inefficiency in the vocal apparatus, or an underlying focal or systemic disease that may not be obvious at time of presentation. Welham and Maclagan reviewing current definitions and concepts of vocal fatigue, suggested five possible mechanisms for the development of vocal fatigue. In brief these include, neuromuscular fatigue, increased vocal fold viscosity, reduced blood circulation, neuromuscular tissue strain and respiratory fatigue.3 MacArdle et al, defined neuromuscular fatigue as “a reduction in the capacity of a muscle to sustain tension under repeated stimulation.”4 In phonation, hypothetically this translates into reduced ability of the adductors and longitudinal tensors to sustain the right amount of tension within the vocal folds during voice production. Neuromuscular fatigue can be either peripheral in origin secondary to inability to clear lactic acid or to replenish the glycogen storage, or centrally through an inhibitory pathway,4 or a defective activator pathway (eg. paresis). Criticism of this hypothesis cite the high ratio of type I to type II fibers in the thyroarytenoid muscle which makes it highly resistant to vocal fatigue.5 The increased vocal fold viscosity hypothesis is based on the relationship between lubrication and/or tissue viscosity and efficiency of vocal fold vibration. With an increase in vocal fold viscosity secondary to prolonged phonatory use or dehydration, there is an increase in the phonation threshold pressure (the pressure needed to initiate oscillation of the vocal folds). This theory has been substantiated by numerous animal and human studies.6–10 Respiratory muscle fatigue is another plausible theory founded on the common knowledge that breathing energizes the oscillator. Reduced breathing capacity, as in patients with obstructive lung disease, may contribute to the development of vocal fatigue. This theory is particularly convincing in singers and other professional voice users in whom even a minor decrease in vital capacity may jeopardize vocal performance.11 A thorough discussion of the association between breathing and phonation is presented in the chapter on respiratory diseases and voice in this book. Another suggested hypothesis for vocal fatigue is reduced blood circulation. A reduction in blood flow might hinder the removal of lactic acid, the dissipation of heat, and the transfer of adequate oxygenation. Last, neuromuscular strain also might contribute to vocal fatigability through repetitive mechanical stress to the non-muscular structures of the vocal folds. This phonation induced stress is particularly produced at high pitches and high intensities and may also affect other ligamentous structures of the larynx.
The self-reported complaint of vocal fatigue is often paralleled with acoustic and stroboscopic changes.12–14 Mann et al showed an increase in perturbation parameters on the first day following the performance of vocally demanding tasks in 16 subjects out of 42. However the authors failed to demonstrate consistent acoustic changes over the course of 6 days, partially due to large intersubject variability and a large number of outliers. Laryngeal videostroboscopic examination proved more sensitivity in detecting effects of excessive vocalization. The most commonly reported findings were free edge irregularities, vocal fold edematous changes, and decrease in mucosal waves and amplitude.13 In a study by Cho et al examining validated indicators of physical and mental fatigue, the authors reported that several acoustic parameters in addition to self-rated symptoms are indicative of the extent of fatigue using the Chalder Fatigue Scale score. VHI changed in association with physical fatigue in women and mental fatigue in men; and harmonic-to-noise ratio, shimmer, and F0 tremor correlated with mental fatigue in men only.12 Thus, both acoustic analysis and stroboscopic examination are valuable tools in substantiating the self-reported symptom of vocal fatigue.
Sleep Deprivation and Voice