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Published on: June 13, 2017
Aging thyroarytenoid and limb skeletal muscle: lessons in contrast
Lisa B Thomas1, Anne L Harrison, Joseph C Stemple
1Rehabilitation Sciences Doctoral Program, University of Kentucky, Lexington, KY 40536-0200, USA. Lisa.Thomas@uky.edu <Lisa.Thomas@uky.edu>
Abstract:
Voice production is vital throughout life because it allows for the communication of basic needs as well as the pursuit and enjoyment of social encounters. Unfortunately, for many older individuals the ability to produce voice is altered. Structural and functional declines in the neuromuscular system occur with aging and likely contribute to the modification of voice. One specific target of the aging process is the thyroarytenoid (TA) muscle, the primary muscle of voice production. The objectives of this overview article are to (1) share current findings related to the aging of limb skeletal muscle, (2) identify age-related morphological and physiological features of TA muscle, (3) compare and contrast age-related changes in TA with those in limb skeletal muscle, and (4) describe therapies for reversing sarcopenia in limb muscle and consider the applicability of these therapies for addressing vocal fold atrophy and age-related voice changes. The article shares current knowledge from the basic sciences related to skeletal muscle aging and compares/contrasts typical muscle aging to TA aging. Current evidence suggests that (1) the TA muscle undergoes notable remodeling with age, (2) aging of the TA is multifactorial, resulting from a myriad of neurologic, metabolic, and hormonal changes, many of which are distinct from the age-related processes of typical limb skeletal muscle, (3) investigation of the aging of the TA and its role in the aging of voice is in its infancy, and (4) potential behavioral and nonbehavioral therapies for reversing aging of the TA must be further examined.
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When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.

