An in vitro investigation of the molecular effects of aging and exercise signaling within human skeletal muscle cells

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dc.contributor.advisorDuplanty, Anthony A.
dc.creatorZumbro, Emily L.
dc.creator.orcid0000-0001-8259-812X
dc.date.accessioned2021-06-23T16:40:15Z
dc.date.created2021-05
dc.date.issued4/23/2021
dc.date.submitted21-May
dc.date.updated2021-06-23T16:40:16Z
dc.description.abstractThe older population is steadily increasing and is expected to double by the year 2050. With this comes the increase in prevalence of chronic disease, sarcopenia being of utmost concern in regard to skeletal muscle (SKM) health. Sarcopenia is associated with additional morbidities, including insulin resistance, resulting in the reduced quality of life in these individuals. Resistance exercise is a common form of treatment for sarcopenia to attenuate the loss of muscle mass but the quality of the muscle may still be suboptimal due to potential mitochondrial dysfunction and oxidative stress. The purpose of the study was to invesitgate the molecular effects of aging in myoblasts related to cell homeostasis, myogenesis, and mitochondrial biogenesis and whether general exercise signaling via the β-2 adrenergic receptor (β2AR) could rescue the dysregulated signaling resulting from aging. Human SKM myoblasts underwent an in vitro continued passaging protocol to represent aging in vivo. Formoterol (FORM), an exercise mimetic, was used to stimulate general exercise signaling. Four conditions were included in this study (n = 6), control (CON), aging (AGED), CON with FORM stimulation (CON+FORM), and AGED with FORM stimulation (AGED+FORM). Extraction of total RNA was conducted once myoblasts reached 85% confluency and was followed by quantitative polymerase chain reaction (qPCR) analyses. Gene expression was analyzed and represented the following categories: (a) cell homeostasis, (b) myogenesis, and (c) mitochondrial biogenesis. The delta-delta cycle threshold (ΔΔCT) method was used to normalize genetic expression followed by one-way anaylysis of variance (ANOVA) for each gene with significance set at p < .05. Aging resulted in a significant increase in atrophy-related gene expression only in addition to non-significant robust effects on genes associated with oxidative stress, protein synthesis, autophagy, substrate utilization, myogenesis, and mitochondrial biogenesis. Formoterol stimulation significantly increased genes related to mitochondrial biogenesis and atrophy in addition to significantly downregulated myogenesis. Additionally, FORM stimulation seems to reduce oxidative stress, though not significantly. Taking all findings into consideration, general exercise signaling representative of combined aerobic and resistance exercise may be beneficial in older individuals to reduce oxidative stress leading to improved intercellular signaling across pathways important for overall SKM health.
dc.format.mimetypeapplication/pdf
dc.identifier.urihttps://hdl.handle.net/11274/13052
dc.language.isoen
dc.subjectAging
dc.subjectSarcopenia
dc.subjectSkeletal muscle
dc.subjectFormoterol
dc.subjectMyoblasts
dc.titleAn in vitro investigation of the molecular effects of aging and exercise signaling within human skeletal muscle cells
dc.typeDissertation
dc.type.materialtext
local.embargo.lift5/1/2024
local.embargo.terms5/1/2024
thesis.degree.departmentKinesiology
thesis.degree.disciplineKinesiology
thesis.degree.grantorTexas Woman's University
thesis.degree.levelDoctoral
thesis.degree.nameDoctor of Philosophy

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