Bailey Peck

Professional football linemen are at risk for sleep disordered breathing (SDB) compared to other types of athletes. It is currently unknown whether collegiate football linemen display a similar risk profile. 1) Determine for the first time whether collegiate football linemen show risk for SDB, and 2) Test the hypothesis that SDB risk is higher in collegiate football linemen compared to an athletic comparison group. Descriptive laboratory study. The Health Risk Assessment Laboratory. Male football linemen (n = 21) and track (n = 22) Division I athletes between the ages of 18 and 22. Participants completed the Multivariable Apnea Prediction (MAP) Index and Epworth Sleepiness Scale (ESS) surveys, validated measures of symptoms of sleep apnea and daytime sleepiness, respectively. Neck and waist circumferences, blood pressure, Mallampati Index (MMPI) and Tonsil Size were determined, followed by body composition assessment using DEXA. Scores from surveys, anthropometric data, MMPI and body composition. Survey data demonstrated a deficiency in sleep quality and efficiency, coinciding with increased self-reported symptoms of apnea (MAP index=0.79) in college linemen relative to track athletes. Neck circumference (45cm), waist circumference (107.07cm), body mass index (36.64kg/m2) and body fat % (30.19%), all of which exceeded the clinical predictors of risk for obstructive sleep apnea, were significantly greater in linemen compared to track athletes. MAP variables were significantly correlated with MMPI, neck circumference, body fat %, body mass index, and systolic blood pressure (r ≥ .31, p < 0.05), indicating that college football linemen are at increased risk for SDB. Risk factors for SDB recognized in professional football linemen are also present at the collegiate level. Screening may minimize present or future risk for SDB, as well as the downstream risk of SDB-associated metabolic and cardiovascular disease.

Unlike the glucocorticoid receptor α (GRα), GR β (GRβ) has a truncated ligand-binding domain that prevents glucocorticoid binding, implicating GRα as the mediator of glucocorticoid-induced skeletal muscle loss. Because GRβ causes glucocorticoid resistance, targeting GRβ may be beneficial in impairing muscle loss as a result of GRα activity. The purpose of this study was to determine how the overexpression of GRβ affects myotube formation and dexamethasone (Dex) responsiveness. We measured GR isoform expression in C₂C₁₂ muscle cells in response to Dex and insulin, and through four days of myotube formation. Next, lentiviral-mediated overexpression of GRβ in C₂C₁₂ was performed, and these cells were characterized for cell fusion and myotube formation, as well as sensitivity to Dex via the expression of ubiquitin ligases. GRβ overexpression increased mRNA levels of muscle regulatory factors and enhanced proliferation in myoblasts. GRβ overexpressing myotubes had an increased fusion index. Myotubes overexpressing GRβ had lower forkhead box O3 (Foxo3a) mRNA levels and a blunted muscle atrophy F-box/Atrogen-1 (MAFbx) and muscle ring finger 1 (MuRF1) response to Dex. We showed that GRβ may serve as a pharmacological target for skeletal muscle growth and protection from glucocorticoid-induced catabolic signaling. Increasing GRβ levels in skeletal muscle may cause a state of glucocorticoid resistance, stabilizing muscle mass during exposure to high doses of glucocorticoids.