Donald Zedalis
Edward Via College of Osteopathic Medicine
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Featured researches published by Donald Zedalis.
Respiratory Medicine | 2009
Trent A. Hargens; Stephen G. Guill; Adrian Aron; Donald Zedalis; John M. Gregg; Sharon M. Nickols-Richardson; William G. Herbert
BACKGROUND Obstructive sleep apnea (OSA) is a disorder characterized by repetitive obstructions of the upper airway. Individuals with OSA experience intermittent hypoxia, hypercapnia, and arousals during sleep, resulting in increased sympathetic activation. Chemoreflex activation, arising from the resultant oscillatory disturbances in blood gases from OSA, exerts control over ventilation, and may induce increases in sympathetic vasoconstriction, contributing to increased long-term risks for hypertension (HTN) and cardiovascular disease (CVD). METHODS To evaluate whether OSA elicits exaggerated ventilatory responses to exercise in young men, 14 overweight men with OSA and 16 overweight men without OSA performed maximal ramping cycle ergometer exercise tests. Oxygen consumption (VO(2)), ventilation, (V(E)), ventilatory equivalents for oxygen (V(E)/VO(2)) and carbon dioxide (V(E)/VCO(2)), and V(E)/VCO(2) slope were measured. RESULTS The VO(2) response to exercise did not differ between groups. The V(E), V(E)/VCO(2), V(E)/VO(2) were higher (p< 0.05, 0.002, and p<0.02, respectively) in the OSA group across all workloads. The V(E)/VCO(2) slope was greater in the OSA group (p<0.05). The V(E)/VCO(2) slope and AHI were significantly correlated (r=0.56, p<0.03). Thus, young, overweight men with OSA exhibit increased ventilatory responses to exercise when compared to overweight controls. This may reflect alterations in chemoreflex sensitivity, and contribute to increased sympathetic drive and HTN risk.
International Journal of Cardiology | 2009
Adrian Aron; Donald Zedalis; John M. Gregg; Francis C. Gwazdauskas; William G. Herbert
There is growing evidence linking obstructive sleep apnea hypopnea syndrome (OSAHS) with multiple cardiovascular and metabolic diseases. Exercise testing is generally available and routinely used to provide valuable information on cardiopulmonary function in healthy and diseased populations. This review summarizes and integrates recent findings on exercise testing in OSAHS and discusses the potential mechanisms that may contribute to the responses that seem to differentiate these patients from apparently healthy subjects and patients with other cardiopulmonary diseases. Although exercise testing is widely used in the evaluation and diagnosis of coronary artery disease patients, recent studies showed distinctive cardiopulmonary responses in OSAHS that raise the possibility of similar applications in this disorder, as well. Several studies illustrated in this review found that OSAHS patients have a reduced exercise capacity, as shown by low peak oxygen uptake achieved. Also, their exercise HR response was reported as significantly lower than in healthy peers, suggesting chronotropic incompetence. Exercise blood pressure response were atypical as well. OSAHS patients had increased systolic and diastolic BP during exercise and a persistently elevated systolic BP during the early post-exercise recovery period. Possible explanations for these responses include cardiac dysfunction, impaired muscle metabolism, chronic sympathetic over-activation, and endothelial dysfunction. Early identification of OSAHS using cardiopulmonary exercise testing (CPXT) shows promise for selecting patients at risk for this disorder in the clinical setting. A uniform definition and measurement of OSAHS together with more rigorous trials are necessary to establish the utility of exercise responses in clinical settings.
North American Journal of Medical Sciences | 2013
Katrina L. Butner; Trent A. Hargens; Anthony S. Kaleth; Larry E. Miller; Donald Zedalis; William G. Herbert
Background: Current research is inconclusive as to whether obstructive sleep apnea severity directly limits exercise capacity and lowers health-related quality of life (HRQoL). Aims: The aim of this study was to evaluate the association of obstructive sleep apnea severity with determinants of exercise capacity and HRQoL. Subjects and Methods: Subjects were evaluated by home somnography and classified as no obstructive sleep apnea (n = 43) or as having mild (n = 27), moderate or severe obstructive sleep apnea (n = 21). Exercise capacity was assessed by a ramping cycle ergometer test, and HRQoL was assessed with the SF-36 questionnaire. Results: Greater obstructive sleep apnea severity was associated with older age, higher body weight, higher body mass index, lower peak aerobic capacity, a higher percentage of peak aerobic capacity at a submaximal exercise intensity of 55 watts, and lower physical component summary score from the SF-36. None of these variables were statistically different among obstructive sleep apnea severity groups after controlling for age and body weight. Obstructive sleep apnea severity was not associated with any cardiorespiratory fitness or HRQoL parameter. Conclusions: Obstructive sleep apnea severity has no independent association with exercise capacity or HRQoL.
Journal of Clinical Hypertension | 2006
Trent A. Hargens; Sharon M. Nickols-Richardson; John M. Gregg; Donald Zedalis; William G. Herbert
Obstructive sleep apnea (OSA) is characterized by repetitive partial and total collapse of the upper airway that induces stressful arousals throughout sleep to reestablish breathing. Although estimates vary, prevalence has been reported as high as 20% in the adult population. OSA is common in several chronic diseases, the most common of which is obesity. Evidence is strong that OSA increases the risk of hypertension and both fatal and nonfatal cardiovascular events. Several mechanisms linking OSA to hypertension have been proposed, with increased sympathetic activation implicated as the prime mediator. This review summarizes recent data on the influence of OSA on blood pressure, the effect of standard OSA therapy on improving blood pressure, and the potential of lifestyle modification for further decreasing hypertension risk. Challenges confronting the investigation of blood pressure outcomes in response to treatment in OSA patients are discussed.
Medicine and Science in Sports and Exercise | 2008
Trent A. Hargens; Stephen G. Guill; Anthony S. Kaleth; Adrian Aron; Donald Zedalis; William G. Herbert
heart rate recovery? Trent A. Hargens;1,4 Stephen G. Guill;1,5 Anthony S. Kaleth;1,2 Adrian Aron;1 Donald Zedalis;3,5 and William G. Herbert FACSM.1 Laboratory for Health and Exercise Sciences, Department of Human Nutrition, Foods and Exercise; Virginia Tech, Blacksburg, VA; 1 Department of Physical Education, Indiana University-Purdue University Indianapolis, IN;2 The Sleep Disorders Network of Southwest Virginia, Christiansburg, VA;3 Human Performance Laboratory, Clinical Exercise Physiology Program; Ball State University, Muncie, IN;4 Edward Via Virginia College of Osteopathic Medicine, Blacksburg, VA.5 Laboratory for Health and Exercise Science Human Performance Laboratory
Medicine and Science in Sports and Exercise | 2006
Adrian Aron; Trent A. Hargens; Stephen G. Guill; Donald Zedalis; John M. Gregg; Sharon M. Nickols-Richardson; William G. Herbert
Exaggerated systolic blood pressure (SBP) responses to graded exercise testing in normotensive adults have been associated with risk of future hypertension. Endothelial dysfunction is one of the mechanisms that lead to functional and structural changes in resistance vessels. Venous occlusion plethysmography (VOP) non-invasively characterizes endothelium-dependent vasodilatory capacity in peripheral arteries (reactive hyperemia: RH). PURPOSE: To determine if an association exists between exaggerated SBP responses to graded exercise and peripheral vascular vasodilatory capacity. METHODS: Subjects were 50 young males (Mean ± SD: age = 22.4 ± 2.6 yr; body fat = 24.3 ± 6.1 %; BMI = 27.7 ± 5.7). Post-occlusive RH was assessed after a 5-min brachial artery occlusion using VOP and standard procedures recommended by the manufacturer (Hokanson EC-6, Bellevue, WA). Each subject performed maximal cycle ergometer exercise tests with a 15 watts/min ramping protocol. Blood pressures (BP) were measured at rest, every 2 min during, and at 15 sec intervals after exercise. RESULTS: During exercise, no relationship was found between any of the exaggerated SBP indices and the measures of peripheral artery status by VOP. Furthermore, when individual SBP responses from peak exercise at the highest vs. lowest tertiles were contrasted, no differences in the VOP measures of vascular status were found. CONCLUSION: Exaggerated SBP response to graded exercise in young adult males seems to be regulated largely by factors other than peripheral vascular status, as assessed by VOP/RH.
Sleep Medicine | 2007
Anthony S. Kaleth; Thomas Chittenden; Brian J. Hawkins; Trent A. Hargens; Steve G. Guill; Donald Zedalis; John M. Gregg; William G. Herbert
Sleep | 2008
Trent A. Hargens; Stephen G. Guill; Donald Zedalis; John M. Gregg; Sharon M. Nickols-Richardson; William G. Herbert
Sleep and Breathing | 2013
Trent A. Hargens; Stephen G. Guill; Anthony S. Kaleth; Sharon M. Nickols-Richardson; Larry E. Miller; Donald Zedalis; John M. Gregg; F.C. Gwazdauskas; William G. Herbert
Journal of transport and health | 2016
J. Erin Mabry; Kathy Hosig; Richard J. Hanowski; Donald Zedalis; John M. Gregg; William G. Herbert