Tony G. Babb, Ph.D.
Tony G. Babb, Ph.D.

Professor of Internal Medicine,
UT Southwestern Medical Center

Director, Pulmonary Physiology Laboratory and the Cardiopulmonary Exercise Laboratory
Effie and Wofford Cain Chair in Cardiopulmonary Research

Dr. Tony G. Babb is a charter member of the IEEM. He is a Professor of Internal Medicine/Pulmonary and Critical Care Medicine at the University of Texas Southwestern Medical Center. Dr. Babb earned his B.S. at Western Kentucky University, his M.S. at the University of Illinois, and his Ph.D. at The Pennsylvania State University. He completed his postdoctoral fellow training at the Mayo Clinic in the Thoracic Diseases Research Unit. He has established a strong national and international reputation for his work in respiratory exercise physiology, particularly as it pertains to pulmonary disease, normal aging, obesity, ventilatory control during exercise, applied respiratory physiology, and clinical cardiopulmonary exercise testing. Dr. Babb is a Fellow of the American College of Sports Medicine (ACSM), an American Thoracic Society Fellow (ATSF), and a member of the American Physiological Society (APS). Currently, his research focuses on investigating the respiratory effects of obesity in children, which is an extension of his prior work on the mechanisms of exertional dyspnea in adults with obesity. His latest project investigates the mechanisms of dyspnea on exertion and exercise intolerance in in patients with heart failure with preserved ejection fraction (HFpEF) and the impact of obesity. Also, he has recently initiated research investigating the mechanisms of exercise intolerance and breathlessness in aged adults with obesity. His projects have been funded by NIH, AHA, ALA, the King Foundation, the Susan Lay Atwell Gift for Pulmonary Research, and Dr. Pepper/Snapple.

Current research focuses on the mechanisms of dyspnea on exertion (DOE) in individuals with obesity. Our studies have shown that one third of otherwise healthy younger adults with obesity suffer from DOE. Although adults with obesity and DOE are generally considered to be deconditioned, our findings continue to challenge this misconception. Additionally, we have shown that excess fat on the chest wall exerts an unfavorable mechanical burden on the respiratory system, particularly during exercise, potentially contributing to DOE. Past studies have also shown that modest weight loss (WL) significantly reduces DOE in women with obesity, and likewise, endurance exercise training (ET) in women with obesity also reduces DOE. Overall, these studies are the first to show that WL and/or ET are effective treatments for DOE in adults with obesity; however, the mechanisms by which WL and ET decrease DOE remain unclear.

Dr. Babb has extended his studies in adults to investigations on the respiratory effects of obesity in children. Over 19% of children 6-11 yr are classified as obese. We have found numerous obesity-related respiratory effects that could influence exercise tolerance and DOE in adults with obesity. However, it is unclear whether the obesity-related respiratory effects in adults can be extended to children. It is possible that they could reduce exercise tolerance, provoke DOE, or contribute to respiratory symptoms. These symptoms could be misdiagnosed as asthma in children with obesity. Obesity-related respiratory symptoms are reported to be wrongly labeled ‘asthma’ in over 50% of patient cases placing children with obesity at risk of unnecessary treatment and potentially a reluctance to exercise, which is counterproductive to WL.

DOE and exercise intolerance are also hallmark symptoms of heart failure with preserved ejection fraction (HFpEF). The mechanisms of these two symptoms are unknown in patients with HFpEF. Potential mechanisms are numerous and multifactorial, including breathing limitations (underlying lung dysfunction), exercise ventilatory limitations (reduced ventilatory reserves, expiratory flow limitation), central cardiovascular limitations (blunted cardiac output, heart stiffness), increased pulmonary capillary wedge pressure (PCW), peripheral vascular/muscle limitations (O2 uptake, oxidative metabolism, & blood flow), autonomic control alterations (altered neural or vascular control), and lastly obesity (reduced lung function, increased work of breathing, etc.). Indeed, the effect of obesity in patients with HFpEF is underappreciated, in contrast to conventional thinking, which assumes that increased PCW alone is responsible for DOE and exercise intolerance in patients with HFpEF. Obesity decreases lung volume subdivisions and exaggerates the age-related decline in maximal expiratory flow increasing the risk of expiratory flow limitation and dynamic hyperinflation during exercise, both responses associated with DOE. Obesity also increases the energy requirement of exercise, ventilatory demand, the work of breathing, and exercise intolerance; all these alterations can also influence DOE. Furthermore, many of the changes noted in patients with HFpEF are common alterations related to obesity (decreased diffusing capacity, decreased muscle blood flow, increased SNA) and most patients with HFpEF patients are obese and older. However, it is unclear whether obesity amplifies HFpEF-related breathing limitations or is a sole contributor to DOE and/or exercise intolerance, but obesity is likely an under recognized but significant contributor to DOE in patients with HFpEF. The overall objective of our latest project (Pulmonary Mechanisms of Dyspnea in HFpEF: Impact of Obesity) is to investigate the mechanisms of DOE and exercise intolerance in patients with HFpEF with and without obesity.


  • B.S., Biology, Western Kentucky University, Bowling Green, KY
  • M.S., Exercise Physiology, University of Illinois, Urbana, IL
  • Ph.D., Exercise Physiology, Pennsylvania State University, University Park, PA
  • Post-Doctoral Fellowship, Thoracic Diseases Research Unit, Mayo Clinic, MN

Professional Associations & Affiliations

  • American College of Sports Medicine, FACSM
  • American Physiological Society
  • American Thoracic Society, ATSF

Contact Information

Phone: 214-345-4622

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