The role of exercise in minimizing postprandial oxidative stress in cigarette smokers
Richard J. Bloomer, Ph.D., Cardiorespiratory/Metabolic Laboratory, The University of Memphis, Memphis, TN
Kelsey Fisher-Wellman, B.S., Cardiorespiratory/Metabolic Laboratory, The University of Memphis, Memphis, TN
Corresponding Author: Richard J. Bloomer, Cardiorespiratory/Metabolic Laboratory, 161F Elma Neal Roane Field House, The University of Memphis, Memphis, TN 38152. Telephone: 901-678-4341. Fax: 901-678-3591. E-mail: rbloomer{at}memphis.edu
 |
Abstract |
|---|
Cigarette smoking continues to pose a significant health burden on society. Two well-described mechanistic links associating smoking with morbidity and mortality include elevated blood lipids and increased oxidative stress. These variables have traditionally been measured while an individual is fasting, but evidence suggests that postprandial lipemia and oxidative stress provide more important information concerning susceptibility to disease, in particular cardiovascular disease. Cigarette smokers have elevated levels of biomarkers of oxidative stress at rest and experience impaired postprandial lipid and glucose metabolism. We have confirmed these findings while noting an exaggerated oxidative stress response to high-fat feeding. Smoking cessation is without question the best approach to minimizing smoking-induced ill health and disease, but success rates among those who attempt to quit are dismal. Other means to decrease a smoker's susceptibility to oxidative stress–related disease are needed. We propose that exercise may aid in attenuating postprandial oxidative stress, and we do so in 3 distinct ways. First, exercise stimulates an increase in endogenous antioxidant enzyme activity. Second, exercise improves blood triglyceride clearance via a reduced chylomicron–triglyceride half-life and an enhanced lipoprotein lipase activity. Third, exercise improves blood glucose clearance via an enhanced glucose 4 transport protein translocation and protein content, as well as insulin–insulin receptor binding and postreceptor signaling. Improvements in antioxidant status, as well as lipid and glucose processing, may aid greatly in minimizing feeding-induced oxidative stress in smokers. If so, and in accordance with the recent joint initiative of the American College of Sports Medicine and the American Medical Association, exercise may be viewed as a "medicine" for cigarette smokers at increased risk for postprandial oxidative stress. Research into this area may provide insight into the potential benefits of exercise for this purpose.
Received: January 14, 2008; Accepted: June 3, 2008
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  K. Keskitalo, U. Broms, M. Heliovaara, S. Ripatti, I. Surakka, M. Perola, J. Pitkaniemi, L. Peltonen, A. Aromaa, and J. Kaprio Association of serum cotinine level with a cluster of three nicotinic acetylcholine receptor genes (CHRNA3/CHRNA5/CHRNB4) on chromosome 15 Hum. Mol. Genet., October 15, 2009; 18(20): 4007 - 4012. [Abstract] [Full Text] [PDF]
|
|