title: Resistance exercise training attenuates alcohol-induced cardiac oxidative stress.
abstract: BACKGROUND
  Myocardial oxidative stress is believed to play an important role in the pathogenesis of alcoholic cardiomyopathy. Strenuous physical exercise has been shown to increase or decrease myocardial oxidative stress depending on the mode and duration of the exercise intervention. Given the possibility of individuals to engage in both alcohol consumption and weight-training exercise, we have examined the effect of resistance exercise training and chronic alcohol consumption on myocardial oxidative stress in rats.
  
  
  METHODS
  Forty Sprague-Dawley rats were randomly assigned to one of four experimental groups: sedentary, sedentary plus alcohol treatment, resistance training, or resistance training plus alcohol treatment. Rats in the alcohol groups received a liquid diet containing alcohol (35% of kilocalorie intake) for 6 weeks. Non-alcohol groups were pair-fed the same liquid diet supplemented with a maltose dextrin caloric substitute. Rats in the resistance training groups were trained to rise onto their hind limbs while wearing lead-weighted vests 30 times per training session, 3 days per week during the 6 week experimental period.
  
  
  RESULTS
  Alcohol treatment in the sedentary animals resulted in greater levels of cardiac malondialdehyde, a marker of lipid peroxidation, and a depressed index of myocardial antioxidant potential compared with all other groups (P<0.05). Hearts from the resistance training plus alcohol animals exhibited malondialdehyde and antioxidant levels similar to sedentary controls, suggesting that resistance training protected against the alcohol-induced myocardial stress.
  
  
  CONCLUSIONS
  These results suggest that resistance training may attenuate the damaging effects of alcohol on the heart and preserve myocardial antioxidant capacity.
authors.affiliation: School of Sport and Exercise Science, University of Northern Colorado Greeley, Denver, CO, USA.
authors.forename: Adam J
authors.initials: AJ
authors.lastname: Chicco
authors.forename: Heidi
authors.initials: H
authors.lastname: McCarty
authors.forename: Adam H
authors.initials: AH
authors.lastname: Reed
authors.forename: Regan R
authors.initials: RR
authors.lastname: Story
authors.forename: Kim C
authors.initials: KC
authors.lastname: Westerlind
authors.forename: Russell T
authors.initials: RT
authors.lastname: Turner
authors.forename: Reid
authors.initials: R
authors.lastname: Hayward
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology; D000434:Alcoholic Beverages / Q000009:adverse effects*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D002492:Central Nervous System Depressants / Q000009:adverse effects*; D000431:Ethanol / Q000009:adverse effects*; D015227:Lipid Peroxidation / Q000502:physiology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000975:Antioxidants; D002492:Central Nervous System Depressants; D000431:Ethanol; D008315:Malondialdehyde