Effect of Resistance Training on Blood Oxidative Stress in Parkinson Disease


Medicine & Science in Sports & Exercise: August 2008 - Volume 40 - Issue 8 - pp 1385-1389
doi: 10.1249/MSS.0b013e31816f1550
CLINICAL SCIENCES: Clinically Relevant

Oxidative stress seems to be involved in the pathogenesis of Parkinson disease (PD). Exercise training can increase endogenous antioxidant protection and decrease the production of reactive oxygen and nitrogen species.

Purpose: To investigate the effect of exercise training on oxidative status in persons with PD.

Methods: Sixteen subjects with PD were match-randomly assigned to resistance exercise (n = 8) or a no-exercise control group (n = 8) on the basis of disease stage (Hoehn and Yahr stages I and II) and sex. Supervised exercise was performed twice weekly for 8 wk, consisting of three sets each of the leg press, leg curl, and calf press. Resting blood samples were taken from subjects before and after the intervention and assayed for markers of oxidative stress [malondialdehyde (MDA) and hydrogen peroxide (H2O2)] and antioxidant capacity (superoxide dismutase, catalase, glutathione peroxidase, and trolox-equivalent antioxidant capacity).

Results: The exercise program was well-tolerated and associated with modest trends toward decreased oxidative stress and increased antioxidant capacity. The two biomarkers of oxidative stress were decreased after exercise training [MDA (15%) and H2O2 (16%)]. With these changes, a postintervention difference was apparent between the resistance exercise training and control groups for H2O2 (P = 0.007), with a trend for difference noted for MDA (P = 0.06). The mean increases in superoxide dismutase (9%) and glutathione peroxidase (15%) noted in the exercise training group were not statistically significant (P > 0.05).

Conclusions: Short-term resistance training may be associated with reduced oxidative stress in subjects with PD. Future studies with larger samples, inclusive of a higher volume of resistance exercise, are needed to extend these findings.

1Department of Health and Sport Sciences, University of Memphis, and 2Department of Neurology, University of Tennessee Health Science Center, Memphis, TN

Address for correspondence: Richard J. Bloomer, Ph.D., Cardiorespiratory/Metabolic Laboratory, University of Memphis, 161F Elma Neal Roane Field House, Memphis, TN 38152; E-mail: rbloomer@memphis.edu.

Submitted for publication December 2007.

Accepted for publication February 2008.

©2008The American College of Sports Medicine