Comparison between Glucose-6-Phosphate Dehydrogenase-Deficient and Normal Individuals after Eccentric Exercise


Medicine & Science in Sports & Exercise: June 2010 - Volume 42 - Issue 6 - pp 1113-1121
doi: 10.1249/MSS.0b013e3181c67ecd
Basic Sciences

Purpose: Theoretically, glucose-6-phosphate dehydrogenase (G6PD)-deficient compared with nondeficient individuals may be less capable of performing physical activities and/or may be more vulnerable to muscle damage and oxidative stress. Therefore, the purpose of the present study was to examine the effects of a resistance muscle-damaging exercise bout on muscle function and damage, redox status in plasma, and erythrocytes and hemolysis.

Methods: Nine males with established G6PD deficiency and nine males with normal G6PD activity performed an eccentric muscle-damaging exercise protocol. Isometric torque, range of motion, delayed onset muscle soreness, and creatine kinase were measured as indices of muscle function and damage. Reduced glutathione, oxidized glutathione, thiobarbituric acid-reactive substances, protein carbonyls, catalase, uric acid, and total antioxidant capacity were measured as indices of blood redox status. Plasma hemoglobin and bilirubin were measured as indices of hemolysis. All measurements conducted before, immediately after, and 1, 2, 3, 4, and 5 d after exercise.

Results: All indices measured confirmed that eccentric exercise induced severe muscle damage, oxidative stress, and hemolysis, peaking at 2 and 3 d postexercise. Lower resting levels of reduced glutathione were detected in the G6PD-deficient group compared with the control group. Nevertheless, both the time course and the magnitude of the changes of the selected muscle performance, redox status (both in plasma and in erythrocytes), and hemolysis indices measured were similar between the two groups.

Conclusions: The present study indicates that G6PD-deficient individuals may participate in high-intensity muscle-damaging activities, without a negative impact on muscle function, blood redox status, and hemolysis.

1Center for Research and Technology, Institute of Human Performance and Rehabilitation, Thessaly, Trikala, GREECE; 2Department of Physical Education and Sport Science, University of Thessaly, Trikala, GREECE; 3Department of Physical Education and Sport Science, Democritus University of Thrace, Komotini, GREECE; and 4School of Sport, Performing Arts and Leisure, Wolverhampton University, Walshall, UNITED KINGDOM

Address for correspondence to: Athanasios Z. Jamurtas, Ph.D., Department of Physical Education and Sports Sciences, University of Thessaly, Karies, 42100, Trikala, Greece; E-mail:

Submitted for publication July 2009.

Accepted for publication October 2009.

©2010The American College of Sports Medicine