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Gender-Related Differences in Muscle Injury, Oxidative Stress, and Apoptosis


Medicine & Science in Sports & Exercise: October 2008 - Volume 40 - Issue 10 - p 1772-1780
doi: 10.1249/MSS.0b013e31817d1cce
BASIC SCIENCES: Original Investigations

Due to its alleged antioxidant properties, 17β-estradiol (E2) may protect against muscle injury, oxidative stress, and apoptosis.

Purpose: This study sought to determine whether such mechanisms existed between genders for muscle injury, oxidative stress, and apoptosis after eccentric exercise.

Methods: Eight men and eight women (no oral contraceptive use; midluteal phase of menstrual cycle) performed 7 × 10 eccentric repetitions of the knee extensors at 150% 1RM. Strength, soreness, and blood samples were taken before exercise and 6, 24, 48, and 72 h after exercise while muscle samples were collected before and 6 and 24 h after exercise. Blood samples were assayed for free E2, lactate dehydrogenase (LDH), superoxide dismutase (SOD), and 8-isoprostane (8-iso). Muscle samples were assayed for mitochondrial apoptosis (e.g., bax, bcl-2, cytochrome c, and cell death), total DNA content, and myofibrillar protein content.

Results: Men reported greater soreness levels at 24, 48, and 72 h after exercise, whereas strength changes were similar among genders. At baseline and independent of exercise, females had higher E2 (P < 0.001) and SOD in conjunction with lower 8-iso levels when compared with men. Bax increased in both genders, whereas bcl-2 increased only in women with no cytochrome c changes for either gender after exercise. The bax/bcl-2 ratio in women significantly decreased after 6 h (P = 0.03) and returned to baseline levels after 24 h. Men exhibited greater cell death at all time points (P < 0.05), whereas myofibrillar protein content and total DNA content decreased in both genders at 24 h after exercise. No changes in LDH were found (P > 0.05).

Conclusions: Although more research is needed, differences between gender may provide greater endogenous protection against oxidative stress and apoptosis.

1Applied Biochemistry and Molecular Physiology Laboratory, Health and Exercise Science Department, University of Oklahoma, Norman, OK; 2Section of Diabetes and Endocrinology, Department of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma City, OK; 3Department of Exercise & Sport Science, University of Mary Hardin-Baylor, Belton, TX; 4Nutritional Sciences, Department of Human Ecology, The University of Texas at Austin, Austin, TX; 5Exercise and Biochemical Nutrition Laboratory, Exercise Nutrition and Resistance Training Research Unit, Department of Health, Human Performance and Recreation, Baylor University, Waco, TX; and 6Institute for Biomedical Studies, Baylor University, Waco, TX

Address for correspondence: Darryn Willoughby, Ph.D., FACSM, Exercise and Biochemical Nutrition Laboratory, PO Box 79713, Baylor University, Waco, TX 76798-7313; E-mail:

Submitted for publication February 2008.

Accepted for publication April 2008.

©2008The American College of Sports Medicine