Middleburg Agricultural Research and Extension Center

 

 

 

 

Oxidative Stress

Oxidation is essential to nearly all cells in the body to provide energy for vital functions. Approximately 95 to 98% of the oxygen consumed is reduced to water during aerobic metabolism, but the remaining fraction may be converted to oxidative by-products-reactive oxygen species that may damage the DNA of genes and contribute to degenerative changes, including aging and cancer.

Under normal conditions natural antioxidant defenses are sufficient to neutralize reactive oxygen species. However, excessive production of reactive oxygen species may overwhelm the antioxidant defense, especially during prolonged aerobic exercise or in times when antioxidant status is compromised by nutritional deficiencies or disease, causing oxidative stress.

Oxidative stress has been suggested to contribute to several equine diseases, including the cartilage defect in osteochondrosis, the membrane damage in exertional rhabdomyolysis, the vascular defect in exercise-induced pulmonary hemorrhage, and degenerative motor neuron disease. Dietary supplementation of antioxidants, especially vitamins E and C, has yielded some encouraging results in exercising horses.

The oxidation rate increases about thirty-fold in horses during strenuous exercise, so the exercising horse is a likely model to observe the balance between proxidant assault and antioxidant defense.
As expected due to the demands of exercise on oxidation, several studies have indicated increased measures of oxidative stress, both in horses in intense, short duration work and prolonged aerobic exercise. In our laboratory, 35 endurance horses competing in 80 and 160 km races exhibited oxidative stress by increased activities of glutathione peroxidase, creatine kinase, aspartate amino transferase, and the depletion of vitamin C and glutathione. Interestingly, plasma vitamin E was maintained in horses throughout 80, 140 and 160 km endurance races. Perhaps plasma vitamin C was depleted in order to conserve the activity of vitamin E in these horses.

Antioxidant Supplementation

Exercising Horses.
Daily dietary supplementation of 5000 IU vitamin E in combination with 7 g of vitamin C, compared to the supplementation of vitamin E only, appeared to have no antioxidant advantage in 34 horses during an 80 km race. Regardless of supplementation, horses had increasing lipid hydroperoxides, glutathione peroxidase, creatine kinase, aspartate amino transferase, and lower glutathione throughout the race. However, compared to our previous work, plasma vitamin C was maintained in horses throughout the race, suggesting that dietary supplementation of vitamin E or vitamin E plus vitamin C may conserve ascorbate status during endurance exercise.

Daily dietary supplementation of 2400 IU vitamin E in combination with 10 g of vitamin C raised serum vitamin E and C concentrations in heavily worked, but not lightly worked, polo ponies. Similarly, heavily worked polo ponies had highest serum ascorbate when supplemented with vitamin E and C, and higher serum ascorbate with vitamin C only, compared to control and vitamin E only.

These studies suggest that supplementation of vitamin E and C, in combination or alone, may conserve or enhance circulating concentrations of vitamin E and especially vitamin C during exercise.

Vitamin E, Mares' Milk and Passive Transfer.
Newborn foals acquire their immunity by nursing and absorbing immunoglobulins (IgG, IgA and IgM) from their dam's first milk, colostrum. Our fat-and-fiber supplemented mares had over 4-times higher IgG in their colostrum, compared to mares fed sweet feed. The vitamin E in the corn oil may have contributed to this effect. Mares supplemented with vitamin E during their last six weeks of pregnancy had higher IgG, IgA and IgM in their colostrum, and their foals had higher IgG in their blood after nursing. Since approximately 27% of all foals born contract infection within the first week of life, enhancing the passive transfer of immunoglobulins from the mare to the foal may boost foal health.

 

FURTHER READING

Hargreaves, B.J., D. S. Kronfeld, J. N. Waldron, M. A. Lopes, L. S. Gay, K. E. Saker, W. L. Cooper, D. J. Sklan, and P. A. Harris. 2002. Antioxidant status and muscle cell leakage during endurance exercise. ICEEP 6. In press.

Hargreaves, B. J., D. S. Kronfeld, J. L. Holland, L. A. Gay, W. L. Cooper, D. J. Sklan and P. A. Harris. 2001. Bioavailability and kinetics of natural and synthetic forms of vitamin E in Thoroughbred horses. p 127-128. Proc. 17th Equine Nutr. Physiol. Soc., Lexington, KY.

Hoffman, R. M., T. M. Hess, C. A. Williams, D. S. Kronfeld, K. M. Griewe-Crandell, J. E. Waldron, P. M. Graham-Thiers, L. S. Gay, R. K. Splan, K. E. Saker and P. A. Harris. 2002. Speed associated with plasma pH, oxygen content, total protein and urea in an 80-km race. ICEEP 6. In press.

Hoffman, R. M., K. L. Morgan, A. Phillips, J. E. Dinger, S. A. Zinn and C. Faustman. 2001. Dietary vitamin E and ascorbic acid influence nutritional status of exercising polo ponies. p 129-130. Proc. 17th Equine Nutr. Physiol. Soc., Lexington, KY.

Hoffman, R. M., K. L. Morgan, M. P. Lynch, S. A. Zinn, C. Faustman and P. A. Harris. 1999. Dietary vitamin E supplemented in the periparturient period influences immunoglobulins in equine colostrum and passive transfer in foals. p 96-97. Proc. 16th Equine Nutr. Physiol. Soc., Raleigh, NC.

Williams, C.A., R. M. Hoffman, D. S. Kronfeld, T. M. Hess, K. E. Saker and P. A. Harris.
2002. Lipoic acid as an antioxidant in mature Thoroughbred geldings: a preliminary study. J. Nutr. Suppl. In press.

Hoffman, R.M., T. M. Hess, C. A. Williams, D. S. Kronfeld, K. M. Griewe-Crandell, J. E. Waldron, P. M. Graham-Thiers, L. S. Gay, R. K. Splan, K. E. Saker, and P. A. Harris. 2002. Dietary grain, behavior and endurance exercise. Proc. ASAS (Abstract). In press.

Williams, C.A., R. M. Hoffman, D. S. Kronfeld, T. M. Hess, J. E. Waldron, R. K. Splan, K. E. Saker, and P. A. Harris. 2002. Oxidative stress and antioxidant supplementation in horses during a competitive endurance ride. Proc. ASAS (Abstract). In press.

 


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