Peter M. Tiidus

Vitamin E Status and Response to Exercise Training

SummaryVitamin E is an important intramembrane antioxidant and membrane stabiliser. Over the past 40 years, vitamin E supplementation has been advocated for athletes in the hope of improving performance, minimising exercise-induced muscle damage and maximising recovery. However, there is currently a lack of conclusive evidence that exercise performance or recovery would benefit in any significant way from dietary vitamin E supplementation. Exceeding current recommended intakes of vitamin E even by several orders of magnitude will result in relatively modest increases in tissue or serum vitamin E concentrations. Most evidence suggests that there is no discernible effect of vitamin E supplementation on performance, training effect or rate of postexercise recovery in either recreational or elite athletes. There is very little evidence, particularly involving humans, that exercise or training will significantly alter tissue or serum vitamin E levels. While there is some evidence that certain indices of tissue peroxidation may be reduced following dietary vitamin E supplementation, the physiological and performance consequences in humans of these relatively minor effects are unknown. Although there appears to be little reason for vitamin E supplementation among athletes, it does not appear that the practice of supplementation is harmful.

Antioxidant and oxidative enzyme adaptations to vitamin E deprivation and training

The effects of endurance training on tissue antioxidant and oxidative enzyme activities were determined in heart, liver, and five skeletal muscles of female rats. Rats were fed either normal (+E) or vitamin E free (-E) diets for 16 wk. For the final 8 wk, subgroups of +E and -E diet animals were trained by treadmill running at 40 m.min-1, 15% grade for 60 min.d-1. No significant differences in training abilities were observed between diet groups. Endurance training significantly increased citrate synthase (CS) activity in all skeletal muscles for both the +E and -E diet animals with no significant difference in degree of response between diet groups. Neither vitamin E deprivation, training, or their combination generally affected the activities of the antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), or glutathione peroxidase (GPX) in skeletal muscles, heart, or liver of the animals. These results suggest that despite an anticipated increase in free radical induced tissue oxidative stress brought about by a combination of vitamin E deprivation and endurance training, antioxidant enzyme adaptations were not evident and the response of citrate synthase to training was not impaired in female rats.

Effects of vitamin e status and exercise training on tissue lipid peroxidation based on two methods of assessment

Abstract Effects of dietary vitamin E deprivation, acute exercise and training on tissue lipid peroxidation as determined via a thiobarbituric acid reactive substances (TBARS) assay and an ion-pairing HPLC assay for malondialdehyde are reported. Female rats were fed diets with (+E) or without (-E) vitamin E for 8 weeks, after which subgroups of rats were exercised for 45 min and immediately sacrificed. Remaining animals continued on their diets, were sedentary or trained for 8 additional weeks, and were sacrificed with or without prior exercise. Little malondialdehyde, as determined by HPLC, was found in liver, heart or muscles (with the exception of white vastus) following any condition. Significant levels of TBARS were found in all tissues following all conditions. Significantly higher levels were found in many tissues with the -E diet and acute exercise. TBARS levels did not correlate with HPLC-determined malondialdehyde levels indicating that determination of the presence and degree of exercise induced lipid peroxidation are specific to each assay and conclusions regarding its occurrence must be made with caution.

Elevated catalase activity in red and white muscles of MyoD gene‐inactivated mice

MyoD is a myogenic transcription factor responsible for skeletal muscle differentiation during development. Muscle antioxidant enzyme status was determined in transgenic MyoD deactivated mice. While catalase activity was significantly (P<0.05) elevated in soleus and extensor digitorum longus muscles from MyoD deactivated mice, superoxide dismutase and glutathione peroxidase activities were not. While this may imply a greater propensity for inherent oxidative stress, soleus glutathione status was similar between MyoD deactivated mouse and control soleus muscles. Catalase activity is localized primarily in peroxisomes. Therefore elevated catalase activity may also indicate the presence of factors associated with peroxisome proliferation in muscles from MyoD gene‐inactivated mice.

Vitamin C and vitamin E status in guinea pig tissues following estrogen administration

Abstract Previous studies reported lower tissue vitamin C levels in rats following estrogen administration. This study examined the effects of two weeks of daily estrogen administration (40 μg β-estradiol 3-benzoate per kg BW) on tissue vitamin C status in male and female guinea pigs, who unlike rats, require dietary vitamin C. Estrogen administration resulted in significant vitamin C loss in heart and liver from both genders and in plantaris muscle from male guinea pigs. However, estrogen administration did not affect vitamin C status in female plantaris or male lung, while resulting in significantly elevated vitamin C level in female lung. Tissue vitamin E status was unaffected by estrogen administration in either gender. Estrogen administration induced GSH loss in some tissues, indicating increased metabolic or oxidative stress and lowered growth rates and nutrient intakes particularly in male guinea pigs. However, tissue glycogen levels were not always affected by estrogen administration. Hence while, the effects of estrogen administration on tissue vitamin C status may in part be due to its effect on metabolism and nutrient intake, these factors cannot fully account for all the effects on tissue vitamin C status seen in this study. It is possible that estrogen administration has other tissue specific effects on vitamin C metabolism in guinea pigs