British Journal of Nutrition

Research Article

Carbohydrate–energy restriction may protect the rat brain against oxidative damage and improve physical performance

S. L. de Oliveiraa1 c1, D. B. Diniza2 and J. Amaya-Farfana3 c1

a1 Department of Nutrition, Federal University of Alagoas, Maceió, AL, Brazil

a2 Department of Nutrition, State University of Ceará, Fortaleza, CE, Brazil

a3 Department of Food and Nutrition, State University of Campinas, SP 13.083-970, Brazil


Chronic energy restriction, α-tocopherol supplementation and their interaction with exhaustive exercise were investigated. Eleven-week-old male Wistar rats (n 6×10) were fed either a control (C), a 30 % carbohydrate-energy-restricted control (R) or an α-tocopherol-supplemented (S) diet for 5 months. The animals in each diet were divided into exercised (E) and non-exercised (NE) groups. Before killing, the exercised rats were required to run to exhaustion (39 (SE 6), 69 (se 11) and 18 (se 2) min for the C, R and S groups, respectively). Lipid peroxidation (thiobarbituric acid-reactive substances; TBARS), protein damage (reactive carbonyls) and α-tocopherol were determined in gastrocnemius, liver, brain an/r plasma. There was no difference in lipid peroxidation between the R and C groups, but in liver and muscle peroxidation appeared significantly lower in the S than the other two diets. TBARS in the brain were similar in all groups. On the other hand, reactive carbonyls showed that both the R and S diets reduced protein damage in the brain, while exhaustive exercise increased it. For liver and muscle, however, reactive carbonyl levels were similar in all groups. α-Tocopherol supplementation increased the vitamin concentrations in liver, muscle and plasma, but exercise decreased them in plasma and brain. Carbohydrate-energy restriction increased (P=0·0025) resistance to exhaustive exercise considerably without depleting stores of α-tocopherol or exacerbating oxidative damage in monitored tissues. It is concluded that while exhaustive exercise promotes a tissue-specific oxidative damage detectable only in brain proteins, both experimental diets tended to ameliorate this condition.