Integrative Medicine > Sugars and Refined Carbohydrates  


Br J Nutr 2003 Jan;89(1):89-96. (Animal Study)


Abstract

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

de Oliveira SL, Diniz DB, Amaya-Farfan J

Department of Nutrition, Federal University of Alagoas, Maceio, AL, Brazil

Chronic energy restriction, alpha-tocopherol supplementation and their interaction with exhaustive exercise were investigated.
Eleven-week-old male Wistar rats (n 6x 10) were fed either a control (C), a 30 % carbohydrate-energy-restricted control (R) or an alpha-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 alpha-tocopherol were determined in gastrocnemius, liver, brain and/or 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.
alpha-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 alpha-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.

PMID: 12568668 [PubMed - indexed for MEDLINE]

Source: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12568668&dopt=Abstract


 

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