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

Abstract

Chronic energy restriction, a-tocopherol supplementation and their interaction with exhaustive exercise were investigated. Eleven-week-old male Wistar rats ðn 6 £ 10Þ were fed either a control (C ), a 30 % carbohydrate-energy-restricted control (R ) or an a-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 atocopherol 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. a-Tocopherol supplementation increased the vitamin concentrations in liver, muscle and plasma, but exercise decreased them in plasma and brain. Carbohydrate-energy restriction increased (P¼ 0·0025) resistance to exhaustive exercise considerably without depleting stores of a-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.

Competition and Food Restriction Effects on Oxidative Stress in Judo

“…In particular, lag phase, an index of the resistance of LDL to in vitro oxidation, is now widely proposed as being a reliable index of the antioxidant status in humans [22].Research on energy restriction has produced diverging results. While some workers have found beneficial effects determined by several indicators of oxidative damage [7], others report no detectable difference with a normal diet. For example, in a recent study, Suzuki et al [29] reported that weight reduction, consisting of both intense exercise and energy restriction, might possibly cause both an increase in oxidative burst activity and decrease in neutrophil phagocytic activity in female judoists.…”

“…This increase of the antioxidant protection was higher after the competition than after the dietary restriction (+ 40 % for the lag phase values at T 3 , + 23% at T 2 for Group A). De Oliveira et al [7] reported that a carbohydrate-energy restriction (30 %) increased resistance to exhaustive exercise considerably in rats without exacerbating oxidative damage. Dietary analysis in our study indicated that the proportion of total calories from carbohydrates were lower than the recommendations for both groups.…”

NFκB-mediated metabolic inflammation in peripheral tissues versus central nervous system

“…Nonetheless, in studying the nutritional control of aging, research has obtained sufficient findings demonstrating that the anti-aging effects of caloric restriction (CR) are attributed to its protection against oxidative stress and inflammation, 89,90 and that the brain benefits the utmost from the anti-oxidative stress action of CR. 91,92 Since the hypothalamus is the primary brain region that directly communicates with the whole body's nutrients and nutritional signals, perhaps unsurprisingly, it contains extra-sensitive properties in reacting to the nutritional oxidative stress and inflammation. 93 Such vulnerability of the hypothalamus has been viewed to be responsible for aging and aging-related diseases, 81 which agrees with the fact that all these problems can be promoted by and all these cytokines are the classical gene products from the NFκB-directed transcriptional program.…”

Caloric restriction or resveratrol supplementation and ageing in a non-human primate: first-year outcome of the RESTRIKAL study in Microcebus murinus

“…However, non-human primates and humans present metabolic responses to a long-term CR and mimetic compound that might differ slightly from what was repeatedly observed in rodents and other lower organisms (Heilbronn et al 2006; Colman et al 2009; Witte et al 2009). For example, CR in mice down-regulates genes involved in oxidative stress and reduces oxidative damage, lipid peroxidation and protein carbonyls (Sohal et al 1994; Dubey et al 1996; Lee et al 1999; de Oliveira et al 2003). In non-human primates, genes involved in protection against oxidative stress are not altered by CR, although protein carbonylation is reduced (Zainal et al 2000).…”