Spices and herbs often contain active phenolic substances endowed with potent antioxidative properties. We had previously shown that curcumin, the yellow pigment in curry, strongly induced HO-1 expression and activity in rat astrocytes. In the CNS, HO-1 has been reported to operate as a fundamental defensive mechanism for neurons exposed to an oxidant challenge. Treatment of astrocytes with curcumin upregulated expression of HO-1 protein at both cytoplasmic and nuclear levels, as shown by immunofluorescence analysis under laser-scanning confocal microscopy. A significant expression of quinone reductase and glutathione S transferase, two members of phase II detoxification enzymes, was found in astrocytes exposed to 5-15 microM curcumin. Moreover, the effects of curcumin on HO-1 activity were explored in cultured hippocampal neurons. Elevated expression of HO-1 mRNA and protein were detected after 6 h incubation with 5-25 microM curcumin. Higher concentrations of curcumin (50-100 microM) caused a substantial cytotoxic effect with no change in HO-1 protein expression. Interestingly, pre-incubation (18 h) with curcumin resulted in an enhanced cellular resistance to glucose oxidase-mediated oxidative damage; this cytoprotective effect was considerably attenuated by zinc protoporphyrin IX, an inhibitor of heme oxygenase activity. This study gives additional support to the possible use of curcumin as a dietary preventive agent against oxidative stress-related diseases.
Carbohydrates (CHO) can be classified on the basis of their glycemic index (GI), and the use of this classification has been increasingly supported by science. Because of its impact on blood glucose and insulin responses following the ingestion of CHO foods, the GI has been studied in many fields of medicine, including sport nutrition. As a new tool in sport nutrition, glycemic index manipulation has been evaluated to improve the first and second phases of glycogen recovery, glycogen load, and exercise metabolism, including control of rebound hypoglycemia and, it is interesting to note, stimulation of lipid oxidation for longer availability of glucose sources during endurance exercise. Although attractive, the use of GI in sport nutrition has received only partial support from available experimental evidence. At the biochemical level, consistent evidence has been attained to suggest that GI manipulation can determine variations in adipocyte lipolysis, plasma free fatty acids levels, and lipid and CHO oxidation rates during exercise. However, when the effects of GI manipulation have been assessed at the functional level, the results have been inconsistent, with evidence of improved exercise performance in some studies, but not in many others. The purpose of the current article is to review the effects and limits of GI manipulation in sport nutrition, and to propose an overall strategy for its application.
Some mitochondrial enzymatic activities (succinate dehydrogenase, NADH cytochrome reductase, cytochrome oxidase) were studied in the gastrocnemius and soleus muscle of the rat. The modifications of the enzyme activity, induced by endurance training, were found to be functions of 1) daily work load and 2) total training time. The treatment with an effective dose of vasodilating substances (papaverine, nicergoline, dipyridamole, and bamethan) showed that 1) nicergoline, bamethan, and dipyridamole were differently able to shorten the time of appearance of the increase in the enzymatic activities; 2) however, long-term treatments with these drugs did not prove able to modify the plateau level of the enzymatic activity increase, for a given amount of endurance training; 3) the pharmacodynamic effect on enzymatic activities was in no way related to the vasodilating effect of these drugs, since the effect was not observed with papaverine. The transition from a given level of endurance training to a lower one led to a proportional decrease of the mitochondrial enzymatic activities, thus pointing out the relation between amount of training and enzymatic activity. The drugs studied were unable to modify the decrease of enzymatic activity induced by lower work load.
Despite the numerous positive effects of physical exercise, some negative physiological changes occur in long-lasting heavy training with transient dysfunction of the immune system, increased inflammation, and oxidative stress. This is the case of elite athletes, who train intensively to compete at the highest levels. However, these athletes can counteract the negative effects of heavy training, reducing acute and chronic inflammations and supporting the immune system, with nutritional and supplementation countermeasures. For this purpose, macronutrient manipulation with an appropriate use of certain supplements can be considered as an intervention to reduce exercise-induced immune changes and inflammatory risk. For example, branched-chain amino acid (BCAA) supplementation may promote such immune responses in skeletal muscle. Furthermore, micronutrients play an important role in immune function; in particular, the antioxidant capacity of several dietary micronutrients (e.g., tocopherols, docosahexaenoate, and flavonoids) is very interesting to support the endogenous antioxidant defense systems of the athletes, counterbalancing the negative effects of oxidative damage due to free radicals. Some of these nutrients have potential anti-inflammatory properties as assessed by the attenuated levels of interleukin-6 (IL-6) and C-reactive protein (CRP). Key Teaching Points: Long-lasting heavy training plan and competition can lead to chronic immune suppression in athletes, increasing infection risk. Chronic exercise increases mobilization of neutrophils, decreases mobilization of lymphocytes, and decreases the absolute and relative numbers of neutrophils at rest. Nutritional deficiencies alter the immuno-system and increase infection risk. Nutrition can influence exercise-induced immune suppression. Elite athletes competing at the highest levels can benefit from nutritional and supplementation support to improve immunity and reduce acute and chronic inflammations.
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