Reinaldo A. Bassit

Branched-chain amino acid supplementation and the immune response of long-distance athletes

OBJECTIVE Intense long-duration exercise has been associated with immunosuppression, which affects natural killer cells, lymphokine-activated killer cells, and lymphocytes. The mechanisms involved, however, are not fully determined and seem to be multifactorial, including endocrine changes and alteration of plasma glutamine concentration. Therefore, we evaluated the effect of branched-chain amino acid supplementation on the immune response of triathletes and long-distance runners. METHODS Peripheral blood was collected prior to and immediately after an Olympic Triathlon or a 30k run. Lymphocyte proliferation, cytokine production by cultured cells, and plasma glutamine were measured. RESULTS After the exercise bout, athletes from the placebo group presented a decreased plasma glutamine concentration that was abolished by branched-chain amino acid supplementation and an increased proliferative response in their peripheral blood mononuclear cells. Those cells also produced, after exercise, less tumor necrosis factor, interleukins-1 and -4, and interferon and 48% more interleukin-2. Supplementation stimulated the production of interleukin-2 and interferon after exercise and a more pronounced decrease in the production of interleukin-4, indicating a diversion toward a Th1 type immune response. CONCLUSIONS Our results indicate that branched-chain amino acid (BCAA) supplementation recovers the ability of peripheral blood mononuclear cells proliferate in response to mitogens after a long distance intense exercise, as well as plasma glutamine concentration. The amino acids also modify the pattern of cytokine production leading to a diversion of the immune response toward a Th1 type of immune response.

Creatine supplementation reduces plasma levels of pro-inflammatory cytokines and PGE2 after a half-ironman competition.

Summary.Objective. The effect of creatine supplementation upon plasma levels of pro-inflammatory cytokines: Interleukin (IL) 1β and IL-6, Tumor Necrosis Factor α (TNFα), and Interferon α (INFα) and Prostaglandin E2 (PGE2) after a half-ironman competition were investigated. Methods. Eleven triathletes, each with at least three years experience of participation in this sport were randomly divided between the control and experimental groups. During 5 days prior to competition, the control group (n = 6) was supplemented with carbohydrate (20 g · d−1) whereas the experimental group (n = 5) received creatine (20 g · d−1) in a double-blind trial. Blood samples were collected 48 h before and 24 and 48 h after competition and were used for the measurement of cytokines and PGE2. Results. Forty-eight hours prior to competition there was no difference between groups in the plasma concentrations (pg · ml−1, mean ± SEM) of IL-6 (7.08 ± 0.63), TNFα (76.50 ± 5.60), INFα (18.32 ± 1.20), IL-1β (23.42 ± 5.52), and PGE2 (39.71 ± 3.8). Twenty-four and 48 h after competition plasma levels of TNFα, INFα, IL-1β and PGE2 were significantly increased (P < 0.05) in both groups. However, the increases in these were markedly reduced following creatine supplementation. An increase in plasma IL-6 was observed only after 24 h and, in this case, there was no difference between the two groups. Conclusion. Creatine supplementation before a long distance triathlon competition may reduce the inflammatory response induced by this form of strenuous of exercise.

Does exercise training interfere with the effects of L-carnitine supplementation?

OBJECTIVE We investigated the effect of L-carnitine supplementation on carnitine content in muscle fiber, glucose, and fatty acid metabolism and on performance in trained rats. METHODS Male Wistar rats received a daily dose of 28 mg/kg, intragastrically, during the last 4 wk of a 6-wk moderate-intensity training program. The contents of carnitine and coenzyme A were evaluated in muscle fiber and its capacity to metabolize labeled glucose, oleate, and pyruvate. The ergogenic effect of the amine was assessed by the evaluation of time until exhaustion in an exercise session. The results were analyzed by analysis of variance and Tukeys post hoc test, and significance was set at P < 0.05. RESULTS In our model, carnitine supplementation increased time until exhaustion (14.0%), similar to that observed for trained rats, but the effect was even greater (30.3% increase) in the supplemented and trained rats. Carnitine supplementation increased oleate decarboxylation (17% for sedentary rats and 119% for trained rats) and decreased glucose (29.7% and 45% for sedentary and trained rats, respectively) and [2-(14)C ]-pyruvate (45.9% and 61% for sedentary and trained rats, respectively) decarboxylation. The flux of [1-(14)C]-pyruvate through the Krebs cycle increased by 32% and 70% for supplemented sedentary and trained rats, respectively. The training protocol also increased [1-(14)C]-pyruvate decarboxylation by 32%. The cytosolic content of free, long-chain, and short-chain acyl-carnitine increased in the soleus muscle obtained from supplemented sedentary rats by 28%, 117%, and 16%, respectively, and 99%, 205%, and 32% for the muscle from supplemented trained rats. CONCLUSIONS This study showed that carnitine supplementation increases fatty acid oxidation in skeletal muscle by a mechanism that includes increasing total carnitine content in soleus muscle mitochondria and the total content of acyl-carnitine. The most interesting finding was that the effect of supplementation was even greater in trained rats that had received 3-wk supplementation of carnitine.

Regulação do metabolismo de glicose e ácido graxo no músculo esquelético durante exercício físico

The glucose-fatty acid cycle explains the preference for fatty acid during moderate and long duration physical exercise. In contrast, there is a high glucose availability and oxidation rate in response to intense physical exercise. The reactive oxygen species (ROS) production during physical exercise suggests that the redox balance is important to regulate of lipids/carbohydrate metabolism. ROS reduces the activity of the Krebs cycle, and increases the activity of mitochondrial uncoupling proteins. The opposite effects happen during moderate physical activity. Thus, some issues is highlighted in the present review: Why does skeletal muscle prefer lipids in the basal and during moderate physical activity? Why does glucose-fatty acid fail to carry out their effects during intense physical exercise? How skeletal muscles regulate the lipids and carbohydrate metabolism during the contraction-relaxation cycle?