Impact of postprandial glycaemia on health and prevention of disease

Postprandial glucose, together with related hyperinsulinemia and lipidaemia, has been implicated in the development of chronic metabolic diseases like obesity, type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). In this review, available evidence is discussed on postprandial glucose in relation to body weight control, the development of oxidative stress, T2DM, and CVD and in maintaining optimal exercise and cognitive performance. There is mechanistic evidence linking postprandial glycaemia or glycaemic variability to the development of these conditions or in the impairment in cognitive and exercise performance. Nevertheless, postprandial glycaemia is interrelated with many other (risk) factors as well as to fasting glucose. In many studies, meal-related glycaemic response is not sufficiently characterized, or the methodology with respect to the description of food or meal composition, or the duration of the measurement of postprandial glycaemia is limited. It is evident that more randomized controlled dietary intervention trials using effective low vs. high glucose response diets are necessary in order to draw more definite conclusions on the role of postprandial glycaemia in relation to health and disease. Also of importance is the evaluation of the potential role of the time course of postprandial glycaemia.

Effect of short-term creatine supplementation on markers of skeletal muscle damage after strenuous contractile activity

The protective effect of short-term creatine supplementation (CrS) upon markers of strenuous contractile activity-induced damage in human and rat skeletal muscles was investigated. Eight Ironman triathletes were randomized into the placebo (Pl; n = 4) and creatine-supplemented (CrS; n = 4) groups. Five days prior to the Ironman competition, the CrS group received creatine monohydrate (20 g day(-1)) plus maltodextrin (50 g) divided in two equal doses. The Pl group received maltodextrin (50 g day(-1)) only. The effect of CrS (5 g day(-1)/kg body weight for 5 days) was also evaluated in a protocol of strenuous contractile activity induced by electrical stimulation in rats. Blood samples were collected before and 36 and 60 h after the competition and were used to determine plasma activities of creatine kinase (CK), lactate dehydrogenase (LDH), aldolase (ALD), glutamic oxaloacetic acid transaminase (GOT), glutamic pyruvic acid transaminase (GPT), and C-reactive protein (CRP) level. In rats, plasma activities of CK and LDH, muscle vascular permeability (MVP) using Evans blue dye, muscle force and fatigue were evaluated. Activities of CK, ALD, LDH, GOT, GTP, and levels of CRP were increased in the Pl group after the competition as compared to basal values. CrS decreased plasma activities of CK, LDH, and ALD, and prevented the rise of GOT and GPT plasma activities. In rats, CrS delayed the fatigue, preserved the force, and prevented the rise of LDH and CK plasma activities and MVP in the gastrocnemius muscle. CrS presented a protective effect on muscle injury induced by strenuous contractile activities.

Creatine supplementation reduces plasma levels of pro-inflammatory cytokines and PGE(2) after a half-ironman competition

Objective. The effect of creatine supplementation upon plasma levels of pro-inflammatory cytokines: Interleukin (IL) 1 beta and IL-6, Tumor Necrosis Factor alpha (TNF alpha), and Interferon alpha (INF alpha) and Prostaglandin E(2) (PGE(2)) 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 (20g center dot d(-1)) whereas the experimental group (n = 5) received creatine (20 center dot d(-1)) in a double-blind trial. Blood samples were collected 48h before and 24 and 48h after competition and were used for the measurement of cytokines and PGE(2). Results. Forty-eight hours prior to competition there was no difference between groups in the plasma concentrations (pg center dot ml(-1), mean +/- SEM) of IL-6 (7.08 +/- 0.63), TNF alpha (76.50 +/- 5.60), INF alpha (18.32 +/- 1.20), IL-1 beta (23.42 +/- 5.52), and PGE(2) (39.71 +/- 3.8). Twenty-four and 48h after competition plasma levels of TNF alpha, INF alpha, IL-1 beta and PGE(2) 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 24h 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.

(Mal) adaptações metabólicas ao treinamento contínuo: concepções não consensuais de terminologia e diagnóstico

Altos desempenhos esportivos demandam treinamentos pesados necessários ao estímulo adaptativo específico a cada esporte. A elevada carga de treino é geralmente acompanhada de discreta fadiga e reduções agudas no desempenho, mas caso acompanhada de períodos apropriados de recuperação, resulta em supercompensação metabólica ao treinamento, refletida como aumento na capacidade aeróbica e/ou força muscular. Visto como contínuo, os processos de intensificação do treinamento e o estresse relacionado à supercompensação, o aumento da sobrecarga ou do estresse poderá, em algum momento, acarretar a quebra da homeostase e a queda temporária da função (supra-alcance - OR ou supra-alcance funcional - FOR). Quando a sobrecarga excessiva de treinamento é combinada com recuperação inadequada há instalação do estado de supratreinamento (OT) ou supra-alcance não funcional (NFOR). O OT excede o OR, cujo pico é também o limiar do OT resultando em desadaptações fisiológicas e queda crônica do desempenho físico. A forma crônica de desadaptação fisiológica ao treinamento físico é chamada de síndrome do supertreinamento (OTS). A própria expressão da síndrome denota a etiologia multifatorial do estado e reconhece que o exercício não é necessariamente seu único fator causal. O diagnóstico de OTS é baseado na recuperação ou não do desempenho. Não há biomarcador objetivo para OTS. A distinção entre OTS e NFOR (supratreinamento extremo) é dependente de desfecho clínico e exclusão diagnóstica de doenças orgânicas, mais comuns na OTS. Também a diferença entre OR e OT é sutil e nenhum de seus marcadores bioquímicos pode ser universalizado. Não há evidências confirmatórias que OR evolui para OT ou que os sintomas de OT são piores dos que os de OR. Apenas pela fadiga aguda e queda de rendimento experimentada em sessões isoladas de treinamento, não é possível diferenciar presentemente os estados de OR e OT. Isto é devido, parcialmente, à variabilidade das respostas individuais ao treinamento e à falta de ambos instrumentos diagnósticos e estudos bem controlados.

EFFECT OF CAFFEINE ON THE METABOLISM OF RATS EXERCISING BY SWIMMING

Several studies have demonstrated that caffeine improves endurance exercise performance but the mechanisms are not fully understood. Possibilities include increased free fatty acid (FFA) oxidation with consequent sparing of muscle glycogen as well as enhancement of neuromuscular function during exercise. The present study was designed to investigate the effects of caffeine on liver and muscle glycogen of 3-month old, male Wistar rats (250-300 g) exercising by swimming. Caffeine (5 mg/kg) dissolved in saline (CAF) or 0.9% sodium chloride (SAL) was administered by oral intubation (1 mu l/g) to fed rats 60 min before exercise. The rats (N = and-IO per group) swam bearing a load corresponding to 5% body weight for 30 or 60 min. FFA levels were significantly elevated to 0.475 +/- 0.10 mEq/l in CAF compared to 0.369 +/- 0.06 mEq/l in SAL rats at the beginning of exercise. During exercise, a significant difference in FFA levels between CAF and SAL rats was observed at 30 min (0.325 +/- 0.06 vs 0.274 +/- 0.05 mEq/l) but not at 60 min (0.424 +/- 0.13 vs 0.385 +/- 0.10 mEq/l). Blood glucose showed an increase due to caffeine only at the end of exercise (CAF = 142.1 +/- 27.4 and SAL = 120.2 +/- 12.9 mg/100 ml). No significant difference in liver or muscle glycogen was observed in CAF as compared to SAL rats, at rest or during exercise. Caffeine increased blood lactate only at the beginning of exercise (CAF = 2.13 +/- 0.2 and SAL = 1.78 +/- 0.2 mmol/l). These data indicate that caffeine (5 mg/kg) has no glycogen-sparing effect on rats exercising by swimming even though the FFA levels of CAF rats were significantly higher at the beginning of exercise.

Influência da pré-eclâmpsia na capacidade funcional de exercício

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Força de reação do solo (vertical) de indivíduos realizando exercício de hidroginástica em ambiente terrestre e aquático

Pós-graduação em Engenharia Mecânica - FEG

Respostas inflamatória, hematológica, de estresse oxidativo, prejuízo muscular e composição corporal em ultramaratona de 217 km

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Efeito do nadar sobre o desempenho do pedal e corrida no triathlon super-sprint

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Maximal power output during incremental cycling test is dependent on the curvature constant of the power-time relationship

The aim of this study was to investigate whether the maximal power output (Pmax) during an incremental test was dependent on the curvature constant (W') of the power-time relationship. Thirty healthy male subjects (maximal oxygen uptake = 3.58 ± 0.40 L·min(-1)) performed a ramp incremental cycling test to determine the maximal oxygen uptake and Pmax, and 4 constant work rate tests to exhaustion to estimate 2 parameters from the modeling of the power-time relationship (i.e., critical power (CP) and W'). Afterwards, the participants were ranked according to their magnitude of W'. The median third was excluded to form a high W' group (HIGH, n = 10), and a low W' group (LOW, n = 10). Maximal oxygen uptake (3.84 ± 0.50 vs. 3.49 ± 0.37 L·min(-1)) and CP (213 ± 22 vs. 200 ± 29 W) were not significantly different between HIGH and LOW, respectively. However, Pmax was significantly greater for the HIGH (337 ± 23 W) than for the LOW (299 ± 40 W). Thus, in physically active individuals with similar aerobic parameters, W' influences the Pmax during incremental testing.

Bioenergetics and neuromuscular determinants of the time to exhaustion at velocity corresponding to (V) over dotO(2)max in recreational long-distance runners

Bertuzzi, R, Bueno, S, Pasqua, LA, Acquesta, FM, Batista, MB, Roschel, H, Kiss, MAPDM, Serrao, JC, Tricoli, V, and Ugrinowitsch, C. Bioenergetics and neuromuscular determinants of the time to exhaustion at velocity corresponding to (V) over dotO(2)max in recreational long-distance runners. J Strength Cond Res 26(8): 2096-2102, 2012-The purpose of this study was to investigate the main bioenergetics and neuromuscular determinants of the time to exhaustion (T-lim) at the velocity corresponding to maximal oxygen uptake in recreational long-distance runners. Twenty runners performed the following tests on 5 different days: (a) maximal incremental treadmill test, (b) 2 submaximal tests to determine running economy and vertical stiffness, (c) exhaustive test to measured the T-lim, (d) maximum dynamic strength test, and (e) muscle power production test. Aerobic and anaerobic energy contributions during the T-lim test were also estimated. The stepwise multiple regression method selected 3 independent variables to explain T-lim variance. Total energy production explained 84.1% of the shared variance (p = 0.001), whereas peak oxygen uptake ((V) over dotO(2)peak) measured during T-lim and lower limb muscle power ability accounted for the additional 10% of the shared variance (p = 0.014). These data suggest that the total energy production, (V) over dotO(2)peak, and lower limb muscle power ability are the main physiological and neuromuscular determinants of T-lim in recreational long-distance runners.

Effects of excess body mass on strength and fatigability of quadriceps in postmenopausal women

Objective: Obesity is a major public health problem leading to, among other things, reduced functional capacity. Moreover, obesity-related declines in functional capacity may be compounded by the detrimental consequences of menopause. The aim of this study was to understand the potential effects of excess body mass on measures of functional capacity in postmenopausal women. Methods: Forty-five postmenopausal women aged 50 to 60 years were divided into two groups according to body mass index (BMI): obese (BMI, >= 30 kg/m(2); n = 19) and nonobese (BMI, 18.5-29.9 kg/m(2); n = 26). To determine clinical characteristics, body composition, bone mineral density, and maximal exercise testing was performed, and a 3-day dietary record was estimated. To assess quadriceps function, isokinetic exercise testing at 60 degrees per second (quadriceps strength) and at 300 degrees per second (quadriceps fatigue) was performed. Results: The absolute value of the peak torque was not significantly different between the groups; however, when the data were normalized by body mass and lean mass, significantly lower values were observed for obese women compared with those in the nonobese group (128% +/- 25% vs 155% +/- 24% and 224% +/- 38% vs 257% +/- 47%, P < 0.05). The fatigue index did not show any significant difference for either group; however, when the data were normalized by the body mass and lean mass, significantly lower values were observed for obese women (69% +/- 16% vs 93% +/- 18% and 120% +/- 25% vs. 135% +/- 23%, P < 0.01). Conclusions: Our results show that despite reduced muscle force, the combination of obesity and postmenopause may be associated with greater resistance to muscle fatigue.

Effects of acute creatine supplementation on iron homeostasis and uric acid-based antioxidant capacity of plasma after wingate test

Background: Dietary creatine has been largely used as an ergogenic aid to improve strength and athletic performance, especially in short-term and high energy-demanding anaerobic exercise. Recent findings have also suggested a possible antioxidant role for creatine in muscle tissues during exercise. Here we evaluate the effects of a 1-week regimen of 20 g/day creatine supplementation on the plasma antioxidant capacity, free and heme iron content, and uric acid and lipid peroxidation levels of young subjects (23.1 +/- 5.8 years old) immediately before and 5 and 60 min after the exhaustive Wingate test. Results: Maximum anaerobic power was improved by acute creatine supplementation (10.5 %), but it was accompanied by a 2.4-fold increase in pro-oxidant free iron ions in the plasma. However, potential iron-driven oxidative insult was adequately counterbalanced by proportional increases in antioxidant ferric-reducing activity in plasma (FRAP), leading to unaltered lipid peroxidation levels. Interestingly, the FRAP index, found to be highly dependent on uric acid levels in the placebo group, also had an additional contribution from other circulating metabolites in creatine-fed subjects. Conclusions: Our data suggest that acute creatine supplementation improved the anaerobic performance of athletes and limited short-term oxidative insults, since creatine-induced iron overload was efficiently circumvented by acquired FRAP capacity attributed to: overproduction of uric acid in energy-depleted muscles (as an end-product of purine metabolism and a powerful iron chelating agent) and inherent antioxidant activity of creatine.

Circulating plasma surfactant protein type B as biological marker of alveolar-capillary barrier damage in chronic heart failure

BACKGROUND: Surfactant protein type B (SPB) is needed for alveolar gas exchange. SPB is increased in the plasma of patients with heart failure (HF), with a concentration that is higher when HF severity is highest. The aim of this study was to evaluate the relationship between plasma SPB and both alveolar-capillary diffusion at rest and ventilation versus carbon dioxide production during exercise. METHODS AND RESULTS: Eighty patients with chronic HF and 20 healthy controls were evaluated consecutively, but the required quality for procedures was only reached by 71 patients with HF and 19 healthy controls. Each subject underwent pulmonary function measurements, including lung diffusion for carbon monoxide and membrane diffusion capacity, and maximal cardiopulmonary exercise test. Plasma SPB was measured by immunoblotting. In patients with HF, SPB values were higher (4.5 [11.1] versus 1.6 [2.9], P=0.0006, median and 25th to 75th interquartile), whereas lung diffusion for carbon monoxide (19.7+/-4.5 versus 24.6+/-6.8 mL/mm Hg per min, P<0.0001, mean+/-SD) and membrane diffusion capacity (28.9+/-7.4 versus 38.7+/-14.8, P<0.0001) were lower. Peak oxygen consumption and ventilation/carbon dioxide production slope were 16.2+/-4.3 versus 26.8+/-6.2 mL/kg per min (P<0.0001) and 29.7+/-5.9 and 24.5+/-3.2 (P<0.0001) in HF and controls, respectively. In the HF population, univariate analysis showed a significant relationship between plasma SPB and lung diffusion for carbon monoxide, membrane diffusion capacity, peak oxygen consumption, and ventilation/carbon dioxide production slope (P<0.0001 for all). On multivariable logistic regression analysis, membrane diffusion capacity (beta, -0.54; SE, 0.018; P<0.0001), peak oxygen consumption (beta, -0.53; SE, 0.036; P=0.004), and ventilation/carbon dioxide production slope (beta, 0.25; SE, 0.026; P=0.034) were independently associated with SPB. CONCLUSIONS: Circulating plasma SPB levels are related to alveolar gas diffusion, overall exercise performance, and efficiency of ventilation showing a link between alveolar-capillary barrier damage, gas exchange abnormalities, and exercise performance in HF.

The importance of growth hormone in the regulation of erythropoiesis, red cell mass, and plasma volume in adults with growth hormone deficiency

Total body water (TBW) is reduced in adult GH deficiency (GHD) largely due to a reduction of extracellular water. It is unknown whether total blood volume (TBV) contributes to the reduced extracellular water in GHD. GH and insulin-like growth factor I (IGF-I) have been demonstrated to stimulate erythropoiesis in vitro, in animal models, and in growing children. Whether GH has a regulatory effect on red cell mass (RCM) in adults is not known. We analyzed body composition by bioelectrical impedance and used standard radionuclide dilution methods to measure RCM and plasma volume (PV) along with measuring full blood count, ferritin, vitamin B12, red cell folate, IGF-I, IGF-binding protein-3, and erythropoietin in 13 adult patients with GHD as part of a 3-month, double blind, placebo-controlled trial of GH (0.036 U/kg.day). TBW and lean body mass significantly increased by 2.5 +/- 0.53 kg (mean +/- SEM; P < 0.004) and 3.4 +/- 0.73 kg (P < 0.004), respectively, and fat mass significantly decreased by 2.4 +/- 0.32 kg (P < 0.001) in the GH-treated group. The baseline RCM of all patients with GHD was lower than the predicted normal values (1635 +/- 108 vs. 1850 +/- 104 mL; P < 0.002). GH significantly increased RCM, PV, and TBV by 183 +/- 43 (P < 0.006), 350 +/- 117 (P < 0.03), and 515 +/- 109 (P < 0.004) mL, respectively. The red cell count increased by 0.36 +/- 0.116 x 10(12)/L (P < 0.03) with a decrease in ferritin levels by 39.1 +/- 4.84 micrograms/L (P < 0.001) after GH treatment. Serum IGF-I and IGF-binding protein-3 concentrations increased by 3.0 +/- 0.43 (P < 0.001) and 1.3 +/- 0.15 (P < 0.001) SD, respectively, but the erythropoietin concentration was unchanged after GH treatment. No significant changes in body composition or blood volume were recorded in the placebo group. Significant positive correlations could be established between changes in TBW and TBV, lean body mass and TBV (r = 0.78; P < 0.04 and r = 0.77; P < 0.04, respectively), and a significant negative correlation existed between changes in fat mass and changes in TBV in the GH-treated group (r = -0.95; P < 0.02). We conclude that 1) erythropoiesis is impaired in GHD; 2) GH stimulates erythropoiesis in adult GHD; and 3) GH increases PV and TBV, which may contribute to the increased exercise performance seen in these patients.