Branched-chain amino acids supplementation enhances exercise capacity and lipid oxidation during endurance exercise after muscle glycogen depletion

Aim. It has been demonstrated that branched-chain amino acids (BCAA) transaminase activation occurs simultaneously with exercise-induced muscle glycogen reduction, suggesting that BCAA supplementation might play an energetic role in this condition. This study aimed to test whether BCAA supplementation enhances exercise capacity and lipid oxidation in glycogen-depleted subjects. Methods. Using a double-blind cross-over design, volunteers (N.=7) were randomly assigned to either the BCAA (300 mg . kg . day (-1)) or the placebo (maltodextrine) for 3 days. On the second day, subjects were submitted to an exercise-induced glycogen depletion protocol. They then performed an exhaustive exercise test on the third day, after which time to exhaustion, respiratory exchange ratio (RER), plasma glucose, free fatty acids (HA), blood ketones and lactate were determined. BCAA supplementation promoted a greater resistance to fatigue when compared to the placebo (+17.2%). Moreover, subjects supplemented with BCAA showed reduced RER and higher plasma glucose levels during the exhaustive exercise test. Results. No significant differences appeared in FFA, blood ketones and lactate concentrations. Conclusion. In conclusion, BCAA supplementation increases resistance to fatigue and enhances lipid oxidation during exercise in glycogen-depleted subjects.

Is acute supramaximal exercise capable of modulating lipoprotein profile in healthy men?

P>Background This study examined the effects of acute supramaximal exercise (similar to 115% VO(2max)) on the blood lipid profile for three different carbohydrate (CHO) storage levels (control, low and high). Methods Six male subjects were randomly divided into three different groups: control, low CHO and high CHO. These groups differed in the diet to which the subjects were submitted before each exercise session. The lipid profile [triglycerides (TG), very low-density lipoprotein (VLDL), high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, TG/HDL-C ratio and total cholesterol) was determined at rest, immediately after exercise and 1 h after exercise bouts. Results The time to exhaustion was lower in the low CHO condition compared with the control and high CHO condition (3 center dot 59 +/- 0 center dot 72; 2 center dot 91 +/- 0 center dot 56; and 4 center dot 26 +/- 0 center dot 69 min; P < 0 center dot 05). The energy expenditure (control: 251 center dot 1 +/- 56 center dot 0 kJ; low CHO: 215 center dot 2 +/- 28 center dot 6 kJ; and high CHO: 310 center dot 4 +/- 64 center dot 9 kJ) was significantly different between the low and high CHO conditions (P < 0 center dot 05). There were no significant changes in the lipid profile for any of the experimental conditions (control, low and high; P < 0 center dot 05). Glucose and insulin levels did not show time-dependent changes in any of the conditions (P > 0 center dot 05). Conclusions These results indicate that a supramaximal exercise session has no significant effects on lipid metabolism.

A low carbohydrate diet affects autonomic modulation during heavy but not moderate exercise

The aim of this study was to examine the effects of low carbohydrate (CHO) availability on heart rate variability (HRV) responses during moderate and severe exercise intensities until exhaustion. Six healthy males (age, 26.5 +/- 6.7 years; body mass, 78.4 +/- 7.7 kg; body fat %, 11.3 +/- 4.5%; (V) over dotO(2max), 39.5 +/- 6.6 mL kg(-1) min(-1)) volunteered for this study. All tests were performed in the morning, after 8-12 h overnight fasting, at a moderate intensity corresponding to 50% of the difference between the first (LT(1)) and second (LT(2)) lactate breakpoints and at a severe intensity corresponding to 25% of the difference between the maximal power output and LT(2). Forty-eight hours before each experimental session, the subjects performed a 90-min cycling exercise followed by 5-min rest periods and subsequent 1-min cycling bouts at 125% (V) over dotO(2max) (with 1-min rest periods) until exhaustion, in order to deplete muscle glycogen. A diet providing 10% (CHO(low)) or 65% (CHO(control)) of energy as carbohydrates was consumed for the following 2 days until the experimental test. The Poicare plots (standard deviations 1 and 2: SD1 and SD2, respectively) and spectral autoregressive model (low frequency LF, and high frequency HF) were applied to obtain HRV parameters. The CHO availability had no effect on the HRV parameters or ventilation during moderate-intensity exercise. However, the SD1 and SD2 parameters were significantly higher in CHO(low) than in CHO(control), as taken at exhaustion during the severe-intensity exercise (P < 0.05). The HF and LF frequencies (ms(2)) were also significantly higher in CHO(low) than in CHO(control) (P < 0.05). In addition, ventilation measured at the 5 and 10-min was higher in CHO(low) (62.5 +/- 4.4 and 74.8 +/- 6.5 L min(-1), respectively, P < 0.05) than in CHO(control) (70.0 +/- 3.6 and 79.6 +/- 5.1 L min(-1), respectively; P < 0.05) during the severe-intensity exercise. These results suggest that the CHO availability alters the HRV parameters during severe-, but not moderate-, intensity exercise, and this was associated with an increase in ventilation volume.

Acute high-intensity exercise with low energy expenditure reduced LDL-c and total cholesterol in men

A reduction in LDL cholesterol and an increase in HDL cholesterol levels are clinically relevant parameters for the treatment of dyslipidaemia, and exercise is often recommended as an intervention. This study aimed to examine the effects of acute, high-intensity exercise (similar to 90% VO(2max)) and varying carbohydrate levels (control, low and high) on the blood lipid profile. Six male subjects were distributed randomly into exercise groups, based on the carbohydrate diets (control, low and high) to which the subjects were restricted before each exercise session. The lipid profile (triglycerides, VLDL, HDL cholesterol, LDL cholesterol and total cholesterol) was determined at rest, and immediately and 1 h after exercise bouts. There were no changes in the time exhaustion (8.00 +/- A 1.83; 7.82 +/- A 2.66; and 9.09 +/- A 3.51 min) and energy expenditure (496.0 +/- A 224.8; 411.5 +/- A 223.1; and 592.1 +/- A 369.9 kJ) parameters with the three varying carbohydrate intake (control, low and high). Glucose and insulin levels did not show time-dependent changes under the different conditions (P > 0.05). Total cholesterol and LDL cholesterol were reduced after the exhaustion and 1 h recovery periods when compared with rest periods only in the control carbohydrate intake group (P < 0.05), although this relation failed when the diet was manipulated. These results indicate that acute, high-intensity exercise with low energy expenditure induces changes in the cholesterol profile, and that influences of carbohydrate level corresponding to these modifications fail when carbohydrate (low and high) intake is manipulated.

Low carbohydrate diet affects the oxygen uptake on-kinetics and rating of perceived exertion in high intensity exercise

The aim of this study was to determine if the carbohydrate (CHO) availability alters the rate of increase in the rating of perceived exertion (RPE) during high intensity exercise and whether this would be associated with physiological changes. Six males performed high intensity exercise after 48 h of controlled, high CHO (80%) and low CHO (10%) diets. Time to exhaustion was lower in the low compared to high CHO diet. The rate of increase in RPE was greater and the VO(2) slow component was lower in the low CHO diet than in the control. There was no significant condition effect for cortisol, insulin, pH, plasma glucose, potassium, or lactate concentrations. Multiple linear regression indicated that the total amplitude of VO(2) and perceived muscle strain accounted for the greatest variance in the rate of increase in RPE. These results suggest that cardiorespiratory variables and muscle strain are important afferent signals from the periphery for the RPE calculations.

Pacing redistributes glycogen within the developing myocardium.

Electrical pacing at physiological rate induces myocardial remodeling associated with regional changes in workload, blood flow and oxygen consumption. However, to what extent energy-producing pathways are also modified within the paced heart remains to be investigated. Pacing could particularly affect glycogen metabolism since hypertrophy stimulates glycolysis and increased workload favors glucose over fat oxidation. In order to test this hypothesis, we used the embryonic chick heart model in which ventricular pacing rapidly resulted in thinning of the ventricle wall and thickening of the atrial wall. Hearts of stage 22HH chick embryos were submitted in ovo to asynchronous and intermittent ventricular pacing delivered at physiological rate during 24 h. The resulting alterations of glycogen content were determined in atrium, ventricle and conotruncus of paced and sham-operated hearts. Hemodynamic parameters of the paced and spontaneously beating hearts were derived from computerized image analysis of video recordings. With respect to sham, paced hearts showed a significant decrease in glycogen content (nmoles glucose units/microg protein; mean+/-S.D.) only in atrium (1.48+/-0.40 v 0.84+/-0.34, n=8) and conotruncus (0.75+/-0.28 v 0.42+/-0.23, n=8). Pacing decreased the end diastolic and stroke volumes by 34 and 44%, respectively. Thus, the rapid glycogen depletion in regions remote from the stimulation site appears to be associated with regional changes in workload and remodeling. These findings underscore the importance of the coupling mechanisms between metabolic pathways and myocardial remodeling in the ectopically paced heart.

Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man.

The metabolic balance method was performed on three men to investigate the fate of large excesses of carbohydrate. Glycogen stores, which were first depleted by diet (3 d, 8.35 +/- 0.27 MJ [1994 +/- 65 kcal] decreasing to 5.70 +/- 1.03 MJ [1361 +/- 247 kcal], 15% protein, 75% fat, 10% carbohydrate) and exercise, were repleted during 7 d carbohydrate overfeeding (11% protein, 3% fat, and 86% carbohydrate) providing 15.25 +/- 1.10 MJ (3642 +/- 263 kcal) on the first day, increasing progressively to 20.64 +/- 1.30 MJ (4930 +/- 311 kcal) on the last day of overfeeding. Glycogen depletion was again accomplished with 2 d of carbohydrate restriction (2.52 MJ/d [602 kcal/d], 85% protein, and 15% fat). Glycogen storage capacity in man is approximately 15 g/kg body weight and can accommodate a gain of approximately 500 g before net lipid synthesis contributes to increasing body fat mass. When the glycogen stores are saturated, massive intakes of carbohydrate are disposed of by high carbohydrate-oxidation rates and substantial de novo lipid synthesis (150 g lipid/d using approximately 475 g CHO/d) without postabsorptive hyperglycemia.

Glycogen storage and muscle glucose transporters (GLUT-4) of mice selectively bred for high voluntary wheel running

To examine the evolution of endurance-exercise behaviour, we have selectively bred four replicate lines of laboratory mice (Mus domesticus) for high voluntary wheel running ('high runner' or HR lines), while also maintaining four non-selected control (C) lines. By generation 16, HR mice ran ∼2.7-fold more than C mice, mainly by running faster (especially in females), a differential maintained through subsequent generations, suggesting an evolutionary limit of unknown origin. We hypothesized that HR mice would have higher glycogen levels before nightly running, show greater depletion of those depots during their more intense wheel running, and have increased glycogen synthase activity and GLUT-4 protein in skeletal muscle. We sampled females from generation 35 at three times (photophase 07:00 h-19:00 h) during days 5-6 of wheel access, as in the routine selection protocol: Group 1, day 5, 16:00 h-17:30 h, wheels blocked from 13:00 h; Group 2, day 6, 02:00 h-03:30 h (immediately after peak running); and Group 3, day 6, 07:00 h-08:30 h. An additional Group 4, sampled 16:00 h-17:30 h, never had wheels. HR individuals with the mini-muscle phenotype (50% reduced hindlimb muscle mass) were distinguished for statistical analyses comparing C, HR normal, and HR mini. HR mini ran more than HR normal, and at higher speeds, which might explain why they have been favored by the selective-breeding protocol. Plasma glucose was higher in Group 1 than in Group 4, indicating a training effect (phenotypic plasticity). Without wheels, no differences in gastrocnemius GLUT-4 were observed. After 5 days with wheels, all mice showed elevated GLUT-4, but HR normal and mini were 2.5-fold higher than C. At all times and irrespective of wheel access, HR mini showed approximately three-fold higher [glycogen] in gastrocnemius and altered glycogen synthase activity. HR mini also showed elevated glycogen in soleus when sampled during peak running. All mice showed some glycogen depletion during nightly wheel running, in muscles and/or liver, but the magnitude of this depletion was not large and hence does not seem to be limiting to the evolution of even-higher wheel running.

Differential contribution of mitochondria, NADPH oxidases, and glycolysis to region-specific oxidant stress in the anoxic-reoxygenated embryonic heart.

The ability of the developing myocardium to tolerate oxidative stress during early gestation is an important issue with regard to possible detrimental consequences for the fetus. In the embryonic heart, antioxidant defences are low, whereas glycolytic flux is high. The pro- and antioxidant mechanisms and their dependency on glucose metabolism remain to be explored. Isolated hearts of 4-day-old chick embryos were exposed to normoxia (30 min), anoxia (30 min), and hyperoxic reoxygenation (60 min). The time course of ROS production in the whole heart and in the atria, ventricle, and outflow tract was established using lucigenin-enhanced chemiluminescence. Cardiac rhythm, conduction, and arrhythmias were determined. The activity of superoxide dismutase, catalase, gutathione reductase, and glutathione peroxidase as well as the content of reduced and oxidized glutathione were measured. The relative contribution of the ROS-generating systems was assessed by inhibition of mitochondrial complexes I and III (rotenone and myxothiazol), NADPH oxidases (diphenylene iodonium and apocynine), and nitric oxide synthases (N-monomethyl-l-arginine and N-iminoethyl-l-ornithine). The effects of glycolysis inhibition (iodoacetate), glucose deprivation, glycogen depletion, and lactate accumulation were also investigated. In untreated hearts, ROS production peaked at 10.8 ± 3.3, 9 ± 0.8, and 4.8 ± 0.4 min (means ± SD; n = 4) of reoxygenation in the atria, ventricle, and outflow tract, respectively, and was associated with arrhythmias. Functional recovery was complete after 30-40 min. At reoxygenation, 1) the respiratory chain and NADPH oxidases were the main sources of ROS in the atria and outflow tract, respectively; 2) glucose deprivation decreased, whereas glycogen depletion increased, oxidative stress; 3) lactate worsened oxidant stress via NADPH oxidase activation; 4) glycolysis blockade enhanced ROS production; 5) no nitrosative stress was detectable; and 6) the glutathione redox cycle appeared to be a major antioxidant system. Thus, the glycolytic pathway plays a predominant role in reoxygenation-induced oxidative stress during early cardiogenesis. The relative contribution of mitochondria and extramitochondrial systems to ROS generation varies from one region to another and throughout reoxygenation.

Fat oxidation kinetics : effect of exercise

ABSTRACT Fat oxidation kinetics: effect of exercise. During graded exercise, absolute whole body fat oxidation rates increase from low to moderate intensities, and then markedly decline at high intensities, implying an exercise intensity (Fatmax) at which the fat oxidation rate is maximal (MFO). The main aim of the present work was to examine the effect of exercise on whole body fat oxidation kinetics. For this purpose, a sinusoidal mathematical model (SIN) has been developped in the first study to provide an accurate description of the shape of fat oxidation kinetics during graded exercise, represented as a function of exercise intensity, and to determine Fatmax and MFO. The SIN model incorporates three independent variables (i.e., dilatation, symmetry, and translation) that correspond to main expected modulations of the basic fat oxidation curve because of factors such as mode of exercise or training status. The results of study 1 showed that the SIN model was a valuable tool to determine Fatmax and MFO, and to precisely characterize and quantify the different shape of fat oxidation kinetics through its three variables. The effectiveness of the SIN model to detect differences in fat oxidation kinetics induced by a specific factor was then confirmed in the second study, which quantitatively described and compared fat oxidation kinetics in two different popular modes of exercise: running and cycling. It was found that the mean fat oxidation kinetics during running was characterized by a greater dilatation and a rightward asymmetry compared with the symmetric parabolic curve in cycling. In the two subsequent studies, the effect of a prior endurance exercise of different intensities and durations on whole body fat oxidation kinetics was examined. Study 3 determined the impact of a 1-h continuous exercise bout at an exercise intensity corresponding to Fatmax on fat oxidation kinetics during a subsequent graded test, while study 4 investigated the effect of an exercise leading to a more pronounced muscle glycogen depletion. The results of these two latter studies showed that fat oxidation rates, MFO, and Fatmax were enhanced following endurance exercise, but were increased to a greater extent with a more severe mucle glycogen depletion, inducing therefore modifications in the postexercise fat oxidation kinetics (i.e., greater dilatation and rightward asymmetry). In perspective, further studies have been suggested 1) to assess physiological meaning of the three independent variables of the SIN model; and 2) to compare the effect of two different training programs on fat oxidation kinetics in obese subjects.

Effect of carbohydrate availability on time to exhaustion in exercise performed at two different intensities

This study examined the effects of pre-exercise carbohydrate availability on the time to exhaustion for moderate and heavy exercise. Seven men participated in a randomized order in two diet and exercise regimens each lasting 3 days with a 1-week interval for washout. The tests were performed at 50% of the difference between the first (LT1) and second (LT2) lactate breakpoint for moderate exercise (below LT2) and at 25% of the difference between the maximal load and LT2 for heavy exercise (above LT2) until exhaustion. Forty-eight hours before each experimental session, subjects performed a 90-min cycling exercise followed by 5-min rest periods and a subsequent 1-min cycling bout at 125% VO2max/1-min rest periods until exhaustion to deplete muscle glycogen. A diet providing 10% (CHOlow) or 65% (CHOmod) energy as carbohydrates was consumed for 2 days until the day of the experimental test. In the exercise below LT2, time to exhaustion did not differ between the CHOmod and the CHOlow diets (57.22 ± 24.24 vs 57.16 ± 25.24 min). In the exercise above LT2, time to exhaustion decreased significantly from 23.16 ± 8.76 min on the CHOmod diet to 18.30 ± 5.86 min on the CHOlow diet (P < 0.05). The rate of carbohydrate oxidation, respiratory exchange ratio and blood lactate concentration were reduced for CHOlow only during exercise above LT2. These results suggest that muscle glycogen depletion followed by a period of a low carbohydrate diet impairs high-intensity exercise performance.

Food-dependent, exercise-induced gastrointestinal distress

Among athletes strenuous exercise, dehydration and gastric emptying (GE) delay are the main causes of gastrointestinal (GI) complaints, whereas gut ischemia is the main cause of their nausea, vomiting, abdominal pain and (blood) diarrhea. Additionally any factor that limits sweat evaporation, such as a hot and humid environment and/or body dehydration, has profound effects on muscle glycogen depletion and risk for heat illness. A serious underperfusion of the gut often leads to mucosal damage and enhanced permeability so as to hide blood loss, microbiota invasion (or endotoxemia) and food-born allergen absorption (with anaphylaxis). The goal of exercise rehydration is to intake more fluid orally than what is being lost in sweat. Sports drinks provide the addition of sodium and carbohydrates to assist with intestinal absorption of water and muscle-glycogen replenishment, respectively. However GE is proportionally slowed by carbohydrate-rich (hyperosmolar) solutions. on the other hand, in order to prevent hyponatremia, avoiding overhydration is recommended. Caregiver's responsibility would be to inform athletes about potential dangers of drinking too much water and also advise them to refrain from using hypertonic fluid replacements.

Effect of fluoride intake on carbohydrate metabolism, glucose tolerance, and insulin signaling

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

Aspectos nutricionais do futebol de competição

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)