Substrate Oxidation Rates Research Articles

Hyperinsulinaemia during exercise does not suppress hepatic glycogen concentrations in patients with type 1 diabetes: a magnetic resonance spectroscopy study

We compared in vivo changes in liver glycogen concentration during exercise between patients with type 1 diabetes and healthy volunteers. We studied seven men with type 1 diabetes (mean +/- SEM diabetes duration 10 +/- 2 years, age 33 +/- 3 years, BMI 24 +/- 1 kg/m(2), HbA(1c) 8.1 +/- 0.2% and VO(2) peak 43 +/- 2 ml [kg lean body mass](-1) min(-1)) and five non-diabetic controls (mean +/- SEM age 30 +/- 3 years, BMI 22 +/- 1 kg/m(2), HbA(1c) 5.4 +/- 0.1% and VO(2) peak 52 +/- 4 ml [kg lean body mass](-1) min(-1), before and after a standardised breakfast and after three bouts (EX1, EX2, EX3) of 40 min of cycling at 60% VO(2) peak. (13)C Magnetic resonance spectroscopy of liver glycogen was acquired in a 3.0 T magnet using a surface coil. Whole-body substrate oxidation was determined using indirect calorimetry. Blood glucose and serum insulin concentrations were significantly higher (p < 0.05) in the fasting state, during the postprandial period and during EX1 and EX2 in subjects with type 1 diabetes compared with controls. Serum insulin concentration was still different between groups during EX3 (p < 0.05), but blood glucose concentration was similar. There was no difference between groups in liver glycogen concentration before or after the three bouts of exercise, despite the relative hyperinsulinaemia in type 1 diabetes. There were also no differences in substrate oxidation rates between groups. In patients with type 1 diabetes, hyperinsulinaemic and hyperglycaemic conditions during moderate exercise did not suppress hepatic glycogen concentrations. These findings do not support the hypothesis that exercise-induced hypoglycaemia in patients with type 1 diabetes is due to suppression of hepatic glycogen mobilisation.

Ferrous Iron Oxidation by Salt-Tolerant &lt;i&gt;“Thiobacillus prosperus”&lt;/i&gt;

Growth on ferrous iron of a new isolate of the halotolerant acidophile “Thiobacillus prosperus” occurred with a substrate oxidation rate similar to that of Acidithiobacillus ferrooxidans, but with a requirement for salt (NaCl). These observations contrast with the previous description of “T. prosperus” in which a salt requirement was not noted and growth on ferrous iron was described as poor. As well as similar capacities for iron oxidation, these species were shown to possess similar clusters of genes (the rus operon) that encode proteins likely to be involved in transfer of electrons from ferrous iron. There were some differences in the organization of the genes and one of them that encodes a cytochrome c in At. ferrooxidans was absent from the “T. prosperus” cluster.

Mechanistic Studies of Ce(IV)-Mediated Oxidation of β-Dicarbonyls: Solvent-Dependent Behavior of Radical Cation Intermediates

The Ce(IV)-initiated oxidation of synthetically relevant beta-diketones and beta-keto silyl enol ethers was explored in three solvents: acetonitrile, methylene chloride, and methanol. The studies presented herein show that the rate of reaction between Ce(IV) and the substrates is dependent upon the polarity of the solvent. Thermochemical studies and analysis are interpreted to be consistent with transition state stabilization by solvent being primarily responsible for the rate of substrate oxidation. Kinetic investigation of radical cations obtained from oxidations of beta-diketones reveals that a more ordered transition state for the radical cation decay is achieved through the direct involvement of methanol in the deprotonation of the intermediate. In the case of radical cations derived from beta-keto silyl enol ethers, experimental data support a mechanism involving unimolecular decay of the intermediate. Remarkably, radical cations derived from beta-diketones and beta-keto silyl enol ethers are surprisingly stable in methylene chloride.

Growth hormone action in puberty: Effects by gender

Objective Adult females receiving GH may be less sensitive to the metabolic effects of GH than males, however these differences are less well studied in adolescence. We aimed to investigate if metabolic effects of GH vary by gender during puberty. Design Sixteen adolescents (8 M/8 F, mean age (SE): 13.1 ± 0.2 yr) with significant short stature due to either GH insufficiency or idiopathic short stature were studied before and after 8 w of daily GH therapy. Differences in rates of protein and glycerol turnover ( 13C leucine and d5-glycerol infusions), substrate oxidation rates (indirect calorimetry), hormones, growth factors, lipid concentrations, body composition (DEXA) and 1 yr growth velocity were measured. Results Protein synthesis rates per kg FFM were similar in boys and girls before and after GH and increased similarly on treatment in both genders. Rates of whole body lipolysis were similar at baseline and increased after GH in both genders comparably. Plasma lipids were similar between boys and girls before and after GH, and triglycerides increased post-GH in both. Insulin increased after GH comparably in both genders, yet no significant difference in glucose or adiponectin concentrations during treatment or between genders was observed. IGF-I concentrations were similar between boys and girls at baseline, but with a more robust increase in males after 8 w of GH (boys: +629 ± 65 ng/ml, girls: +331 ± 67, p = 0.007). Body composition changes and bone mineral density were similar between genders after GH. HT SDS increased comparably after 1 yr (boys −2.2 ± 0.09 to −1.77 ± 0.11, p = 0.0002; girls −2.49 ± 0.24 to −2.02 ± 0.25, p = 0.04). There were no gender differences on the linear growth responses after 12 mo. Conclusions As compared to girls, boys had: (1) similar sensitivity to GH for protein synthesis, lipolysis, lipid concentrations and body composition changes as well as comparable glucose and adiponectin concentrations; (2) higher IGF-I responses to 8 w of GH. Differences in IGF-I during GH treatment may account in part for the gender differences in physique and strength that develop during human puberty; however, using conventional doses of GH, these differences do not translate into differences in linear growth after 12 mo. Contrary to adults, these data do not support the need for different GH dosing depending on gender during puberty.

High-level medium-chain triglyceride feeding and energy expenditure in normal-weight women

The objective of this study was to assess how short-term feeding of high levels of dietary medium-chain triglyceride (MCT) affect energy expenditure and postprandial substrate oxidation rates in normal-weight, premenopausal women. Eight healthy women were fed both a MCT-rich and an isocaloric long-chain triglyceride (LCT)-rich diet for two 1-week periods separated by a minimum of 21 days. The energy intake in each diet was 45% carbohydrates, 40% fat, and 15% protein. The 2 diets had either 60.81% or 1.11% of total fat energy from MCT with the remaining fat energy intake from LCT. On days 1 and 7 of each diet, resting metabolic rate and postprandial energy expenditure (EE) were measured by indirect calorimetry with a ventilated hood. Results indicated on days 1 and 7, there were no significant differences between diets for resting metabolic rate or mean postprandial EE. On both days 1 and 7, fat oxidation for the MCT-rich diet was significantly greater (0.0001 </= p </= 0.04) than that for the LCT-rich diet at different time points across the 5.5 h postprandial period. In conclusion, for premenopausal, normal-weight women consuming a diet with 25% of the energy content from MCT, there were no changes in resting metabolic rate, transient increases in postprandial energy expenditure, and significant increases in postprandial fat oxidation.

Impaired Mitochondrial Substrate Oxidation in Muscle of Insulin-Resistant Offspring of Type 2 Diabetic Patients

Insulin resistance is the best predictor for the development of diabetes in offspring of type 2 diabetic patients, but the mechanism responsible for it remains unknown. Recent studies have demonstrated increased intramyocellular lipid, decreased mitochondrial ATP synthesis, and decreased mitochondrial density in the muscle of lean, insulin-resistant offspring of type 2 diabetic patients. These data suggest an important role for mitochondrial dysfunction in the pathogenesis of type 2 diabetes. To further explore this hypothesis, we assessed rates of substrate oxidation in the muscle of these same individuals using (13)C magnetic resonance spectroscopy (MRS). Young, lean, insulin-resistant offspring of type 2 diabetic patients and insulin-sensitive control subjects underwent (13)C MRS studies to noninvasively assess rates of substrate oxidation in muscle by monitoring the incorporation of (13)C label into C(4) glutamate during a [2-(13)C]acetate infusion. Using this approach, we found that rates of muscle mitochondrial substrate oxidation were decreased by 30% in lean, insulin-resistant offspring (59.8 +/- 5.1 nmol x g(-1) x min(-1), P = 0.02) compared with insulin-sensitive control subjects (96.1 +/- 16.3 nmol x g(-1) x min(-1)). These data support the hypothesis that insulin resistance in skeletal muscle of insulin-resistant offspring is associated with dysregulation of intramyocellular fatty acid metabolism, possibly because of an inherited defect in the activity of mitochondrial oxidative phosphorylation.

Plasma concentrations of free triiodothyronine predict weight change in euthyroid persons

Background:Factors that influence energy metabolism and substrate oxidation, such as thyroid hormones (THs), may be important regulators of body weight.Objective:We investigated associations of THs cross-sectionally with obesity, energy expenditure, and substrate oxidation and prospectively with weight change.Design:Euthyroid, nondiabetic, healthy, adult Pima Indians (n= 89; 47 M, 42 F) were studied. Percentage body fat (%BF) was measured by using dual-energy X-ray absorptiometry; sleeping metabolic rate (SMR), respiratory quotient, and substrate oxidation rates were measured in a respiratory chamber. Thyroid-stimulating hormone (TSH), free thyroxine (T4), free triiodothyronine (T3), and leptin concentrations were measured in fasting plasma samples.Results:TSH, but neither free T3nor free T4, was associated with %BF and leptin concentrations (r= 0.27 and 0.29, respectively; both: P≤ 0.01). In multiple regression analyses adjusted for age, sex, fat mass, and fat-free mass, free T3was a positive predictor of SMR (P= 0.02). After adjustment for age, sex, %BF, and energy balance, free T3was a negative predictor of 24-h respiratory quotient (P< 0.05) and a positive predictor of 24-h lipid oxidation rate (P= 0.006). Prospectively, after an average follow-up of 4 ± 2 y, the mean increase in weight was 3 ± 9 kg. Baseline T3concentrations were associated with absolute and annual percentage of changes in weight (r= −0.27, P= 0.02, and r= −0.28, P= 0.009, for the age- and sex-adjusted associations, respectively).Conclusions:In euthyroid Pima Indians, lower free T3but not free T4concentrations were an independent predictor of SMR and lipid oxidation and a predictor of weight gain. This finding indicates that control of T4-to-T3conversion may play a role in body weight regulation.

A single 1-h bout of evening exercise increases basal FFA flux without affecting VLDL-triglyceride and VLDL-apolipoprotein B-100 kinetics in untrained lean men

Our group (Magkos F, Wright DC, Patterson BW, Mohammed BS, Mittendorfer B, Am J Physiol Endocrinol Metab 290: E355-E362, 2006) has recently demonstrated that a single, prolonged bout of moderate-intensity cycling (2 h at 60% of peak oxygen consumption) in the evening increases basal whole-body free fatty acid (FFA) flux and fat oxidation, decreases hepatic VLDL-apolipoprotein B-100 (apoB-100) secretion, and enhances removal efficiency of VLDL-triglyceride (TG) from the circulation the following day in untrained, healthy, lean men. In the present study, we investigated the effect of a single, shorter-duration bout of the same exercise (1 h cycling at 60% of peak oxygen consumption) on basal FFA, VLDL-TG, and VLDL-apoB-100 kinetics in seven untrained, healthy, lean men by using stable isotope-labeled tracer techniques. Basal FFA rate of appearance in plasma and plasma FFA concentration were approximately 55% greater (P < 0.05) the morning after exercise than rest, whereas resting metabolic rate and whole-body substrate oxidation rates were not different after rest and exercise. Exercise had no effect on plasma VLDL-TG and VLDL-apoB-100 concentrations, hepatic VLDL-TG and VLDL-apoB-100 secretion rates, and VLDL-TG and VLDL-apoB-100 plasma clearance rates (all P > 0.05). We conclude that in untrained, healthy, lean men 1) the exercise-induced changes in basal whole-body fat oxidation, VLDL-TG, and VLDL-apoB-100 metabolism during the late phase of recovery from exercise are related to the duration of the exercise bout; 2) single sessions of typical recreational activities appear to have little effect on basal, fasting plasma TG homeostasis; and 3) there is a dissociation between systemic FFA availability and VLDL-TG and VLDL-apoB-100 secretion by the liver.

Chronic Activation of Peroxisome Proliferator-Activated Receptor-α with Fenofibrate Prevents Alterations in Cardiac Metabolic Phenotype without Changing the Onset of Decompensation in Pacing-Induced Heart Failure

Severe heart failure (HF) is characterized by profound alterations in cardiac metabolic phenotype, with down-regulation of the free fatty acid (FFA) oxidative pathway and marked increase in glucose oxidation. We tested whether fenofibrate, a pharmacological agonist of peroxisome proliferator-activated receptor-alpha, the nuclear receptor that activates the expression of enzymes involved in FFA oxidation, can prevent metabolic alterations and modify the progression of HF. We administered 6.5 mg/kg/day p.o. fenofibrate to eight chronically instrumented dogs over the entire period of high-frequency left ventricular pacing (HF + Feno). Eight additional HF dogs were not treated, and eight normal dogs were used as a control. [3H]Oleate and [14C]Glucose were infused intravenously to measure the rate of substrate oxidation. At 21 days of pacing, left ventricular end-diastolic pressure was significantly lower in HF + Feno (14.1 +/- 1.6 mm Hg) compared with HF (18.7 +/- 1.3 mm Hg), but it increased up to 25 +/- 2 mm Hg, indicating end-stage failure, in both groups after 29 +/- 2 days of pacing. FFA oxidation was reduced by 40%, and glucose oxidation was increased by 150% in HF compared with control, changes that were prevented by fenofibrate. Consistently, the activity of myocardial medium chain acyl-CoA dehydrogenase, a marker enzyme of the FFA beta-oxidation pathway, was reduced in HF versus control (1.46 +/- 0.25 versus 2.42 +/- 0.24 micromol/min/gram wet weight (gww); p < 0.05) but not in HF + Feno (1.85 +/- 0.18 micromol/min/gww; N.S. versus control). Thus, preventing changes in myocardial substrate metabolism in the failing heart causes a modest improvement of cardiac function during the progression of the disease, with no effects on the onset of decompensation.

Effects of a palatinose-based liquid diet (Inslow) on glycemic control and the second-meal effect in healthy men

Postprandial hyperglycemia induces prolonged hyperinsulinemia, which is a risk factor for type 2 diabetes mellitus. Foods with a low glycemic index blunt the rapid rise in postprandial plasma glucose and insulin levels. We herein investigated the effects of a novel, palatinose-based liquid diet (Inslow, Meiji Dairy Products, Tokyo, Japan) on postprandial plasma glucose and insulin levels and on the rate of substrate oxidation in 7 healthy men. Furthermore, to examine the effects of Inslow on the second-meal effect, we quantified our subjects' postprandial plasma glucose, insulin, and free fatty acid levels for up to 7 hours after they ingested a breakfast containing Inslow or control formula, followed by a standard lunch 5 hours later. Our results showed that peak plasma glucose and insulin levels 30 minutes after Inslow loading were lower than after control formula loading. Postprandial fat oxidation rates in the Inslow group were higher than in the control formula group ( P < .05). In the second-meal effect study, plasma glucose and insulin levels after lunch in the Inslow group were lower than in the control formula group ( P < .01), although the peak levels in these groups were not different. The free fatty acid concentration in the Inslow group immediately before lunch was significantly lower than in the control formula group ( P < .05). In conclusion, consumption of Inslow at breakfast appears to improve patient glycemic control by reducing their postprandial plasma glucose and insulin levels after lunch (second-meal effect).

Severity of insulin resistance in critically ill medical patients

Critical illness is characterized by a hypermetabolic state associated with increased mortality, which is partly ascribed to the occurrence of hyperglycemia caused by enhanced endogenous glucose production and insulin resistance (IR). Insulin resistance is well described in patients after surgery and trauma. However, it is less clearly quantified in critically ill medical patients. In this clinical cohort study, IR (M value) was quantified in 40 critically ill medical patients and 25 matched, healthy controls by isoglycemic hyperinsulinemic clamps after an overnight fast on the day after admission to a medical intensive care unit. Energy and substrate metabolism were measured by using indirect calorimetry in the patients before and during the clamp. The severity of illness was assessed by the acute physiology and chronic health evaluation (APACHE) III score. M values of critically ill medical patients were significantly lower compared with healthy controls (2.29 ± 1.0 and 7.6 ± 2.9 mg/kg per minute, respectively; P < .001) and were closely related to APACHE III scores ( r = −0.43, P < .01), body mass index ( r = −0.41, P < .01), and resting energy expenditure ( r = 0.40, P < .05). The M value was not associated with age, basal glucose concentrations, and respiratory quotient, and it did not differ among patients with various admission diagnoses. In conclusion, insulin sensitivity was found to be reduced by 70% in critically ill medical patients. The severity of IR was associated with the severity of illness, body mass index, and resting energy expenditure, but not with substrate oxidation rates. In addition, the severity of IR did not vary among patients with different admission diagnoses.

Ruthenium(VI)-Catalyzed Oxidation of Alcohols by Hexacyanoferrate(III): An Example of Mixed Order

The absorbance decay of hexacyanoferrate(III) as a function of time shows a progressive deviation from zero to first order. This variation follows an experimental rate law that has been analyzed. The change in reaction order is due to a change in the relative rate of substrate oxidation with respect to that of catalyst regeneration.

Kinetic model of mitochondrial Krebs cycle: unraveling the mechanism of salicylate hepatotoxic effects.

This paper studies the effect of salicylate on the energy metabolism of mitochondria using in silico simulations. A kinetic model of the mitochondrial Krebs cycle is constructed using information on the individual enzymes. Model parameters for the rate equations are estimated using in vitro experimental data from the literature. Enzyme concentrations are determined from data on respiration in mitochondrial suspensions containing glutamate and malate. It is shown that inhibition in succinate dehydrogenase and alpha-ketoglutarate dehydrogenase by salicylate contributes substantially to the cumulative inhibition of the Krebs cycle by salicylates. Uncoupling of oxidative phosphorylation has little effect and coenzyme A consumption in salicylates transformation processes has an insignificant effect on the rate of substrate oxidation in the Krebs cycle. It is found that the salicylate-inhibited Krebs cycle flux can be increased by flux redirection through addition of external glutamate and malate, and depletion in external alpha-ketoglutarate and glycine concentrations.

A low-calorie diet improves the rate of nutrient oxidation, lowers body fat, and maintains lean mass in morbidly obese Brazilian women

To assess the effect of a low calorie diet on the resting metabolic rate (RMR), substrate oxidation, body composition, and to compare measured and calculated RMR of obese Brazilian women, we selected 19 patients aged 31 ± 9 years, with a body mass index of 51 ± 8 kg/m 2, for admission to the Metabolic Unit of the University Hospital for 8 weeks, who were then submitted to a 3.3 to 4.2 MJ/d (800-1000 kcal/d) diet. Weight, height, and circumferences were measured on the first and last days of the study. Body composition was assessed by bioelectrical impedance, and RMR and substrate oxidation rate by indirect calorimetry. A decrease in body weight (134 ± 23 kg vs 121 ± 21 kg, P < .05), waist (136 ± 17 cm vs 123 ± 17 cm, P < .05), and hip circumference (149 ± 14 cm vs 137 ± 16 cm, P < .05) occurred during the study. Mean RMR measured by indirect calorimetry (10.6 ± 1.7 MJ/d; 2540 ± 420 kcal/d) was 16% higher ( P < .05) than that calculated by Harris-Benedict and World Health Organization equations (8.7 ± 0.9 MJ/d; 2070 ± 210 kcal/d and 9.0 ± 1.4 MJ/d; 2161 ± 344 kcal/d, respectively) at the beginning, but not at the end of the study. Lipid oxidation rate was 45% of RMR at the beginning of the study, reaching 59% at the end ( P > .05). Present data suggest that equations to estimate RMR of obese females are reliable after a low-calorie diet and weight loss. Resting metabolic rate was correlated with fat-free mass and body fat. A low-calorie diet with balanced macronutrients is effective for weight loss, leading to a maintenance of lipid oxidation rate and to a reduction of carbohydrate and protein oxidation rates. The low-calorie diet reduced body fat and maintained lean mass.

Effets de la puberté sur la balance glucido-lipidique lors de l’exercice de l’enfant obèse

The aim of the present study was to investigate effect of puberty on substrate oxidation rates using a graded exercise test to exhaustion. Two groups of obese adolescent males (34 prepubertal: body mass index (BMI) = 25,94 +/- 2,63; Z-score = 4,43 +/- 1,83; and 26 postpubertal: BMI = 31,14 +/- 4,88; Z-score = 5,264 +/- 1,76) performed an exercise test on a cycle ergometer. The test consisted in a series of graded exercises on a cycle ergometer. Stage duration was 3 min 30 s. Fat and carbohydrate rates were calculated during the last 30 s of each stage using stoichiometric equations, and this permitted us to calculate substrate oxidation according to exercise intensity. Lipid oxidation rates are significantly higher in the postpubertal group. When the fat oxidation rates are reported relative to fat free mass, fat oxidation rates are higher in the prepubertal group. Puberty decreases significantly the capacity of fat free mass to oxidize fat for a same level of exercise.

Sex-specific effect of the Val1483Ile polymorphism in the fatty acid synthase gene (FAS) on body mass index and lipid profile in Caucasian children

A Val1483Ile polymorphism in the human fatty acid sythase gene (FAS) has recently been shown to be associated with lower percentage of body fat and substrate oxidation rates in Pima Indians, but its role in other populations has not been described. Here, we investigate the effect of this variant on obesity in Caucasian children and adolescents. In total, 738 Caucasian children and adolescents aged 6-17 years of the Leipzig Schoolchildren cohort, which constitutes an unselected representative German population and 205 obese children (body mass index (BMI) 2.71+/-0.04 SDS) were genotyped for genotype-phenotype associations. The frequency of the Ile-allele was lower in German Caucasians compared with Pima Indians (0.03 compared to 0.10). Using generalized linear regression models, there was no effect of the polymorphism on BMI in the whole normal population. However, we identified a significant interaction effect between sex and genotype (P=0.004). Subsequent sex stratified analyses revealed a lower BMI SDS in boys with Ile/Val genotype compared to Val/Val (-0.36+/-0.29 vs 0.09+/-0.05, P<0.05), while an opposite effect was observed in girls (0.48+/-0.19 vs 0.09+/-0.05, P<0.05). In genotype-phenotype associations in obese children, the polymorphism did not affect parameters of insulin, glucose, or lipid metabolism in the whole population. Again, however, obese boys with Ile/Val genotype had significantly higher high-density lipoprotein (HDL) cholesterol levels (1.46+/-0.07 vs 1.23+/-0.03 mmol/l, P<0.05). In conclusion, our findings suggest a sex-specific protective effect of the Val1483Ile polymorphism in FAS for obesity in Caucasian boys. In addition, the polymorphism may be associated with a beneficial lipid profile in obese boys.

Bicarbonate kinetics in Indian males

Measurement of rates of in vivo substrate oxidation such as that of glucose, fatty acids and amino acids, are based on tracer (14C or 13C) data, and often depend on the isotopic content of expired CO2. The recovery of tracer-labelled CO 2 generated from the oxidation of 13C labelled substrates may not be 100% over short term. This can lead to underestimation of oxidation rate of substrates, and consequently a correction for the incomplete recovery of tracer has to be applied by the determination of the recovery of 13CO2 in the breath during tracer bicarbonate infusions. We have studied the recovery of tracer-labelled bicarbonate using a bolus administration model, and further characterized kinetics of bicarbonate using a three-compartment model, to assess which compartmental fluxes changed during the change from a fasted state to fed state. Recovery of bicarbonate was lower at 69% and 67% (fasted and fed state) than the value of 71% and 74% found during earlier longer term of continuous infusions. During feeding, there was a 20-fold increase in the flux of bicarbonate between the central compartment and the compartment that was equivalent to the viscera. This study shows that the difference between the fasted and fed state recovery of tracer bicarbonate similar to that obtained with continuous infusions, and that bicarbonate fluxes show large changes between different compartments in the body depending on metabolic state.

Fat Oxidation Rates are Higher Over a Wide Range of Intensities in Rowing Compared to Cycling Ergometry

The relative contribution of carbohydrate and fat oxidation to whole body energy production during exercise is dependent on oxygen availability. Continuous incremental exercise is associated with a progressive increase in carbohydrate oxidation and a decrease in fat oxidation. The exercise modality, more specifically the muscle mass recruited, is also thought to be an important contributor to substrate selection. PURPOSE: The purpose of this study was to determine the rates of fat oxidation and the cross-over point for substrate utilisation over a wide range of intensities during incremental rowing and cycle ergometry. METHODS: Thirteen moderately trained male rowers [age, 23.2 ± 1.6 yrs; height, 1.82 ± 0.02 m; body mass, 77.0 ± 1.6 kg] performed a continuous incremental exercise test to exhaustion on an electronicaly braked cycle ergometer and an air braked rowing ergometer. The exercise intensity began at 95W and increased in 35W increments every 3-min. Rates of substrate oxidation and the relative contribution to energy expenditure were calculated for the same absolute (W) and relative (%VO2peak) intensity by indirect calorimetry during the last 2-min of each 3-min stage. RESULTS: Peak oxygen consumption was similar for the rowing (57.5 ± 1.5 ml kg min−1) and cycle (55.7 ± 1.6 ml kg min−1) ergometer tests. Peak fat oxidation was higher in rowing (0.72 ± 0.05 g.min−1) than cycling (0.51 ± 0.04 g.min−1, p=0.008) and occurred during the first stage. The rate of fat oxidation was greater during rowing at the same absolute (p=0.019) and relative (p=0.001) exercise intensities up to ∼93%VO2peak. The crossover point for substrate utilisation occurred at a higher relative exercise intensity for rowing than cycling (57.8 ± 2.1 vs. 42.1 ± 3.6 %VO2peak, p=0.003). CONCLUSION: The rate of fat oxidation is higher during rowing exercise than cycling, across a range of exercise intensities, despite similar oxygen uptake. It is possible that the greater muscle mass recruited during rowing may distribute the metabolic stress and facilitate fat oxidation. These results indicate that when prescribing exercise to optimise fat oxidation, the exercise modality should be such that it recruits a larger muscle mass.

The Impact of Carbohydrate Ingestion on the Regulation of Fat Oxidation Following Exercise

The level of obesity has reached epidemic proportions in recent years. Fat is an important fuel for muscle metabolism during recovery from exercise. A comprehensive understanding of the effect of carbohydrate on post-exercise lipid oxidation could have important implications for exercise recommendations to prevent weight gain. PURPOSE: To determine the impact of carbohydrate ingestion on the regulation of fat oxidation following a glycogen depleting bout of exercise. METHODS: Six trained males (age 22.7 ± 3.4 yrs; VO2peak 55.8 ± 5.0ml·kg−1. min−1) volunteered to participate in the study. On two separate days, subjects cycled at 75%VO2peak for 90 mins. Upon completion of exercise, subjects consumed either a carbohydrate drink (10% solution; 1.5g kg−1) or a flavoured placebo. Substrate oxidation rates were measured at 1-hr post exercise using indirect calorimetry. RESULTS:The relative exercise intensity was similar for the carbohydrate (72 ± 2%VO2peak) and placebo (73 ± 2%VO2peak) trials. Total energy expenditure during exercise was similar for the two trials. Post exercise carbohydrate ingestion increased the rate of carbohydrate oxidation at 1-hr recovery (0.30 ± 0.02 vs. 0.17 ± 0.02 g.min−1). The rate of fat oxidation was decreased in comparison to placebo (0.12 ± 0.02 vs. 0.07 ± 0.02 g.min−1) but the rate of whole body energy expenditure was similar between trials. CONCLUSIONS: The ingestion of a large amount of carbohydrate in the recovery from prolonged exercise significantly decreased, but did not suppress, fat oxidation. It has been proposed that the rate of fat oxidation is determined by the availability of glucose, rather than the rate of lipolysis. These results indicate that factors other than carbohydrate availability control post-exercise fat oxidation. Further research on the regulation of malonyl-CoA and triglyceride re-esterification following exercise is required.

The Effect of Pre-Exercise Dietary Manipulation on ATP Utilisation and Metabolism During Simulated Duathlon Performance

Duathlon is a multi-sport event that has received little attention in terms of dietary intervention studies but presents an ideal form of exercise in which the development of appropriate nutritional strategies might benefit performance. PURPOSE: This study investigated the effect of high carbohydrate and high fat meals on the metabolic responses to simulated duathlon time trials. METHODS: Nine male subjects of mean (SD) age 28.6 (5.9) y, body mass 76.8 (8.5) kg, height 1.80 (0.7) m, and VO2max4.8 (0.6) 1.min-1 completed three laboratory simulated duathlon time trials (5 km run, 30 km cycle, and 5 km run). Subjects fasted overnight before each duathlon and were randomly given isoenergetic meals (3998±2.2kJ) 3.5 hours before the start of exercise. The meals consisted of predominantly low carbohydrate (LCHO: 50 g), high carbohydrate (CHO: 214.8 g) or a fasting (F) condition, in which subjects ate nothing. Respiratory gas analysis was used to calculate substrate oxidation rates (Frayn 1983) and ATP utilisation was calculated using standard stoichiometric calculations. Significant differences in all of the data between conditions and over time were identified using a General Linear Model ANOVA with Repeated Measures and significance was accepted at p< 0.05. RESULTS: Time to complete the duathlon (101.9±6.8, 101.0±7.1, 102.4±7.1 min for the F, CHO and LCHO respectively) was not significantly affected by the pre-exercise meals (P>0.05). Total ATP utilisation (92.5±7.7, 94.8±5.3, 92.6±9.2 mol. min−1 for F, CHO and LCHO respectively) was also unaffected by the pre-exercise meals although there were significant changes in the rate of ATP use as a result of a change in exercise modality (p<0.01). Carbohydrate oxidation rate was significantly increased following CHO (p<0.01) and significantly reduced following LCHO meal (P>0.01). Conversely fat oxidation rate was suppressed (p<0.05) as a consequence of the availability of carbohydrate following CHO and increased following LCHO (p<0.01). CONCLUSIONS: Despite changes in substrate availability and differences in the oxidation rates of both carbohydrate and fat, duathlon performance and the rate at which ATP is utilised are not altered as a result of acute pre-exercise macronutrient manipulation.