Endogenous Carbohydrate Oxidation Research Articles

High-fat ketogenic diets and ketone monoester supplements differentially affect substrate metabolism during aerobic exercise.

Chronically adhering to high-fat ketogenic diets or consuming ketone monoester supplements elicits ketosis. Resulting changes in substrate metabolism appear to be drastically different between ketogenic diets and ketone supplements. Consuming a ketogenic diet increases fatty acid oxidation with concomitant decreases in endogenous carbohydrate oxidation. Increased fat oxidation eventually results in an accumulation of circulating ketone bodies, which are metabolites of fatty acids that serve as an alternative source of fuel. Conversely, consuming ketone monoester supplements rapidly increases circulating ketone body concentrations that typically exceed those achieved by adhering to ketogenic diets. Rapid increases in ketone body concentrations with ketone monoester supplementation elicit a negative feedback inhibition that reduces fatty acid mobilization during aerobic exercise. Supplement-derived ketosis appears to have minimal impact on sparing of muscle glycogen or minimizing of carbohydrate oxidation during aerobic exercise. This review will discuss the substrate metabolic and associated aerobic performance responses to ketogenic diets and ketone supplements.

Increased exogenous but unaltered endogenous carbohydrate oxidation with combined fructose-maltodextrin ingested at 120 g h−1 versus 90 g h−1 at different ratios

PurposeThis study aimed to investigate whether carbohydrate ingestion during 3 h long endurance exercise in highly trained cyclists at a rate of 120 g h−1 in 0.8:1 ratio between fructose and glucose-based carbohydrates would result in higher exogenous and lower endogenous carbohydrate oxidation rates as compared to ingestion of 90 g h−1 in 1:2 ratio, which is the currently recommended approach for exercise of this duration.MethodsEleven male participants (V̇O2peak 62.6 ± 7 mL kg−1 min−1, gas exchange threshold (GET) 270 ± 17 W and Respiratory compensation point 328 ± 32 W) completed the study involving 4 experimental visits consisting of 3 h cycling commencing after an overnight fast at an intensity equivalent to 95% GET. During the trials they received carbohydrates at an average rate of 120 or 90 g h−1 in 0.8:1 or 1:2 fructose-maltodextrin ratio, respectively. Carbohydrates were naturally high or low in 13C stable isotopes enabling subsequent calculations of exogenous and endogenous carbohydrate oxidation rates.ResultsExogenous carbohydrate oxidation rates were higher in the 120 g h−1 condition (120–180 min: 1.51 ± 0.22 g min−1) as compared to the 90 g h−1 condition (1.29 ± 0.16 g min−1; p = 0.026). Endogenous carbohydrate oxidation rates did not differ between conditions (2.15 ± 0.30 and 2.20 ± 0.33 g min−1 for 120 and 90 g h−1 conditions, respectively; p = 0.786).ConclusionsThe results suggest that carbohydrate ingestion at 120 g h−1 in 0.8:1 fructose-maltodextrin ratio as compared with 90 g h−1 in 1:2 ratio offers higher exogenous carbohydrate oxidation rates but no additional sparing of endogenous carbohydrates. Further studies should investigate potential performance effects of such carbohydrate ingestion strategies.

Endogenous versus exogenous carbohydrate oxidation measured by stable isotopes in pre-pubescent children plus 13C abundances in foods consumed three days prior

PurposeThe purposes of the present study were to (a) examine resting metabolism, substrate utilization, and endogenous versus exogenous carbohydrate (CHO) oxidation before and after 30-g rapidly-digesting carbohydrate (RDC) ingestion using indirect calorimetry and breath test analysis of stable isotope concentrations in pre-pubescent children and (b) report the 13C abundances in foods consumed for three days prior. MethodsNineteen children (n = 10 boys, n = 9 girls) at Tanner stage I or II participated (mean age ± 95% CI = 9.84 ± 0.77 y) in this study. Food was administered to the children for three days preceding their scheduled breath tests. Breath tests and indirect calorimetry were performed after an 8-h fast before and 60 min following consumption of a 30-g simple RDC drink consisting of maltodextrin and sucrose. Open circuit spirometry and indirect calorimetry monitored resting metabolism and CHO oxidation. Separate breath samples were taken every 15 min. Samples of all foods and breath samples were analyzed for 13C and 12C abundances with a stable-isotope mass spectrometer. Results13C in expired breath samples were −23.81 ± 1.64‰ at baseline and increased every 15 min after consumption of the CHO drink (p < 0.001–0.009). Cumulative total, endogenous, and exogenous CHO utilization increased during the post-prandial period (p < 0.001). Endogenous CHO oxidation was consistently greater than exogenous CHO oxidation (p < 0.001–0.002).Blood glucose was elevated from baseline at 30- and 60-min post-prandial (p < 0.001). Insulin did not change over time (p = 0.184). ConclusionsThe foods provided during the 3-day controlled diet effectively minimized 13C variation prior to metabolic testing. The 13C abundances of foods reported herein should serve as practical recommendations to reduce 13C intake before breath tests. While endogenous CHO oxidation remained greater in proportion to exogenous CHO oxidation, these findings suggest that even a relatively small amount of RDC can increase exogenous CHO oxidation and blood glucose in normal-weight children. To further examine shifts in endogenous versus exogenous CHO utilization, we recommend that future studies take steps to minimize 13C variation before breath tests and examine changes in substrate metabolism at rest and during exercise in normal weight and overweight pre-pubescent children. Clinical trial registration numberNCT03185884.

Sports Drink Intake Pattern Affects Exogenous Carbohydrate Oxidation during Running.

This study aimed to determine whether the pattern of carbohydrate sports drink ingestion during prolonged submaximal running affects exogenous carbohydrate oxidation rates and gastrointestinal (GI) comfort. Twelve well-trained male runners (27 ± 7 yr; 67.9 ± 6.7 kg; V˙O2peak, 68 ± 7 mL·kg·min) completed two exercise trials of 100 min steady-state running at 70%V˙O2peak. In each of the trials, 1 L of a 10% dextrose solution, enriched with [U-C] glucose, was consumed as either 200 mL every 20 min (CHO-20) or 50 mL every 5 min (CHO-5). Expired breath and venous blood samples were collected at rest and every 20 min during exercise. Subjective scales of GI comfort were recorded at regular intervals. Average exogenous carbohydrate oxidation rates were 23% higher during exercise in CHO-20 (0.38 ± 0.11 vs 0.31 ± 0.11 g·min; P = 0.017). Peak exogenous carbohydrate oxidation was also higher in CHO-20 (0.68 ± 0.14 g·min vs 0.61 ± 0.14 g·min; P = 0.004). During exercise, total carbohydrate oxidation (CHO-20, 2.15 ± 0.47; CHO-5, 2.23 ± 0.45 g·min, P = 0.412) and endogenous carbohydrate oxidation (CHO-20, 1.78 ± 0.45; CHO-5, 1.92 ± 0.40 g·min; P = 0.148) were not different between trials. Average serum glucose (P = 0.952) and insulin (P = 0.373) concentrations were not different between trials. There were no differences in reported symptoms of GI comfort and stomach bloatedness (P > 0.05), with only 3% of reported scores classed as severe (≥5 out of 10). Ingestion of a larger volume of carbohydrate solution at less frequent intervals during prolonged submaximal running increased exogenous carbohydrate oxidation rates. Neither drinking pattern resulted in increased markers of GI discomfort to a severe level.

Acute Hypoxia Suppresses Exogenous Glucose Oxidation, Lowers Fat Oxidation, and Increases Muscle Glycogenolysis During Steady-state Aerobic Exercise (P08-084-19)

ObjectivesLowlanders performing steady-state aerobic exercise during high-altitude (HA) sojourns, hypoxia mediates increased endogenous carbohydrate oxidation compared to sea level (SL). At SL, ingesting carbohydrate during exercise spares endogenous carbohydrate stores and improves endurance. However, it is unclear whether that strategy is effective at HA, as data from a recent study suggests exogenous glucose oxidation is suppressed during aerobic exercise performed 5 hr after arriving at HA. This observation has not been replicated. The objective of this study was to determine substrate oxidative responses to exogenous carbohydrate ingestion during steady-state aerobic exercise at SL and HA. MethodsUsing a randomized, crossover design, native lowlanders (n = 8 males, mean ± SD, age: 23 ± 2 yr, body mass: 87 ± 10 kg, and VO2peak: SL 4.3 ± 0.2 L/min and HA 2.9 ± 0.2 L/min) consumed 145 g (1.8 g/min) of glucose while performing 80 min of metabolically-matched (SL: 1.66 ± 0.14 L/min 347 ± 29 kcal, HA: 1.59 ± 0.10 L/min, 369 ± 39 kcal) treadmill exercise at SL (757 mmHg) and HA (460 mmHg) conditions after a 5 hr exposure. Total carbohydrate and fat oxidation rates (g/min) during exercise were determined by indirect calorimetry, and exogenous, muscle- and hepatic-derived glucose oxidation by tracer technique using breath and blood measurements of 13C-glucose. ResultsTotal carbohydrate oxidation was higher (P < 0.05) at HA (2.15 ± 0.32) compared to SL (1.39 ± 0.14). Exogenous glucose oxidation was lower (P < 0.05) at HA (0.35 ± 0.07) than SL (0.44 ± 0.05). Muscle glycogen oxidation was higher at HA (1.67 ± 0.26) compared to SL (0.83 ± 0.13). There was no difference in hepatic glycogen oxidation between SL (0.13 ± 0.03) and HA (0.13 ± 0.04). Fat oxidation was lower at HA (0.05 ± 0.07) than SL (0.31 ± 0.08). ConclusionsThese data confirm that acute hypoxic exposure suppresses exogenous carbohydrate oxidation during steady-state exercise. Coupled with observations that fat oxidation was reduced and muscle glycogenolysis accelerated in hypoxia, these findings suggest that ingesting carbohydrate during exercise upon acute hypoxia exposure is not an effective strategy for attenuating oxidation of endogenous carbohydrate stores. Funding SourcesViews expressed are the authors and do not reflect the official policy of the Army, DoD, or the U.S. Government. Supported by USAMRMC.

Exercising with low muscle glycogen content increases fat oxidation and decreases endogenous, but not exogenous carbohydrate oxidation

BackgroundInitiating aerobic exercise with low muscle glycogen content promotes greater fat and less endogenous carbohydrate oxidation during exercise. However, the extent exogenous carbohydrate oxidation increases when exercise is initiated with low muscle glycogen is unclear. PurposeDetermine the effects of muscle glycogen content at the onset of exercise on whole-body and muscle substrate metabolism. MethodsUsing a randomized, crossover design, 12 men (mean ± SD, age: 21 ± 4 y; body mass: 83 ± 11 kg; VO2peak: 44 ± 3 mL/kg/min) completed 2 cycle ergometry glycogen depletion trials separated by 7-d, followed by a 24-h refeeding to elicit low (LOW; 1.5 g/kg carbohydrate, 3.0 g/kg fat) or adequate (AD; 6.0 g/kg carbohydrate, 1.0 g/kg fat) glycogen stores. Participants then performed 80 min of steady-state cycle ergometry (64 ± 3% VO2peak) while consuming a carbohydrate drink (95 g glucose +51 g fructose; 1.8 g/min). Substrate oxidation (g/min) was determined by indirect calorimetry and 13C. Muscle glycogen (mmol/kg dry weight), pyruvate dehydrogenase (PDH) activity, and gene expression were assessed in muscle. ResultsInitiating steady-state exercise with LOW (217 ± 103) or AD (396 ± 70; P < 0.05) muscle glycogen did not alter exogenous carbohydrate oxidation (LOW: 0.84 ± 0.14, AD: 0.87 ± 0.16; P > 0.05) during exercise. Endogenous carbohydrate oxidation was lower and fat oxidation was higher in LOW (0.75 ± 0.29 and 0.55 ± 0.10) than AD (1.17 ± 0.29 and 0.38 ± 0.13; all P < 0.05). Before and after exercise PDH activity was lower (P < 0.05) and transcriptional regulation of fat metabolism (FAT, FABP, CPT1a, HADHA) was higher (P < 0.05) in LOW than AD. ConclusionInitiating exercise with low muscle glycogen does not impair exogenous carbohydrate oxidative capacity, rather, to compensate for lower endogenous carbohydrate oxidation acute adaptations lead to increased whole-body and skeletal muscle fat oxidation.

No Effect of Protein Coingestion on Exogenous Glucose Oxidation during Exercise

We examined the hypothesis that protein coingestion with glucose during endurance exercise increases exogenous glucose oxidation rate and gut comfort and lowers perceived exertion. In a randomized crossover design, eight male cyclists rode 150 min at 50% of peak power on three occasions while ingesting solutions containing the following: 8% ¹³C-enriched glucose and 2% milk protein concentrate (protein-glucose), glucose only (glucose), or noncaloric placebo (water). All solutions contained sodium citrate ([⁺Na] 60 mmol·L⁻¹) and flavor and were ingested at 150 mL·15 min⁻¹. The exogenous carbohydrate oxidation rate was determined using stable isotope method and indirect calorimetry. Protein coingestion had no effect on the exogenous glucose oxidation rate but increased endogenous carbohydrate oxidation rate (16%; 90% confidence limits ±7%), relative to glucose. Total carbohydrate and fat oxidation rates were increased (25%; ±6%) and decreased (17%; ±4%), respectively, by protein coingestion relative to water, but the effect relative to glucose was trivial. The plasma glucose concentration relative to glucose (mean ± SD; 6.1 ± 0.8 mmol·L⁻¹) was 5.8% (±3%) lower with protein coingestion; there were no clear differences in glucose concentration for the remaining comparisons or for lactate concentration. Perceived exertion was not altered by protein coingestion; however, there was a small decrease in nausea with the protein-glucose solution relative to water (-0.14 ± 0.08 U); other protein-affected comparisons were without note. Adding protein to a glucose-sodium solution ingested during exercise had neutral effect on exogenous carbohydrate oxidation and perception and little effect on metabolic measures associated with endurance performance. We conclude that previously reported effects of protein coingestion on endurance capacity were unlikely due to increased exogenous carbohydrate provision.

L-Arginine but not l-glutamine likely increases exogenous carbohydrate oxidation during endurance exercise

The addition of L-arginine or L-glutamine to glucose-electrolyte solutions can increase intestinal water, glucose, and sodium absorption in rats and humans. We evaluated the utility of L-arginine and L-glutamine in energy-rehydration beverages through assessment of exogenous glucose oxidation and perceptions of exertion and gastrointestinal distress during endurance exercise. Eight cyclists rode 150 min at 50% of peak power on four occasions while ingesting solutions at a rate of 150 mL 15 min(-1) that contained (13)C-enriched glucose (266 mmol L(-1)) and sodium citrate ([Na(+)] 60 mmol L(-1)), and either: 4.25 mmol L(-1) L-arginine or 45 mmol L(-1) L-glutamine, and as controls glucose only or no glucose. Relative to glucose only, L-arginine invoked a likely 12% increase in exogenous glucose oxidation (90% confidence limits: ± 8%); however, the effect of L-glutamine was possibly trivial (4.5 ± 7.3%). L-Arginine also led to very likely small reductions in endogenous fat oxidation rate relative to glucose (12 ± 4%) and L-glutamine (14 ± 4%), and relative to no glucose, likely reductions in exercise oxygen consumption (2.6 ± 1.5%) and plasma lactate concentration (0.20 ± 0.16 mmol L(-1)). Effects on endogenous and total carbohydrate oxidation were inconsequential. Compared with glucose only, L-arginine and L-glutamine caused likely small-moderate effect size increases in perceptions of stomach fullness, abdominal cramp, exertion, and muscle tiredness during exercise. Addition of L-arginine to a glucose and electrolyte solution increases the oxidation of exogenous glucose and decreases the oxygen cost of exercise, although the mechanisms responsible and impact on endurance performance require further investigation. However, L-arginine also increases subjective feelings of gastrointestinal distress, which may attenuate its other benefits.

Lower oxidation of a high molecular weight glucose polymer vs. glucose during cycling

We previously reported no difference in the oxidation rate of a high molecular weight glucose polymer (GP) vs. maltodextrin (8kDa) during exercise; however, the ingestion rate (1.8g·min(-1)) was above the glucose absorption-oxidation maxima (∼1.0g·min(-1)), possibly masking either faster gastric emptying of the GP and delivery to the circulation observed at rest or physical properties of the GP that might slow intestinal absorption. Therefore, we asked whether GP oxidation could be differentially affected when ingested at a lower rate (0.8g·min(-1)). Eight cyclists performed three 150-min rides at 50% peak power while ingesting solutions containing 8% GP (500-750kDa, 21 mosm·kg(-1)), 8% glucose (469 mosm·kg(-1)), or water. The exogenous carbohydrate oxidation rate was determined using stable isotope methodology and indirect calorimetry. Glucose and GP were oxidized on average at 0.54g·min(-1) (coefficient of variation (CV) 37%) and 0.41g·min(-1) (CV 60%), respectively, which equated to a moderate (effect size) reduction of 24% (90% confidence limits:±22%) with GP. The endogenous carbohydrate oxidation rate with glucose (1.04g·min(-1); CV 68%) was not clearly different from GP (15%; 90% confidence limits:±24%) and total carbohydrate oxidation rate was not affected. Plasma glucose concentration was 8.3% lower (±7.0%, moderate) and nausea 0.4 units higher (±0.4 units, moderate) with GP vs. glucose. To conclude, the oxidation rate of GP when ingested below the glucose absorption-oxidation maxima is slower than glucose. Further work could determine the physical properties of the carbohydrate and (or) physiological mechanism determining this response. Meanwhile, utility of the glucose polymer over glucose or maltodextrin in energy beverages appears limited.

Fructose-maltodextrin ratio in a carbohydrate-electrolyte solution differentially affects exogenous carbohydrate oxidation rate, gut comfort, and performance

Solutions containing multiple carbohydrates utilizing different intestinal transporters (glucose and fructose) show enhanced absorption, oxidation, and performance compared with single-carbohydrate solutions, but the impact of the ratio of these carbohydrates on outcomes is unknown. In a randomized double-blind crossover, 10 cyclists rode 150 min at 50% peak power, then performed an incremental test to exhaustion, while ingesting artificially sweetened water or one of three carbohydrate-salt solutions comprising fructose and maltodextrin in the respective following concentrations: 4.5 and 9% (0.5-Ratio), 6 and 7.5% (0.8-Ratio), and 7.5 and 6% (1.25-Ratio). The carbohydrates were ingested at 1.8 g/min and naturally (13)C-enriched to permit evaluation of oxidation rate by mass spectrometry and indirect calorimetry. Mean exogenous carbohydrate oxidation rates were 1.04, 1.14, and 1.05 g/min (coefficient of variation 20%) in 0.5-, 0.8-, and 1.25-Ratios, respectively, representing likely small increases in 0.8-Ratio of 11% (90% confidence limits; ± 4%) and 10% (± 4%) relative to 0.5- and 1.25-Ratios, respectively. Comparisons of fat and total and endogenous carbohydrate oxidation rates between solutions were unclear. Relative to 0.5-Ratio, there were moderate improvements to peak power with 0.8- (3.6%; 99% confidence limits ± 3.5%) and 1.25-Ratio (3.0%; ± 3.7%) but unclear with water (0.4%; ± 4.4%). Increases in stomach fullness, abdominal cramping, and nausea were lowest with the 0.8- followed by the 1.25-Ratio solution. At high carbohydrate-ingestion rate, greater benefits to endurance performance may result from ingestion of 0.8- to 1.25-Ratio fructose-maltodextrin solutions. Small perceptible improvements in gut comfort favor the 0.8-Ratio and provide a clearer suggestion of mechanism than the relationship with exogenous carbohydrate oxidation.

Exogenous glucose oxidation is reduced with carbohydrate feeding during exercise after starvation

Lean healthy individuals are characterized by the ability to rapidly adapt metabolism to acute changes in substrate availability and metabolic rate. However, in glucose-intolerance/insulin-resistant conditions, such as that induced by starvation, the flexibility of tissues to rapidly respond to change in substrate availability is diminished. We asked whether the conundrum of increased glucose demand by the contracting skeletal muscle during prolonged exercise and the glucose intolerance of starvation would result in the obstruction of oxidative disposal of ingested 13C-labeled glucose during exercise. Seven lean, healthy, physically active individuals (2 women, 5 men) completed a randomized crossover study comparing the effects of the normal-fed condition vs a 67-hour water-only fast on the metabolic response to carbohydrate ingestion during 80 minutes of exercise at 56% of maximum oxygen uptake. Compared with the normal condition, fasting resulted in a large overall increase in the rate of fat oxidation (mean effect, 71%; 95% confidence limit, ±22%) and moderate reductions in both exogenous (−54%, ±10%) and endogenous (−40%, ±19%) glucose oxidation rates during exercise. Over the course of exercise, fat oxidation was impermeable to change in the fasting condition, but increased moderately (33%, ±19%) in the normal condition. These changes were associated with a large increase in plasma free fatty-acid concentration (120%, ±64%) and a moderate increase in blood lactate concentration (58%, ±50%). In contrast, large reductions in resting blood glucose (−21%, ±14%) and moderate reductions in plasma insulin concentrations (−47%, ±26%) were observed in the fast condition; but this effect was reversed for glucose (30%, ± 24%) and negated for insulin by the end of exercise. To conclude, a 67-hour fast leads to an impermeable increase in fat oxidation, suppression of both exogenous and endogenous carbohydrate oxidation, and a metabolic response consistent with resistance to contraction-induced exogenous glucose uptake and oxidation.

Oxidation of Maltose and Trehalose during Prolonged Moderate-Intensity Exercise

The aim of the present study was to compare the effects of trehalose (TRE) and maltose (MAL) ingestion on exogenous carbohydrate oxidation rates and blood metabolite responses during prolonged moderate-intensity cycling exercise. Nine trained subjects performed three randomly assigned bouts of exercise separated by at least 1 wk. Each trial consisted of 150 min of cycling at 55% of maximal power output (Wmax) while ingesting a solution providing either 1.1 g x min(-1) TRE, 1.1 g x min(-1) MAL, or water (WAT). Total carbohydrate oxidation rates were significantly higher (P < 0.05) in both the MAL (2.09 +/- 0.18 g x min(-1)) and TRE (1.92 +/- 0.32 g x min(-1)) trials compared with the WAT trial (1.62 +/- 0.28 g x min(-1)). Peak exogenous carbohydrate oxidation was significantly higher in the MAL trial compared with the TRE trial (1.01 +/- 0.24 and 0.73 +/- 0.22 g x min(-1), respectively, P < 0.05). The MAL trial resulted in significantly reduced endogenous carbohydrate oxidation rates compared with the WAT trial (1.20 +/- 0.25 and 1.62 +/- 0.28 g x min(-1), respectively, P < 0.05). When compared with the WAT trial, total fat oxidation for the same period was significantly reduced in both carbohydrate trials (0.91 +/- 0.19, 0.68 +/- 0.19, and 0.79 +/- 0.19 g x min(-1) for WAT, MAL, and TRE, respectively, P < 0.05) and tended to be lower in MAL compared with TRE (P < 0.06). Both solutions maintained high plasma glucose concentrations. MAL had a "sparing" effect on endogenous carbohydrate stores. The reduced exogenous carbohydrate oxidation rate of TRE compared to MAL is probably due to a reduced enzymatic hydrolysis rate within the small intestine, causing a slower availability.

Comparison of exogenous glucose, fructose and galactose oxidation during exercise using C-labelling

Six subjects exercised for 120 min on a cycle ergometer (65 (se 3) % VO2max) when ingesting a placebo or glucose, fructose or galactose (100 g in 1000 ml water) labelled with 13C. The oxidation of energy substrates including exogenous hexoses was compared using indirect respiratory calorimetry and 13CO2 production at the mouth. Total carbohydrate progressively decreased and total fat oxidation increased over the 120 min exercise period in the four experimental situations. During the 120 min of exercise, the amount of fructose oxidized (38.8 (se 2.6) g; 9.0 (se 0.6) % energy yield) was not significantly (approximately 4 %) lower than that of exogenous glucose (40.5 (se 3.4) g; 9.2 (se 0.8) % energy yield), while that of galactose (23.7 (se 3.5) g; 5.5 (se 0.9) % energy yield) was only 59 % and 61 % that of glucose and fructose, respectively. When compared with the placebo, the ingestion and oxidation of the three hexoses did not significantly modify fat oxidation or total carbohydrate oxidation, but it significantly reduced (9-13 %) endogenous carbohydrate oxidation. The present data indicate that fructose and exogenous glucose ingested during exercise could be oxidized at a similar rate, but that the oxidation rate of galactose was only approximately 60 % that of the exogenous glucose and fructose, presumably because of a preferential incorporation of galactose into liver glycogen (Leloir pathway). The reduction in endogenous carbohydrate oxidation was, however, similar with the three hexoses.

Glucose Polymer Molecular Weight Does Not Affect Exogenous Carbohydrate Oxidation

To compare the effects of high (HMW) versus low molecular weight (LMW) glucose polymer solutions on the pattern of substrate oxidation during exercise. Eight cyclists (VO(2max): 63 +/- 8 mL.kg(-1).min(-1)) performed three 150-min cycling trials at 64 +/- 5% VO(2max) while ingesting 11.25% HMW (500-750 kg.mol(-1), 21 mOsm.kg(-1)) or LMW (8 kg.mol(-1), 110 mOsm.kg(-1)) solutions providing 1.8 g of carbohydrate per minute, or plain water. Substrate oxidation was determined using stable-isotope methods and indirect calorimetry. Exogenous carbohydrate oxidation rate was not affected by carbohydrate molecular weight (P = 0.89, peak rate: 0.93 x// 1.37 g.min(-1)). There was no effect of carbohydrate molecular weight on endogenous carbohydrate or fat oxidation rates (P = 0.30), plasma free fatty acid (P = 0.14), lactate (P = 0.38), or glucose concentrations (P = 0.98), nor were there any serious gastrointestinal complaints reported for either of the two solutions during exercise. Despite previous reports of faster gastric emptying and glycogen resynthesis suggesting enhanced glucose delivery, a markedly hypotonic HMW glucose polymer solution had no effect on exogenous and endogenous substrate oxidation rates during exercise, relative to a LMW glucose polymer solution. These data are consistent with there being no effect of carbohydrate structure or solution osmolality or viscosity on exogenous glucose oxidation and that ingested glucose polymers can only be oxidized on average up to 1.0 g.min during exercise.

Regulation of fuel metabolism by preexercise muscle glycogen content and exercise intensity.

To date, the results of studies that have examined the effects of altering preexercise muscle glycogen content and exercise intensity on endogenous carbohydrate oxidation are equivocal. Differences in the training status of subjects between investigations may, in part, explain these inconsistent findings. Accordingly, we determined the relative effects of exercise intensity and carbohydrate availability on patterns of fuel utilization in the same subjects who performed a random order of four 60-min rides, two at 45% and two at 70% of peak O(2) uptake (Vo(2 peak)), after exercise-diet intervention to manipulate muscle glycogen content. Preexercise muscle glycogen content was 596 +/- 43 and 202 +/- 21 mmol/kg dry mass (P < 0.001) for high-glycogen (HG) and low-glycogen (LG) conditions, respectively. Respiratory exchange ratio was higher for HG than LG during exercise at both 45% (0.85 +/- 0.01 vs. 0.74 +/- 0.01; P < 0.001) and 70% (0.90 +/- 0.01 vs. 0.79 +/- 0.01; P < 0.001) of Vo(2 peak). The contribution of whole body muscle glycogen oxidation to energy expenditure differed between LG and HG for exercise at both 45% (5 +/- 2 vs. 45 +/- 5%; P < 0.001) and 70% (25 +/- 3 vs. 60 +/- 3%; P < 0.001) of Vo(2 peak). Yet, despite marked differences in preexercise muscle glycogen content and its subsequent utilization, rates of plasma glucose disappearance were similar under all conditions. We conclude that, in moderately trained individuals, muscle glycogen availability (low vs. high) does not influence rates of plasma glucose disposal during either low- or moderate-intensity exercise.

Oxidation of combined ingestion of glucose and fructose during exercise.

The purpose of the present study was to examine whether combined ingestion of a large amount of fructose and glucose during cycling exercise would lead to exogenous carbohydrate oxidation rates >1 g/min. Eight trained cyclists (maximal O(2) consumption: 62 +/- 3 ml x kg(-1) x min(-1)) performed four exercise trials in random order. Each trial consisted of 120 min of cycling at 50% maximum power output (63 +/- 2% maximal O(2) consumption), while subjects received a solution providing either 1.2 g/min of glucose (Med-Glu), 1.8 g/min of glucose (High-Glu), 0.6 g/min of fructose + 1.2 g/min of glucose (Fruc+Glu), or water. The ingested fructose was labeled with [U-(13)C]fructose, and the ingested glucose was labeled with [U-(14)C]glucose. Peak exogenous carbohydrate oxidation rates were approximately 55% higher (P < 0.001) in Fruc+Glu (1.26 +/- 0.07 g/min) compared with Med-Glu and High-Glu (0.80 +/- 0.04 and 0.83 +/- 0.05 g/min, respectively). Furthermore, the average exogenous carbohydrate oxidation rates over the 60- to 120-min exercise period were higher (P < 0.001) in Fruc+Glu compared with Med-Glu and High-Glu (1.16 +/- 0.06, 0.75 +/- 0.04, and 0.75 +/- 0.04 g/min, respectively). There was a trend toward a lower endogenous carbohydrate oxidation in Fruc+Glu compared with the other two carbohydrate trials, but this failed to reach statistical significance (P = 0.075). The present results demonstrate that, when fructose and glucose are ingested simultaneously at high rates during cycling exercise, exogenous carbohydrate oxidation rates can reach peak values of approximately 1.3 g/min.

A Soybean Peptide Isolate Diet Promotes Postprandial Carbohydrate Oxidation and Energy Expenditure in Type II Diabetic Mice

The aim of the present study was to determine the effects of dietary proteins on the oxidation of dietary carbohydrate and lipids in type II diabetic mice. KK-A(y) strain mice were provided free access to a high fat diet (30% of energy as fat) for an initial 4-wk period to induce diabetes. To reduce body weight gain, the mice were subsequently fed restrictive isoenergetic and isonitrogenous diets (35% of energy as protein and 5% as fat) based on either casein or soy protein isolate hydrolysate (SPI-H) for 4 wk. To measure exogenous carbohydrate and lipid oxidation, the mice were fed a diet containing (13)C-glucose or (13)C-triolein while they were in a respiratory chamber for 72 h. Postprandial energy expenditure was higher in the SPI-H than in the casein group; this difference was due to an increase in postprandial exogenous and endogenous carbohydrate oxidation. There were no differences in 24-h energy expenditure between dietary groups. Oxidation of exogenous carbohydrate tended to be higher (P = 0.054) in the SPI-H group during the 24 h of measurement. Fecal excretion of (13)C-glucose was lower but the excretion of lipid was higher in mice fed the SPI-H diet than in casein-fed mice. These results indicate that in type II diabetic mice, dietary SPI-H not only inhibits the absorption of dietary lipids and increases the absorption of dietary carbohydrates but also augments postprandial energy expenditure, which is accompanied by a postprandial increase in oxidation of dietary carbohydrates.

Dose-response relationship between fat ingestion and oxidation: quantitative estimation using whole-body calorimetry and 13C isotope ratio mass spectrometry.

To determine dose-dependent relationship between ingested fat and its oxidation in the immediate post-prandial period in humans. Subjects were randomly selected for the study at the Dunn Clinical Nutrition Centre, Cambridge, UK. Subjects ingested naturally enriched 13C corn-oil doses (range 20-140g) in a whole-body indirect calorimeter, and were studied for 8 h. Ingested fat oxidation was estimated from the subject's breath 13C enrichment and total carbon dioxide production. Total fat and carbohydrate oxidation were estimated from non-protein oxygen and carbon dioxide exchanges. Endogenous fat oxidation was estimated as the difference between total fat and ingested fat oxidation. The amount of fat dose oxidized was nonlinearly related to the amount ingested. On average, 25.6+/-2.7% of the mean fat dose was oxidized. A significant (r = - 0.72, P < 0.001) inverse correlation was found between the amount of fat dose and the proportion oxidized. Endogenous carbohydrate oxidation was negatively and significantly correlated to fat dose oxidized (r= -0.61, P < 0.01), but it was not correlated to endogenous fat oxidation. There was a nonlinear relationship between amount of fat dose and its quantity that was oxidized in the immediate post-prandial period. The inverse relationship between the size of the fat load and the proportion that was oxidized post-prandially implies increased dietary fat storage beyond about 50 g in a normal resting adult. This has important implications for 13CO2-based studies.

Effect of diets high or low in unavailable and slowly digestible carbohydrates on the pattern of 24-h substrate oxidation and feelings of hunger in humans

The pattern of substrate utilization with diets containing a high or a low proportion of unavailable and slowly digestible carbohydrates may constitute an important factor in the control, time course, and onset of hunger in humans. We tested the hypothesis that isoenergetic diets differing only in their content of unavailable carbohydrates would result in different time courses of total, endogenous, and exogenous carbohydrate oxidation rates. Two diets with either a high (H diet) or a low (L diet) content of unavailable carbohydrates were fed to 14 healthy subjects studied during two 24-h periods in a metabolic chamber. Substrate utilization was assessed by whole-body indirect calorimetry. In a subgroup of 8 subjects, endogenous and exogenous carbohydrate oxidation were assessed by prelabeling the body glycogen stores with [(13)C]carbohydrate. Subjective feelings of hunger were estimated with use of visual analogue scales. Total energy expenditure and substrate oxidation did not differ significantly between the 2 diets. However, there was a significant effect of diet (P: = 0.03) on the carbohydrate oxidation pattern: the H diet elicited a lower and delayed rise of postprandial carbohydrate oxidation and was associated with lower hunger feelings than was the L diet. The differences in hunger scores between the 2 diets were significantly associated with the differences in the pattern of carbohydrate oxidation among diets (r = -0.67, P: = 0. 006). Exogenous and endogenous carbohydrate oxidation were not significantly influenced by diet. The pattern of carbohydrate utilization is involved in the modulation of hunger feelings. The greater suppression of hunger after the H diet than after the L diet may be helpful, at least over the short term, in individuals attempting to better control their food intake.

Treatment with Growth Hormone and Insulin-Like Growth Factor-1 in Septicemia: Effects on Carbohydrate Metabolism

Growth hormone (GH) and insulin-like growth factor-1 (IGF-1) may be beneficial against the protein catabolism seen in injury and septicemia. Further understanding of their effects on carbohydrate metabolism is needed. In a septic porcine model receiving total parenteral nutrition, pretreatment with GH or IGF-1 (or no treatment in controls) was followed by an infusion of live Escherichia coli bacteria. Endogenous glucose production, carbohydrate oxidation, glucose and lactate fluxes over the liver, gastrointestinal organs, kidney, and hindleg were determined. Endogenous glucose production increased during septicemia in the GH group. The metabolic acidosis induced by septicemia was augmented by GH, but attenuated by IGF-1. The alanine and lactate levels were significantly higher in the GH- than in the IGF-1-treated animals during septicemia. IGF-1 pretreatment appeared to induce favorable effects while GH pretreatment might produce unfavorable effects on carbohydrate metabolism in septic piglets.