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Biomedical subjects

S C Dennis

Publications and source records attributed to S C Dennis.

At least 19 recordsLinked to original sources

Advantages of a smaller bodymass in humans when distance-running in warm, humid conditions.

Using a 65-kg athlete running a 2 h 10 min marathon as an example, we estimated that imbalances between approximately 1400 W of heat production and dissipation would occur in ambient temperatures of 17 degrees C at 90% relative humidity (rh) to 37 degrees C at 50% rh. Because heat production during running depends on body mass and heat loss depends on surface area, intercepts between predicted heat production and maximal heat loss with increasing speeds depend on an athlete's body mass. At 35 degrees C and 60% rh, a 45-kg athlete could maintain thermal balance by running a 2 h 13 min marathon at 19.1 km x h(-1) but a 75-kg athlete would only be able run a 3 h 28 min marathon at 12.2 km x h(-1). In both cases, the production of 970-1020 W of heat would necessitate the evaporation of at least 1.5-1.6 l of sweat per hour. A lower metabolic heat production in lighter runners at any given speed may be one reason why smallness of stature is an asset in distance running.

Adult

Effects of ingesting a sports bar versus glucose polymer on substrate utilisation and ultra-endurance performance.

The purpose of this study was to determine whether the ingestion of a sports bar (BAR) containing a mixture of fat (7 g), protein (14 ) and carbohydrate (CHO; 19 ) improved ulta-endurance cycling performance compared to when an equicaloric amount of CHO was consumed. On two occasions separated by a minimum of 7 days, six highly trained (peak power output [PPO] 414 +/- 8 W) endurance cyclists rode for 330 min at approximately 50% of PPO (203 +/- 8 W) while ingesting either the BAR or just CHO, before performing a 400 k] time trial as fast as possible. Rates of fat oxidation were significantly greater at the end of the submaximal ride when subjects ingested the BAR compared to CHO (1.09 +/- 0.08 vs 0.73 +/- 0.08g x min(-1); P<0.05), and accordingly total fat oxidation was significantly higher (280 +/- 24 vs 203 +/- 25 g, P < 0.05). However, two subjects failed to complete the time trial after they consumed the BAR during the prolonged, submaximal ride, whereas all subjects managed to finish the time trial when ingesting CHO. In conclusion, ingestion of the sports bar enhanced fat metabolism during prolonged, submaximal exercise, but impaired subsequent high-intensity time-trial performance.

Adult

Effects of different interval-training programs on cycling time-trial performance.

PURPOSE: We have investigated the effect of varying the intensity of interval training on 40-km time-trial performance in 20 male endurance cyclists (peak oxygen uptake 4.8+/-0.6 L x min(-1), mean +/- SD). METHODS: Cyclists performed a 25-kJ sprint test, an incremental test to determine peak aerobic power (PP) and a simulated 40-km time-trial on a Kingcycle ergometer. They were then randomly assigned to one of five types of interval-training session: 12x30 s at 175% PP, 12x60 s at 100% PP, 12x2 min at 90% PP, 8x4 min at 85% PP, or 4x8 min at 80% PP. Cyclists completed 6 sessions over 3 wk, in addition to their usual aerobic base training. All laboratory tests were then repeated. RESULTS: Performances in the time trial were highly reliable when controlled for training effects (coefficient of variation = 1.1%). The percent improvement in the time trial was modeled as a polynomial function of the rank order of the intensity of the training intervals, a procedure validated by simulation. The cubic trend was strong and statistically significant (overall correlation = 0.70, P = 0.005) and predicted greatest enhancement for the intervals performed at 85% PP (2.8%, 95% CI = 4.3-1.3%) and at 175% PP (2.4%, 95% CI = 4.0-0.7%). Intervals performed at 100% PP and 80% PP did not produce statistically significant enhancements of performance. Quadratic and linear trends were weak or insubstantial. CONCLUSIONS: Interval training with work bouts close to race-pace enhance 1-h endurance performance; work bouts at much higher intensity also appear to improve performance, possibly by a different mechanism.

Adult

Effects of medium-chain triaclyglycerol ingested with carbohydrate on metabolism and exercise performance.

The effects of ingesting different amounts of medium-chain triacylglycerol (MCT) and carbohydrate (CHO) on gastric symptoms, fuel metabolism, and exercise performance were measured in 9 endurance-trained cyclists. Participants, 2 hr after a standardized lunch, cycled for 2 hr at 63% of peak oxygen consumption and then performed a simulated 40-km time trial (Ttrial). During the rides, participants ingested either 10% 14C-glucose (GLU), 10% 14C-GLU + 1.72% MCT (LO-MCT), or 10% 14C-GLU +3.44% MCT (HI-MCT) solutions: 400 ml at the start of exercise and then 100 ml every 10 min. MCT ingestion did not affect gastrointestinal symptoms. It only raised serum free fatty acid (FFA) and beta-hydroxybutyrate concentrations. Higher FFA and beta-hydroxybutyrate concentrations with MCT ingestion did not affect fuel oxidation or T-trial performance. The high CHO content of the pretrial lunch increased starting plasma insulin levels, which may have promoted CHO oxidation despite elevated circulating FFA concentrations with MCT ingestion.

3-Hydroxybutyric Acid

Fuel metabolism during ultra-endurance exercise.

Cyclists either ingested 300 ml 100 g/l U-[14C] glucose solution every 30 min during 6 h rides at 55% of VO2max (n=6) or they consumed unlabelled glucose and were infused with U-[14C] lactate (n=5). Maintenance of euglycaemia limited rises in circulating free fatty acids, noradrenaline and adrenaline concentrations to 0.9+/-0. 1 mM, 27+/-4 nM and 2.0+/-0.5 nM, respectively, and sustained the oxidation of glucose and lactate. As muscle glycogen oxidation declined from 100+/-13 to 71+/-9 micromol/min/kg in the last 3 h of exercise, glucose and lactate oxidation and interconversion rates remained at approximately 60 and 50 and at about 4 and 5 micromol/min/kg, respectively. Continued high rates of carbohydrate oxidation led to a total oxidation of around 270 g glucose, 130 g plasma lactate and 530 g muscle glycogen. Oxidation of some 530 g of muscle glycogen far exceeded the predicted (about 250 g) initial glycogen content of the active muscles and suggested that there must have been a considerable diffusion of unlabelled lactate from glycogen breakdown in inactive muscle fibres to adjacent active muscle fibres via the interstitial fluid that did not equilibrate with 14C lactate in the circulation.

Beverages

Influence of muscle glycogen content on metabolic regulation.

Euglycemia was maintained in 13 subjects with low muscle glycogen [low glycogen, euglycemic (LGE), n = 8; low glycogen, euglycemic, hyperinsulinemic (LGEI), n = 5] and 6 subjects with normal muscle glycogen (NGE), whereas hyperglycemia was maintained in 8 low muscle glycogen subjects (LGH). All subjects cycled for 145 min at 70% of maximal oxygen uptake during the infusions. Insulin was infused in LGEI at 0.2 mU.kg-1.min-1. During exercise, respiratory exchange ratio (RER) was lower and norepinephrine higher in LGE than in NGE. In LGEI and LGH, RER at the start of exercise was the same as in LGE but did not decrease as in LGE. Free fatty acids (FFA) were higher and plasma insulin concentrations lower in LGE than NGE, LGEI, or LGH over the first 45 min of exercise. Rate of glucose infusion (Ri) and rate of glucose oxidation (Rox) were higher in LGH and LGEI than in NGE or LGE, and Ri matched Rox in all groups except LGH, in which Ri was greater than Rox. Muscle glycogen disappearance was greater in NGE than LGE, LGEI, or LGH, but the latter three groups did not differ. In conclusion, this study showed that low muscle glycogen content results in a decrease in RER, an increase in FFA, fat oxidation, and norepinephrine both at rest and during exercise, and does not affect Rox when euglycemia is maintained by infusion of glucose alone. Rox was increased only during insulin and hyperglycemia.

Adult

Preexercise muscle glycogen content affects metabolism during exercise despite maintenance of hyperglycemia.

Trained cyclists with low muscle glycogen (LGH; n = 8) or normal glycogen (NGH; n = 5) exercised for 145 min at 70% of maximal oxygen uptake during a hyperglycemic clamp. Respiratory exchange ratio was higher in NGH than LGH, and free fatty acid concentrations were lower in NGH than LGH. Areas under the curve for insulin and lactate were lower in LGH than NGH. Total glucose infusion and total glucose oxidation were not different between NGH and LGH, and total glucose oxidation amounted to 65 and 66% of total glucose infusion in NGH and LGH, respectively. Rates of glucose oxidation rose during exercise, reaching peaks of 9.2 +/- 1.7 and 8.3 +/- 1.1 mmol/min in NGH and LGH, respectively. Muscle glycogen disappearance was greater in NGH than LGH. Thus 1) low muscle glycogen content does not cause increased glucose oxidation, even during hyperglycemia; instead there is an increase in fat oxidation, 2) there is an upper limit to the rate of glucose oxidation during exercise with hyperglycemia irrespective of muscle glycogen status, and 3) net muscle glycogen utilization is determined by muscle glycogen content at the start of exercise, even during hyperglycemia.

Adult

Skeletal muscle buffering capacity and endurance performance after high-intensity interval training by well-trained cyclists.

Skeletal muscle buffering capacity (beta m), enzyme activities and exercise performance were measured before and after 4 weeks of high-intensity, submaximal interval training (HIT) undertaken by six well-trained competitive cyclists [mean maximal oxygen consumption (VO2max) = 66.2 ml.kg-1.min-1]. HIT replaced a portion of habitual endurance training and consisted of six sessions, each of six to eight repetitions of 5 min duration at 80% of peak sustained power output (PPO) separated by 1 min of recovery. beta m increased from 206.6 (17.9) to 240.4 (34.1) mumol H+.g muscle dw-1.pH-1 after HIT (P = 0.05). PPO, time to fatigue at 150% PPO (TF150) and 40-km cycle time trial performance (TT40) all significantly improved after HIT (P < 0.05). In contrast, there was no change in the activity of either phosphofructokinase or citrate synthase. In addition, beta m correlated significantly with TT40 performance before HIT (r = -0.82, P < 0.05) and the relationship between change in beta m and change in TT40 was close to significance (r = -0.74). beta m did not correlate with TF150. These results indicate that beta m may be an important determinant of relatively short-duration (< 60 min) endurance cycling activity and responds positively to just six sessions of high-intensity, submaximal interval training.

Adult

Metabolic and performance adaptations to interval training in endurance-trained cyclists.

This study examined the effects of sustained high-intensity interval training (HIT) on the athletic performances and fuel utilisation of eight male endurance-trained cyclists. Before HIT, each subject undertook three baseline peak power output Wpeak tests and two simulated 40-km time-trial cycling performance (TT40) tests, of which the variabilities were 1.5 (1.3)% and 1.0 (0.5)%, respectively [mean (SD)]. Over 6 weeks, the cyclists then replaced 15 (2)% of their 300 (66) km.week-1 endurance training with 12 HIT sessions, each consisting of six to nine 5-min rides at 80% of Wpeak, separated by a l-min recovery. HIT increased Wpeak from 404 (40) to 424 (53) W (P < 0.01) and improved TT40 speeds from 42.0 (3.6) to 43.0 (4.2) km.h-1 (P < 0.05). Faster TT40 performances were due to increases in both the absolute work rates from 291 (43) to 327 (51) W (P < 0.05) and the relative work rates from 72.6 (5.3)% of pre-HIT Wpeak to 78.1 (2.8)% of post-HIT Wpeak (P < 0.05). HIT decreased carbohydrate (CHO) oxidation, plasma lactate concentration and ventilation when the cyclists rode at the same absolute work rates of 60, 70 and 80% of pre-HIT Wpeak (P < 0.05), but not when they exercised at the same relative (% post-HIT Wpeak) work rates. Thus, the ability of the cyclists to sustain higher percentages of Wpeak in TT40 performances after HIT was not due to lower rates of CHO oxidation. Higher relative work rates in the TT40 rides following HIT increased the estimated rates of CHO oxidation from approximately 4.3 to approximately 5.1 g.min-1.

Adaptation, Physiological

Time course of the effects of a high-fat diet and voluntary exercise on muscle enzyme activity in Long-Evans rats.

This study examined the time course of the effects of a high-fat diet and voluntary running exercise on rat skeletal muscle carnitine acyltransferase (CAT), beta-hydroxy-acyl-CoA dehydrogenase (HAD), and citrate synthase (CS) activities. Sixty male Long-Evans rats were randomly allocated to receive either a standard (12% fat by energy) laboratory chow diet (CHOW) or a high-fat (76% by energy) diet (HFD) and placed in running wheels for up to 6 weeks. Energy intakes and weekly voluntary running distances were similar in the CHOW and HFD rats. In both groups, weekly training distance more than doubled from week 4 to week 6. However, increased training had little influence on soleus (s) CAT(s), HAD(s), and CS(s) activities. CAT(s) and HAD(s) activities were higher in the HFD rats than in the CHOW rats from 2 weeks onward (p < 0.005), and CS(s) activities were not different between groups and remained constant over time. In contrast, increased training distance after 4 weeks in the CHOW rats resulted in an increase in deep vastus (v) CAT(v) activities to values similar to those in HFD rats prior to increases in training volume (p < 0.005) but had no effect on their HAD(v) and CS(v) activities. Increases in HAD(v) and CS(v) activities with increased training volume were only seen in the HFD rats (p < 0.005). HAD(v) activities and HAD/CS(v) activity ratios correlated with training distance in the HFD rats only (p < 0.001 and p < 0.01, respectively). These results suggest that a high-fat diet improves the beta-oxidation capacity of rat predominantly slow-twitch soleus muscle and enhances the effects of modest levels of training on the mitochondrial density and beta-oxidation capacity of rat deep vastus mixed fast- and slow-twitch muscles.

3-Hydroxyacyl CoA Dehydrogenases

Nutritional strategies to minimize fatigue during prolonged exercise: fluid, electrolyte and energy replacement.

While the presence of palatable (20 mmol l-1) concentrations of NaCl in drinks containing carbohydrate consumed during intense exercise would not be expected to promote absorption or significantly help maintain fluid balance, there is no doubt that athletes should ingest some from of carbohydrate (other than fructose) during moderate-intensity exercise lasting > 90 min. As only approximately 20 g of ingested carbohydrate is oxidized in the first hour of exercise, athletes should probably consume 100 ml every 10 min of a dilute (3-5 g 100 ml-1) carbohydrate solution and thereafter increase the carbohydrate concentration to approximately 10 g 100 ml-1 to match the peak (approximately 1 g min-1) rates of plasma glucose oxidation. Drinking more than those amounts of carbohydrate may increase muscle glycogen oxidation by attenuating the fall in plasma insulin concentration and thereby delaying fat mobilization, especially at relatively low (55% of peak oxygen consumption) intensity exercise. As carbohydrate ingestion does not slow the rate of glycogen utilization in working muscle, it is also advisable for endurance athletes to start exercise with an adequate supply of muscle glycogen, irrespective of whether or not they ingest carbohydrate during exercise. While carbohydrate ingestion 'spares' conversion of liver glycogen to plasma glucose and prevents hypoglycemia, it does not delay the fatigue associated with a low (approximately 20 mmol kg-1) glycogen content in working muscle. Conversely, increases in glycogen content of working muscle at the start of exercise have no effect on the rates of plasma glucose oxidation. Higher initial rates of glycogen utilization by active muscles in 'carbohydrate-loaded' subjects decrease the indirect oxidation (via lactate) of non-working muscle glycogen, rather than the conversion of liver glycogen to plasma glucose. Hence, athletes should ingest carbohydrate during endurance exercise even if they have 'carbohydrate-loaded' before exercise.

Dietary Carbohydrates

Nutritional strategies for promoting fat utilization and delaying the onset of fatigue during prolonged exercise.

Carbohydrate ingestion before and during endurance exercise delays the onset of fatigue (reduced power output). Therefore, endurance athletes are recommended to ingest diets high in carbohydrate (70% of total energy) during competition and training. However, increasing the availability of plasma free fatty acids has been shown to slow the rate of muscle and liver glycogen depletion by promoting the utilization of fat. Ingested fat, in the form of long-chain (C16-22) triacylglycerols, is largely unavailable during acute exercise, but medium-chain (C8-10) triacylglycerols are rapidly absorbed and oxidized. We have shown that the ingestion of medium-chain triacylglycerols in combination with carbohydrate spares muscle carbohydrate stores during 2 h of submaximal (< 70% VO2 peak) cycling exercise, and improves 40 km time-trial performance. These data suggest that by combining carbohydrate and medium-chain triacylglycerols as a pre-exercise supplement and as a nutritional supplement during exercise, fat oxidation will be enhanced, and endogenous carbohydrate will be spared. We have also examined the chronic metabolic adaptations and effects on substrate utilization and endurance performance when athletes ingest a diet that is high in fat (> 70% by energy). Dietary fat adaptation for a period of at least 2-4 weeks has resulted in a nearly two-fold increase in resistance to fatigue during prolonged, low- to moderate-intensity cycling (< 70% VO2 peak). Moreover, preliminary studies suggest that mean cycling 20 km time-trial performance following prolonged submaximal exercise is enhanced by 80 s after dietary fat adaptation and 3 days of carbohydrate loading. Thus the relative contribution of fuel substrate to prolonged endurance activity may be modified by training, pre-exercise feeding, habitual diet, or by artificially altering the hormonal milieu or the availability of circulating fuels. The time course and dose-response of these effects on maximizing the oxidative contribution of fat for exercise metabolism and in exercise performance have not been systematically studied during moderate- to high-intensity exercise in humans.

Adipose Tissue

Training techniques to improve fatigue resistance and enhance endurance performance.

Despite their best efforts, sports scientists have found it difficult to persuade elite athletes to experiment with their training regimens. Thus, until recently, exercise physiologists have had limited impact on the training practices of successful athletes, with most of the innovations in the training patterns of the best athletes coming from the empirical observations of top-level coaches. One form of training recognized by sports scientists and used by athletes for several decades in interval/transition training. Such training consists of a number of exercise bouts alternated with short rest intervals of more slowly paced activity and is thought to improve the fatigue resistance of the active muscles by exposing them to sustained, high-intensity exercise at the athlete's maximal steady-state pace. Few scientific studies, however, have examined the effects of transition training on the performances of competitive athletes. This paper identifies the physiological factors associated with successful endurance performance, and summarizes the results of investigations on competitive endurance cyclists which examined the time-course of changes in performance in response to a sustained, high-intensity interval training programme.

Adult

Could women outrun men in ultramarathon races?

To test a hypothesis that the differences in running performances between men and women narrow with increasing race distance, recent best running speeds (m.s-1) of 28 female ultramarathon runners over racing distances from 5 to 90 km were compared with those of male runners matched for 56 km race time, age and training. These comparisons revealed that the men ran faster than the women over 5 to 42.2 km (P < 0.01-0.05), but not in a 90-km race (2.82 +/- 0.04 vs 2.90 +/- 0.09 m.s-1). Declines in the men's and women's running speeds with increasing race distances were best fitted by Y = 2.9.exp.(-0.01.X) + 1.7 and Y = 2.1.exp.(-0.01.X) + 2.0 equations (r = -0.99). Differences between the exponential declines in the men's and women's running speeds over longer race distances were best fitted by a linear Y = -0.006 (X-66) equation (r = -0.98, P < 0.001). The negative slope and the X-axis intercept of this equation at 66 km supports the hypothesis that women ultramarathon runners have greater fatigue resistance than do equally trained men whose performances are superior up to the marathon distance.

Adult

Carbohydrate-loading and exercise performance. An update.

This review suggests that there is little or no effect of elevating pre-exercise muscle glycogen contents above normal resting values on a single exhaustive bout of high-intensity exercise lasting less than 5 minutes. Nor is there any benefit of increasing starting muscle glycogen content on moderate-intensity running or cycling lasting 60 to 90 minutes. In such exercise substantial quantities of glycogen remain in the working muscles at the end of exercise. However, elevated starting muscle glycogen content will postpone fatigue by approximately equal to 20% in endurance events lasting more than 90 minutes. During this type of exercise, exhaustion usually coincides with critically low (25 mmol/kg wet weight) muscle glycogen contents, suggesting the supply of energy from glycogen utilisation cannot be replaced by an increased oxidation of blood glucose. Glycogen supercompensation may also improve endurance performance in which a set distance is covered as quickly as possible. In such exercise, high carbohydrate diets have been reported to improve performance by 2 to 3%.

Dietary Carbohydrates

Fuel kinetics during intense running and cycling when fed carbohydrate.

On two occasions, six well-trained, male competitive triathletes performed, in random order, two experimental trials consisting of either a timed ride to exhaustion on a cycle ergometer or a run to exhaustion on a motor-driven treadmill at 80% of their respective peak cycling and peak running oxygen (VO2 max) uptakes. At the start of exercise, subjects drank 250 ml of a 15 g.100 ml-1 w/v [U-14C]glucose solution and, thereafter, 150 ml of the same solution every 15 min. Despite identical metabolic rates [VO2 3.51 (0.06) vs 3.51 (0.10) 1.min-1; values are mean (SEM) for the cycling and running trials, respectively], exercise times to exhaustion were significantly longer during cycling than running [96 (14) vs 63 (11) min; P < 0.05]. The superior cycling than running endurance was not associated with any differences in either the rate of blood glucose oxidation [3.8 (0.1) vs 3.9 (0.4) mmol.min-1], or the rate of ingested glucose oxidation [2.0 (0.1) vs 1.7 (0.2) mmol.min-1] at the last common time point (40 min) before exhaustion, despite higher blood glucose concentrations at exhaustion during running than cycling [7.0 (0.9) vs 5.8 (0.5) mmol.l-1; P < 0.05]. However, the final rate of total carbohydrate (CHO) oxidation was significantly greater during cycling than running [24.0 (0.8) vs 21.7 (1.4) mmol C6.min-1; P < 0.01]. At exhaustion, the estimated contribution to energy production from muscle glycogen had declined to similar extents in both cycling and running [68 (3) vs 65 (5)%]. These differences between the rates of total CHO oxidation and blood glucose oxidation suggest that the direct and/or indirect (via lactate) oxidation of muscle glycogen was greater in cycling than running.

Adult

Fuel substrate turnover and oxidation and glycogen sparing with carbohydrate ingestion in non-carbohydrate-loaded cyclists.

This study examined the effects of ingesting 500 ml/h of either a 10% carbohydrate (CHO) drink (CI) or placebo (PI) on splanchnic glucose appearance rate (endogenous + exogenous) (Ra), plasma glucose oxidation and muscle glycogen utilisation in 17, non-carbohydrate-loaded, male, endurance-trained cyclists who rode for 180 min at 70% of maximum oxygen uptake. Mean muscle glycogen content at the start of exercise was 130 +/- 6 mmol/kg ww; (mean +/- SEM). Total CHO oxidation was similar in CI and PI subjects and declined during the trial. Ra increased significantly during the trial (P < 0.05) in both groups. Plasma glucose oxidation also increased significantly during the trial, reaching a plateau in the PI subjects, but was significantly (P < 0.05) higher in CI than PI subjects at the end of exercise [(98 +/- 14 vs. 72 +/- 10 micromol/min/kg fat-free mass) (FFM) (1.34 +/- 0.19 vs. 0.93 +/- 0. 13 g/min)]. However, mean endogenous Ra was significantly (P < 0.05) lower in the CI than PI subjects throughout exercise (35 +/- 7 vs. 54 +/- 6 micromol/min/kg FFM), as was the oxidation of endogenous plasma glucose, which remained almost constant in CI subjects, and reached values at the end of exercise of 42 +/- 13 and 72 +/- 10 micromol/min/kg FFM in the CI and PI groups respectively. Of the 150 g CHO ingested during the trial, 50% was oxidised. Muscle glycogen disappearance was identical during the first 2 h of exercise in both groups and continued at the same rate in PI subjects, however no net muscle glycogen disappearance occurred during the final hour in CI subjects. We conclude that ingestion of 500 ml/h of a 10% CHO solution during prolonged exercise in non carbohydrate loaded subjects has a marked liver glycogen-sparing effect or causes a reduction in gluconeogenesis, or both, maintains plasma glucose concentration and has a muscle glycogen-sparing effect.

Adult

Fuel substrate kinetics of carbohydrate loading differs from that of carbohydrate ingestion during prolonged exercise.

This study compared fuel substrate kinetics in trained cyclists who ingested a 10% carbohydrate (CHO) drink without prior CHO-loading ([NLC] n=9) with those in cyclists who ingested a water placebo after CHO-loading ([CLP] n=7) during 180 minutes of cycling at 70% maximum oxygen consumption (Vo2 max). Muscle glycogen at the start of exercise was 194 +/- 4 and 124 +/- 8 mmol/kg wet weight (mean +/- SEM) in CLP and NLC subjects, respectively . Total CHO oxidation was similar. Total rate of appearance of glucose from endogenous (Raend) and exogenous (Raexog) origin and plasma glucose oxidation increased significantly (P<.05), with NLC subjects ending significantly higher than CLP subjects (104 +/- 17 v 79 +/- 9 and 115 +/- 16 v 74 +/- 11 micromol/min/kg fat-free mass [FFM], respectively). However, Raend was lower (P<.05) in NLC than in CLP subjects (40 +/- 10 v 79 +/- 9 micromol/min/kg FFM), as was endogenous plasma glucose oxidation (42 +/- 13 v 75 +/- 11 micromol/min kg FFM). Muscle glycogen disappearance was identical in the first hour, but declined thereafter in NLC subjects. Two NLC subjects with the lowest muscle glycogen content were unable to complete the trial despite CHO ingestion. We conclude that with respect to the groups studied (1) CHO loading before exercise reduces the relative contribution of plasma glucose oxidation to total CHO oxidation, but may prolong time to exhaustion as a function of higher muscle glycogen concentration; (2) CHO ingestion has a liver glycogen-sparing effect, causes a reduction in gluconeogenesis, or both, that should delay the onset of hypoglycemia; (3) the progressive increase in plasma glucose oxidation that occurs during prolonged exercise is related to muscle glycogen status and occurs irrespective of whether CHO is ingested: (4) the effects of CHO ingestion and CHO-loading on fuel substrate kinetics are different.

Adult