The effect of a preexercise meal on time to fatigue during prolonged cycling exercise.

PURPOSE AND METHODS: Seven subjects exercised to exhaustion on a bicycle ergometer at a workload corresponding to an intensity of 70% maximal oxygen uptake (VO2max). On one occasion (FED), subjects consumed a preexercise carbohydrate (CHO) containing breakfast (100 g CHO) 3 h before exercise. On the other occasion (FASTED), subjects exercised after an overnight fast. Exercise time to fatigue was significantly longer (P < 0.05) when subjects consumed the breakfast (136+/-14 min) compared with when they exercised in the fasted state (109+/-12 min). RESULTS: Pre- and post-exercise muscle glycogen concentrations, respiratory exchange ratio, carbohydrate and fat oxidation, and lactate and insulin concentrations were not significantly different between the two trials. Insulin concentrations decreased significantly (P < 0.05) from 4.7+/-0.05 microIU.mL(-1) to 2.8+/-0.4 microIU.mL(-1) in FED and from 6.6+/-0.6 microIU.mL(-1) to 3.7+/-0.6 microIU.mL(-1) in FASTED subjects and free fatty acid concentrations (FFA) increased significantly (P < 0.05) from 0.09+/-0.02 mmol.L(-1) to 1.4+/-0.6 mmol.L(-1) in FED and from 0.17+/-0.02 mmol.L(-) to 0.74+/-0.27 mmol.L(-1) in FASTED subjects over the duration of the trials. CONCLUSIONS: In conclusion, the important finding of this study is the increased time to fatigue when subjects ingested the CHO meal with no negative effects ascribed to increased insulin concentrations and decreased FFA concentrations after CHO ingestion.

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.

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.

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.

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.

Glucose kinetics during prolonged exercise in euglycaemic and hyperglycaemic subjects.

To determine the limits to oxidation of exogenous glucose by skeletal muscle, the effects of euglycaemia (plasma glucose 5 mM, ET) and hyperglycaemia (plasma glucose 10 mM, HT) on fuel substrate kinetics were evaluated in 12 trained subjects cycling at 70% of maximal oxygen uptake (VO2, max) for 2 h. During exercise, subjects ingested water labelled with traces of U-14C-glucose so that the rates of plasma glucose oxidation (Rox) could be determined from plasma 14C-glucose and expired 14CO2 radioactivities, and respiratory gas exchange. Simultaneously, 2-3H-glucose was infused at a constant rate to estimate rates of endogenous glucose turnover (Ra), while unlabelled glucose (25% dextrose) was infused to maintain plasma glucose concentration at either 5 or 10 mM. During ET, endogenous liver glucose Ra (total Ra minus the rate of infusion) declined from 22.4 +/- 4.9 to 6.5 +/- 1.4 mumol/min per kg fat-free mass [FFM] (P < 0.05) and during HT it was completely suppressed. In contrast, Rox increased to 152 +/- 21 and 61 +/- 10 mumol/min per kg FFM at the end of HT and ET respectively (P < 0.05). HT (i.e., plasma glucose 10 mM) and hyperinsulinaemia (24.5 +/- 0.9 microU/ml) also increased total carbohydrate oxidation from 203 +/- 7 (ET) to 310 +/- 3 mumol/min per kg FFM (P < 0.0001) and suppressed fat oxidation from 51 +/- 3 (ET) to 18 +/- 2 mumol/min per kg FFM (P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of glucose ingestion or glucose infusion on fuel substrate kinetics during prolonged exercise.

To determine if bypassing both intestinal absorption and hepatic glucose uptake by intravenous glucose infusion might increase the rate of muscle glucose oxidation above 1 g.min-1, ten endurance-trained subjects were studied during 125 min of cycling at 70% of peak oxygen uptake (VO2peak). During exercise the subjects ingested either a 15 g.100 ml-1 U-14C labelled glucose solution or H2O labelled with a U-14C glucose tracer for the determination of the rates of plasma glucose oxidation (Rox) and exogenous carbohydrate (CHO) oxidation from plasma 14C glucose and 14CO2 specific activities, and respiratory gas exchange. Simultaneously, 2-3H glucose was infused at a constant rate to measure glucose turnover, while unlabelled glucose (25% dextrose) was infused into those subjects not ingesting glucose to maintain plasma glucose concentration at 5 mmol.l-1. Despite similar plasma glucose concentrations [ingestion 5.3 (SEM 0.13) mmol.l-1; infusion 5.0 (0.09) mmol.l-1], compared to glucose infusion, CHO ingestion significantly increased plasma insulin concentrations [12.9 (1.0) vs 4.8 (0.5) mU.l-1; P < 0.05], raised total Rox values [9.5 (1.2) vs 6.2 (0.7) mmol.125 min-1 kg fat free mass-1 (FFM); P < 0.05] and rates of CHO oxidation [37.2 (2.8) vs 24.1 (3.9) mmol.125 min-1 kg FFM-1; P < 0.05]. An increased reliance on CHO metabolism with CHO ingestion was associated with a decrease in fat oxidation. Whereas the contribution from fat oxidation to energy production increased to 51 (10)% with glucose infusion, it only reached 18 (4)% with glucose ingestion (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)