Effects of carbohydrate ingestion before and during exercise on glucose kinetics and performance.

We investigated the effect of carbohydrate (CHO) ingestion before and during exercise and in combination on glucose kinetics, metabolism and performance in seven trained men, who cycled for 120 min (SS) at approximately 63% of peak power output, followed by a 7 kJ/kg body wt time trial (TT). On four separate occasions, subjects received either a placebo beverage before and during SS (PP); placebo 30 min before and 2 g/kg body wt of CHO in a 6.4% CHO solution throughout SS (PC); 2 g/kg body wt of CHO in a 25.7% CHO beverage 30 min before and placebo throughout SS (CP); or 2 g/kg body wt of CHO in a 25.7% CHO beverage 30 min before and 2 g/kg of CHO in a 6.4% CHO solution throughout SS (CC). Ingestion of CC and CP markedly (>8 mM) increased plasma glucose concentration ([glucose]) compared with PP and PC (5 mM). However, plasma [glucose] fell rapidly at the onset of SS so that after 80 min it was similar (6 mM) between all treatments. After this time, plasma [glucose] declined in both PP and CP (P < 0.05) but was well maintained in both CC and PC. Ingestion of CC and CP increased rates of glucose appearance (R(a)) and disappearance (R(d)) compared with PP and PC at the onset of, and early during, SS (P < 0.05). However, late in SS, both glucose R(a) and R(d) were higher in CC and PC compared with other trials (P < 0.05). Although calculated rates of glucose oxidation were different when comparing the four trials (P < 0.05), total CHO oxidation and total fat oxidation were similar. Despite this, TT was improved in CC and PC compared with PP (P < 0.05). We conclude that 1) preexercise ingestion of CHO improves performance only when CHO ingestion is maintained throughout exercise, and 2) ingestion of CHO during 120 min of cycling improves subsequent TT performance.     

Effects of 4- and 8-h preexercise feedings on substrate use and performance

Seven well-trained male cyclists were studied during 105 min of cycling (65% of maximal oxygen uptake) and a 15-min "performance ride" to compare the effects of 4- and 8-h preexercise carbohydrate (CHO) feedings on substrate use and performance. A high CHO meal was given 1) 4-h preexercise (M-4), 2) 8-h preexercise (M-8), 3) 4-h preexercise with CHO feedings during exercise (M-4CHO), and 4) 8-h preexercise with CHO feedings during exercise (M-8CHO). Blood samples were obtained at 0, 15, 60, 105, and 120 min and analyzed for lactate, glucose, insulin, and glycerol. Total work output during the performance ride was similar for the M-4 (217,893 +/- 13,348 N/m) and M-8 trials (216,542 +/- 13,905) and was somewhat higher for the M-4CHO (223,994 +/- 14,387) and M-8CHO (224,702 +/- 15,709) trials (P = 0.059, NS). Glucose was significantly elevated throughout exercise, and insulin levels were significantly elevated at 15 and 60 min during M-4CHO and M-8CHO compared with M-4 and M-8 trials. Glycerol levels were significantly lower during the CHO feeding trials compared with placebo and were not significantly different during exercise when the subject had fasted an additional 4 h. The results of this study suggest that when preexercise meals are ingested 4 or 8 h before submaximal cycling exercise, substrate use and performance are similar.     

Enhanced leg exercise endurance with a high-carbohydrate diet and dihydroxyacetone and pyruvate

The effects of dietary supplementation of dihydroxyacetone and pyruvate (DHAP) on metabolic responses and endurance capacity during leg exercise were determined in eight untrained males (20-30 yr). During the 7 days before exercise, a high-carbohydrate diet was consumed (70% carbohydrate, 18% protein, 12% fat; 35 kcal/kg body weight). One hundred grams of either Polycose (placebo) or dihydroxyacetone and pyruvate (treatment, 3:1) were substituted for a portion of carbohydrate. Dietary conditions were randomized, and subjects consumed each diet separated by 7-14 days. After each diet, cycle ergometer exercise (70% of peak oxygen consumption) was performed to exhaustion. Biopsy of the vastus lateralis muscle was obtained before and after exercise. Blood samples were drawn through radial artery and femoral vein catheters at rest, after 30 min of exercise, and at exercise termination. Leg endurance was 66 +/- 4 and 79 +/- 2 min after placebo and DHAP, respectively (P less than 0.01). Muscle glycogen at rest and exhaustion did not differ between diets. Whole leg arteriovenous glucose difference was greater (P less than 0.05) for DHAP than for placebo at rest (0.36 +/- 0.05 vs. 0.19 +/- 0.07 mM) and after 30 min of exercise (1.06 +/- 0.14 vs. 0.65 +/- 0.10 mM) but did not differ at exhaustion. Plasma free fatty acids, glycerol, and beta-hydroxybutyrate were similar during rest and exercise for both diets. Estimated total glucose oxidation during exercise was 165 +/- 17 and 203 +/- 15 g after placebo and DHAP, respectively (P less than 0.05). It is concluded that feeding of DHAP for 7 days in conjunction with a high carbohydrate diet enhances leg exercise endurance capacity by increasing glucose extraction by muscle.     

Acute glucocorticoid effects on glycogen utilization, O2 uptake, and endurance

This study was undertaken to determine the effects of increased substrate availability (glycogen + plasma fatty acids) by glucocorticoids on energy metabolism during exercise to exhaustion. Female rats received a single subcutaneous injection of cortisol acetate (CA) (100 mg.kg body wt-1) 21 h before treadmill running (30.8 m/min). At the start of exercise in the CA-treated rats, plasma fatty acids and liver glycogen were increased by 40%. Glycogen levels were also increased by CA treatment in slow-twitch soleus (61%), fast-twitch white vastus (38%), and fast-twitch red vastus lateralis (85%) muscles. Exercise time to exhaustion was increased by CA treatment (114 +/- 5 vs. 95 +/- 6 min, P less than 0.05). During the exercise, total glycogen depletion was greater in the CA-treated than in the control animals, whereas estimated relative rates of carbohydrate utilization (R = 0.90) were similar. However, while running the CA-treated group consumed 11% more O2 than the controls (P less than 0.05). These results show that a single injection of glucocorticoids is capable of improving endurance. Yet the increased O2 uptake during exercise may have minimized the impact of the initial increased availability of carbohydrates and fatty acids in prolonging exercise capacity. This decreased running economy by the CA-treated runners may be secondary to alterations in energy production or utilization.     

Effect of a divided caffeine dose on endurance cycling performance, postexercise urinary caffeine concentration, and plasma paraxanthine.

This study compared the effects of a single and divided dose of caffeine on endurance performance and on postexercise urinary caffeine and plasma paraxanthine concentrations. Nine male cyclists and triathletes cycled for 90 min at 68% of maximal oxygen uptake, followed by a self-paced time trial (work equivalent to 80% of maximal oxygen uptake workload over 30 min) with three randomized, balanced, and double-blind interventions: 1) placebo 60 min before and 45 min into exercise (PP); 2) single caffeine dose (6 mg/kg) 60 min before exercise and placebo 45 min into exercise (CP); and 3) divided caffeine dose (3 mg/kg) 60 min before and 45 min into exercise (CC). Time trial performance was unchanged with caffeine ingestion (P = 0.08), but it tended to be faster in the caffeine trials (CP: 24.2 min and CC: 23.4 min) compared with placebo (PP: 28.3 min). Postexercise urinary caffeine concentration was significantly lower in CC (3.8 micro g/ml) compared with CP (6.8 micro g/ml). Plasma paraxanthine increased in a dose-dependent fashion and did not peak during exercise. In conclusion, dividing a caffeine dose provides no ergogenic effect over a bolus dose but reduces postexercise urinary concentration.     

Effect of carbohydrate feedings during high-intensity exercise

To determine the upper limits of steady-state exercise performance and carbohydrate oxidation late in exercise, seven trained men were studied on two occasions during prolonged cycling that alternated every 15 min between approximately 60% and approximately 85% of VO2max. When fed a sweet placebo throughout exercise, plasma glucose and respiratory exchange ratio (R) declined (P less than 0.05) from 5.0 +/- 0.1 mM and 0.91 +/- 0.01 after 30 min (i.e., at 85% VO2max) to 3.7 +/- 0.3 mM and 0.79 +/- 0.01 at fatigue (i.e., when the subjects were unable to continue exercise at 60% VO2max). Carbohydrate feeding throughout exercise (1 g/kg at 10 min, then 0.6 g/kg every 30 min) increased plasma glucose to approximately 6 mM and partially prevented this decline in carbohydrate oxidation, allowing the men to perform 19% more work (2.74 +/- 0.13 vs. 2.29 +/- 0.09 MJ, P less than 0.05) before fatiguing. Even when fed carbohydrate, however, by the 3rd h of exercise, R had fallen from 0.92 to 0.87, accompanied by a reduction in exercise intensity from approximately 85% to approximately 75% VO2max (both P less than 0.05). These data indicate that carbohydrate feedings enable trained cyclists to exercise at up to 75% VO2max and to oxidize carbohydrate at up to 2 g/min during the later stages of prolonged intense exercise.     

Glycogen depletion during prolonged exercise: influence of glucose, fructose, or placebo

We examined the influence of various carbohydrates of fuel homeostasis and glycogen utilization during prolonged exercise. Seventy-five grams of glucose, fructose, or placebo were given orally to eight healthy males 45 min before ergometer exercise performed for 2 h at 55% of maximal aerobic power (VO2max). After glucose ingestion, the rises in plasma glucose (P less than 0.01) and insulin (P less than 0.001) were 2.4- and 5.8-fold greater than when fructose was consumed. After 30 min of exercise following glucose ingestion, the plasma glucose concentration had declined to a nadir of 3.9 +/- 0.3 mmol/l, and plasma insulin had returned to basal levels. The fall in plasma glucose was closely related to the preexercise glucose (r = 0.98, P less than 0.001) and insulin (r = 0.66, P less than 0.05) levels. The rate of endogenous glucose production and utilization rose similarly by 2.8-fold during exercise in fructose group and were 10-15% higher than in placebo group (P less than 0.05). Serum free fatty acid levels were 1.5- to 2-fold higher (P less than 0.01) after placebo than carbohydrate ingestion. Muscle glycogen concentration in the quadriceps femoris fell in all three groups by 60-65% (P less than 0.001) during exercise. These data indicate that fructose ingestion, though causing smaller perturbations in plasma glucose, insulin, and gastrointestinal polypeptide (GIP) levels than glucose ingestion, was no more effective than glucose or placebo in sparing glycogen during a long-term exercise.     

Effect of carbohydrate ingestion on glucose kinetics and muscle metabolism during intense endurance exercise.

There has been recent interest in the potential performance and metabolic effects of carbohydrate ingestion during exercise lasting approximately 1 h. In this study, 13 well-trained men ingested in randomized order either a 6% glucose solution (CHO trial) or a placebo (Con trial) during exercise to exhaustion at 83+/-1% peak oxygen uptake. In six subjects, vastus lateralis muscle was sampled at rest, at 32 min, and at exhaustion, and in six subjects, glucose kinetics was determined by infusion of [6,6-(2)H]glucose in both trials and ingestion of [6-(3)H]glucose in the CHO trial. Of the 84 g of glucose ingested during exercise in the CHO trial, only 22 g appeared in the peripheral circulation. This resulted in a small (12 g) but significant (P<0.05) increase in glucose uptake without influencing carbohydrate oxidation, muscle glycogen use, or time to exhaustion (CHO: 68.1+/-4.1 min; Con: 69.6+/-5.5 min). Decreases in muscle phosphocreatine content and increases in muscle inosine monophosphate and lactate content during exercise were similar in the two trials. Although endogenous glucose production during exercise was partially suppressed in the CHO trial, it remained significantly above preexercise levels throughout exercise. In conclusion, only 26% of the ingested glucose appeared in the peripheral circulation. Glucose ingestion increased glucose uptake and partially reduced endogenous glucose production but had no effect on carbohydrate oxidation, muscle metabolism, or time to exhaustion during exercise at 83% peak oxygen uptake.     

Comparison of the effects of pre-exercise feeding of glucose, glycerol and placebo on endurance and fuel homeostasis in man

Six men were studied during exercise to exhaustion on a cycle ergometer at 73% of VO2max following ingestion of glycerol, glucose or placebo. Five of the subjects exercised for longer on the glucose trial compared to the placebo trial (p less than 0.1; 108.8 vs 95.9 min). Exercise time to exhaustion on the glucose trial was longer (p less than 0.01) than on the glycerol trial (86.0 min). No difference in performance was found between the glycerol and placebo trials. The ingestion of glucose (lg X kg-1 body weight) 45 min before exercise produced a 50% rise in blood glucose and a 3-fold rise in plasma insulin at zero min of exercise. Total carbohydrate oxidation was increased by 26% compared to placebo and none of the subjects exhibited a fall in blood glucose below 4 mmol X 1-1 during the exercise. The ingestion of glycerol (lg X kg-1 body weight) 45 min before exercise produced a 340-fold increase in blood glycerol concentration at zero min of exercise, but did not affect resting blood glucose or plasma insulin levels; blood glucose levels were up to 14% higher (p less than 0.05) in the later stages of exercise and at exhaustion compared to the placebo or glucose trials. Both glycerol and glucose feedings lowered the magnitude of the rise in plasma FFA during exercise compared to placebo. Levels of blood lactate and alanine during exercise were not different on the 3 dietary treatments.(ABSTRACT TRUNCATED AT 250 WORDS)     

Partial restoration of dietary fat induced metabolic adaptations to training by 7 days of carbohydrate diet.

We tested the hypothesis that a shift to carbohydrate diet after prolonged adaptation to fat diet would lead to decreased glucose uptake and impaired muscle glycogen breakdown during exercise compared with ingestion of a carbohydrate diet all along. We studied 13 untrained men; 7 consumed a high-fat (Fat-CHO; 62% fat, 21% carbohydrate) and 6 a high-carbohydrate diet (CHO; 20% fat, 65% carbohydrate) for 7 wk, and thereafter both groups consumed the carbohydrate diet for an eighth week. Training was performed throughout. After 8 wk, during 60 min of exercise (71 +/- 1% pretraining maximal oxygen uptake) average leg glucose uptake (1.00 +/- 0.07 vs. 1.55 +/- 0.21 mmol/min) was lower (P < 0.05) in Fat-CHO than in CHO. The rate of muscle glycogen breakdown was similar (4.4 +/- 0.5 vs. 4.2 +/- 0.7 mmol. min(-1). kg dry wt(-1)) despite a significantly higher preexercise glycogen concentration (872 +/- 59 vs. 688 +/- 43 mmol/kg dry wt) in Fat-CHO than in CHO. In conclusion, shift to carbohydrate diet after prolonged adaptation to fat diet and training causes increased resting muscle glycogen levels but impaired leg glucose uptake and similar muscle glycogen breakdown, despite higher resting levels, compared with when the carbohydrate diet is consumed throughout training.     

Substrate usage during prolonged exercise following a preexercise meal

The effect of a high-carbohydrate meal 4 h before 105 min of exercise at 70% of maximal O2 uptake was determined in seven endurance-trained cyclists and compared with exercise following a 16-h fast. The preexercise meal produced a transient elevation of plasma insulin and blood glucose, which returned to fasting basal levels prior to the initiation of exercise. The meal also resulted in a 42% elevation (P less than 0.05) of glycogen within the vastus lateralis at the beginning of exercise. The 1st h of exercise when subjects were fed was characterized by a 13-25% decline (P less than 0.05) in blood glucose concentration, a suppression of the normal increase in plasma free fatty acids and blood glycerol, and a 45% (P less than 0.05) greater rate of carbohydrate oxidation compared with exercise when subjects were fasted. After 105 min of exercise, there were no significant differences when subjects were fed or fasted regarding blood glucose levels, rate of carbohydrate oxidation, or muscle glycogen concentration. The greater muscle glycogen utilization (97 +/- 18 vs. 64 +/- 8 mmol glucosyl units X kg-1; P less than 0.05) and carbohydrate oxidation when subjects were fed appeared to be derived from the glycogen synthesized following the meal. These results indicate that preexercise feedings alter substrate availability despite a return of plasma insulin to fasting levels prior to exercise and that these effects persist until the 2nd h of exercise.     

Acute pantothenic acid and cysteine supplementation does not affect muscle coenzyme A content, fuel selection, or exercise performance in healthy humans

Reduced skeletal muscle free coenzyme A (CoASH) availability may decrease the contribution of fat oxidation to ATP production during high-intensity, submaximal exercise or, alternatively, limit pyruvate dehydrogenase complex (PDC) flux and thereby carbohydrate oxidation. Here we attempted to increase the muscle CoASH pool in humans, via pantothenic acid and cysteine feeding, in order to elucidate the role of CoASH availability on muscle fuel metabolism during exercise. On three occasions, eight healthy male volunteers (age 22.9 ± 1.4 yr, body mass index 24.2 ± 1.5 kg/m(2)) cycled at 75% maximal oxygen uptake (Vo(2max)) to exhaustion, followed by a 15-min work output performance test. Muscle biopsies were obtained at rest, and after 60 min and 91.3 ± 3.1 min of exercise (time to exhaustion on baseline visit) on each occasion. Two weeks following the first visit (baseline), 1 wk of oral supplementation with either 3 g/day of a placebo control (glucose polymer; CON) or 1.5 g/day each of d-pantothenic acid and l-cysteine (CP) was carried out prior to the second and third visits in a randomized, counterbalanced, double-blind manner, leaving a 3-wk gap in total between each visit. Resting muscle CoASH content was not altered by supplementation in any visit. Following 60 min of exercise, muscle CoASH content was reduced by 13% from rest in all three visits (P < 0.05), and similar changes in the respiratory exchange ratio, glycogenolysis (～235 mmol/kg dry muscle), PCr degradation (～57 mmol/kg dry muscle), and lactate (～25 mmol/kg dry muscle) and acetylcarnitine (～12 mmol(.)kg/dry muscle) accumulation was observed during exercise when comparing visits. Furthermore, no difference in work output was observed when comparing CON and CP. Acute feeding with pantothenic acid and cysteine does not alter muscle CoASH content and consequently does not impact on muscle fuel metabolism or performance during exercise in humans.     

Effects of carbohydrate supplementation on force output and time to exhaustion during static leg contractions superimposed with electromyostimulation

The purpose of this study was to investigate the effects of carbohydrate ingestion on force output and time to exhaustion using single leg static contractions superimposed with brief periods of electromyostimulation. Six trained male subjects participated in a randomized, counterbalanced, double-blind study. The subjects were randomly assigned to placebo (PL) or carbohydrate (CHO). The subjects in CHO consumed 1 g of carbohydrate per kilogram of body mass loading dose and 0.17 g of carbohydrate per kilogram of body mass every 6 minutes during the exercise protocol. The PL received an equal volume of a solution made of saccharin and aspartame. The exercise protocol consisted of repeated 20-second static contractions of quadriceps muscle at 50% maximal voluntary contraction followed by 40-second rest until failure occurred. Importantly, the force output during quadriceps maximal voluntary contraction strength with superimposed electromyostimulation was measured in the beginning and every 5 minutes during the last 3 seconds of static contractions throughout the exercise protocol. Venous blood samples were taken preexercise, immediately postexercise, and at 5 minutes postexercise and analyzed for blood lactate. Our results indicate that time to exhaustion (PL = 16.0 ± 8.1 minutes; CHO = 29.0 ± 13.1 minutes) and force output (PL = 3,638.7 ± 524.5 N; CHO = 5,540.1 ± 726.1 N) were significantly higher (p < 0.05) in CHO compared with that in PL. Data suggest that carbohydrate ingestion before and during static muscle contractions can increase force output and increase time to exhaustion. Therefore, our data suggest that carbohydrate supplementation before and during resistance exercise might help increase the training volume of athletes.     

Enhancement of arm exercise endurance capacity with dihydroxyacetone and pyruvate

The effects of dietary supplementation of dihydroxyacetone and pyruvate (DHAP) on endurance capacity and metabolic responses during arm exercise were determined in 10 untrained males (20-26 yr). Subjects performed arm ergometer exercise (60% peak O2 consumption) to exhaustion after consumption of standard diets (55% carbohydrate, 15% protein, 30% fat; 35 kcal/kg) containing either 100 g of Polycose (placebo, P) or DHAP (3:1, treatment) substituted for a portion of carbohydrate. The two diets were administered in a random order, and each was consumed for a 7-day period. Biopsy of the triceps muscle was obtained immediately before and after exercise. Blood samples were drawn through radial artery and axillary vein catheters at rest, after 60 min of exercise, and at exercise termination. Arm endurance was 133 +/- 20 min after P and 160 +/- 22 min after DHAP (P less than 0.01). Triceps glycogen at rest was 88 +/- 8 (P) and 130 +/- 19 mmol/kg (DHAP) (P less than 0.05). Whole arm arteriovenous glucose difference (mmol/l) was greater (P less than 0.05) for DHAP than P at rest (0.60 +/- 0.12 vs. 0.05 +/- 0.09) and after 60 min of exercise (1.00 +/- 0.12 vs. 0.36 +/- 0.11), but it did not differ at exhaustion. Neither respiratory exchange ratio nor respiratory quotient differed between trials at rest, after 60 min of exercise, or at exhaustion. Plasma free fatty acid, glycerol, beta-hydroxybutyrate, catecholamines, and insulin were similar during rest and exercise for both diets. Feeding DHAP for 7 days increased arm muscle glucose extraction before and during exercise, thereby enhancing submaximal arm endurance capacity.     

Improvements in exercise performance: effects of carbohydrate feedings and diet

In an effort to determine the effects of carbohydrate (CHO) feedings immediately before exercise in both the fasted and fed state, 10 well-trained male cyclists [maximum O2 consumption (VO2 max), 4.35 +/- 0.11 l/min)] performed 45 min of cycling at 77% VO2 max followed by a 15-min performance ride on an isokinetic cycle ergometer. After a 12-h fast, subjects ingested 45 g of liquid carbohydrate (LCHO), solid carbohydrate confectionery bar (SCHO), or placebo (P) 5 min before exercise. An additional trial was performed in which a high-CHO meal (200 g) taken 4 h before exercise was combined with a confectionery bar feeding (M + SCHO) immediately before the activity. At 10 min of exercise, serum glucose values were elevated by 18 and 24% during SCHO and LCHO, respectively, compared with P. At 0 and 45 min no significant differences were observed in muscle glycogen concentration or total use between the four trials. Total work produced during the final 15 min of exercise was significantly greater (P less than 0.05) during M + SCHO (194,735 +/- 9,448 N X m), compared with all other trials and significantly greater (P less than 0.05) during LCHO and SCHO (175,204 +/- 11,780 and 176,013 +/- 10,465 N X m, respectively) than trial P (159,143 +/- 11,407 N X m). These results suggest that, under conditions when CHO stores are less than optimal, exercise performance is enhanced with the ingestion of 45 g of CHO 5 min before 1 h of intense cycling.(ABSTRACT TRUNCATED AT 250 WORDS)     

Muscle glycogen storage postexercise: effect of mode of carbohydrate administration

The primary purpose of this study was to determine whether gastric emptying limits the rate of muscle glycogen storage during the initial 4 h after exercise when a carbohydrate supplement is provided. A secondary purpose was to determine whether liquid (L) and solid (S) carbohydrate (CHO) feedings result in different rates of muscle glycogen storage after exercise. Eight subjects cycled for 2 h on three separate occasions to deplete their muscle glycogen stores. After each exercise bout they received 3 g CHO/kg body wt in L (50% glucose polymer) or S (rice/banana cake) form or by intravenous infusion (I; 20% sterile glucose). The L and S supplements were divided into two equal doses and administered immediately after and 120 min after exercise, whereas the I supplement was administered continuously during the first 235 min of the 240-min recovery period. Blood samples were drawn from an antecubital vein before exercise, during exercise, and throughout recovery. Muscle biopsies were taken from the vastus lateralis immediately after and 120 and 240 min after exercise. Blood glucose and insulin declined during exercise and increased significantly above preexercise levels during recovery in all treatments. The increase in blood glucose during the I treatment, however, was three times greater than during the L or S treatments. The average insulin response of the L treatment (61.7 +/- 4.9 microU/ml) was significantly greater than that of the S treatment (47.5 +/- 4.2 microU/ml) but not that of the I (55.3 +/- 4.5 microU/ml) treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Epinephrine inhibits exogenous glucose utilization in exercising horses.

This study examined the effects of preexercise glucose administration, with and without epinephrine infusion, on carbohydrate metabolism in horses during exercise. Six horses completed 60 min of treadmill exercise at 55 +/- 1% maximum O(2) uptake 1) 1 h after oral administration of glucose (2 g/kg; G trial); 2) 1 h after oral glucose and with an intravenous infusion of epinephrine (0.2 micromol. kg(-1). min(-1); GE trial) during exercise, and 3) 1 h after water only (F trial). Glucose administration (G and GE) caused hyperinsulinemia and hyperglycemia ( approximately 8 mM). In GE, plasma epinephrine concentrations were three- to fourfold higher than in the other trials. Compared with F, the glucose rate of appearance was approximately 50% and approximately 33% higher in G and GE, respectively, during exercise. The glucose rate of disappearance was approximately 100% higher in G than in F, but epinephrine infusion completely inhibited the increase in glucose uptake associated with glucose administration. Muscle glycogen utilization was higher in GE [349 +/- 44 mmol/kg dry muscle (dm)] than in F (218 +/- 28 mmol/kg dm) and G (201 +/- 35 mmol/kg dm). We conclude that 1) preexercise glucose augments utilization of plasma glucose in horses during moderate-intensity exercise but does not alter muscle glycogen usage and 2) increased circulating epinephrine inhibits the increase in glucose rate of disappearance associated with preexercise glucose administration and increases reliance on muscle glycogen for energy transduction.     

Maximum O2 uptake, O2 debt and deficit, and muscle metabolites in Thoroughbred horses

This study determined maximal O2 uptake (VO2max), maximal O2 deficit, and O2 debt in the Thoroughbred racehorse exercising on an inclined treadmill. In eight horses the O2 uptake (VO2) vs. speed relationship was linear until 10 m/s and VO2max values ranged from 131 to 153 ml.kg-1.min-1. Six of these horses then exercised at 120% of their VO2max until exhaustion. VO2, CO2 production (VCO2), and plasma lactate (La) were measured before and during exercise and through 60 min of recovery. Muscle biopsies were collected before and at 0.25, 0.5, 1, 1.5, 2, 5, 10, 15, 20, 40, and 60 min after exercise. Muscle concentrations of adenosine 5'-triphosphate (ATP), phosphocreatine (PC), La, glucose 6-phosphate (G-6-P), and creatine were determined, and pH was measured. The O2 deficit was 128 +/- 32 (SD) ml/kg (64 +/- 13 liters). The O2 debt was 324 +/- 62 ml/kg (159 +/- 37 liters), approximately two to three times comparative values for human beings. Muscle [ATP] was unchanged, but [PC] was lower (P less than 0.01) than preexercise values at less than or equal to 10 min of recovery. [PC] and VO2 were negatively correlated during both the fast and slow phases of VO2 during recovery. Muscle [La] and [G-6-P] were elevated for 10 min postexercise. Mean muscle pH decreased from 7.05 (preexercise) to 6.75 at 1.5 min recovery, and the mean peak plasma La value was 34.5 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)     

Preexercise carbohydrate ingestion, glucose kinetics, and muscle glycogen use: effect of the glycemic index.

Eight trained men cycled at 70% peak oxygen uptake for 120 min followed by a 30-min performance cycle after ingesting either a high-glycemic index (HGI), low-glycemic index (LGI), or placebo (Con) meal 30 min before exercise. Ingestion of HGI resulted in an elevated (P<0.01) blood glucose concentration compared with LGI and Con. At the onset of exercise, blood glucose fell (P<0.05) such that it was lower (P<0.05) in HGI compared with LGI and Con at 15 and 30 min during exercise. Plasma insulin concentration was higher (P<0.01) throughout the rest period after ingestion of HGI compared with LGI and Con. Plasma free fatty acid concentrations were lower (P<0.05) throughout exercise in HGI compared with LGI and Con. The rates of [6,6-(2)H]glucose appearance and disappearance were higher (P<0.05) at rest after ingestion and throughout exercise in HGI compared with LGI and Con. Carbohydrate oxidation was higher (P<0.05) throughout exercise, whereas glycogen use tended (P = 0.07) to be higher in HGI compared with LGI and Con. No differences were observed in work output during the performance cycle when comparing the three trials. These results demonstrate that preexercise carbohydrate feeding with a HGI, but not a LGI, meal augments carbohydrate utilization during exercise but does not effect exercise performance.     

Prolactin Release during Exercise in Normal and Adrenodemedullated Untrained Rats Submitted to Central Cholinergic Blockade with Atropine

To study the role of the central cholinergic system in pituitary prolactin (PRL) release during exercise we injected atropine (5 x 10(-7) mol) into the lateral cerebral ventricle of intact or adrenodemedullated (ADM) untrained rats, at rest or submitted to exercise on a treadmill (18 m x min(-1), 5% grade) until exhaustion. The rats were implanted with chronic jugular catheters for blood sampling and with unilateral intracerebroventricular (icv) cannulas placed in the right lateral ventricle. Blood prolactin concentrations were measured before and every 10 min after the start of exercise for a period of 60 min. After the animals started running, plasma prolactin levels rose rapidly in both normal and ADM rats, reaching near maximum at 10 min. Close to exhaustion (19.8 +/- 2.9 min for intact rats and 23.5 +/- 4.1 min for ADM) they were still high, remained increased until 30 min, and returned to preexercise levels at 40 min. Icv injections of atropine decreased the time to exhaustion by 67% in intact rats and by 96.2% in ADM and also reduced the exercise-induced PRL release in both intact (50%) and ADM rats (90%). The results showed that prolactin release induced by exercise was dependent on the exercise workload and could be observed as early as after 10 min of running, remaining increased until 30 min. These data indicate that adrenodemedullation does not affect prolactin secretion induced by exercise, although adrenodemedullated rats proved to be more sensitive to the reducing effect of central cholinergic blockade on their maximal capacity for exercise.