Effect of different carbohydrate drinks on whole body carbohydrate storage after exhaustive exercise.

Seven untrained male subjects participated in a double-blind, crossover study conducted to determine the efficacy of different carbohydrate drinks in promoting carbohydrate storage in the whole body and skeletal muscle during recovery from exhaustive exercise. The postabsorptive subjects first completed an exercise protocol designed to deplete muscle fibers of glycogen, then consumed 330 ml of one of three carbohydrate drinks (18.5% glucose polymer, 18.5% sucrose, or 12% sucrose; wt/vol) and also received a primed constant infusion of [1-(13)C]glucose for 2 h. Nonoxidative glucose disposal (3.51 +/- 0.28, 18.5% glucose polymer; 2.96 +/- 0.32, 18.5% sucrose; 2.97 +/- 0.16, 12% sucrose; all mmol. kg(-1). h(-1)) and storage of muscle glycogen (5.31 +/- 1.11, 18.5% glucose polymer; 4.07 +/- 1.05, 18.5% sucrose; 3.45 +/- 0.85, 12% sucrose; all mmol. kg wet wt(-1). h(-1); P < 0.05) were greater after consumption of the glucose polymer drink than after either sucrose drink. The results suggest that the consumption of a glucose polymer drink (containing 61 g carbohydrate) promotes a more rapid storage of carbohydrate in the whole body, skeletal muscle in particular, than an isoenergetic sucrose drink.     

Effects of recovery beverages on glycogen restoration and endurance exercise performance

The restorative capacities of a high carbohydrate-protein (CHO-PRO) beverage containing electrolytes and a traditional 6% carbohydrate-electrolyte sports beverage (SB) were assessed after glycogen-depleting exercise. Postexercise ingestion of the CHO-PRO beverage, in comparison with the SB, resulted in a 55% greater time to exhaustion during a subsequent exercise bout at 85% maximum oxygen consumption (VO(2)max). The greater recovery after the intake of the CHO-PRO beverage could be because of a greater rate of muscle glycogen storage. Therefore, a second study was designed to investigate the effects of after exercise CHO-PRO and SB supplements on muscle glycogen restoration. Eight endurance-trained cyclists (VO(2)max = 62.1 +/- 2.2 ml.kg(-1) body wt.min(-1)) performed 2 trials consisting of a 2-hour glycogen-depletion ride at 65-75% VO(2)max. Carbohydrate-protein (355 ml; approximately 0.8 g carbohydrate (CHO).kg(-1) body wt and approximately 0.2 g protein.kg(-1) body wt) or SB (355 ml; approximately 0.3 g CHO.kg(-1) body wt) was provided immediately and 2 hours after exercise. Trials were randomized and separated by 7-15 days. Ingestion of the CHO-PRO beverage resulted in a 17% greater plasma glucose response, a 92% greater insulin response, and a 128% greater storage of muscle glycogen (159 +/- 18 and 69 +/- 32 micromol.g(-1) dry weight for CHO-PRO and SB, respectively) compared with the SB (p < 0.05). These findings indicate that the rate of recovery is coupled with the rate of muscle glycogen replenishment and suggest that recovery supplements should be consumed to optimize muscle glycogen synthesis as well as fluid replacement.     

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)     

Muscle glycogen storage after different amounts of carbohydrate ingestion

The purpose of this study was to determine whether the rate of muscle glycogen storage could be enhanced during the initial 4-h period postexercise by substantially increasing the amount of the carbohydrate consumed. Eight subjects cycled for 2 h on three separate occasions to deplete their muscle glycogen stores. Immediately and 2 h after exercise they consumed either 0 (P), 1.5 (L), or 3.0 g glucose/kg body wt (H) from a 50% glucose polymer solution. Blood samples were drawn from an antecubital vein before exercise, during exercise, and throughout recovery. Muscle biopsies were taken from the vastus lateralis immediately, 2 h, and 4 h after exercise. Blood glucose and insulin declined significantly during exercise in each of the three treatments. They remained below the preexercise concentrations during recovery in the P treatment but increased significantly above the preexercise concentrations during the L and H treatments. By the end of the 4 h-recovery period, blood glucose and insulin were still significantly above the preexercise concentrations in both treatments. Muscle glycogen storage was significantly increased above the basal rate (P, 0.5 mumol.g wet wt-1.h-1) after ingestion of either glucose polymer supplement. The rates of muscle glycogen storage, however, were not different between the L and H treatments during the first 2 h (L, 5.2 +/- 0.9 vs. H, 5.8 +/- 0.7 mumol.g wet wt-1.h-1) or the second 2 h of recovery (L, 4.0 +/- 0.9 vs. H, 4.5 +/- 0.6 mumol.g wet wt-1. h-1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Carbohydrate metabolism during intense exercise when hyperglycemic

The effects of hyperglycemia on muscle glycogen use and carbohydrate metabolism were evaluated in eight well-trained cyclists (average maximal O2 consumption 4.5 +/- 0.1 l/min) during 2 h of exercise at 73 +/- 2% of maximal O2 consumption. During the control trial (CT), plasma glucose concentration averaged 4.2 +/- 0.2 mM and plasma insulin remained between 6 and 9 microU/ml. During the hyperglycemic trial (HT), 20 g of glucose were infused intravenously after 8 min of exercise, after which a variable-rate infusion of 18% glucose was used to maintain plasma glucose at 10.8 +/- 0.4 mM throughout exercise. Plasma insulin remained low during the 1st h of HT, yet it increased significantly (to 16-24 microU/ml; P less than 0.05) during the 2nd h. The amount of muscle glycogen utilized in the vastus lateralis during exercise was similar during HT and CT (75 +/- 8 and 76 +/- 7 mmol/kg, respectively). As exercise duration increased, carbohydrate oxidation declined during CT but increased during HT. Consequently, after 2 h of exercise, carbohydrate oxidation was 40% higher during HT than during CT (P less than 0.01). The rate of glucose infusion required to maintain hyperglycemia (10 mM) remained very stable at 1.6 +/- 0.1 g/min during the 1st h. However, during the 2nd h of exercise, the rate of glucose infusion increased (P less than 0.01) to 2.6 +/- 0.1 g/min (37 mg.kg body wt-1.min-1) during the final 20 min of exercise. We conclude that hyperglycemia (i.e., 10 mM) in humans does not alter muscle glycogen use during 2 h of intense cycling.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of carbohydrate ingestion on exercise metabolism

Five male cyclists were studied during 2 h of cycle ergometer exercise (70% VO2 max) on two occasions to examine the effect of carbohydrate ingestion on muscle glycogen utilization. In the experimental trial (CHO) subjects ingested 250 ml of a glucose polymer solution containing 30 g of carbohydrate at 0, 30, 60, and 90 min of exercise; in the control trial (CON) they received an equal volume of a sweet placebo. No differences between trials were seen in O2 uptake or heart rate during exercise. Venous blood glucose was similar before exercise in both trials, but, on average, was higher during exercise in CHO [5.2 +/- 0.2 (SE) mmol/l] compared with CON (4.8 +/- 0.1, P less than 0.05). Plasma insulin levels were similar in both trials. Muscle glycogen levels were also similar in CHO and CON both before and after exercise; accordingly, there was no difference between trials in the amount of glycogen used during the 2 h of exercise (CHO = 62.8 +/- 10.1 mmol/kg wet wt, CON = 56.9 +/- 10.1). The results of this study indicate that carbohydrate ingestion does not influence the utilization of muscle glycogen during prolonged strenuous exercise.     

Muscle glycogen utilization during prolonged strenuous exercise when fed carbohydrate

The purpose of this study was to determine whether the postponement of fatigue in subjects fed carbohydrate during prolonged strenuous exercise is associated with a slowing of muscle glycogen depletion. Seven endurance-trained cyclists exercised at 71 +/- 1% of maximal O2 consumption (VO2max), to fatigue, while ingesting a flavored water solution (i.e., placebo) during one trial and while ingesting a glucose polymer solution (i.e., 2.0 g/kg at 20 min and 0.4 g/kg every 20 min thereafter) during another trial. Fatigue during the placebo trial occurred after 3.02 +/- 0.19 h of exercise and was preceded by a decline (P less than 0.01) in plasma glucose to 2.5 +/- 0.5 mM and by a decline in the respiratory exchange ratio (i.e., R; from 0.85 to 0.80; P less than 0.05). Glycogen within the vastus lateralis muscle declined at an average rate of 51.5 +/- 5.4 mmol glucosyl units (GU) X kg-1 X h-1 during the first 2 h of exercise and at a slower rate (P less than 0.01) of 23.0 +/- 14.3 mmol GU X kg-1 X h-1 during the third and final hour. When fed carbohydrate, which maintained plasma glucose concentration (4.2-5.2 mM), the subjects exercised for an additional hour before fatiguing (4.02 +/- 0.33 h; P less than 0.01) and maintained their initial R (i.e., 0.86) and rate of carbohydrate oxidation throughout exercise. The pattern of muscle glycogen utilization, however, was not different during the first 3 h of exercise with the placebo or the carbohydrate feedings. The additional hour of exercise performed when fed carbohydrate was accomplished with little reliance on muscle glycogen (i.e., 5 mmol GU X kg-1 X h-1; NS) and without compromising carbohydrate oxidation. We conclude that when they are fed carbohydrate, highly trained endurance athletes are capable of oxidizing carbohydrate at relatively high rates from sources other than muscle glycogen during the latter stages of prolonged strenuous exercise and that this postpones fatigue.     

Effect of carbohydrate supplements and water on exercise metabolism in the heat

Carbohydrate (CHO) supplements of different concentrations were compared with water to determine their effects on thermal regulation and plasma volume maintenance while subjects exercised for 2 h in the heat and to determine their impact on carbohydrate utilization. Trained cyclists (n = 12) rode at 48.8 +/- 0.8% maximal O2 consumption in an environmental chamber maintained at 33.0 +/- 0.1 degree C and 51.7 +/- 1.4% relative humidity on three separate occasions. During each exercise bout the subjects received 3 ml/kg body wt of H2O, a 2.0% glucose polymer (LC) solution, or an 8.5% glucose polymer (HC) solution every 15 min. Muscle biopsies from the vastus lateralis were obtained before and after the H2O and HC trials only. Rectal temperature and heart rate, but not O2 consumption, rose from the 10- to 120-min period of exercise. No differences among treatments were found for these variables. There were also no significant differences among treatments for percent changes in plasma volume and blood volume. Plasma glucose and insulin were unchanged during the H2O and LC trials but were significantly elevated during the HC trial. In addition, CHO oxidation was significantly greater during the HC trial than during the H2O trial from 60 to 120 min of exercise. However, the reduction in muscle glycogen during the HC trial (206.5 +/- 23.6 mumol/g protein) was significantly less (P less than 0.05) than during the H2O trial (342.3 +/- 41.9 mumol/g protein).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of carbohydrate ingestion on metabolism during running and cycling.

The effects of carbohydrate or water ingestion on metabolism were investigated in seven male subjects during two running and two cycling trials lasting 60 min at individual lactate threshold using indirect calorimetry, U-14C-labeled tracer-derived measures of the rates of oxidation of plasma glucose, and direct determination of mixed muscle glycogen content from the vastus lateralis before and after exercise. Subjects ingested 8 ml/kg body mass of either a 6.4% carbohydrate-electrolyte solution (CHO) or water 10 min before exercise and an additional 2 ml/kg body mass of the same fluid after 20 and 40 min of exercise. Plasma glucose oxidation was greater with CHO than with water during both running (65 +/- 20 vs. 42 +/- 16 g/h; P < 0.01) and cycling (57 +/- 16 vs. 35 +/- 12 g/h; P < 0.01). Accordingly, the contribution from plasma glucose oxidation to total carbohydrate oxidation was greater during both running (33 +/- 4 vs. 23 +/- 3%; P < 0.01) and cycling (36 +/- 5 vs. 22 +/- 3%; P < 0.01) with CHO ingestion. However, muscle glycogen utilization was not reduced by the ingestion of CHO compared with water during either running (112 +/- 32 vs. 141 +/- 34 mmol/kg dry mass) or cycling (227 +/- 36 vs. 216 +/- 39 mmol/kg dry mass). We conclude that, compared with water, 1) the ingestion of carbohydrate during running and cycling enhanced the contribution of plasma glucose oxidation to total carbohydrate oxidation but 2) did not attenuate mixed muscle glycogen utilization during 1 h of continuous submaximal exercise at individual lactate threshold.     

Heat stress increases muscle glycogen use but reduces the oxidation of ingested carbohydrates during exercise.

The aim of the present study was to test the hypothesis that the oxidation rate of ingested carbohydrate (CHO) is impaired during exercise in the heat compared with a cool environment. Nine trained cyclists (maximal oxygen consumption 65 +/- 1 ml x kg body wt(-1) x min(-1)) exercised on two different occasions for 90 min at 55% maximum power ouptput at an ambient temperature of either 16.4 +/- 0.2 degrees C (cool trial) or 35.4 +/- 0.1 degrees C (heat trial). Subjects received 8% glucose solutions that were enriched with [U-13C]glucose for measurements of exogenous glucose, plasma glucose, liver-derived glucose and muscle glycogen oxidation. Exogenous glucose oxidation during the final 30 min of exercise was significantly (P < 0.05) lower in the heat compared with the cool trial (0.76 +/- 0.06 vs. 0.84 +/- 0.05 g/min). Muscle glycogen oxidation during the final 30 min of exercise was increased by 25% in the heat (2.07 +/- 0.16 vs. 1.66 +/- 0.09 g/min; P < 0.05), and liver-derived glucose oxidation was not different. There was a trend toward a higher total CHO oxidation and a lower plasma glucose oxidation in the heat although this did not reach statistical significance (P = 0.087 and P = 0.082, respectively). These results demonstrate that the oxidation rate of ingested CHO is reduced and muscle glycogen utilization is increased during exercise in the heat compared with a cool environment.     

Effect of carbohydrate ingestion on glycogen resynthesis in human liver and skeletal muscle, measured by (13)C MRS

This study investigated the effect of carbohydrate (CHO) ingestion on postexercise glycogen resynthesis, measured simultaneously in liver and muscle (n = 6) by (13)C magnetic resonance spectroscopy, and subsequent exercise capacity (n = 10). Subjects cycled at 70% maximal oxygen uptake for 83 +/- 8 min on six separate occasions. At the end of exercise, subjects ingested 1 g/kg body mass (BM) glucose, sucrose, or placebo (control). Resynthesis of glycogen over a 4-h period after treatment ingestion was measured on the first three occasions, and subsequent exercise capacity was measured on occasions four through six. No glycogen was resynthesized during the control trial. Liver glycogen resynthesis was evident after glucose (13 +/- 8 g) and sucrose (25 +/- 5 g) ingestion, both of which were different from control (P < 0.01). No significant differences in muscle glycogen resynthesis were found among trials. A relationship between the CHO load (g) and change in liver glycogen content (g) was evident after 30, 90, 150, and 210 min of recovery (r = 0.59-0. 79, P < 0.05). Furthermore, a modest relationship existed between change in liver glycogen content (g) and subsequent exercise capacity (r = 0.53, P < 0.05). However, no significant difference in mean exercise time was found (control: 35 +/- 5, glucose: 40 +/- 5, and sucrose: 46 +/- 6 min). Therefore, 1 g/kg BM glucose or sucrose is sufficient to initiate postexercise liver glycogen resynthesis, which contributes to subsequent exercise capacity, but not muscle glycogen resynthesis.     

Hypohydration does not impair skeletal muscle glycogen resynthesis after exercise

The purpose of this investigation was to examine the effects of moderate hypohydration (HY) on skeletal muscle glycogen resynthesis after exhaustive exercise. On two occasions, eight males completed 2 h of intermittent cycle ergometer exercise (4 bouts of 17 min at 60% and 3 min at 80% of maximal O2 consumption/10 min rest) to reduce muscle glycogen concentrations (control values 711 +/- 41 mumol/g dry wt). During one trial, cycle exercise was followed by several hours of light upper body exercise in the heat without fluid replacement to induce HY (-5% body wt); in the second trial, sufficient water was ingested during the upper body exercise and heat exposure to maintain euhydration (EU). In both trials, 400 g of carbohydrate were ingested at the completion of exercise and followed by 15 h of rest while the desired hydration level was maintained. Muscle biopsy samples were obtained from the vastus lateralis immediately after intermittent cycle exercise (T1) and after 15 h of rest (T2). During the HY trial, the muscle water content was lower (P less than 0.05) at T1 and T2 (288 +/- 9 and 265 +/- 5 ml/100 g dry wt, respectively; NS) than during EU (313 +/- 8 and 301 +/- 4 ml/100 g dry wt, respectively; NS). Muscle glycogen concentration was not significantly different during EU and HY at T1 (200 +/- 35 vs. 251 +/- 50 mumol/g dry wt) or T2 (452 +/- 34 vs. 491 +/- 35 mumol/g dry wt). These data indicate that, despite reduced water content during the first 15 h after heavy exercise, skeletal muscle glycogen resynthesis is not impaired.     

Muscle glycogen synthesis after exercise: effect of time of carbohydrate ingestion

The time of ingestion of a carbohydrate supplement on muscle glycogen storage postexercise was examined. Twelve male cyclists exercised continuously for 70 min on a cycle ergometer at 68% VO2max, interrupted by six 2-min intervals at 88% VO2max, on two separate occasions. A 25% carbohydrate solution (2 g/kg body wt) was ingested immediately postexercise (P-EX) or 2 h postexercise (2P-EX). Muscle biopsies were taken from the vastus lateralis at 0, 2, and 4 h postexercise. Blood samples were obtained from an antecubital vein before and during exercise and at specific times after exercise. Muscle glycogen immediately postexercise was not significantly different for the P-EX and 2P-EX treatments. During the first 2 h postexercise, the rate of muscle glycogen storage was 7.7 mumol.g wet wt-1.h-1 for the P-EX treatment, but only 2.5 mumol.g wet wt-1.h-1 for the 2P-EX treatment. During the second 2 h of recovery, the rate of glycogen storage slowed to 4.3 mumol.g wet wt-1.h-1 during treatment P-EX but increased to 4.1 mumol.g wet wt-1.h-1 during treatment 2P-EX. This rate, however, was still 45% slower (P less than 0.05) than that for the P-EX treatment during the first 2 h of recovery. This slower rate of glycogen storage occurred despite significantly elevated plasma glucose and insulin levels. The results suggest that delaying the ingestion of a carbohydrate supplement post-exercise will result in a reduced rate of muscle glycogen storage.     

Effect of carbohydrate supplementation on postexercise GLUT-4 protein expression in skeletal muscle.

The effect of carbohydrate supplementation on skeletal muscle glucose transporter GLUT-4 protein expression was studied in fast-twitch red and white gastrocnemius muscle of Sprague-Dawley rats before and after glycogen depletion by swimming. Exercise significantly reduced fast-twitch red muscle glycogen by 50%. During a 16-h exercise recovery period, muscle glycogen returned to control levels (25.0 +/- 1.4 micromol/g) in exercise-fasted rats (24.2 +/- 0. 3 micro). However, when carbohydrate supplementation was provided during and immediately postexercise by intubation, muscle glycogen increased 77% above control (44.4 +/- 2.1 micromol/g). Exercise-fasting resulted in an 80% increase in fast-twitch red muscle GLUT-4 mRNA but only a 43% increase in GLUT-4 protein concentration. Conversely, exercise plus carbohydrate supplementation elevated fast-twitch red muscle GLUT-4 protein concentration by 88% above control, whereas GLUT-4 mRNA was increased by only 40%. Neither a 16-h fast nor carbohydrate supplementation had an effect on fast-twitch red muscle GLUT-4 protein concentration or on GLUT-4 mRNA in sedentary rats, although carbohydrate supplementation increased muscle glycogen concentration by 40% (35.0 +/- 0.9 micromol/g). GLUT-4 protein in fast-twitch white muscle followed a pattern similar to fast-twitch red muscle. These results indicate that carbohydrate supplementation, provided with exercise, will enhance GLUT-4 protein expression by increasing translational efficiency. Conversely, postexercise fasting appears to upregulate GLUT-4 mRNA, possibly to amplify GLUT-4 protein expression on an increase in glucose availability. These regulatory mechanisms may help control muscle glucose uptake in accordance with glucose availability and protect against postexercise hypoglycemia.     

Early postexercise muscle glycogen recovery is enhanced with a carbohydrate-protein supplement.

In the present study, we tested the hypothesis that a carbohydrate-protein (CHO-Pro) supplement would be more effective in the replenishment of muscle glycogen after exercise compared with a carbohydrate supplement of equal carbohydrate content (LCHO) or caloric equivalency (HCHO). After 2.5 +/- 0.1 h of intense cycling to deplete the muscle glycogen stores, subjects (n = 7) received, using a rank-ordered design, a CHO-Pro (80 g CHO, 28 g Pro, 6 g fat), LCHO (80 g CHO, 6 g fat), or HCHO (108 g CHO, 6 g fat) supplement immediately after exercise (10 min) and 2 h postexercise. Before exercise and during 4 h of recovery, muscle glycogen of the vastus lateralis was determined periodically by nuclear magnetic resonance spectroscopy. Exercise significantly reduced the muscle glycogen stores (final concentrations: 40.9 +/- 5.9 mmol/l CHO-Pro, 41.9 +/- 5.7 mmol/l HCHO, 40.7 +/- 5.0 mmol/l LCHO). After 240 min of recovery, muscle glycogen was significantly greater for the CHO-Pro treatment (88.8 +/- 4.4 mmol/l) when compared with the LCHO (70.0 +/- 4.0 mmol/l; P = 0.004) and HCHO (75.5 +/- 2.8 mmol/l; P = 0.013) treatments. Glycogen storage did not differ significantly between the LCHO and HCHO treatments. There were no significant differences in the plasma insulin responses among treatments, although plasma glucose was significantly lower during the CHO-Pro treatment. These results suggest that a CHO-Pro supplement is more effective for the rapid replenishment of muscle glycogen after exercise than a CHO supplement of equal CHO or caloric content.     

Postexercise muscle glycogen resynthesis in obese insulin-resistant Zucker rats.

We determined the effect of an acute bout of swimming (8 x 30 min) followed by either carbohydrate administration (0.5 mg/g glucose ip and ad libitum access to chow; CHO) or fasting (Fast) on postexercise glycogen resynthesis in soleus muscle and liver from female lean (ZL) and obese insulin-resistant (ZO) Zucker rats. Resting soleus muscle glycogen concentration ([glycogen]) was similar between genotypes and was reduced by 73 (ZL) and 63% (ZO) after exercise (P < 0.05). Liver [glycogen] at rest was greater in ZO than ZL (334 +/- 31 vs. 247 +/- 16 micromol/g wet wt; P < 0.01) and fell by 44 and 94% after exercise (P < 0.05). The fractional activity of glycogen synthase (active/total) increased immediately after exercise (from 0.22 +/- 0.05 and 0.32 +/- 0.04 to 0.63 +/- 0.08 vs. 0.57 +/- 0.05; P < 0.01 for ZL and ZO rats, respectively) and remained elevated above resting values after 30 min of recovery. During this time, muscle [glycogen] in ZO increased 68% with CHO (P < 0.05) but did not change in Fast. Muscle [glycogen] was unchanged in ZL from postexercise values after both treatments. After 6 h recovery, GLUT-4 protein concentration was increased above resting levels by a similar extent for both genotypes in both fasted (approximately 45%) and CHO-supplemented (approximately 115%) rats. Accordingly, during this time CHO refeeding resulted in supercompensation in both genotypes (68% vs. 44% for ZL and ZO). With CHO, liver [glycogen] was restored to resting levels in ZL but remained at postexercise values for ZO after both treatments. We conclude that the increased glucose availability with carbohydrate refeeding after glycogen-depleting exercise resulted in glycogen supercompensation, even in the face of muscle insulin-resistance.     

Muscle glycogen depletion and subsequent replenishment affect anaerobic capacity of horses.

The purpose of this study was to determine the effect of muscle glycogen depletion and subsequent replenishment on anaerobic capacity of horses. In a blinded crossover study, seven fit horses performed glycogen-depleting exercise on two occasions. Horses were infused after glycogen-depleting exercise with either 6 g/kg body wt of glucose as a 13.5% solution in 0.9% NaCl (Glu) or with 0.9% NaCl (Sal) of equivalent volume. Subsequently, horses performed a high-speed exercise test (120% of maximal rate of oxygen consumption) to estimate maximum accumulated oxygen deficit. Replenishment of muscle glycogen was greater (P < 0.05) in Glu [from 24.7 +/- 7.2 (SE) to 116.5 +/- 7 mmol/kg wet wt before and after infusion, respectively] than in Sal (from 23.4 +/- 7.2 to 47.8 +/- 5.7 mmol/kg wet wt before and after infusion, respectively). Run time to fatigue during the high-speed exercise test (97.3 +/- 8.2 and 70.8 +/- 8.3 s, P < 0.05), maximal accumulated oxygen deficit (105.7 +/- 9.3 and 82.4 +/- 10.3 ml O(2) equivalent/kg, P < 0.05), and blood lactate concentration at the end of the high-speed exercise test (11.1 +/- 1.4 and 9.2 +/- 3.7 mmol/l, P < 0.05) were greater for Glu than for Sal, respectively. We concluded that decreased availability of skeletal muscle glycogen stores diminishes anaerobic power generation and capacity for high-intensity exercise in horses.     

Muscle glycogen resynthesis during recovery from cycle exercise: no effect of additional protein ingestion.

In the present study, we have investigated the effect of carbohydrate and protein hydrolysate ingestion on muscle glycogen resynthesis during 4 h of recovery from intense cycle exercise. Five volunteers were studied during recovery while they ingested, immediately after exercise, a 600-ml bolus and then every 15 min a 150-ml bolus containing 1) 1.67 g. kg body wt(-1). l(-1) of sucrose and 0.5 g. kg body wt(-1). l(-1) of a whey protein hydrolysate (CHO/protein), 2) 1.67 g. kg body wt(-1). l(-1) of sucrose (CHO), and 3) water. CHO/protein and CHO ingestion caused an increased arterial glucose concentration compared with water ingestion during 4 h of recovery. With CHO ingestion, glucose concentration was 1-1.5 mmol/l higher during the first hour of recovery compared with CHO/protein ingestion. Leg glucose uptake was initially 0.7 mmol/min with water ingestion and decreased gradually with no measurable glucose uptake observed at 3 h of recovery. Leg glucose uptake was rather constant at 0.9 mmol/min with CHO/protein and CHO ingestion, and insulin levels were stable at 70, 45, and 5 mU/l for CHO/protein, CHO, and water ingestion, respectively. Glycogen resynthesis rates were 52 +/- 7, 48 +/- 5, and 18 +/- 6 for the first 1.5 h of recovery and decreased to 30 +/- 6, 36 +/- 3, and 8 +/- 6 mmol. kg dry muscle(-1). h(-1) between 1.5 and 4 h for CHO/protein, CHO, and water ingestion, respectively. No differences could be observed between CHO/protein and CHO ingestion ingestion. It is concluded that coingestion of carbohydrate and protein, compared with ingestion of carbohydrate alone, did not increase leg glucose uptake or glycogen resynthesis rate further when carbohydrate was ingested in sufficient amounts every 15 min to induce an optimal rate of glycogen resynthesis.     

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.     

Metabolic and performance responses to constant-load vs. variable-intensity exercise in trained cyclists.

We studied glucose oxidation (Glu(ox)) and glycogen degradation during 140 min of constant-load [steady-state (SS)] and variable-intensity (VI) cycling of the same average power output, immediately followed by a 20-km performance ride [time trial (TT)]. Six trained cyclists each performed four trials: two experimental bouts (SS and VI) in which muscle biopsies were taken before and after 140 min of exercise for determination of glycogen and periodic acid-Schiff's staining; and two similar trials without biopsies but incorporating the TT. During two of the experimental rides, subjects ingested a 5 g/100 ml [U-(14)C]glucose solution to determine rates of Glu(ox). Values were similar between SS and VI trials: O(2) consumption (3.08 +/- 0.02 vs. 3.15 +/- 0.03 l/min), energy expenditure (901 +/- 40 vs. 904 +/- 58 J x kg(-1) x min(-1)), heart rate (156 +/- 1 vs. 160 +/- 1 beats/min), and rating of perceived exertion (12.6 +/- 0.6 vs. 12.7 +/- 0.7). However, the area under the curve for plasma lactate concentration vs. time was significantly greater during VI than SS (29.1 +/- 3.9 vs. 24.6 +/- 3. 7 mM/140 min; P = 0.03). VI resulted in a 49% reduction in total muscle glycogen utilization vs. 65% for SS, while total Glu(ox) was higher (99.2 +/- 5.3 vs. 83.9 +/- 5.2 g/140 min; P < 0.05). The number of glycogen-depleted type I muscle fibers at the end of 140 min was 98% after SS but only 59% after VI. Conversely, the number of type II fibers that showed reduced periodic acid-Schiff's staining was 1% after SS vs. 10% after VI. Despite these metabolic differences, subsequent TT performance was similar (29.14 +/- 0.9 vs. 30.5 +/- 0.9 min for SS vs. VI). These results indicate that whole body metabolic and cardiovascular responses to 140 min of either SS or VI exercise at the same average intensity are similar, despite differences in skeletal muscle carbohydrate metabolism and recruitment.