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)     

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.     

Effect of fat adaptation and carbohydrate restoration on metabolism and performance during prolonged cycling.

For 5 days, eight well-trained cyclists consumed a random order of a high-carbohydrate (CHO) diet (9.6 g. kg(-1). day(-1) CHO, 0.7 g. kg(-1). day(-1) fat; HCHO) or an isoenergetic high-fat diet (2.4 g. kg(-1). day(-1) CHO, 4 g. kg(-1). day(-1) fat; Fat-adapt) while undertaking supervised training. On day 6, subjects ingested high CHO and rested before performance testing on day 7 [2 h cycling at 70% maximal O(2) consumption (SS) + 7 kJ/kg time trial (TT)]. With Fat-adapt, 5 days of high-fat diet reduced respiratory exchange ratio (RER) during cycling at 70% maximal O(2) consumption; this was partially restored by 1 day of high CHO [0.90 +/- 0.01 vs. 0.82 +/- 0.01 (P < 0.05) vs. 0.87 +/- 0.01 (P < 0.05), for day 1, day 6, and day 7, respectively]. Corresponding RER values on HCHO trial were [0. 91 +/- 0.01 vs. 0.88 +/- 0.01 (P < 0.05) vs. 0.93 +/- 0.01 (P < 0.05)]. During SS, estimated fat oxidation increased [94 +/- 6 vs. 61 +/- 5 g (P < 0.05)], whereas CHO oxidation decreased [271 +/- 16 vs. 342 +/- 14 g (P < 0.05)] for Fat-adapt compared with HCHO. Tracer-derived estimates of plasma glucose uptake revealed no differences between treatments, suggesting muscle glycogen sparing accounted for reduced CHO oxidation. Direct assessment of muscle glycogen utilization showed a similar order of sparing (260 +/- 26 vs. 360 +/- 43 mmol/kg dry wt; P = 0.06). TT performance was 30.73 +/- 1.12 vs. 34.17 +/- 2.48 min for Fat-adapt and HCHO (P = 0.21). These data show significant metabolic adaptations with a brief period of high-fat intake, which persist even after restoration of CHO availability. However, there was no evidence of a clear benefit of fat adaptation to cycling performance.     

Coingestion of carbohydrate with protein does not further augment postexercise muscle protein synthesis

The present study was designed to assess the impact of coingestion of various amounts of carbohydrate combined with an ample amount of protein intake on postexercise muscle protein synthesis rates. Ten healthy, fit men (20 +/- 0.3 yr) were randomly assigned to three crossover experiments. After 60 min of resistance exercise, subjects consumed 0.3 g x kg(-1) x h(-1) protein hydrolysate with 0, 0.15, or 0.6 g x kg(-1) x h(-1) carbohydrate during a 6-h recovery period (PRO, PRO + LCHO, and PRO + HCHO, respectively). Primed, continuous infusions with L-[ring-(13)C(6)]phenylalanine, L-[ring-(2)H(2)]tyrosine, and [6,6-(2)H(2)]glucose were applied, and blood and muscle samples were collected to assess whole body protein turnover and glucose kinetics as well as protein fractional synthesis rate (FSR) in the vastus lateralis muscle over 6 h of postexercise recovery. Plasma insulin responses were significantly greater in PRO + HCHO compared with PRO + LCHO and PRO (18.4 +/- 2.9 vs. 3.7 +/- 0.5 and 1.5 +/- 0.2 U.6 h(-1) x l(-1), respectively, P < 0.001). Plasma glucose rate of appearance (R(a)) and disappearance (R(d)) increased over time in PRO + HCHO and PRO + LCHO, but not in PRO. Plasma glucose R(a) and R(d) were substantially greater in PRO + HCHO vs. both PRO and PRO + LCHO (P < 0.01). Whole body protein breakdown, synthesis, and oxidation rates, as well as whole body protein balance, did not differ between experiments. Mixed muscle protein FSR did not differ between treatments and averaged 0.10 +/- 0.01, 0.10 +/- 0.01, and 0.11 +/- 0.01%/h in the PRO, PRO + LCHO, and PRO + HCHO experiments, respectively. In conclusion, coingestion of carbohydrate during recovery does not further stimulate postexercise muscle protein synthesis when ample protein is ingested.     

Decreased PDH activation and glycogenolysis during exercise following fat adaptation with carbohydrate restoration

Five days of a high-fat diet while training, followed by 1 day of carbohydrate (CHO) restoration, increases rates of whole body fat oxidation and decreases CHO oxidation during aerobic cycling. The mechanisms responsible for these shifts in fuel oxidation are unknown but involve up- and downregulation of key regulatory enzymes in the pathways of skeletal muscle fat and CHO metabolism, respectively. This study measured muscle PDH and HSL activities before and after 20 min of cycling at 70% VO2peak and 1 min of sprinting at 150% peak power output (PPO). Estimations of muscle glycogenolysis were made during the initial minute of exercise at 70% VO2peak and during the 1-min sprint. Seven male cyclists undertook this exercise protocol on two occasions. For 5 days, subjects consumed in random order either a high-CHO (HCHO) diet (10.3 g x kg(-1) x day(-1) CHO, or approximately 70% of total energy intake) or an isoenergetic high-fat (FAT-adapt) diet (4.6 g x kg(-1) x day(-1) FAT, or 67% of total energy) while undertaking supervised aerobic endurance training. On day 6 for both treatments, subjects ingested an HCHO diet and rested before their experimental trials on day 7. This CHO restoration resulted in similar resting glycogen contents (FAT-adapt 873 +/- 121 vs. HCHO 868 +/- 120 micromol glucosyl units/g dry wt). However, the respiratory exchange ratio was lower during cycling at 70% VO2peak in the FAT-adapt trial, which resulted in an approximately 45% increase and an approximately 30% decrease in fat and CHO oxidation, respectively. PDH activity was lower at rest and throughout exercise at 70% VO2peak (1.69 +/- 0.25 vs. 2.39 +/- 0.19 mmol x kg wet wt(-1) x min(-1)) and the 1-min sprint in the FAT-adapt vs. the HCHO trial. Estimates of glycogenolysis during the 1st min of exercise at 70% VO2peak and the 1-min sprint were also lower after FAT-adapt (9.1 +/- 1.1 vs. 13.4 +/- 2.1 and 37.3 +/- 5.1 vs. 50.5 +/- 2.7 glucosyl units x kg dry wt(-1) x min(-1)). HSL activity was approximately 20% higher (P = 0.12) during exercise at 70% VO2peak after FAT-adapt. Results indicate that previously reported decreases in whole body CHO oxidation and increases in fat oxidation after the FAT-adapt protocol are a function of metabolic changes within skeletal muscle. The metabolic signals responsible for the shift in muscle substrate use during cycling at 70% VO2peak remain unclear, but lower accumulation of free ADP and AMP after the FAT-adapt trial may be responsible for the decreased glycogenolysis and PDH activation during sprinting.     

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)     

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.     

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)     

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.     

Effects of depletion exercise and light training on muscle glycogen supercompensation in men

Supercompensated muscle glycogen can be achieved by using several carbohydrate (CHO)-loading protocols. This study compared the effectiveness of two "modified" CHO-loading protocols. Additionally, we determined the effect of light cycle training on muscle glycogen. Subjects completed a depletion (D, n = 15) or nondepletion (ND, n = 10) CHO-loading protocol. After a 2-day adaptation period in a metabolic ward, the D group performed a 120-min cycle exercise at 65% peak oxygen uptake (VO2 peak) followed by 1-min sprints at 120% VO2 peak to exhaustion. The ND group performed only 20-min cycle exercise at 65% VO2 peak. For the next 6 days, both groups ate the same high-CHO diets and performed 20-min daily cycle exercise at 65% VO2 peak followed by a CHO beverage (105 g of CHO). Muscle glycogen concentrations of the vastus lateralis were measured daily with 13C magnetic resonance spectroscopy. On the morning of day 5, muscle glycogen concentrations had increased 1.45 (D) and 1.24 (ND) times baseline (P < 0.001) but did not differ significantly between groups. However, on day 7, muscle glycogen of the D group was significantly greater (p < 0.01) than that of the ND group (130 +/- 7 vs. 104 +/- 5 mmol/l). Daily cycle exercise decreased muscle glycogen by 10 +/- 2 (D) and 14 +/- 5 mmol/l (ND), but muscle glycogen was equal to or greater than preexercise values 24 h later. In conclusion, a CHO-loading protocol that begins with a glycogen-depleting exercise results in significantly greater muscle glycogen that persists longer than a CHO-loading protocol using only an exercise taper. Daily exercise at 65% VO2 peak for 20 min can be performed throughout the CHO-loading protocol without negatively affecting muscle glycogen supercompensation.     

Ingestion of a high-glycemic index meal increases muscle glycogen storage at rest but augments its utilization during subsequent exercise.

The aim of this study was to compare the effect of preexercise breakfast containing high- and low-glycemic index (GI) carbohydrate (CHO) (2.5g CHO/kg body mass) on muscle glycogen metabolism. On two occasions, 14 days apart, seven trained men ran at 71% maximal oxygen uptake for 30 min on a treadmill. Three hours before exercise, in a randomized order, subjects consumed either isoenergetic high- (HGI) or low-GI (LGI) CHO breakfasts that provided (per 70 kg body mass) 3.43 MJ energy, 175 g CHO, 21 g protein, and 4 g fat. The incremental areas under the 3-h plasma glucose and serum insulin response curves after the HGI meal were 3.9- (P < 0.05) and 1.4-fold greater (P < 0.001), respectively, than those after the LGI meal. During the 3-h postprandial period, muscle glycogen concentration increased by 15% (P < 0.05) after the HGI meal but remained unchanged after the LGI meal. Muscle glycogen utilization during exercise was greater in the HGI (129.1 +/- 16.1 mmol/kg dry mass) compared with the LGI (87.9 +/- 15.1 mmol/kg dry mass; P < 0.01) trial. Although the LGI meal contributed less CHO to muscle glycogen synthesis in the 3-h postprandial period compared with the HGI meal, a sparing of muscle glycogen utilization during subsequent exercise was observed in the LGI trial, most likely as a result of better maintained fat oxidation.     

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.     

Effects of postexercise carbohydrate-protein feedings on muscle glycogen restoration.

The purpose of this investigation was to determine the effects of postexercise eucaloric carbohydrate-protein feedings on muscle glycogen restoration after an exhaustive cycle ergometer exercise bout. Seven male collegiate cyclists [age = 25.6 +/- 1.3 yr, height = 180.9 +/- 3.2 cm, wt = 75.4 +/- 4.0 kg, peak oxygen uptake (VO(2 peak)) = 4.20 +/- 0.2 l/min] performed three trials, each separated by 1 wk: 1) 100% alpha-D-glucose [carbohydrate (CHO)], 2) 70% carbohydrate-20% protein (PRO)-10% fat, and 3) 86% carbohydrate-14% amino acid (AA). All feedings were eucaloric, based on 1.0 g. kg body wt(-1). h(-1) of CHO, and administered every 30 min during a 4-h muscle glycogen restoration period in an 18% wt/vol solution. Muscle biopsies were obtained immediately and 4 h after exercise. Blood samples were drawn immediately after the exercise bout and every 0.5 h for 4 h during the restoration period. Increases in muscle glycogen concentrations for the three feedings (CHO, CHO-PRO, CHO-AA) were 118 mmol/kg dry wt; however, no differences among the feedings were apparent. The serum glucose and insulin responses did not differ throughout the restoration period among the three feedings. These results suggest that muscle glycogen restoration does not appear to be enhanced with the addition of proteins or amino acids to an eucaloric CHO feeding after exhaustive cycle exercise.     

Impaired muscle glycogen resynthesis after eccentric exercise

Eight men performed 10 sets of 10 eccentric contractions of the knee extensor muscles with one leg [eccentrically exercised leg (EL)]. The weight used for this exercise was 120% of the maximal extension strength. After 30 min of rest the subjects performed two-legged cycling [concentrically exercised leg (CL)] at 74% of maximal O2 uptake for 1 h. In the 3 days after this exercise four subjects consumed diets containing 4.25 g CHO/kg body wt, and the remainder were fed 8.5 g CHO/kg. All subjects experienced severe muscle soreness and edema in the quadriceps muscles of the eccentrically exercised leg. Mean (+/- SE) resting serum creatine kinase increased from a preexercise level of 57 +/- 3 to 6,988 +/- 1,913 U/l on the 3rd day of recovery. The glycogen content (mmol/kg dry wt) in the vastus lateralis of CL muscles averaged 90, 395, and 592 mmol/kg dry wt at 0, 24, and 72 h of recovery. The EL muscle, on the other hand, averaged 168, 329, and 435 mmol/kg dry wt at these same intervals. Subjects receiving 8.5 g CHO/kg stored significantly more glycogen than those who were fed 4.3 g CHO/kg. In both groups, however, significantly less glycogen was stored in the EL than in the CL.     

Influence of muscle glycogen availability on ERK1/2 and Akt signaling after resistance exercise in human skeletal muscle.

Two pathways that have been implicated for cellular growth and development in response to muscle contraction are the extracellular signal-regulated kinase (ERK1/2) and Akt signaling pathways. Although these pathways are readily stimulated after exercise, little is known about how nutritional status may affect stimulation of these pathways in response to resistance exercise in human skeletal muscle. To investigate this, experienced cyclists performed 30 repetitions of knee extension exercise at 70% of one repetition maximum after a low (2%) or high (77%) carbohydrate (LCHO or HCHO) diet, which resulted in low or high (approximately 174 or approximately 591 mmol/kg dry wt) preexercise muscle glycogen content. Muscle biopsies were taken from the vastus lateralis before, approximately 20 s after, and 10 min after exercise. ERK1/2 and p90 ribosomal S6 kinase phosphorylation increased (P < or = 0.05) 10 min after exercise, regardless of muscle glycogen availability. Akt phosphorylation was elevated (P < 0.05) 10 min after exercise in the HCHO trial but was unaffected after exercise in the LCHO trial. Mammalian target of rapamycin phosphorylation was similar to that of Akt during each trial; however, change or lack of change was not significant. In conclusion, the ERK1/2 pathway appears to be unaffected by muscle glycogen content. However, muscle glycogen availability appears to contribute to regulation of the Akt pathway, which may influence cellular growth and adaptation in response to resistance exercise in a low-glycogen state.     

Fiber type-specific muscle glycogen sparing due to carbohydrate intake before and during exercise.

The effect of carbohydrate intake before and during exercise on muscle glycogen content was investigated. According to a randomized crossover study design, eight young healthy volunteers (n = 8) participated in two experimental sessions with an interval of 3 wk. In each session subjects performed 2 h of constant-load bicycle exercise ( approximately 75% maximal oxygen uptake). On one occasion (CHO), they received carbohydrates before ( approximately 150 g) and during (1 g.kg body weight(-1).h(-1)) exercise. On the other occasion they exercised after an overnight fast (F). Fiber type-specific relative glycogen content was determined by periodic acid Schiff staining combined with immunofluorescence in needle biopsies from the vastus lateralis muscle before and immediately after exercise. Preexercise glycogen content was higher in type IIa fibers [9.1 +/- 1 x 10(-2) optical density (OD)/microm(2)] than in type I fibers (8.0 +/- 1 x 10(-2) OD/microm(2); P < 0.0001). Type IIa fiber glycogen content decreased during F from 9.6 +/- 1 x 10(-2) OD/microm(2) to 4.5 +/- 1 x 10(-2) OD/microm(2) (P = 0.001), but it did not significantly change during CHO (P = 0.29). Conversely, in type I fibers during CHO and F the exercise bout decreased glycogen content to the same degree. We conclude that the combination of carbohydrate intake both before and during moderate- to high-intensity endurance exercise results in glycogen sparing in type IIa muscle fibers.     

High rates of muscle glycogen resynthesis after exhaustive exercise when carbohydrate is coingested with caffeine.

We determined the effect of coingestion of caffeine (Caff) with carbohydrate (CHO) on rates of muscle glycogen resynthesis during recovery from exhaustive exercise in seven trained subjects who completed two experimental trials in a randomized, double-blind crossover design. The evening before an experiment subjects performed intermittent exhaustive cycling and then consumed a low-CHO meal. The next morning subjects rode until volitional fatigue. On completion of this ride subjects consumed either CHO [4 g/kg body mass (BM)] or the same amount of CHO + Caff (8 mg/kg BM) during 4 h of passive recovery. Muscle biopsies and blood samples were taken at regular intervals throughout recovery. Muscle glycogen levels were similar at exhaustion [ approximately 75 mmol/kg dry wt (dw)] and increased by a similar amount ( approximately 80%) after 1 h of recovery (133 +/- 37.8 vs. 149 +/- 48 mmol/kg dw for CHO and Caff, respectively). After 4 h of recovery Caff resulted in higher glycogen accumulation (313 +/- 69 vs. 234 +/- 50 mmol/kg dw, P < 0.001). Accordingly, the overall rate of resynthesis for the 4-h recovery period was 66% higher in Caff compared with CHO (57.7 +/- 18.5 vs. 38.0 +/- 7.7 mmol x kg dw(-1) x h(-1), P < 0.05). After 1 h of recovery plasma Caff levels had increased to 31 +/- 11 microM (P < 0.001) and at the end of the recovery reached 77 +/- 11 microM (P < 0.001) with Caff. Phosphorylation of CaMK(Thr286) was similar after exercise and after 1 h of recovery, but after 4 h CaMK(Thr286) phosphorylation was higher in Caff than CHO (P < 0.05). Phosphorylation of AMP-activated protein kinase (AMPK)(Thr172) and Akt(Ser473) was similar for both treatments at all time points. We provide the first evidence that in trained subjects coingestion of large amounts of Caff (8 mg/kg BM) with CHO has an additive effect on rates of postexercise muscle glycogen accumulation compared with consumption of CHO alone.     

Direct assessment of muscle glycogen storage after mixed meals in normal and type 2 diabetic subjects

To understand the day-to-day pathophysiology of impaired muscle glycogen storage in type 2 diabetes, glycogen concentrations were measured before and after the consumption of sequential mixed meals (breakfast: 190.5 g carbohydrate, 41.0 g fat, 28.8 g protein, 1253 kcal; lunch: 203.3 g carbohydrate, 48.1 g fat, 44.0 g protein, 1497.5 kcal) by use of natural abundance (13)C magnetic resonance spectroscopy. Subjects with diet-controlled type 2 diabetes (n = 9) and age- and body mass index-matched nondiabetic controls (n = 9) were studied. Mean fasting gastrocnemius glycogen concentration was significantly lower in the diabetic group (57.1 +/- 3.6 vs. 68.9 +/- 4.1 mmol/l; P < 0.05). After the first meal, mean glycogen concentration in the control group rose significantly from basal (97.1 +/- 7.0 mmol/l at 240 min; P = 0.005). After the second meal, the high level of muscle glycogen concentration in the control group was maintained, with a further rise to 108.0 +/- 11.6 mmol/l by 480 min. In the diabetic group, the postprandial rise was markedly lower than that of the control group (65.9 +/- 5.2 mmol/l at 240 min, P < 0.005, and 70.8 +/- 6.7 mmol/l at 480 min, P = 0.01) despite considerably greater serum insulin levels (752.0 +/- 109.0 vs. 372.3 +/- 78.2 pmol/l at 300 min, P = 0.013). This was associated with a significantly greater postprandial hyperglycemia (10.8 +/- 1.3 vs. 5.3 +/- 0.2 mmol/l at 240 min, P < 0.005). Basal muscle glycogen concentration correlated inversely with fasting blood glucose (r = -0.55, P < 0.02) and fasting serum insulin (r = -0.57, P < 0.02). The increment in muscle glycogen correlated with initial increment in serum insulin only in the control group (r = 0.87, P < 0.002). This study quantitates for the first time the subnormal basal muscle glycogen concentration and the inadequate glycogen storage after meals in type 2 diabetes.     

Adding fat calories to meals after exercise does not alter glucose tolerance.

A single session of exercise increases insulin sensitivity for hours and even days, and dietary carbohydrate ingested after exercise alters the magnitude and duration of this effect. Although increasing systemic fatty acid availability is associated with insulin resistance, it is uncertain whether increasing dietary fat availability after exercise alters the exercise-induced increase in insulin sensitivity. The purpose of this study was to determine whether adding fat calories to meals after exercise alters glucose tolerance the next day. Seven healthy men cycled 90 min at 66 +/- 2% peak oxygen uptake followed by a maximum of five high-intensity intervals. During the hours after exercise, subjects ingested three meals containing either low-fat (5% energy from fat) or high-fat (45% energy from fat) foods (Low-Fat and High-Fat groups, respectively). Each diet contained the same amount of carbohydrate and protein. An oral glucose tolerance test was performed the next morning. Muscle glycogen and intramuscular triglyceride (IMTG) concentrations were measured in muscle biopsy samples obtained immediately before exercise and the next morning. The day after exercise, muscle glycogen concentration was identical in High-Fat and Low-Fat (393 +/- 70 and 379 +/- 38 mmol/kg dry wt). At the same time, IMTG concentration was approximately 20% greater during High-Fat compared with Low-Fat (42.5 +/- 3.4 and 36.3 +/- 3.3 mmol/kg dry wt; P < 0.05). Despite the addition of approximately 165 g of fat to meals after exercise ( approximately 1,500 kcal) and a resultant elevation in IMTG concentration, glucose tolerance was identical in High-Fat and Low-Fat (composite index: 8.7 +/- 1.0 and 8.4 +/- 1.0). In summary, as long as meals ingested in the hours after exercise contain the same carbohydrate content, the addition of approximately 1500 kcal from fat to these meals did not alter muscle glycogen resynthesis or glucose tolerance the next day.     

Manipulation of dietary carbohydrates after prolonged effort modifies muscle sarcoplasmic reticulum responses in exercising males

The hypothesis tested was that disturbances in the sarcoplasmic reticulum (SR) Ca2+-cycling responses to exercise would associate with muscle glycogen reserves. Ten untrained males [peak O2 consumption (VO2 peak) = 3.41 +/- 0.20 (SE) l/min] performed a standardized cycle test (approximately 70% VO2 peak) on two occasions, namely, following 4 days of a high (Hi CHO)- and 4 days of a low (Lo CHO)-carbohydrate diet. Both Hi CHO and Lo CHO were preceded by a session of prolonged exercise designed to deplete muscle glycogen. SR Ca2+ cycling in crude homogenates prepared from vastus lateralis samples indicated higher (P < 0.05) Ca2+ uptake (microM x g protein(-1) x min(-1)) in Hi CHO compared with Lo CHO at 30 min (2.93 +/- 0.10 vs. 2.23 +/- 0.12) and at 67 min (2.77 +/- 0.16 vs. 2.10 +/- 0.12) of exercise, the point of fatigue in Lo CHO. Similar effects (P < 0.05) were noted between conditions for maximal Ca2+-ATPase (microM x g protein(-1) x min(-1)) at 30 min (142 +/- 8.5 vs. 107 +/- 5.0) and at 67 min (130 +/- 4.5 vs. 101 +/- 4.7). Both phase 1 and phase 2 Ca2+ release were 23 and 37% higher (P < 0.05) at 30 min of exercise and 15 and 34% higher (P < 0.05), at 67 min during Hi CHO compared with Lo CHO, respectively. No differences between conditions were observed at rest for any of these SR properties. Total muscle glycogen (mmol glucosyl units/kg dry wt) was higher (P < 0.05) in Hi CHO compared with Lo CHO at rest (+36%), 30 min (+53%), and at 67 min (+44%) of cycling. These results indicate that exercise-induced reductions in SR Ca2+-cycling properties occur earlier in exercise during low glycogen states compared with high glycogen states.