Preexercise medium-chain triglyceride ingestion does not alter muscle glycogen use during exercise.

This investigation determined whether ingestion of a tolerable amount of medium-chain triglycerides (MCT; approximately 25 g) reduces the rate of muscle glycogen use during high-intensity exercise. On two occasions, seven well-trained men cycled for 30 min at 84% maximal O(2) uptake. Exactly 1 h before exercise, they ingested either 1) carbohydrate (CHO; 0.72 g sucrose/kg) or 2) MCT+CHO [0.36 g tricaprin (C10:0)/kg plus 0.72 g sucrose/kg]. The change in glycogen concentration was measured in biopsies taken from the vastus lateralis before and after exercise. Additionally, glycogen oxidation was calculated as the difference between total carbohydrate oxidation and the rate of glucose disappearance from plasma (R(d) glucose), as measured by stable isotope dilution techniques. The change in muscle glycogen concentration was not different during MCT+CHO and CHO (42.0 +/- 4.6 vs. 38.8 +/- 4.0 micromol glucosyl units/g wet wt). Furthermore, calculated glycogen oxidation was also similar (331 +/- 18 vs. 329 +/- 15 micromol. kg(-1). min(-1)). The coingestion of MCT+CHO did increase (P < 0.05) R(d) glucose at rest compared with CHO (26.9 +/- 1.5 vs. 20.7 +/- 0. 7 micromol.kg(-1). min(-1)), yet during exercise R(d) glucose was not different during the two trials. Therefore, the addition of a small amount of MCT to a preexercise CHO meal did not reduce muscle glycogen oxidation during high-intensity exercise, but it did increase glucose uptake at rest.     

Effect of training status on fuel selection during submaximal exercise with glucose ingestion.

In this study, an oral glucose load was enriched with a [U-(13)C]glucose tracer to determine differences in substrate utilization between endurance-trained (T) and untrained (UT) subjects during submaximal exercise at the same relative and absolute workload when glucose is ingested. Six highly trained cyclists/triathletes [maximal workload (Wmax), 400 +/- 9 W] and seven UT subjects (Wmax, 296 +/- 8 W) were studied during 120 min of cycling exercise at 50% Wmax ( approximately 55% maximal O(2) consumption). The T subjects performed a second trial at the mean workload of the UT group (148 +/- 4 W). Before exercise, 8.0 ml/kg of a (13)C-enriched glucose solution (80 g/l) was ingested. During exercise, boluses of 2.0 ml/kg of the same solution were administered every 15 min. Measurements were made in the 90- to 120-min period when a steady state was present in breath (13)CO(2) and plasma glucose (13)C enrichment. Energy expenditure was higher in T than in UT subjects (58 vs. 47 kJ/min, respectively; P < 0.001) at the same relative intensity. This was completely accounted for by an increased fat oxidation (0.57 vs. 0.40 g/min; P < 0.01). At the same absolute intensity, fat oxidation contributed more to energy expenditure in the T compared with the UT group (44 vs. 33%, respectively; P < 0.01). The reduction in carbohydrate oxidation in the T group was explained by a diminished oxidation rate of muscle glycogen (indirectly assessed by using tracer methodology at 0.72 +/- 0.1 and 1.03 +/- 0.1 g/min, respectively; P < 0.01) and liver-derived glucose (0.15 +/- 0.03 and 0.22 +/- 0.02 g/min, respectively; P < 0.05). Exogenous glucose oxidation rates were similar during all trials (+/-0.70 g/min).     

Training decreases muscle glycogen turnover during exercise

The present study was undertaken to determine the effects of endurance training on glycogen kinetics during exercise. A new model describing glycogen kinetics was applied to quantitate the rates of synthesis and degradation of glycogen. Trained and untrained rats were infused with a 25% glucose solution with 6-³H-glucose and U-¹⁴C-lactate at 1.5 and 0.5 μCi · min⁻¹ (where 1 Ci = 3.7 × 10¹⁰ Bq), respectively, during rest (30 min) and exercise (60 min). Blood samples were taken at 10-min intervals starting just prior to isotopic infusion, until the cessation of exercise. Tissues harvested after the cessation of exercise were muscle (soleus, deep, and superficial vastus lateralis, gastrocnemius), liver, and heart. Tissue glycogen was quantitated and analyzed for incorporation of ³H and ¹⁴C via liquid scintillation counting. There were no net decreases in muscle glycogen concentration from trained rats, whereas muscle glycogen concentration decreased to as much as 64% (P < 0.05) in soleus in muscles from untrained rats after exercise. Liver glycogen decreased in both trained (30%) and untrained (40%) rats. Glycogen specific activity increased in all tissues after exercise indicating isotope incorporation and, thus, glycogen synthesis during exercise. There were no differences in muscle glycogen synthesis rates between trained and untrained rats after exercise. However, training decreased muscle glycogen degradation rates in total muscle (i.e., the sum of the degradation rates of all of the muscles sampled) tenfold (P < 0.05). We have applied a model to describe glycogen kinetics in relation to glucose and lactate metabolism during exercise in trained and untrained rats. Training significantly decreases muscle glycogen degradation rates during exercise. Accepted: 22 May 1998     

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.     

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.     

Carbohydrate ingestion and muscle glycogen depletion during marathon and ultramarathon racing

Two studies were undertaken to characterize the effects of carbohydrate ingestion on fuel/hormone response to exercise and muscle glycogen utilization during prolonged competitive exercise. In study 1, eighteen subjects were divided into three groups, matched for maximum oxygen consumption (VO2max) and blood lactate turnpoint. All subjects underwent a 3-day carbohydrate (CHO) depletion phase, followed by 3 days of CHO loading (500-600 g.day-1). During the race, the groups drank either 2% glucose (G), 8% glucose polymer (GP), or 8% fructose (F). Muscle biopsies were performed before and after the race and venous blood was sampled before and at regular intervals during the race. In study 2, eighteen subjects divided into 2 matched groups ingested either a 4% G or 10% GP solution during a 56 km race. Despite significantly greater CHO ingestion by GP and F in study 1 and by GP in study 2, blood glucose, free fatty acids and insulin concentrations, muscle glycogen utilization and running performance were not different between groups. These studies show (i) that hypoglycaemia is uncommon in athletes competing in races of up to 56 km provided they CHO-load before and ingest a minimum of 10 g CHO.h-1 during competition; (ii) that neither the amount (10 g vs 40 g.h-1) nor the type of carbohydrate (G vs GP vs F) has any effect on the extent of muscle glycogen depletion or running performance in matched subjects racing over distances up to 56 km.     

Role of submaximal exercise in promoting creatine and glycogen accumulation in human skeletal muscle.

We examined the effect of glycogen-depleting exercise on subsequent muscle total creatine (TCr) accumulation and glycogen resynthesis during postexercise periods when the diet was supplemented with carbohydrate (CHO) or creatine (Cr) + CHO. Fourteen subjects performed one-legged cycling exercise to exhaustion. Muscle biopsies were taken from the exhausted (Ex) and nonexhausted (Nex) limbs after exercise and after 6 h and 5 days of recovery, during which CHO (CHO group, n = 7) or Cr + CHO (Cr+CHO group, n = 7) supplements were ingested. Muscle TCr concentration ([TCr]) was unchanged in both groups 6 h after supplementation commenced but had increased in the Ex (P < 0.001) and Nex limbs (P < 0.05) of the Cr+CHO group after 5 days. Greater TCr accumulation was achieved in the Ex limbs (P < 0.01) of this group. Glycogen was increased above nonexercised concentrations in the Ex limbs of both groups after 5 days, with the concentration being greater in the Cr+CHO group (P = 0.06). Thus a single bout of exercise enhanced muscle Cr accumulation, and this effect was restricted to the exercised muscle. However, exercise also diminished CHO-mediated insulin release, which may have attenuated insulin-mediated muscle Cr accumulation. Ingesting Cr with CHO also augmented glycogen supercompensation in the exercised muscle.     

Menstrual cycle phase and sex influence muscle glycogen utilization and glucose turnover during moderate-intensity endurance exercise

Numerous studies from our and other laboratories have shown that women have a lower respiratory exchange ratio (RER) during exercise than equally trained men, indicating a greater reliance on fat oxidation. Differences in estrogen concentration between men and women likely play a role in this sex difference. Differing estrogen and progesterone concentrations during the follicular (FP) and luteal (LP) phases of the female menstrual cycle suggest that fuel use may also vary between phases. The purpose of the current study was to determine the effect of menstrual cycle phase and sex upon glucose turnover and muscle glycogen utilization during endurance exercise. Healthy, recreationally active young women (n = 13) and men (n = 11) underwent a primed constant infusion of [6,6-2H]glucose with muscle biopsies taken before and after a 90-min cycling bout at 65% peak O2 consumption. LP women had lower glucose rate of appearance (Ra, P = 0.03), rate of disappearance (Rd, P = 0.03), and metabolic clearance rate (MCR, P = 0.04) at 90 min of exercise and lower proglycogen (P = 0.04), macroglycogen (P = 0.04), and total glycogen (P = 0.02) utilization during exercise compared with FP women. Men had a higher RER (P = 0.02), glucose Ra (P = 0.03), Rd (P = 0.03), and MCR (P = 0.01) during exercise compared with FP women, and men had a higher RER at 75 and 90 min of exercise (P = 0.04), glucose Ra (P = 0.01), Rd (P = 0.01), and MCR (P = 0.001) and a greater PG utilization (P = 0.05) compared with LP women. We conclude that sex, and to a lesser extent menstrual cycle, influence glucose turnover and glycogen utilization during moderate-intensity endurance exercise.     

Recruitment of single muscle fibers during submaximal cycling exercise.

In literature, an inconsistency exists in the submaximal exercise intensity at which type II fibers are activated. In the present study, the recruitment of type I and II fibers was investigated from the very beginning and throughout a 45-min cycle exercise at 75% of the maximal oxygen uptake, which corresponded to 38% of the maximal dynamic muscle force. Biopsies of the vastus lateralis muscle were taken from six subjects at rest and during the exercise, two at each time point. From the first biopsy single fibers were isolated and characterized as type I and II, and phosphocreatine-to-creatine (PCr/Cr) ratios and periodic acid-Schiff (PAS) stain intensities were measured. Cross sections were cut from the second biopsy, individual fibers were characterized as type I and II, and PAS stain intensities were measured. A decline in PCr/Cr ratio and in PAS stain intensity was used as indication of fiber recruitment. Within 1 min of exercise both type I and, although to a lesser extent, type II fibers were recruited. Furthermore, the PCr/Cr ratio revealed that the same proportion of fibers was recruited during the whole 45 min of exercise, indicating a rather constant recruitment. The PAS staining, however, proved inadequate to fully demonstrate fiber recruitment even after 45 min of exercise. We conclude that during cycling exercise a greater proportion of type II fibers is recruited than previously reported for isometric contractions, probably because of the dynamic character of the exercise. Furthermore, the PCr/Cr ratio method is more sensitive in determining fiber activation than the PAS stain intensity method.     

Effect of epinephrine on glucose disposal during exercise in humans: role of muscle glycogen

This study examined the effect of epinephrine on glucose disposal during moderate exercise when glycogenolytic flux was limited by low preexercise skeletal muscle glycogen availability. Six male subjects cycled for 40 min at 59 +/- 1% peak pulmonary O2 uptake on two occasions, either without (CON) or with (EPI) epinephrine infusion starting after 20 min of exercise. On the day before each experimental trial, subjects completed fatiguing exercise and then maintained a low carbohydrate diet to lower muscle glycogen. Muscle samples were obtained after 20 and 40 min of exercise, and glucose kinetics were measured using [6,6-2H]glucose. Exercise increased plasma epinephrine above resting concentrations in both trials, and plasma epinephrine was higher (P < 0.05) during the final 20 min in EPI compared with CON. Muscle glycogen levels were low after 20 min of exercise (CON, 117 +/- 25; EPI, 122 +/- 20 mmol/kg dry matter), and net muscle glycogen breakdown and muscle glucose 6-phosphate levels during the subsequent 20 min of exercise were unaffected by epinephrine infusion. Plasma glucose increased with epinephrine infusion (i.e., 20-40 min), and this was due to a decrease in glucose disposal (R(d)) (40 min: CON, 33.8 +/- 3; EPI, 20.9 +/- 4.9 micromol. kg(-1). min(-1), P < 0.05), because the exercise-induced rise in glucose rate of appearance was similar in the trials. These results show that glucose R(d) during exercise is reduced by elevated plasma epinephrine, even when muscle glycogen availability and utilization are low. This suggests that the effect of epinephrine does not appear to be mediated by increased glucose 6-phosphate, secondary to enhanced muscle glycogenolysis, but may be linked to a direct effect of epinephrine on sarcolemmal glucose transport.     

Effects of pre-exercise carbohydrate feedings on muscle glycogen use during exercise in well-trained runners

The purpose of this study was to examine the effects of pre-exercise glucose and fructose feedings on muscle glycogen utilization during exercise in six well-trained runners (VO2max = 68.2 +/- 3.4 ml X kg-1 X min-1). On three separate occasions, the runners performed a 30 min treadmill run at 70% VO2max. Thirty minutes prior to exercise each runner ingested 75 g of glucose (trial G), 75 g of fructose (trial F) or 150 ml of a sweetened placebo (trial C). During exercise, no differences were observed between any of the trials for oxygen uptake, heart rate or perceived exertion. Serum glucose levels were elevated as a result of the glucose feeding (P less than 0.05) reaching peak levels at 30 min post-feeding (7.90 +/- 0.24 mmol X l-1). With the onset of exercise, glucose levels dropped to a low of 5.89 +/- 0.85 mmol X l-1 at 15 min of exercise in trial G. Serum glucose levels in trials F and C averaged 6.21 +/- 0.31 mmol X l-1 and 5.95 +/- 0.23 mmol X l-1 respectively, and were not significantly different (P less than 0.05). There were also no differences in serum glucose levels between any of the trials at 15 and 30 min of exercise.     

Increased submaximal insulin-stimulated glucose uptake in mouse skeletal muscle after treadmill exercise.

The primary purpose of this study was to determine the effect of prior exercise on insulin-stimulated glucose uptake with physiological insulin in isolated muscles of mice. Male C57BL/6 mice completed a 60-min treadmill exercise protocol or were sedentary. Paired epitrochlearis, soleus, and extensor digitorum longus (EDL) muscles were incubated with [3H]-2-deoxyglucose without or with insulin (60 microU/ml) to measure glucose uptake. Insulin-stimulated glucose uptake for paired muscles was calculated by subtracting glucose uptake without insulin from glucose uptake with insulin. Muscles from other mice were assessed for glycogen and AMPK Thr172 phosphorylation. Exercised vs. sedentary mice had decreased glycogen in epitrochlearis (48%, P < 0.001), soleus (51%, P < 0.001), and EDL (41%, P < 0.01) and increased AMPK Thr172 phosphorylation (P < 0.05) in epitrochlearis (1.7-fold), soleus (2.0-fold), and EDL (1.4-fold). Insulin-independent glucose uptake was increased 30 min postexercise vs. sedentary in the epitrochlearis (1.2-fold, P < 0.001), soleus (1.4-fold, P < 0.05), and EDL (1.3-fold, P < 0.01). Insulin-stimulated glucose uptake was increased (P < 0.05) approximately 85 min after exercise in the epitrochlearis (sedentary: 0.266 +/- 0.045 micromol x g(-1) x 15 min(-1); exercised: 0.414 +/- 0.051) and soleus (sedentary: 0.102 +/- 0.049; exercised: 0.347 +/- 0.098) but not in the EDL. Akt Ser473 and Akt Thr308 phosphorylation for insulin-stimulated muscles did not differ in exercised vs. sedentary. These results demonstrate enhanced submaximal insulin-stimulated glucose uptake in the epitrochlearis and soleus of mice 85 min postexercise and suggest that it will be feasible to probe the mechanism of enhanced postexercise insulin sensitivity by using genetically modified mice.