Oxidation and metabolic effects of fructose or glucose ingested before exercise

The aim of this study was to compare the effects of fructose (F) and glucose (G) intake before exercise on oxidation of the ingested substrate, glycogen utilization, work output, and metabolic changes. Ten trained subjects ingested F or G (1 g/kg), both of which were naturally enriched in 13C. After 1 h of rest, they exercised on an ergometer at 61% of their maximal oxygen uptake (VO2 max) for 45 min, which was immediately followed by 15 min at their maximal voluntary output. During the resting hour, blood insulin and glucose were lower (p less than 0.05) and respiratory quotient and blood lactate higher (p less than 0.01) after F. During exercise, the differences disappeared, apart from a transient but moderate (4.3 mmol/l) hypoglycemia after G compared to F. No difference between F and G was observed for uric acid, glycerol, FFA, and glucagon. Glycogen decrements in the vastus lateralis muscle were 67 +/- 9 (F) and 97 +/- 15 (G) mmol/kg, values not significantly different from each other (P greater than 0.05). The maximal voluntary work produced during the last 15 min did not differ between treatments. During the 2 h after sugar ingestion, 30 +/- 3 g of F and 26 +/- 3 g of G were oxidized to 13CO2. These findings indicate that fructose ingested before exercise was utilized at least as well as glucose, allowed a more stable glycemia, and did not modify performance.     

Oxidation of carbohydrate ingested during prolonged endurance exercise.

Classic studies conducted in the 1920s and 1930s established that the consumption of a high carbohydrate (CHO) diet before exercise and the ingestion of glucose during exercise delayed the onset of fatigue, in part by preventing the development of hypoglycaemia. For the next 30 to 40 years, however, interest in CHO ingestion during exercise waned. Indeed, it was not until the reintroduction of the muscle biopsy technique into exercise physiology in the 1960s that a series of studies on CHO utilisation during exercise appeared. Investigations by Scandinavian physiologists showed that muscle glycogen depletion during prolonged exercise coincided with the development of fatigue. Despite this finding, attempts to delay fatigue during prolonged exercise focused principally on techniques that would increase muscle glycogen storage before exercise. The possibility that CHO ingestion during exercise might also delay the development of muscle glycogen depletion and hence, at least potentially, fatigue, was not extensively investigated. This, in part, can be explained by the popular belief that water replacement to prevent dehydration and hyperthermia was of greater importance than CHO replacement during prolonged exercise. This position was strengthened by studies in the early 1970s which showed that the ingestion of CHO solutions delayed gastric emptying compared with water, and might therefore exacerbate dehydration. As a result, athletes were actively discouraged from ingesting even mildly concentrated (greater than 5 g/100ml) CHO solutions during exercise. Only in the early 1980s, when commercial interest in the sale of CHO products to athletes was aroused, did exercise physiologists again begin to study the effects of CHO ingestion during exercise. These studies soon established that CHO ingestion during prolonged exercise could delay fatigue; this finding added urgency to the search for the optimum CHO type for ingestion during exercise. Whereas in the earlier studies, estimates of CHO oxidation were made using respiratory gas exchange measurements, investigations since the early 1970s have employed stable 13C and radioactive 14C isotope techniques to determine the amount of ingested CHO that is oxidised during exercise. Most of the early interest was in glucose ingestion during exercise. These studies showed that significant quantities of ingested glucose can be oxidised during exercise. Peak rates of glucose oxidation occur approximately 75 to 90 minutes after ingestion and are unaffected by the time of glucose ingestion during exercise. Rates of oxidation also appear not to be influenced to a major extent by the use of different feeding schedules.(ABSTRACT TRUNCATED AT 400 WORDS)     

The effects of glucose, fructose, and sucrose ingestion during exercise

The purpose of this study was to compare the physiological, sensory, and exercise performance responses to ingestion of 6% glucose, 6% fructose, and 6% sucrose solutions during cycling exercise. Twelve subjects completed three sessions consisting of 115 min of intermittent cycle ergometer exercise at 65-80% of VO2max followed by a timed performance bout requiring the completion of 600 pedal revolutions. During each of five 4-min rest periods, subjects consumed 3 ml.kg LBM-1 of one of the beverages. Beverages were presented in counterbalanced, double-blind fashion. Heart rate, VO2, plasma urate, plasma lactate, respiratory exchange ratio, and carbohydrate combustion rates changed similarly among beverage treatment. However, fructose was associated with lower plasma glucose and serum insulin, a larger loss of plasma volume, greater gastrointestinal distress and relative perceived exertion ratings, and higher plasma or serum concentrations of free fatty acids, fructose, and cortisol values than sucrose or glucose (P less than 0.05). Compared to sucrose and glucose, fructose feeding also resulted in lower lactate and HR values during the performance bout (P less than 0.05). Mean +/- SE cycling performance times were faster with sucrose and glucose than with fructose: 419.4 +/- 21.0 s, 423.9 +/- 21.2 s, and 488.3 +/- 21.1 s, respectively (P less than 0.05). Relative to 6% solutions of sucrose and glucose, ingestion of a 6% fructose beverage is associated with gastrointestinal distress, compromised physiological response, and reduced exercise capacity.     

Oxidation of combined ingestion of maltodextrins and fructose during exercise

PURPOSE: To determine whether combined ingestion of maltodextrin and fructose during 150 min of cycling exercise would lead to exogenous carbohydrate oxidation rates higher than 1.1 g.min. METHODS: Eight trained cyclists VO2max: 64.1 +/- 3.1 mL.kg.min) performed three exercise trials in a random order. Each trial consisted of 150 min cycling at 55% maximum power output (64.2+/-3.5% VO2max) while subjects received a solution providing either 1.8 g.min of maltodextrin (MD), 1.2 g.min of maltodextrin + 0.6 g.min of fructose (MD+F), or plain water. To quantify exogenous carbohydrate oxidation, corn-derived MD and F were used, which have a high natural abundance of C. RESULTS: Peak exogenous carbohydrate oxidation (last 30 min of exercise) rates were approximately 40% higher with combined MD+F ingestion compared with MD only ingestion (1.50+/-0.07 and 1.06+/-0.08 g.min, respectively, P<0.05). Furthermore, the average exogenous carbohydrate oxidation rate during the last 90 min of exercise was higher with combined MD+F ingestion compared with MD alone (1.38+/-0.06 and 0.96+/-0.07 g.min, respectively, P<0.05). CONCLUSIONS: The present study demonstrates that with ingestion of large amounts of maltodextrin and fructose during cycling exercise, exogenous carbohydrate oxidation can reach peak values of approximately 1.5 g.min, and this is markedly higher than oxidation rates from ingesting maltodextrin alone.     

Effects of caffeine, fructose, and glucose ingestion on muscle glycogen utilization during exercise

Five competitive cyclists were used to determine the effects of fluid intake (16 ml.kg-1) consisting of: (i) non-nutrient control (CON); (ii) fructose (1 g.kg-1) before exercise (FRU); (iii) caffeine (5 mg.kg-1) before exercise (CAF); (iv) glucose (1 g.kg-1) during exercise (GLU); and (v) fructose/caffeine before and glucose during exercise (CFG) on blood glucose, free fatty acids, muscle glycogen, and other parameters. Exercise consisted of 90 min of cycling at 65 to 70% VO2max. Following exercise, blood glucose was found to be significantly (P less than 0.05) higher for CFG and GLU (117 and 109 mg%) compared to CON, CAF, and FRU (92, 89, and 86 mg%). Blood free fatty acids rose (P less than 0.05) further for CON (1,336), CAF (1,126), and FRU (1,034) over CFG (737) and GLU (714 mumol.l-1). Muscle glycogen utilization was greater (P less than 0.05) for CON (91) vs CAF (63) and GLU (62 mumol/g-1 wet muscle weight). It was concluded that GLU and CAF decrease muscle glycogen utilization, FRU is likely to cause gastric upset, and ingestion of multiple substances produces the greatest variability in muscle glycogen utilization and may provide added endurance benefits in some individuals.     

Comparison of fructose and glucose ingestion before and during endurance cycling to exhaustion

BACKGROUND: Pre-exercise and exercise ingestion of fructose and glucose during cycling exercise were compared. METHODS: Experimental design: Seventeen trained subjects ingested a placebo prior to and during a cycling test to exhaustion at 75% VO2max (control group = CG). One week later, subjects were matched on exercise time to exhaustion (ETE) and assigned to a fructose group (FG) or a glucose group (GG). Subjects then performed a second cycling test to exhaustion, ingesting fructose or glucose doses. For all groups (CG, FG and GG), blood was drawn before and at timed intervals during exercise to determine glucose, lactate and free fatty acid (FFA) levels. RESULTS: The ETE for CG was less than either FG (p<0.02) or GG (p<0.001) but FG and GG were similar. FG and GG did not show any differences in blood lactate or blood FFA during the ETE. However, CG FFA levels were higher than those of FG (p<0.02) prior to exercise. CONCLUSIONS: This study demonstrated that fructose and glucose are of equal value in prolonging ETE in endurance cycling Ingesting fructose before and during exercise apparently provided a more constant supply of glucose to be available to the working muscles. The more stable blood glucose levels with fructose ingestion may be beneficial in reducing perceived exhaustion, and thereby allowing for an enhancement in exercise performance.     

Effects of oral curcumin ingested before or after eccentric exercise on markers of muscle damage and inflammation

We examined the effect of curcumin (CUR) ingestion before or after exercise on changes in muscle damage and inflammatory responses after exercise. We conducted two parallel experiments with different CUR ingestion timings using a double‐blind crossover. In Exp. 1, ten healthy men ingested 180 mg d^?1 of CUR or placebo (PLA) 7 days before exercise. In Exp. 2, ten other healthy men ingested 180 mg d^?1 of CUR or PLA 7 days after exercise. They performed 30 maximal isokinetic (120°s^?1) eccentric contractions of the elbow flexors using an isokinetic dynamometer, and this was repeated with the other arm ≥4 weeks later. Maximal voluntary contraction (MVC) torque of the elbow flexors, elbow joint range of motion (ROM), muscle soreness, and serum creatine kinase (CK) activity were measured before, immediately after, and 1‐7 days after exercise. Plasma interleukin‐8 (IL‐8) was measured before, immediately after, 12 hours after, and 1‐7 days after exercise. The changes were compared over time. In Exp. 1, no significant differences were found between CUR and PLA subjects for each parameter. However, increases in IL‐8 were significantly reduced 12 hours after exercise when CUR was ingested before exercise. In Exp. 2, compared to the PLA subjects, MVC torque and ROM were higher 3‐7 days and 2‐7 days after exercise (P < 0.05), respectively, whereas muscle soreness and CK activity were lower 3‐6 days and 5‐7 days after exercise (P < 0.05), respectively, in CUR subjects. CUR ingestion before exercise could attenuate acute inflammation, and after exercise could attenuate muscle damage and facilitate faster recovery.     

RPE, blood glucose, and carbohydrate oxidation during exercise: effects of glucose feedings

This study examined the effects of glucose ingestion on differentiated and undifferentiated ratings of perceived exertion (RPE) during prolonged cycling exercise. On two occasions, seven trained males cycled for 180 min on a Monark cycle ergometer at 70% peak VO2 (VO2peak). Subjects consumed an 8% glucose/electrolyte drink (G) or a flavored water placebo (P) every 15 min throughout exercise. Measurement of RPE, ventilation (VE), oxygen uptake (VO2), respiration rate (RR), respiratory exchange ratio (RER), heart rate (HR), and venous blood sample collection preceded ingestion of the drink. Subjects were homogenous with respect to height, weight, and VO2peak. RPE for the legs and overall body were significantly attenuated (P less than 0.05) during the last 45 min of exercise. Plasma glucose and insulin were higher (P less than 0.05) in G than in P at virtually all time points. CHO oxidation and work rate were maintained throughout exercise in G but not during the last 30 min of exercise in P (P less than 0.05). Percent changes in plasma volume, plasma lactate, HR, VE, RR, and RPE for the chest were not different between conditions (P greater than 0.05). The data suggest that ingestion of carbohydrate beverages during endurance cycling can maintain plasma glucose and CHO oxidation during the latter stages of prolonged exercise. As a result, it appears that a relationship exists between attenuation of ratings of perceived exertion (especially in the legs), blood glucose, and CHO oxidation late in prolonged exercise. The mechanism for this probably involves the increased availability of blood-borne glucose to serve as substrate for brain and/or muscle energy metabolism during a time when endogenous stores of carbohydrate are low.     

Dose-response effects of ingested carbohydrate on exercise metabolism in women

PURPOSE: The effect of different quantities of carbohydrate (CHO) intake on CHO metabolism during prolonged exercise was examined in endurance-trained females. METHOD: On four occasions, eight females performed 2 h of cycling at approximately 60% .VO2max with ingestion of beverages containing low (LOW, 0.5 g.min(-1)), moderate (MOD, 1.0 g.min(-1)), or high (HIGH, 1.5 g.min(-1)) amounts of CHO, or water only (WAT). Test solutions contained trace amounts of [U-13C] glucose. Indirect calorimetry combined with measurement of expired 13CO2 and plasma 13C enrichment enabled calculation of exogenous CHO, liver-derived glucose, and muscle glycogen oxidation during the last 30 min of exercise. RESULTS: The highest rates of exogenous CHO oxidation were observed in MOD, with no further increases in HIGH (peak rates of 0.33 +/- 0.02, 0.50 +/- 0.03, and 0.48 +/- 0.05 g.min(-1) for LOW, MOD, and HIGH, respectively; P < 0.05 for LOW vs MOD and HIGH). Endogenous CHO oxidation was lowest in MOD (0.99 +/- 0.06, 0.82 +/- 0.08, 0.70 +/- 0.07, and 0.89 +/- 0.09 g.min(-1); P < 0.05 for MOD vs all other trials). Compared with WAT, CHO ingestion reduced liver glucose oxidation during exercise by approximately 30% (P < 0.05 for WAT vs all CHO). Differential rates of muscle glycogen oxidation were observed with different CHO doses (0.57 +/- 0.07, 0.53 +/- 0.08, 0.41 +/- 0.07, and 0.60 +/- 0.09 g.min(-1) for WAT, LOW, MOD, and HIGH respectively; P < 0.05 for MOD vs HIGH). CONCLUSION: In endurance-trained women, the highest rates of exogenous CHO oxidation and greatest endogenous CHO sparing was observed when CHO was ingested at moderate rates (1.0 g.min(-1), 60 g.h(-1)) during exercise.     

Effect of fructose ingestion on muscle glycogen usage during exercise

Eight healthy males were studied to compare the effects of preexercise fructose and glucose ingestion on muscle glycogen usage during exercise. Subjects performed three randomly assigned trials, each involving 30 min of cycling exercise at 75% VO2max. Forty-five min prior to commencing each trial, subjects ingested either 50 g of glucose (G), 50 g of fructose (F), or sweet placebo (C). No differences in VO2 or respiratory exchange ratio were observed between the trials. Blood glucose was elevated (P less than 0.05) as a result of the glucose feeding. With the onset of exercise, blood glucose declined rapidly during G, reaching a nadir of 3.18 +/- 0.15 (SE) mmol X 1(-1) at 20 min of exercise. This value was lower (P less than 0.05) than the corresponding values in F (3.79 +/- 0.20) and C (3.99 +/- 0.18). No differences in exercise blood glucose levels were observed between F and C. Muscle glycogen utilization was greater (P less than 0.05) during G (55.4 +/- 3.3 mmol X kg-1 w.w.) than C (42.8 +/- 4.2). No difference was observed between F (45.6 +/- 4.3) and C. There was a trend (P = 0.07) for muscle glycogen usage to be lower during F than G. These results suggest that the adverse effects of preexercise glucose ingestion are, in general, not observed with either fructose or sweet placebo.     

Muscle glycogen synthesis before and after exercise

The importance of carbohydrates as a fuel source during endurance exercise has been known for 60 years. With the advent of the muscle biopsy needle in the 1960s, it was determined that the major source of carbohydrate during exercise was the muscle glycogen stores. It was demonstrated that the capacity to exercise at intensities between 65 to 75% VO2max was related to the pre-exercise level of muscle glycogen, i.e. the greater the muscle glycogen stores, the longer the exercise time to exhaustion. Because of the paramount importance of muscle glycogen during prolonged, intense exercise, a considerable amount of research has been conducted in an attempt to design the best regimen to elevate the muscle's glycogen stores prior to competition and to determine the most effective means of rapidly replenishing the muscle glycogen stores after exercise. The rate-limiting step in glycogen synthesis is the transfer of glucose from uridine diphosphate-glucose to an amylose chain. This reaction is catalysed by the enzyme glycogen synthase which can exist in a glucose-6-phosphate-dependent, inactive form (D-form) and a glucose-6-phosphate-independent, active form (I-form). The conversion of glycogen synthase from one form to the other is controlled by phosphorylation-dephosphorylation reactions. The muscle glycogen concentration can vary greatly depending on training status, exercise routines and diet. The pattern of muscle glycogen resynthesis following exercise-induced depletion is biphasic. Following the cessation of exercise and with adequate carbohydrate consumption, muscle glycogen is rapidly resynthesised to near pre-exercise levels within 24 hours. Muscle glycogen then increases very gradually to above-normal levels over the next few days. Contributing to the rapid phase of glycogen resynthesis is an increase in the percentage of glycogen synthase I, an increase in the muscle cell membrane permeability to glucose, and an increase in the muscle's sensitivity to insulin. The slow phase of glycogen synthesis appears to be under the control of an intermediate form of glycogen synthase that is highly sensitive to glucose-6-phosphate activation. Conversion of the enzyme to this intermediate form may be due to the muscle tissue being constantly exposed to an elevated plasma insulin concentration subsequent to several days of high carbohydrate consumption. For optimal training performance, muscle glycogen stores must be replenished on a daily basis. For the average endurance athlete, a daily carbohydrate consumption of 500 to 600g is required. This results in a maximum glycogen storage of 80 to 100 mumol/g wet weight.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effect of fructose 1,6-diphosphate infusion on the hormonal response to exercise

Exogenous fructose 1,6-diphosphate (FDP), a glycolytic intermediate, has recently been demonstrated to accelerate ATP production, prevent glycogen breakdown, stimulate glycogen synthesis, and synthesize free fatty acids in animals and humans. To assess the effects of FDP on the hormonal and metabolic response to exercise, ten trained males (34 +/- 7 yr) underwent 1 h of continuous exercise at 70% VO2max followed by 20 W.min-1 increments to exhaustion. Two hundred fifty mg.kg-1 body weight FDP or placebo was infused in randomized, double-blind, crossover fashion. No differences were observed in heart rate, blood pressure, gas exchange data, perceived effort, or glucose, insulin, free fatty acid, lactate, beta-hydroxybutyrate, glycerol, and glucagon concentration at rest, during exercise, or upon exhaustion. In contrast to the previously reported bioenergetic effects of FDP under conditions in which glycolysis is impeded (acidosis, hypoxia, and ischemia), FDP did not affect the gas exchange, hormonal, or substrate response to moderately high intensity exercise in healthy normals.     

Prediction of glucose oxidation rate during exercise

Recently, the relationship between percentage maximal heart rate vs. glucose oxidation rate has been proposed as a tool for estimating glucose oxidation rate during exercise in insulin-dependent diabetic patients. The reliability of this relationship and its applicability to long-term exercise is evaluated. Eight healthy volunteers performed a graded cycloergometric exercise (10-min steps at 30, 50, 70, 90 % of ventilatory threshold). Heart rate and glucose oxidation rate (by indirect calorimetry) were measured during the last 5 min of each step. Volunteers underwent then three 1-hour constant intensity rides at 40, 60, 80 % of ventilatory threshold. Heart rate was recorded continuously; glucose oxidation rate was determined over 15-min periods. The percentage maximal heart rate vs. glucose oxidation rate relationship obtained from the graded exercise matched that previously reported. Independently of intensity, glucose oxidation rates observed during the 1-hr rides were linearly related to the estimated ones (R (2) > 0.96, p < 0.001), being, however, progressively over-estimated in subsequent exercise periods. The proposed correction yields values close to the identity line (y = 1.001 . x; R2 = 0.974, p < 0.001), the difference between observed and "corrected" values amounting to 0.23 +/- 2.17 mg . min (-1) . kg (-1). In conclusion, glucose oxidation rate can be estimated from heart rate, once proper correction factors are applied for long duration exercises.     

Control of hepatic glucose production during exercise

Major advancements have occurred recently in study of the mechanisms of regulation of glycogenolysis and gluconeogenesis in perfused livers and isolated hepatocytes. Many questions remain unanswered, however, with respect to the control of these processes in the live exercising animal. Additional studies will be necessary to determine the relative roles of alpha- and beta-adrenergic receptor-mediated effects of circulating catecholamines, of glucagon, glucocorticoids, angiotensin II, vasopressin, insulin, and of the direct sympathetic innervation in regulation of hepatic glycogenolysis and gluconeogenesis during exercise.