Effect Of Carbohydrate Feeding Research Articles

Effect of carbohydrate feeding on the bone metabolic response to running.

Bone resorption is increased after running, with no change in bone formation. Feeding during exercise might attenuate this increase, preventing associated problems for bone. This study investigated the immediate and short-term bone metabolic responses to carbohydrate (CHO) feeding during treadmill running. Ten men completed two 7-day trials, once being fed CHO (8% glucose immediately before, every 20 min during, and immediately after exercise at a rate of 0.7 g CHO·kg body mass−1·h−1) and once being fed placebo (PBO). On day 4 of each trial, participants completed a 120-min treadmill run at 70% of maximal oxygen consumption (V̇o2 max). Blood was taken at baseline (BASE), immediately after exercise (EE), after 60 (R1) and 120 (R2) min of recovery, and on three follow-up days (FU1-FU3). Markers of bone resorption [COOH-terminal telopeptide region of collagen type 1 (β-CTX)] and formation [NH2-terminal propeptides of procollagen type 1 (P1NP)] were measured, along with osteocalcin (OC), parathyroid hormone (PTH), albumin-adjusted calcium (ACa), phosphate, glucagon-like peptide-2 (GLP-2), interleukin-6 (IL-6), insulin, cortisol, leptin, and osteoprotogerin (OPG). Area under the curve was calculated in terms of the immediate (BASE, EE, R1, and R2) and short-term (BASE, FU1, FU2, and FU3) responses to exercise. β-CTX, P1NP, and IL-6 responses to exercise were significantly lower in the immediate postexercise period with CHO feeding compared with PBO (β-CTX: P = 0.028; P1NP: P = 0.021; IL-6: P = 0.036), although there was no difference in the short-term response (β-CTX: P = 0.856; P1NP: P = 0.721; IL-6: P = 0.327). No other variable was significantly affected by CHO feeding during exercise. We conclude that CHO feeding during exercise attenuated the β-CTX and P1NP responses in the hours but not days following exercise, indicating an acute effect of CHO feeding on bone turnover.

The effect of carbohydrate feeding during cycling on run performance within a simulated Olympic-distance triathlon

Introduction: The purpose of the present study was to examine the effects of carbohydrate ingestion during the cycle leg of a simulated Olympic-distance triathlon (1500-m swim, 40-km cycle, 10-km run) on subsequent running performance. Methods: Five well-trained triathletes (4 male, 1 female) volunteered to participate (mean±SD age: 23.6±4.2 y, body mass: 63.0±7.6 kg and VO2max: 64.0±9.0 ml kg-1 min-1). Participants attended three separate testing sessions separated by at least five days. The first session involved a 1500-m swim time-trial (STT) followed approximately 30 min later by a graded cycle test to exhaustio nfor the evaluation of maximal aerobic power (MAP). The two subsequent sessions required participants to complete a simulated Olympic-distance triathlon involving a 1500-m pool swim to within 5% of the STT, a 40-km stationary cycle at 75% of MAP and a 10-km running time trial. Participants randomly consumed either a 14.4% carbohydrate drink containing 1.2 g min-1 of glucose and 0.6 g min-1 of fructose (CHO) or a fruit squash placebo (PLA) throughout the cycle leg of the triathlon. Fingertip blood samples were collected after every 5 km of the cycle leg and at the end of the run and were subsequently analysed for blood glucose (GLU) and lactate (LAC) concentrations. Rating of perceived exertion (RPE) and perceived stomach upset (PSU) were also measured after each 5-km cycle period and at the end of the run. Heart rate (HR) was measured throughout the cycle leg only. Results and conclusion: The 10-km run time was 4.2% faster following CHO (38 min 08 s ± 2 min 46 s) compared with PLA (39 min 44 s ±3 min 13 s; P 0.05) and significantly lower RPE scores in the CHO compared with the PLA trial (P < 0.05). These results show that a 10-km run at the end of an Olympic-distance triathlon may be significantly improved following ingestion of a 14.4% glucose-fructose beverage at a rate of 1.8 g min−1 compared with a fruit squash placebo, with no additional gastro-intestinal stress. This improvement in run performance in the CHO trial may be due to muscle and liver glycogen sparing during the cycle leg, which increased carbohydrate metabolism in the latter stages of the triathlon.

No effect of carbohydrate feeding on 16 km cycling time trial performance

The aim of this study is to investigate the effects of CHO ingestion during high intensity exercise performance lasting approximately 25 min. Twelve endurance trained male cyclists (age 19-41 years; body mass 73.2 +/- 4.2 kg; VO(2)max 66.4 +/- 6.2 ml kg(-1) min(-1)) completed a simulated 16 km time trial (457 +/- 37 kJ) time trial in the lab on three occasions. Once they received a 6% carbohydrate electrolyte solution (CHO) and twice they received the same electrolyte containing placebo drink (PLA). Carbohydrate or placebo drinks were ingested 5 min before the start (4 ml kg(-1)) and at 25, 50, and 75% of completion of the time trial (1.4 ml kg(-1)). The CHO drink was a 6% sucrose-glucose-electrolyte solution. No differences were observed in the time to complete the time trials with either treatment. Time in min:s were 25:30 +/- 1:34 and 25:27 +/- 1:46 for the two placebo trials and 25:38 +/- 1:59 in the CHO trial. Power output during the time trials was also remarkably similar: 300 +/- 37 W, 301 +/- 39 W and 299 +/- 40 W, respectively. Pacing strategies and heart rate were identical in all three trials. From the two placebo trials, a coefficient of variation for this performance task was calculated to be 1.1%. Data from this study provides evidence that carbohydrate ingestion during short high intensity exercise (approximately 30 min, 85-90% VO(2)max) does not improve performance. Furthermore, this study found a very low coefficient of variation (1.1%) for a simulated 16 km time trial.

Effect of carbohydrate feeding on insulin action in skeletal muscle after surgical trauma in the rat

Metabolic stress after surgery is associated with peripheral insulin resistance. Recent studies have suggested that preoperative glucose can ameliorate postoperative decreases in insulin-stimulated glucose disposal. In the present experiments, we used a bowel-resection model of surgical trauma to test the hypothesis that elevations of serum insulin induced by preoperative oral glucose or ad libitum feeding affects postoperative insulin-stimulated glucose uptake in skeletal muscle. Insulin-stimulated glucose transport was measured in vitro in soleus muscles after surgical trauma in fasted rats given oral glucose or water before surgery. Insulin-stimulated glucose transport was also assessed in vitro in fasted or fed traumatized rats and non-traumatized control animals. In addition, stress hormones (glucagon, corticosterone, and adrenaline) were measured before and after surgical trauma in fasted rats and rats fed ad libitum. In vitro skeletal-muscle insulin sensitivity and responsiveness were reduced postoperatively in fasted animals that received oral glucose loads before bowel resections and in rats fed ad libitum or fasted before surgery versus non-traumatized rats (all P < 0.05). Stress-hormone concentrations after trauma did not differ between fed and fasted animals. In the current study, insulin sensitivity and responsiveness were reduced in isolated skeletal muscles after bowel resection, but neither preoperative glucose supplementation nor free intake of mixed nutrients ameliorated the development of postoperative insulin resistance.

CARBOHYDRATE FEEDINGS IMPROVE 1 H TIME TRIAL CYCLING PERFORMANCE* 221

Carbohydrate (CHO) feedings have been shown to improve endurance performance at moderate intensities (60-75% VO2max) and of more than 2 h duration. The effects of carbohydrate feedings during high intensity exercise (i.e. ≥ 80% VO2max) of shorter duration (-1 h) are less clear. The purpose of the present study therefore was to investigate the effect of a ingestion of a 7.6% CHO solution during exercise on time trial performance of approximately 1 h. On two occasions nineteen endurance trained cyclists completed an exercise test requiring the accomplishment a set amount of work as fast as possible under strictly standardized conditions. This test has been shown to be highly reproducible (coefficient of variation 3.35%, Jeukendrup et al. MSSE 27 in press 1995). At the start and during the trials they drank either a 7.6% CHO solution or artificially flavored and colored water (placebo). The rate of CHO ingestion was about 1 g/min in the carbohydrate trial. Time to complete the set amount of work was significantly reduced and thus performance was significantly increased (P<0.001) with the CHO drink by 2.3%. Time to complete the set amount of work was 58.74 ± 0.52 min with CHO and 60.15 ± 0.65 min with placebo. Average workload during the time trials was 297.5 ± 1.4 W and 291.0 ± 10.3 W respectively. Subjects exercised at 76.4 ± 0.7% of their maximal work rate (Wmax) with CHO and at 74.8% Wmax with placebo. It was concluded that carbohydrate feedings ingested at a rate of ≈ 1 g/min during exercise improve time trial cycling performance of about 1 h duration.

Carbohydrates, Branched-Chain Amino Acids, and Endurances: The Central Fatigue Hypothesis

The mechanisms of central fatigue are largely unexplored, but the central fatigue hypothesis suggests that increased brain serotonin (5-HT) can cause a deterioration in sport and exercise performance. There is now convincing evidence that exercise-induced increases in the plasma free tryptophan (f-TRP)/branched-chain amino acids (BCCA) ratio are associated with increased brain 5-HT and the onset of fatigue during prolonged exercise. Furthermore, when drugs are administered to alter brain 5-HT, they have the predicted effects on exercise performance. The influence of nutritional manipulations of f-TRP/BCCA on performance is less well established. The effects of BCCA supplementation on exercise performance are mixed, and the published studies often suffer from methodological flaws. Alternatively, dramatic reductions in f-TRP/BCCA and enhanced performance accompany carbohydrate feedings during prolonged exercise. However, it is difficult to distinguish between the effects of carbohydrate feedings on mechanisms that reside in the brain versus the muscles themselves.

Central and peripheral factors in fatigue.

The causes of fatigue during muscular exercise include factors that reside in the brain (central mechanisms) as well as the muscles themselves (peripheral mechanisms). Central fatigue is largely unexplored, but there is increasing evidence that increased brain serotonin (5-HT) can lead to central (mental) fatigue, thereby causing a deterioration in sport and exercise performance. Although there are also strong theoretical grounds for a beneficial role of nutrition in delaying central fatigue, the data are much more tenuous. Dietary supplementation with branched-chain amino acids (BCAA) in low doses produces small and probably inconsequential effects on peripheral markers of brain 5-HT synthesis (plasma free tryptophan/BCAA), whereas larger doses are likely to be unpalatable, reduce the absorption of water in the gut, and may increase potentially toxic ammonia concentrations in the plasma. Alternatively, carbohydrate supplementation results in large reductions in plasma free tryptophan/BCAA and exercise time to fatigue is significantly longer, but it is difficult to distinguish between the effects of carbohydrate feedings on central fatigue mechanisms and the well-established beneficial effects of carbohydrate supplements on the contracting muscle. These data support the exciting possibility that relationships exist among nutrition, brain neurochemistry and sport performance. However, while the evidence is intriguing and makes good intuitive sense, our knowledge in this area is rudimentary at best.

Changes in circulating insulin-like growth factor-binding protein-1 (IGFBP-1) during prolonged exercise: effect of carbohydrate feeding

Changes in circulating insulin-like growth factor-binding protein-1 (IGFBP-1) during prolonged exercise: effect of carbohydrate feeding

Carbohydrate Ingestion during Exercise: Effects on Muscle Glycogen Resynthesis after Exercise

To determine the effect of carbohydrate feeding on muscle glycogen resynthesis, 8 male cyclists pedaled for 2 hrs on a cycle ergometer at 70% of VO2max while consuming either a 10% carbohydrate solution (CHO) or a nonnutritive sweet placebo (No CHO). Muscle biopsies were obtained from the vastus lateralis prior to, immediately postexercise, and at 2, 4, and 24 hrs of recovery. Blood samples were taken before and at the end of exercise, and at specified times during recovery. During both trials food intake was withheld for the first 2 hrs of recovery, but at 2 hrs postexercise a 24% carbohydrate solution was ingested. The rate of muscle glycogen resynthesis during the first 2 hrs of recovery was similar for the CHO and No CHO trials. Following ingestion of the 24% carbohydrate supplement, the rates of muscle glycogen resynthesis increased similarly in both trials. These similar rates of resynthesis following ingestion of the carbohydrate supplement were obtained despite significantly greater serum glucose and insulin levels during the No CHO trial. The results indicate that the carbohydrate feedings taken during exercise had little effect on postexercise muscle glycogen resynthesis.

No effect of carbohydrate feeding on glycogen synthase in human muscle during exercise.

The effect of carbohydrate (CHO) feedings on exercise-mediated changes in glycogen synthase fractional (GSF) activity has been investigated. Subjects cycled at approximately 70% of maximal oxygen uptake on two occasions: the first to fatigue (135 +/- 17 min; mean +/- SE) (control, CON), and the second at the same workload and duration as the first, but with the addition of frequent ingestion of CHO during exercise (0.27 g kg-1 body weight every 15 min). Biopsies were taken from the quadriceps femoris muscle before and immediately after exercise. Plasma glucose and insulin decreased during CON exercise, but remained elevated throughout CHO exercise (end of exercise: glucose = 4.4 +/- 0.2 mM CON vs. 5.8 +/- 0.2 CHO, P < 0.01; insulin = 9 +/- 1 uU ml-1 CON vs. 19 +/- 3 CHO, P < 0.05). Glycogen decreased to approximately 10% of the basal value during CON and to approximately 20% during CHO, and there was no significant difference in net glycogenolysis between treatments. GSF activity averaged 0.25 +/- 0.03 and 0.22 +/- 0.05 at rest, and increased to 0.51 +/- 0.08 and 0.48 +/- 0.09 after exercise in CON and CHO, respectively (P > 0.05 between treatments). It is concluded that under the present conditions CHO feedings do not alter the exercise-mediated changes in GSF activity. The increase in GSF during exercise is attributed at least in part to the decrease in muscle glycogen (which increases the suitability of GS as substrate for GS phosphatase).

Effect of carbohydrate feedings on muscle glycogen utilization and exercise performance

Ten men were studied during 4 h of cycling to determine the effect of solid carbohydrate (CHO) feedings on muscle glycogen utilization and exercise performance. In the experimental trial (E) the subjects ingested 43 g of sucrose in solid form along with 400 ml of water at 0, 1, 2 and 3 h of exercise. During the control trial (C) they received 400 ml of an artificially sweetened drink without solid CHO. No differences in VO2, heart rate, or total energy expenditure were observed between trials; however, respiratory exchange ratios were significantly (P less than 0.05) higher during E. Blood glucose was significantly (P less than 0.05) elevated 20 min post-feeding in E; however, by 50 min no differences were observed between trials until 230 min (E = 4.5 +/- 0.2 mmol X l-1 vs C = 3.9 +/- 0.2, means +/- SE; P less than 0.05). Muscle glycogen utilization was significantly (P less than 0.05) lower during E (100.7 +/- 10.2 mmol X kg-1 w.w.) than C (126.2 +/- 5.5). During a sprint (100% VO2max) ride to exhaustion at the end of each trial, subjects performed 45% longer when fed CHO (E = 126.8 +/- 24.7 s vs C = 87.2 +/- 17.5; P less than 0.05). It was concluded that repeated solid CHO feedings maintain blood glucose levels, reduce muscle glycogen depletion during prolonged exercise, and enhance sprint performance at the end of such activity.

Effects of carbohydrate feeding on blood coagulation, fibrinolysis and platelet adhesiveness — relations to serum lipids and lipoproteins

An isocaloric diet containing 93 calorie % glucose was given for 23 days to 9 obese subjects and 2 normal controls. The influence on blood coagulation, fibrinolysis and platelet function as well as serum lipids and lipoproteins were: Factor II-VII-X activity, fibrinogen dn plasminogen decreased while factor V and factor VIII, antithrombin III, a 1 antitrypsin and α 2 macroglobulin, did not change. Recalcification time of platelet-rich and platelet-poor plasma, Russel viper venom (RVV) clotting time and activated partial thromboplastin time (APTT) were shortened. No one of the factors known to influence on clotting was found to be responsible for the shortening of the clotting times. Platelet adhesiveness decreased unexpectedly. Fibrinolytic activity in plasma and in euglobulin before and after stasis of the arm did not change sifnificantly. Serum cholesterol, low density lipoproteins (LDL) and high density lipoproteins (HDL) decreased while serum triglycerides and very low density lipoproteins (VLDL) increased - the latter preferentially in the obese group with large fat cells. The reduction in HDL caused by the diet was correlated to the decrease in factor II-VII-X and fibrinogen. A strong correlation was found between LDL and platelet adhesiveness and a causal relationship may exist. According to conventional ideas the shortening of clotting times should tend to increase and the lowering of platelet adhesiveness to decrease the tendency to thrombosis. The results of the present work demonstrate the danger in drawing conclusions from studying only one factor in the complicated scheme of hemostasis.

The effect of carbohydrate feeding on the induction of δ-aminolevulinic acid synthetase

Allylisopropylacetamide (AIA), when administered to rats, induces high levels of hepatic mitochondrial δ-aminolevulinic acid synthetase (ALA synthetase). The activity of this enzyme can be quantitated in porphyric rat liver, since the freshly prepared mitochondria from porphyric rat liver are permeable to succinyl-coenzyme A and do not have high deacylase activity. Administration of carbohydrate to rats markedly inhibits the induction of ALA synthetase by AIA. Since ALA synthetase is thought to be the rate controlling enzyme in hepatic porphyrin biosynthesis, diet is a regulatory factor in hepatic porphyrin synthesis in porphyria. The previously observed effects of diet on porphyrin precursor excretion in both experimental and human acute intermittent porphyria are best explained by the effect of diet on the hepatic ALA synthetase level. The application of the theory of “catabolite repression” to the present findings is discussed.

Effects of carbohydrate feeding on serum lipids and lipoproteins in the rat.

Fasting in the rat is accompanied by an increase in serum cholesterol concentration reflecting an increase in high-density lipoproteins. The feeding of carbohydrate results in decreases in both low- and high-density lipoproteins, the former occurring acutely, and the latter occurring more slowly. In the fasting rat the injection of protamine, an antiheparin agent, produces an increase in all serum lipids, but the increase occurs in the low-density lipoproteins. In the rat fed carbohydrate this lipemia-inducing effect of protamine is practically abolished. The feeding of carbohydrate has no effect, however, on the rate of clearance of intravenously administered chylomicrons. These phenomena are discussed in relation to current theories of lipid transport.

An experiment on the absorption of glucose given by rectum

For many years it has been accepted by clinicians that glucose given by rectum is absorbed immediately into the blood, and surgeons constantly use such a procedure as a part of their postoperative therapy. Because of the difficulties attending the procedure there are comparatively few controlled experiments on the effect of glucose so administered in the literature. The effect of carbohydrate feeding on acetonuria has been clearly demonstrated by many experiments during the past few years, and it was determined to test the rectal absorption of glucose by studies of the effect produced upon experimental acetonuria.The subject of the experiment (one of the authors, D. C. W.) was a man 5 ft. 9 1/4 in. tall who weighed 165 pounds, and whose basal metabolism, as measured by the portable Benedict calorimeter was 1700 calories. He received the diet recently discussed by Hubbard and Wright1 for four days. This diet furnished 2,142 calories—twenty per cent. more than the basal requirement—and consisted of 54 grams...