Evidence of disturbed sleep and mood state in well-trained athletes during short-term intensified training with and without a high carbohydrate nutritional intervention.

Few studies have investigated the effects of exercise training on sleep physiology in well-trained athletes. We investigated changes in sleep markers, mood state and exercise performance in well-trained cyclists undergoing short-term intensified training and carbohydrate nutritional intervention. Thirteen highly-trained male cyclists (age: 25 ± 6y, [Formula: see text]O2max: 72 ± 5 ml/kg/min) participated in two 9-day periods of intensified training while undergoing a high (HCHO) or moderate (CON) carbohydrate nutritional intervention before, during and after training sessions. Sleep was measured each night via wristwatch actigraphy. Mood state questionnaires were completed daily. Performance was assessed with maximal oxygen uptake ([Formula: see text]. Percentage sleep time fell during intensified training (87.9 ± 1.5 to 82.5 ± 2.3%; p < 0.05) despite an increase in time in bed (456 ± 50 to 509 ± 48 min; p = 0.02). Sleep efficiency decreased during intensified training (83.1 ± 5.3 to 77.8 ± 8.6%; p < 0.05). Actual sleep time was significantly higher in CON than HCHO throughout intensified training. Mood disturbance increased during intensified training and was higher in CON than HCHO (p < 0.05). Performance in the [Formula: see text] exercise protocol fell significantly with intensified training. The main findings of this study were that 9-days of intensified training in highly-trained cyclists resulted in significant and progressive declines in sleep quality, mood state and maximal exercise performance.

Fat burners: nutrition supplements that increase fat metabolism.

The term 'fat burner' is used to describe nutrition supplements that are claimed to acutely increase fat metabolism or energy expenditure, impair fat absorption, increase weight loss, increase fat oxidation during exercise, or somehow cause long-term adaptations that promote fat metabolism. Often, these supplements contain a number of ingredients, each with its own proposed mechanism of action and it is often claimed that the combination of these substances will have additive effects. The list of supplements that are claimed to increase or improve fat metabolism is long; the most popular supplements include caffeine, carnitine, green tea, conjugated linoleic acid, forskolin, chromium, kelp and fucoxanthin. In this review the evidence for some of these supplements is briefly summarized. Based on the available literature, caffeine and green tea have data to back up its fat metabolism-enhancing properties. For many other supplements, although some show some promise, evidence is lacking. The list of supplements is industry-driven and is likely to grow at a rate that is not matched by a similar increase in scientific underpinning.

Exercise training increases adipose tissue GLUT4 expression in patients with type 2 diabetes.

We investigated the effects of exercise training on adipose tissue and skeletal muscle GLUT4 expression in patients with type 2 diabetes (T2D). Muscle and adipose tissue samples were obtained before and after 4-weeks of exercise training in seven patients with T2D [47 ± 2 years, body mass index (BMI) 28 ± 2]. Seven control subjects (54 ± 4, BMI 30 ± 2) were recruited for baseline comparison. Adipose tissue GLUT4 protein expression was 43% lower (p < 0.05) in patients with T2D compared with control subjects and exercise training increased (p < 0.05) adipose tissue GLUT4 expression by 36%. Skeletal muscle GLUT4 protein expression was not different between control subjects and patients with T2D. Exercise training increased (p < 0.05) skeletal muscle GLUT4 protein expression by 20%. In conclusion, 4-weeks of exercise training increased GLUT4 expression in adipose tissue and skeletal muscle of patients with T2D, although the functional benefits of this adaptation appear to be dependent on an optimal ß-cell function.

Multiple transportable carbohydrates enhance gastric emptying and fluid delivery.

This study compared the effects of ingesting water (WATER), an 8.6% glucose solution (GLU) and an 8.6% glucose+fructose solution (2:1 ratio, GLU+FRU) on gastric emptying (GE), fluid delivery, and markers of hydration status during moderate intensity exercise. Eight male subjects (age=24+/-2 years, weight=74.5+/-1.2 kg, VO2max=62.6+/-2.5 mL/kg/min) performed three 120 min cycling bouts at 61% VO2max. Subjects ingested GLU, GLU+FRU (both delivering 1.5 g/min carbohydrate), or WATER throughout exercise, ingesting 2.1 L. Serial dye dilution measurements of GE were made throughout exercise and subjects ingested 5.00 g of D2O and 150 mg of 13C-acetate at 60 min to obtain measures of fluid uptake and GE, respectively. GLU+FRU resulted in faster rates of deuterium accumulation, an earlier time to peak in the 13C enrichment of expired air and a faster rate of GE compared with GLU. GLU+FRU also attenuated the rise in heart rate that occurred in GLU and WATER and resulted in lower ratings of perceived exertion. There was a greater loss in body weight with GLU corrected for fluid intake. These data suggest that ingestion of a combined GLU+FRU solution increases GE and "fluid delivery" compared with a glucose only solution.

Influence of body position when considering the ecological validity of laboratory time-trial cycling performance.

The aims of this study were to compare the physiological demands of laboratory- and road-based time-trial cycling and to examine the importance of body position during laboratory cycling. Nine male competitive but non-elite cyclists completed two 40.23-km time-trials on an air-braked ergometer (Kingcycle) in the laboratory and one 40.23-km time-trial (RD) on a local road course. One laboratory time-trial was conducted in an aerodynamic position (AP), while the second was conducted in an upright position (UP). Mean performance speed was significantly higher during laboratory trials (UP and AP) compared with the RD trial (P < 0.001). Although there was no difference in power output between the RD and UP trials (P > 0.05), power output was significantly lower during the AP trial than during both the RD (P = 0.013) and UP trials (P = 0.003). Similar correlations were found between AP power output and RD power output (r = 0.85, P = 0.003) and between UP power output and RD power output (r = 0.87, P = 0.003). Despite a significantly lower power output in the laboratory AP condition, these results suggest that body position does not affect the ecological validity of laboratory-based time-trial cycling.

The ecological validity of laboratory cycling: Does body size explain the difference between laboratory- and field-based cycling performance?

Previous researchers have identified significant differences between laboratory and road cycling performances. To establish the ecological validity of laboratory time-trial cycling performances, the causes of such differences should be understood. Hence, the purpose of the present study was to quantify differences between laboratory- and road-based time-trial cycling and to establish to what extent body size [mass (m) and height (h)] may help to explain such differences. Twenty-three male competitive, but non-elite, cyclists completed two 25 mile time-trials, one in the laboratory using an air-braked ergometer (Kingcycle) and the other outdoors on a local road course over relatively flat terrain. Although laboratory speed was a reasonably strong predictor of road speed (R2 = 69.3%), a significant 4% difference (P < 0.001) in cycling speed was identified (laboratory vs. road speed: 40.4 +/- 3.02 vs. 38.7 +/- 3.55 km x h(-1); mean +/- s). When linear regression was used to predict these differences (Diff) in cycling speeds, the following equation was obtained: Diff (km x h(-1)) = 24.9 - 0.0969 x m - 10.7 x h, R2 = 52.1% and the standard deviation of residuals about the fitted regression line = 1.428 (km . h-1). The difference between road and laboratory cycling speeds (km x h(-1)) was found to be minimal for small individuals (mass = 65 kg and height = 1.738 m) but larger riders would appear to benefit from the fixed resistance in the laboratory compared with the progressively increasing drag due to increased body size that would be experienced in the field. This difference was found to be proportional to the cyclists' body surface area that we speculate might be associated with the cyclists' frontal surface area.

Optimal power-to-mass ratios when predicting flat and hill-climbing time-trial cycling.

The purpose of this article was to establish whether previously reported oxygen-to-mass ratios, used to predict flat and hill-climbing cycling performance, extend to similar power-to-mass ratios incorporating other, often quick and convenient measures of power output recorded in the laboratory [maximum aerobic power (W(MAP)), power output at ventilatory threshold (W(VT)) and average power output (W(AVG)) maintained during a 1 h performance test]. A proportional allometric model was used to predict the optimal power-to-mass ratios associated with cycling speeds during flat and hill-climbing cycling. The optimal models predicting flat time-trial cycling speeds were found to be (W(MAP)m(-0.48))(0.54), (W(VT)m(-0.48))(0.46) and (W(AVG)m(-0.34))(0.58) that explained 69.3, 59.1 and 96.3% of the variance in cycling speeds, respectively. Cross-validation results suggest that, in conjunction with body mass, W(MAP) can provide an accurate and independent prediction of time-trial cycling, explaining 94.6% of the variance in cycling speeds with the standard deviation about the regression line, s=0.686 km h(-1). Based on these models, there is evidence to support that previously reported VO2-to-mass ratios associated with flat cycling speed extend to other laboratory-recorded measures of power output (i.e. Wm(-0.32)). However, the power-function exponents (0.54, 0.46 and 0.58) would appear to conflict with the assumption that the cyclists' speeds should be proportional to the cube root (0.33) of power demand/expended, a finding that could be explained by other confounding variables such as bicycle geometry, tractional resistance and/or the presence of a tailwind. The models predicting 6 and 12% hill-climbing cycling speeds were found to be proportional to (W(MAP)m(-0.91))(0.66), revealing a mass exponent, 0.91, that also supports previous research.

Measurement of substrate oxidation during exercise by means of gas exchange measurements.

Measures of substrate oxidation have traditionally been calculated from indirect calorimetry measurements using stoichiometric equations. Although this has proven to be a solid technique and it has become one of the standard techniques to measure whole body substrate metabolism, there are also several limitations that have to be considered. When indirect calorimetry is used during exercise most of the assumptions on which the method is based hold true although changes in the size of the bicarbonate pool at higher exercise intensities may invalidate the calculations of carbohydrate and fat oxidation. Most of the existing equations are based on stoichiometric equations of glucose oxidation and the oxidation of a triacylglycerol that is representative of human adipose tissue. However, in many exercise conditions, glycogen and not glucose is the predominant carbohydrate substrate. Therefore we propose slightly modified equations for the calculation of carbohydrate and fat oxidation for use during low to high intensity exercise. Studies that investigated fat oxidation over a wide range of intensities and that determined the exercise intensity at which fat oxidation is maximal have provided useful insights in the variation in fat oxidation between individuals and in the factors that affect fat oxidation. Fat oxidation during exercise can be influenced by exercise intensity and duration, diet, exercise training, exercise mode and gender. Although a number of important factors regulating fat oxidation have been identified, it is apparent that a considerable degree of inter-subject variability in substrate utilization persists and cannot be explained by the aforementioned factors. Future research should investigate the causes of the large inter-individual differences in fat metabolism between individuals and their links with various disease states.

Measurement of exogenous carbohydrate oxidation: a comparison of [U-14C]glucose and [U-13C]glucose tracers.

The purpose of this study was to assess the level of agreement between two techniques commonly used to measure exogenous carbohydrate oxidation (CHO(EXO)). To accomplish this, seven healthy male subjects (24 +/- 3 yr, 74.8 +/- 2.1 kg, V(O2(max)) 62 +/- 4 ml x kg(-1) x min(-1)) exercised at 50% of their peak power for 120 min on two occasions. During these exercise bouts, subjects ingested a solution containing either 144 g glucose (8.7% wt/vol glucose) or water. The glucose solution contained trace amounts of both [U-13C]glucose and [U-14C]glucose to allow CHO(EXO) to be quantified simultaneously. The water trial was used to correct for background 13C enrichment. 13C appearance in the expired air was measured using isotope ratio mass spectrometry, whereas 14C appearance was quantified by trapping expired CO(2) in solution (using hyamine hydroxide) and adding a scintillator before counting radioactivity. CHO(EXO) measured with [13C]glucose ([13C]CHO(EXO)) was significantly greater than CHO(EXO) measured with [14C]glucose ([14C]CHO(EXO)) from 30 to 120 min. There was a 15 +/- 4% difference between [13C]CHO(EXO) and [14C]CHO(EXO) such that the absolute difference increased with the magnitude of CHO(EXO). Further investigations suggest that the difference is not because of losses of CO2 from the trapping solution before counting or an underestimation of the "strength" of the trapping solution. Previous research suggests that the degree of isotopic fractionation is small (S. C. Kalhan, S. M. Savin, and P. A. Adam. J Lab Clin Med89: 285-294, 1977). Therefore, the explanation for the discrepancy in calculated CHO(EXO) remains to be fully understood.

Effect of prolonged exercise and carbohydrate ingestion on type 1 and type 2 T lymphocyte distribution and intracellular cytokine production in humans.

The present study was undertaken to examine the role of the exercise-induced stress hormone response on the regulation of type 1 and type 2 T lymphocyte intracellular cytokine production. Subjects performed 2.5 h of cycling exercise at 65% maximal O2 uptake while ingesting a 6.4% carbohydrate (CHO) solution, 12.8% CHO solution, or a placebo. Peripheral whole blood samples were stimulated and stained for T lymphocyte surface antigens (CD4 and CD8). Cells were then permeabilized, stained for intracellular cytokines, and analyzed using flow cytometry. Exercise resulted in a decrease (P < 0.05) in the number and percentage of IFN-gamma positive CD4+ and CD8+ T lymphocytes. These stimulated cells produced less IFN-gamma immediately postexercise (P < 0.05) and 2-h postexercise (P < 0.05) compared with preexercise. However, CHO ingestion, which attenuated the exercise-induced stress hormone response compared with placebo (P < 0.05), prevented both the decrease in the number and percentage of IFN-gamma-positive CD4+ and CD8+ T lymphocytes and the suppression of IFN-gamma production from stimulated CD4+ and CD8+ T lymphocytes. There was no effect of exercise on the number of, or cytokine production from, IL-4-positive CD4+ or CD8+ T lymphocytes. These data provide support for the role of exercise-induced elevations in stress hormones in the regulation of type 1 T lymphocyte cytokine production and distribution.

Leukocyte heat shock protein expression before and after intensified training.

The purpose of the current research was to test the hypothesis that exercise induced leukocyte heat shock protein (HSP) expression is increased during periods of intensified exercise training. Seven male endurance cyclists carried out tests of maximal oxygen consumption and endurance capacity. These standard exercise tests were carried out prior to and following 6 days of prescribed intensified training. Sampled leukocytes were examined for Hsp27 and Hsp70 expression using a Fluorescence Activated Cell Scanner (EPICS XL, Coulter). During a period of overreaching, as signified by a drop in time to fatigue following the intensified training period (p = 0.02), the number of extracellular Hsp27 positive granulocytes increased in response to the VO(2)max test. Acute, intracellular HSP responses were observed in both baseline and overreached conditions. The present study showed that a period of intensified training caused adaptations in the acute heat shock protein exercise response, reflected by a greater increase of cell surface HSP positive leukocytes following heavy training.

No differences in cycling efficiency between world-class and recreational cyclists.

The aim of this experiment was to compare the efficiency of elite cyclists with that of trained and recreational cyclists. Male subjects (N = 69) performed an incremental exercise test to exhaustion on an electrically braked cycle ergometer. Cadence was maintained between 80 - 90 rpm. Energy expenditure was estimated from measures of oxygen uptake (VO (2)) and carbon dioxide production (VCO(2)) using stoichiometric equations. Subjects (age 26 +/- 7 yr, body mass 74.0 +/- 6.3 kg, Wpeak 359 +/- 40 W and VO(2)peak 62.3 +/- 7.0 mL/kg/min) were divided into 3 groups on the basis of their VO (2)peak (< 60.0 (Low, N = 26), 60 - 70 (Med, N = 27) and > 70 (High, N = 16) mL/kg/min). All data are mean +/- SE. Despite the wide range in aerobic capacities gross efficiency (GE) at 165 W (GE (165)), GE at the same relative intensity (GE (final)), delta efficiency (DE) and economy (EC) were similar between all groups. Mean GE (165) was 18.6 +/- 0.3 %, 18.8 +/- 0.4 % and 17.9 +/- 0.3 % while mean DE was 22.4 +/- 0.4 %, 21.6 +/- 0.4 % and 21.2 +/- 0.5 % (for Low, Medium and High, respectively). There was no correlation between GE (165), GE (final), DE or EC and VO(2)peak. Based on these data, we conclude that there are no differences in efficiency and economy between elite cyclists and recreational level cyclists.

Relation between plasma lactate concentration and fat oxidation rates over a wide range of exercise intensities.

Increasing exercise intensities will induce an increase in glycolytic flux. High glycolytic activity is associated with reduced fat oxidation rates and increased accumulation of lactate. Both lactate and hydrogen ions have been shown to be directly related to the decreased fat oxidation rates. The aim of the present study was to determine whether the exercise intensity at which maximal fat oxidation rates occur coincides with the intensity at which lactate starts to accumulate in plasma. Thirty-three moderately trained endurance athletes performed a graded exercise test to exhaustion on a cycle-ergometer with 35 W increments every three minutes. Expired gas analysis was performed throughout the test and stoichiometric equations were used to calculate fat oxidation rates. The intensity which elicited maximal fat oxidation (Fat (max)) and the intensity at which fat oxidation rates became negligible (Fat (min)) were determined. Blood samples for lactate analysis were collected at the end of each stage of the graded exercise test. The intensity at which lactate concentration increased above baseline (LIAB) and the lactate threshold (LT-D) were determined (D-max method). Fat (max) was located at 63 +/- 9 % V.O (2)max and LIAB at 61 +/- 5 % V.O (2)max and there appeared to be no statistical difference between the two intensities. Fat (max) and LIAB were significantly correlated. Fat (min) and LT-D were also significantly correlated but were located at different intensities (82 +/- 7 and 87 +/- 9 % V.O (2)max respectively). The data of the present study showed that accumulation of lactate in plasma is strongly correlated to the reduction seen in fatty acid oxidation with increasing exercise intensities. The first rise of lactate concentration occurred at the same intensity as the intensity which elicited maximal fat oxidation rates.

Higher dietary carbohydrate content during intensified running training results in better maintenance of performance and mood state.

The aim of this study was to determine whether consumption of a diet containing 8.5 g carbohydrate (CHO) x kg(-1) x day(-1) (high CHO; HCHO) compared with 5.4 g CHO x kg(-1) x day(-1) (control; Con) during a period of intensified training (IT) would result in better maintenance of physical performance and mood state. In a randomized cross-over design, seven trained runners [maximal O(2) uptake (Vo(2 max)) 64.7 +/- 2.6 ml x kg(-1) x min(-1)] performed two 11-day trials consuming either the Con or the HCHO diet. The last week of both trials consisted of IT. Performance was measured with a preloaded 8-km all-out run on the treadmill and 16-km all-out runs outdoors. Substrate utilization was measured using indirect calorimetry and continuous [U-(13)C]glucose infusion during 30 min of running at 58 and 77% Vo(2 max). Time to complete 8 km was negatively affected by the IT: time significantly increased by 61 +/- 23 and 155 +/- 38 s in the HCHO and Con trials, respectively. The 16-km times were significantly increased (by 8.2 +/- 2.1%) during the Con trial only. The Daily Analysis of Life Demands of Athletes questionnaire showed significant deterioration in mood states in both trials, whereas deterioration in global mood scores, as assessed with the Profile of Mood States, was more pronounced in the Con trial. Scores for fatigue were significantly higher in the Con compared with the HCHO trial. CHO oxidation decreased significantly from 1.7 +/- 0.2 to 1.2 +/- 0.2 g/min over the course of the Con trial, which was completely accounted for by a decrease in muscle glycogen oxidation. These findings indicate that an increase in dietary CHO content from 5.4 to 8.5 g CHO x kg(-1)x day(-1) (41 vs. 65% total energy intake, respectively) allowed better maintenance of physical performance and mood state over the course of training, thereby reducing the symptoms of overreaching.

Modulation of carbohydrate and fat utilization by diet, exercise and environment.

At rest and during exercise carbohydrate and fat are the predominant substrates. They are oxidized simultaneously but the relative contribution of these two substrates is dependent on a variety of factors including the exercise intensity and duration, diet, environmental conditions and training status. Changes in carbohydrate metabolism during the transition from rest to exercise and from low- to high-intensity exercise are mainly due to allosteric regulation. The factors that up-regulate fat metabolism in the transition to moderate-intensity exercise and the factors that result in a down-regulation of fat metabolism at higher intensities are incompletely understood. Substrate use is further modulated by the endocrine milieu (e.g. catecholamines, insulin, cortisol) and possibly cytokines (e.g. interleukin-6). With increasing duration of exercise there are marked increases in fat metabolism and decreases in carbohydrate metabolism and this has been ascribed mainly to substrate availability. Both acute food intake and chronic diets also have profound effects on substrate utilization. An increase in carbohydrate intake will rapidly suppress fat metabolism and increase carbohydrate metabolism whereas such an adaptation to a high-fat diet may take several days. The environmental conditions can also alter substrate use; high ambient temperatures can increase glycogen breakdown as a result of increased body core temperature and increased circulation catecholamines. Low temperatures can also increase carbohydrate metabolism, especially when shivering. In addition to these factors adaptation to training, in particular endurance training, will reduce the reliance on carbohydrate metabolism and increase fat oxidation, especially from intramuscular triacylglycerol stores.

Maximal fat oxidation during exercise in trained men.

Fat oxidation increases from low to moderate exercise intensities and decreases from moderate to high exercise intensities. Recently, a protocol has been developed to determine the exercise intensity, which elicits maximal fat oxidation rates (Fat(max)). The main aim of the present study was to establish the reliability of the estimation of Fat(max) using this protocol (n = 10). An additional aim was to determine Fat(max) in a large group of endurance-trained individuals (n = 55). For the assessment of reliability, subjects performed three graded exercise tests to exhaustion on a cycle ergometer. Tests were performed after an overnight fast and diet and exercise regime on the day before all tests were similar. Fifty-five male subjects performed the graded exercise test on one occasion. The typical error (root mean square error and CV) for Fat(max) and Fat(min) was 0.23 and 0.33 l O(2) x min(-1) and 9.6 and 9.4 % respectively. Maximal fat oxidation rates of 0.52 +/- 0.15 g x min(-1) were reached at 62.5 +/- 9.8 % VO(2)max, while Fat(min) was located at 86.1 +/- 6.8 % VO(2)max. When the subjects were divided in two groups according to their VO(2)max, the large spread in Fat(max) and maximal fat oxidation rates remained present. The CV of the estimation of Fat(max) and Fa(min) is 9.0 - 9.5 %. In the present study the average intensity of maximal fat oxidation was located at 63 % VO(2)max. Even within a homogeneous group of subjects, there was a relatively large inter-individual variation in Fat(max) and the rate of maximal fat oxidation.

Effects of pre-exercise ingestion of differing amounts of carbohydrate on subsequent metabolism and cycling performance.

Studies on the effect of the pre-exercise ingestion of carbohydrate on metabolism and performance have produced conflicting results, perhaps because of differences in the designs of the studies. The purpose of the present study was to examine the effects of ingesting differing amounts of glucose pre-exercise on the glucose and insulin responses during exercise and on time-trial (TT) performance. Nine well-trained male cyclists completed four exercise trials separated by at least 3 days. At 45 min before the start of exercise subjects consumed 500 ml of a beverage containing either 0 g (PLAC), 25 g (LOW), 75 g (MED) or 200 g (HIGH) of glucose. The exercise trials consisted of 20 min of submaximal steady-state exercise (SS) at 65% of maximal power output immediately followed by a [mean (SEM)] 691 (12) kJ TT. Plasma insulin concentrations at the onset of exercise were significantly higher ( P<0.05) in MED and HIGH compared with LOW and PLAC. Plasma glucose concentration fell rapidly ( P<0.05) during SS exercise in all glucose trials, but remained steady in PLAC. No difference in plasma glucose concentration was observed between the glucose trials at any time. Hypoglycaemia (less than 3.5 mmol.l(-1)) was observed in six subjects during SS but only after ingesting glucose pre-exercise. However, there was no difference in TT performance between the four trials. The ingestion of 0, 25, 75 or 200 g of glucose 45 min before a 20 min submaximal exercise bout did not affect subsequent TT performance. In addition, mild rebound hypoglycaemia following pre-exercise glucose ingestion did not negatively affect performance.

Effects of pre-exercise ingestion of trehalose, galactose and glucose on subsequent metabolism and cycling performance.

The glycaemic and insulinaemic responses to different carbohydrates vary and these have been suggested to affect performance. The purpose of the present study was to determine the effects of pre-exercise ingestion of glucose (GLU), galactose (GAL) and trehalose (TRE) on metabolic responses at rest and during exercise and on subsequent time-trial (TT) performance. Eight well-trained male cyclists completed three exercise trials separated by at least 3 days. At 45 min before the start of exercise subjects consumed 500 ml of a beverage containing 75 g of either glucose, galactose or trehalose. The exercise trials consisted of 20 min of submaximal steady-state exercise (SS) at 65% of maximal power output immediately followed by a [mean (SEM)] 702 (25) kJ TT. Plasma glucose concentration 15 min postprandial was significantly higher in GLU compared to GAL and TRE ( P<0.05). This was accompanied by a more than twofold greater rise in plasma insulin concentration in GLU compared to GAL and TRE (118% and 145%, respectively). During SS exercise four subjects in GLU and one subject in TRE developed a rebound hypoglycaemia (plasma glucose concentration less than 3.5 mmol.l(-1)). No differences were observed in TT performance between the three trials. Pre-exercise ingestion of trehalose and galactose resulted in lower plasma glucose and insulin responses prior to exercise and reduced the prevalence of rebound hypoglycaemia. Despite the attenuated insulin and glucose responses at rest and during exercise following pre-exercise ingestion of galactose and trehalose, there was no difference in TT performance compared with pre-exercise ingestion of glucose.

Effects of oral creatine supplementation on high intensity, intermittent exercise performance in competitive squash players.

The purpose of this study was to determine the effects of oral creatine supplementation on high intensity, intermittent exercise performance in competitive squash players. Nine squash players (mean +/- SEM VO2max = 61.9 +/- 2.1 ml x kg(-1) x min(-1); body mass = 73 +/- 3 kg) performed an on-court "ghosting" routine that involved 10 sets of 2 repetitions of simulated positional play, each set interspersed with 30 s passive recovery. A double blind, crossover design was utilised whereby experimental and control groups supplemented 4 times daily for 5 d with 0.075 g x kg(-1) body mass of creatine monohydrate and maltodextrine, respectively, and a 4 wk washout period separated the crossover of treatments. The experimental group improved mean set sprint time by 3.2 +/- 0.8% over and above the changes noted for the control group (P = 0.004 and 95% Cl = 1.4 to 5.1%). Sets 2 to 10 were completed in a significantly shorter time following creatine supplementation compared to the placebo condition (P < 0.05). In conclusion, these data support existing evidence that creatine supplementation improves high intensity, intermittent exercise performance. In addition, the present study provides new evidence that oral creatine supplementation improves exercise performance in competitive squash players.