The effect of pre-exercise galactose and glucose ingestion on high-intensity endurance cycling.

This study evaluated the effects of the pre-exercise (30 minutes) ingestion of galactose (Gal) or glucose (Glu) on endurance capacity as well as glycemic and insulinemic responses. Ten trained male cyclists completed 3 randomized high-intensity cycling endurance tests. Thirty minutes before each trial, cyclists ingested 1 L of either 40 g of glucose, 40 g of galactose, or a placebo in a double-blind manner. The protocol comprised 20 minutes of progressive incremental exercise (70-85% maximal power output [Wmax]); ten 90-second bouts at 90% Wmax, separated by 180 seconds at 55% Wmax; and 90% Wmax until exhaustion. Blood samples were drawn throughout the protocol. Times to exhaustion were longer with Gal (68.7 ± 10.2 minutes, p = 0.005) compared with Glu (58.5 ± 24.9 minutes), with neither being different to placebo (63.9 ± 16.2 minutes). Twenty-eight minutes after Glu consumption, plasma glucose and serum insulin concentrations were higher than with Gal and placebo (p < 0.001). After the initial 20 minutes of exercise, plasma glucose concentrations increased to a relative hyperglycemia during the Gal and placebo, compared with Glu condition. Higher plasma glucose concentrations during exercise, and the attenuated serum insulin response at rest, may explain the significantly longer times to exhaustion produced by Gal compared with Glu. However, neither carbohydrate treatment produced significantly longer times to exhaustion than placebo, suggesting that the pre-exercise ingestion of galactose and glucose alone is not sufficient to support this type of endurance performance

The effect of pre-exercise galactose and glucose ingestion on high-intensity endurance cycling.

This study evaluated the effects of the pre-exercise (30 minutes) ingestion of galactose (Gal) or glucose (Glu) on endurance capacity as well as glycemic and insulinemic responses. Ten trained male cyclists completed 3 randomized high-intensity cycling endurance tests. Thirty minutes before each trial, cyclists ingested 1 L of either 40 g of glucose, 40 g of galactose, or a placebo in a double-blind manner. The protocol comprised 20 minutes of progressive incremental exercise (70-85% maximal power output [Wmax]); ten 90-second bouts at 90% Wmax, separated by 180 seconds at 55% Wmax; and 90% Wmax until exhaustion. Blood samples were drawn throughout the protocol. Times to exhaustion were longer with Gal (68.7 ± 10.2 minutes, p = 0.005) compared with Glu (58.5 ± 24.9 minutes), with neither being different to placebo (63.9 ± 16.2 minutes). Twenty-eight minutes after Glu consumption, plasma glucose and serum insulin concentrations were higher than with Gal and placebo (p < 0.001). After the initial 20 minutes of exercise, plasma glucose concentrations increased to a relative hyperglycemia during the Gal and placebo, compared with Glu condition. Higher plasma glucose concentrations during exercise, and the attenuated serum insulin response at rest, may explain the significantly longer times to exhaustion produced by Gal compared with Glu. However, neither carbohydrate treatment produced significantly longer times to exhaustion than placebo, suggesting that the pre-exercise ingestion of galactose and glucose alone is not sufficient to support this type of endurance performance

The effects of low and high glycemic index foods on exercise performance and beta-endorphin responses

Τhe aim of this study was to examine the effects of the consumption of foods of various glycemic index values on performance, β-endorphin levels and substrate (fat and carbohydrate) utilization during prolonged exercise. Eight untrained healthy males underwent, in a randomized counterbalanced design, three experimental conditions under which they received carbohydrates (1.5 gr. kg-1 of body weight) of low glycemic index (LGI), high glycemic index (HGI) or placebo. Food was administered 30 min prior to exercise. Subjects cycled for 60 min at an intensity corresponding to 65% of VO2max, which was increased to 90% of VO2max, then they cycled until exhaustion and the time to exhaustion was recorded. Blood was collected prior to food consumption, 15 min prior to exercise, 0, 20, 40, and 60 min into exercise as well as at exhaustion. Blood was analyzed for β-endorphin, glucose, insulin, and lactate. The mean time to exhaustion did not differ between the three conditions (LGI = 3.2 ± 0.9 min; HGI = 2.9 ± 0.9 min; placebo = 2.7 ± 0.7 min). There was a significant interaction in glucose and insulin response (P < 0.05) with HGI exhibiting higher values before exercise. β-endorphin increased significantly (P < 0.05) at the end of exercise without, however, a significant interaction between the three conditions. Rate of perceived exertion, heart rate, ventilation, lactate, respiratory quotient and substrate oxidation rate did not differ between the three conditions. The present study indicates that ingestion of foods of different glycemic index 30 min prior to one hour cycling exercise does not result in significant changes in exercise performance, β-endorphin levels as well as carbohydrate and fat oxidation during exercise

Preexercise glucose ingestion and glucose kinetics during exercise

The present study was undertaken to examine the effects of glucose ingestion before exercise on liver glucose output and muscle glucose uptake during exercise. On two occasions, at least 1 wk apart, six trained men (peak pulmonary O2 uptake = 5.11 +/- 0.17 l/min) ingested 400 ml of a solution containing either 75 g glucose [carbohydrate (CHO)] or a sweet placebo [control (Con)] 30 min before 60 min of exercise at 71 +/- 1% peak pulmonary O2 uptake. Glucose kinetics (rates of appearance and disappearance) were measured by a primed continuous infusion of [6,6–2H2]glucose. Liver glucose output was derived from total glucose appearance and the appearance of ingested glucose from the gut. After glucose ingestion, plasma glucose increased to 6.4 +/- 0.4 mmol/l immediately before exercise, fell to 4.2 +/- 0.5 mmol/l after 20 min of exercise, and then increased to a higher value than in the Con group (5.4 +/- 0.3 vs. 4.7 +/- 0.1 mmol/l; P &lt; 0.05) after 60 min of exercise. In the CHO group, plasma insulin was higher immediately before exercise (P &lt; 0.05) and, despite falling during exercise, remained higher than in the Con group after 60 min of exercise (57.0 +/- 11.4 vs. 24.8 +/- 1.7 pmol/l; P &lt; 0.05). The rapid fall in plasma glucose in the CHO group was the result of a higher muscle glucose uptake with the onset of exercise (P &lt; 0.05), which could not be matched by the glucose rate of appearance. Liver glucose output was decreased by glucose ingestion, and although it increased during the early stages of exercise in the CHO group, it did not rise above the basal values and was reduced by 62% over the 60 min of exercise compared with the Con group. In summary, preexercise glucose ingestion results in increased muscle glucose uptake and reduced liver glucose output during exercise. </jats:p

Ro 31-6045, the inactive analogue of the protein kinase C inhibitor Ro 31-8220, blocks in vivo activation of p70s6k/p85s6k: implications for the analysis of S6K signalling

AbstractThe mitogen-stimulated protein kinase p70s6k/p85s6k (S6K) plays an essential role in cell proliferation and growth, with inhibitors of the S6K signalling pathway showing promise as anti-tumour therapeutics. Here, we report that the bisindolylmaleimide derivative Ro 31-6045, previously reported to be inactive as a kinase inhibitor, inhibited S6K activity in vivo with an IC50=8 μM. Structure/function analysis using mutant forms of S6K indicates that Ro 31-6045 inhibition is independent of the upstream activator mTOR. Ro 31-6045 will prove useful in elucidating the complex activation mechanism of S6K and its independence from mTOR will allow confirmation of functional data obtained using the mTOR inhibitor rapamycin