Probiotic supplementation increases carbohydrate metabolism in trained male cyclists: a randomized, double-blind, placebo-controlled crossover trial.

We hypothesized that probiotic supplementation (PRO) increases the absorption and oxidation of orally ingested maltodextrin during 2 h endurance cycling, thereby sparing muscle glycogen for a subsequent time trial (simulating a road race). Measurements were made of lipid and carbohydrate oxidation, plasma metabolites and insulin, gastrointestinal (GI) permeability, and subjective symptoms of discomfort. Seven male cyclists were randomized to PRO (bacterial composition given in methods) or placebo for 4 wk, separated by a 14-day washout period. After each period, cyclists consumed a 10% maltodextrin solution (initial 8 mL/kg bolus and 2 mL/kg every 15 min) while exercising for 2 h at 55% maximal aerobic power output, followed by a 100-kJ time trial. PRO resulted in small increases in peak oxidation rates of the ingested maltodextrin (0.84 ± 0.10 vs. 0.77 ± 0.09 g/min; P = 0.016) and mean total carbohydrate oxidation (2.20 ± 0.25 vs. 1.87 ± 0.39 g/min; P = 0.038), whereas fat oxidation was reduced (0.40 ± 0.11 vs. 0.55 ± 0.10 g/min; P = 0.021). During PRO, small but significant increases were seen in glucose absorption, plasma glucose, and insulin concentration and decreases in nonesterified fatty acid and glycerol. Differences between markers of GI damage and permeability and time-trial performance were not significant (P > 0.05). In contrast to the hypothesis, PRO led to minimal increases in absorption and oxidation of the ingested maltodextrin and small reductions in fat oxidation, whereas having no effect on subsequent time-trial performance.

Passive heat therapy in sedentary humans increases skeletal muscle capillarization and eNOS content but not mitochondrial density or GLUT4 content.

Passive heat therapy (PHT) has been proposed as an alternative intervention to moderate-intensity continuous training (MICT) in individuals who are unable or unwilling to exercise. This study aimed to make the first comparison of the effect of PHT and MICT on 1) skeletal muscle capillarization and endothelial-specific endothelial nitric oxide synthase (eNOS) content and 2) mitochondrial density, glucose transporter 4 (GLUT4), and intramuscular triglyceride (IMTG) content. Twenty young sedentary males (21 ± 1 yr, body mass index 25 ± 1 kg/m2) were allocated to either 6 wk of PHT (n = 10; 40-50 min at 40°C in a heat chamber, 3×/wk) or MICT (n = 10; time-matched cycling at ~65% V̇o2peak). Muscle biopsies were taken from the vastus lateralis muscle before and after training. Immunofluorescence microscopy was used to assess changes in skeletal muscle mitochondrial density (mitochondrial marker cytochrome c oxidase subunit 4), GLUT4, and IMTG content, capillarization, and endothelial-specific eNOS content. V̇o2peak and whole body insulin sensitivity were also assessed. PHT and MICT both increased capillary density (PHT 21%; MICT 12%), capillary-fiber perimeter exchange index (PHT 15%; MICT 12%) (P < 0.05), and endothelial-specific eNOS content (PHT 8%; MICT 12%) (P < 0.05). However, unlike MICT (mitochondrial density 40%; GLUT4 14%; IMTG content 70%) (P < 0.05), PHT did not increase mitochondrial density (11%, P = 0.443), GLUT4 (7%, P = 0.217), or IMTG content (1%, P = 0.957). Both interventions improved aerobic capacity (PHT 5%; MICT 7%) and whole body insulin sensitivity (PHT 15%; MICT 36%) (P < 0.05). Six-week PHT in young sedentary males increases skeletal muscle capillarization and eNOS content to a similar extent as MICT; however, unlike MICT, PHT does not affect skeletal muscle mitochondrial density, GLUT4, or IMTG content. NEW & NOTEWORTHY The effect of 6-wk passive heat therapy (PHT) compared with moderate-intensity continuous training (MICT) was investigated in young sedentary males. PHT induced similar increases in skeletal muscle capillarization and endothelial-specific endothelial nitric oxide synthase content to MICT. Unlike MICT, PHT did not improve skeletal muscle mitochondrial density, glucose transporter 4, or intramuscular triglyceride content. These microvascular adaptations were paralleled by improvements in V̇o2peak and insulin sensitivity, suggesting that microvascular adaptations may contribute to functional improvements following PHT.

Co-ingestion of leucine with protein does not further augment post-exercise muscle protein synthesis rates in elderly men.

Leucine has been suggested to have the potential to modulate muscle protein metabolism by increasing muscle protein synthesis. The objective of this study was to investigate the surplus value of the co-ingestion of free leucine with protein hydrolysate and carbohydrate following physical activity in elderly men. Eight elderly men (mean age 73 +/- 1 years) were randomly assigned to two cross-over treatments consuming either carbohydrate and protein hydrolysate (CHO+PRO) or carbohydrate, protein hydrolysate with additional leucine (CHO+PRO+leu) after performing 30 min of standardized physical activity. Primed, continuous infusions with L-[ring-(13)C(6)]phenylalanine and L-[ring-(2)H(2)]tyrosine were applied, and blood and muscle samples were collected to assess whole-body protein turnover as well as protein fractional synthetic rate in the vastus lateralis muscle over a 6 h period. Whole-body protein breakdown and synthesis rates were not different between treatments. Phenylalanine oxidation rates were significantly lower in the CHO+PRO+leu v. CHO+PRO treatment. As a result, whole-body protein balance was significantly greater in the CHO+PRO+leu compared to the CHO+PRO treatment (23.8 (SEM 0.3) v. 23.2 (SEM 0.3) micromol/kg per h, respectively; P < 0.05). Mixed muscle fractional synthetic rate averaged 0.081 (SEM 0.003) and 0.082 (SEM 0.006) %/h in the CHO+PRO+leu and CHO+PRO treatment, respectively (NS). Co-ingestion of leucine with carbohydrate and protein following physical activity does not further elevate muscle protein fractional synthetic rate in elderly men when ample protein is ingested.

Combined ingestion of protein and carbohydrate improves protein balance during ultra-endurance exercise.

The aims of this study were to compare different tracer methods to assess whole body protein turnover during 6 h of prolonged endurance exercise when carbohydrate was ingested throughout the exercise period and to investigate whether addition of protein can improve protein balance. Eight endurance-trained athletes were studied on two different occasions at rest (4 h), during 6 h of exercise at 50% of maximal O2 uptake (in sequential order: 2.5 h of cycling, 1 h of running, and 2.5 h of cycling), and during subsequent recovery (4 h). Subjects ingested carbohydrate (CHO trial; 0.7 g CHO.kg(-1.)h(-1)) or carbohydrate/protein beverages (CHO + PRO trial; 0.7 g CHO.kg(-1).h(-1) and 0.25 g PRO.kg(-1).h(-1)) at 30-min intervals during the entire study. Whole body protein metabolism was determined by infusion of L-[1-13C]leucine, L-[2H5]phenylalanine, and [15N2]urea tracers with sampling of blood and expired breath. Leucine oxidation increased from rest to exercise [27 +/- 2.5 vs. 74 +/- 8.8 (CHO) and 85 +/- 9.5 vs. 200 +/- 16.3 mg protein.kg(-1).h(-1) (CHO + PRO), P < 0.05], whereas phenylalanine oxidation and urea production did not increase with exercise. Whole body protein balance during exercise with carbohydrate ingestion was negative (-74 +/- 8.8, -17 +/- 1.1, and -72 +/- 5.7 mg protein.kg(-1).h(-1)) when L-[1-13C]leucine, L-[2H5]phenylalanine, and [15N2]urea, respectively, were used as tracers. Addition of protein to the carbohydrate drinks resulted in a positive or less-negative protein balance (-32 +/- 16.3, 165 +/- 4.6, and 151 +/- 13.4 mg protein.kg(-1).h(-1)) when L-[1-13C]leucine, L-[2H5]phenylalanine, and [15N2]urea, respectively, were used as tracers. We conclude that, even during 6 h of exhaustive exercise in trained athletes using carbohydrate supplements, net protein oxidation does not increase compared with the resting state and/or postexercise recovery. Combined ingestion of protein and carbohydrate improves net protein balance at rest as well as during exercise and postexercise recovery.

Creatine supplementation increases glycogen storage but not GLUT-4 expression in human skeletal muscle.

It has been speculated that creatine supplementation affects muscle glucose metabolism in humans by increasing muscle glycogen storage and up-regulating GLUT-4 protein expression. In the present study, we assessed the effects of creatine loading and prolonged supplementation on muscle glycogen storage and GLUT-4 mRNA and protein content in humans. A total of 20 subjects participated in a 6-week supplementation period during which creatine or a placebo was ingested. Muscle biopsies were taken before and after 5 days of creatine loading (20 g.day(-1)) and after 6 weeks of continued supplementation (2 g.day(-1)). Fasting plasma insulin concentrations, muscle creatine, glycogen and GLUT-4 protein content as well as GLUT-4, glycogen synthase-1 (GS-1) and glycogenin-1 (Gln-1) mRNA expression were determined. Creatine loading significantly increased total creatine, free creatine and creatine phosphate content with a concomitant 18 +/- 5% increase in muscle glycogen content (P<0.05). The subsequent use of a 2 g.day(-1) maintenance dose for 37 days did not maintain total creatine, creatine phosphate and glycogen content at the elevated levels. The initial increase in muscle glycogen accumulation could not be explained by an increase in fasting plasma insulin concentration, muscle GLUT-4 mRNA and/or protein content. In addition, neither muscle GS-1 nor Gln-1 mRNA expression was affected. We conclude that creatine ingestion itself stimulates muscle glycogen storage, but does not affect muscle GLUT-4 expression.

Effects of creatine loading and prolonged creatine supplementation on body composition, fuel selection, sprint and endurance performance in humans.

Most research on creatine has focused on short-term creatine loading and its effect on high-intensity performance capacity. Some studies have investigated the effect of prolonged creatine use during strength training. However, studies on the effects of prolonged creatine supplementation are lacking. In the present study, we have assessed the effects of both creatine loading and prolonged supplementation on muscle creatine content, body composition, muscle and whole-body oxidative capacity, substrate utilization during submaximal exercise, and on repeated supramaximal sprint, as well as endurance-type time-trial performance on a cycle ergometer. Twenty subjects ingested creatine or a placebo during a 5-day loading period (20 g.day(-1)) after which supplementation was continued for up to 6 weeks (2 g.day(-1)). Creatine loading increased muscle free creatine, creatine phosphate (CrP) and total creatine content ( P <0.05). The subsequent use of a 2 g.day(-1) maintenance dose, as suggested by an American College of Sports Medicine Roundtable, resulted in a decline in both the elevated CrP and total creatine content and maintenance of the free creatine concentration. Both short- and long-term creatine supplementation improved performance during repeated supramaximal sprints on a cycle ergometer. However, whole-body and muscle oxidative capacity, substrate utilization and time-trial performance were not affected. The increase in body mass following creatine loading was maintained after 6 weeks of continued supplementation and accounted for by a corresponding increase in fat-free mass. This study provides definite evidence that prolonged creatine supplementation in humans does not increase muscle or whole-body oxidative capacity and, as such, does not influence substrate utilization or performance during endurance cycling exercise. In addition, our findings suggest that prolonged creatine ingestion induces an increase in fat-free mass.