Glycogen Resynthesis Research Articles

Supplementation Strategies for Strength and Power Athletes: Carbohydrate, Protein, and Amino Acid Ingestion.

It is a common belief amongst strength and power athletes that nutritional supplementation strategies aid recovery by shifting the anabolic/catabolic profile toward anabolism. Factors such as nutrient quantity, nutrient quality, and nutrient timing significantly impact upon the effectiveness of nutritional strategies in optimizing the acute responses to resistance exercise and the adaptive response to resistance training (i.e., muscle growth and strength expression). Specifically, the aim of this review is to address carbohydrates (CHOs), protein (PRO), and/or amino acids (AAs) supplementation strategies, as there is growing evidence suggesting a link between nutrient signaling and the initiation of protein synthesis, muscle glycogen resynthesis, and the attenuation of myofibrillar protein degradation following resistance exercise. Collectively, the current scientific literature indicates that nutritional supplementation strategies utilizing CHO, PRO, and/or AA represents an important approach aimed at enhancing muscular responses for strength and power athletes, primarily increased muscular hypertrophy and enhanced strength expression. There appears to be a critical interaction between resistance exercise and nutrient-cell signaling associated with the principle of nutrient timing (i.e., pre-exercise, during, and post-exercise). Recommendations for nutritional supplementation strategies to promote muscular responses for strength and athletes are provided.

Decreased pancreatic amylase activity after acute high-intensity exercise and its effects on post-exercise muscle glycogen recovery.

Our prior results showed that an acute bout of endurance exercise for 6h, but not 1h, decreased pancreatic amylase activity, indicating that acute endurance exercise may affect carbohydrate digestive capacity in an exercise duration-dependent manner. Here, we investigated the effects of acute endurance exercise of different intensities on mouse pancreatic amylase activity. Male C57BL/6J mice performed low- or high-intensity running exercise for 60min at either 10 (Ex-Low group) or 20m/min (Ex-High group). The control group comprised sedentary mice. Immediately after acute exercise, pancreatic amylase activity was significantly decreased in the Ex-High group and not the Ex-Low group in comparison with the control group. To determine whether the decreased amylase activity induced by high-intensity exercise influenced muscle glycogen recovery after exercise, we investigated the rates of muscle glycogen resynthesis in Ex-High group mice administered either oral glucose or starch solution (2.0mg/g body weight) immediately after exercise. The starch-fed mice exhibited significantly lower post-exercise glycogen accumulation rates in the 2-h recovery period compared with the glucose-fed mice. This difference in the glycogen accumulation rate was absent for starch- and glucose-fed mice in the sedentary (no exercise) control group. Furthermore, the plasma glucose AUC during early post-exercise recovery (0-60min) was significantly lower in the starch-fed mice than in the glucose-fed mice. Thus, our findings suggest that acute endurance exercise diminishes the carbohydrate digestive capacity of the pancreas in a manner dependent on exercise intensity, with polysaccharides leading to delayed muscle glycogen recovery after exercise.

Ketone Monoester Followed by Carbohydrate Ingestion after Glycogen-Lowering Exercise Does Not Improve Subsequent Endurance Cycle Time Trial Performance.

Relative to carbohydrate (CHO) alone, exogenous ketones followed by CHO supplementation during recovery from glycogen-lowering exercise have been shown to increase muscle glycogen resynthesis. However, whether this strategy improves subsequent exercise performance is unknown. The objective of this study was to assess the efficacy of ketone monoester (KME) followed by CHO ingestion after glycogen-lowering exercise on subsequent 20 km (TT20km) and 5 km (TT5km) best-effort time trials. Nine recreationally active men (175.6 ± 5.3 cm, 72.9 ± 7.7 kg, 28 ± 5 y, 12.2 ± 3.2% body fat, VO2max = 56.2 ± 5.8 mL· kg BM-1·min-1; mean ± SD) completed a glycogen-lowering exercise session, followed by 4 h of recovery and subsequent TT20km and TT5km. During the first 2 h of recovery, participants ingested either KME (25 g) followed by CHO at a rate of 1.2 g·kg-1·h-1 (KME + CHO) or an iso-energetic placebo (dextrose) followed by CHO (PLAC + CHO). Blood metabolites during recovery and performance during the subsequent two-time trials were measured. In comparison to PLAC + CHO, KME + CHO displayed greater (p < 0.05) blood beta-hydroxybutyrate concentration during the first 2 h, lower (p < 0.05) blood glucose concentrations at 30 and 60 min, as well as greater (p < 0.05) blood insulin concentration 2 h following ingestion. However, no treatment differences (p > 0.05) in power output nor time to complete either time trial were observed vs. PLAC + CHO. These data indicate that the metabolic changes induced by KME + CHO ingestion following glycogen-lowering exercise are insufficient to enhance subsequent endurance time trial performance.

A novel genetic model provides a unique perspective on the relationship between postexercise glycogen concentration and increases in the abundance of key metabolic proteins after acute exercise.

Some acute exercise effects are influenced by postexercise (PEX) diet, and these diet-effects are attributed to differential glycogen resynthesis. However, this idea is challenging to test rigorously. Therefore, we devised a novel genetic model to modify muscle glycogen synthase 1 (GS1) expression in rat skeletal muscle with an adeno-associated virus (AAV) short hairpin RNA knockdown vector targeting GS1 (shRNA-GS1). Contralateral muscles were injected with scrambled shRNA (shRNA-Scr). Muscles from exercised (2-hour-swim) and time-matched sedentary (Sed) rats were collected immediately postexercise (IPEX), 5-hours-PEX (5hPEX), or 9-hours-PEX (9hPEX). Rats in 5hPEX and 9hPEX experiments were refed (RF) or not-refed (NRF) chow. Muscles were analyzed for glycogen, abundance of metabolic proteins (pyruvate dehydrogenase kinase 4, PDK4; peroxisome proliferator-activated receptor γ coactivator-1α, PGC1α; hexokinase II, HKII; glucose transporter 4, GLUT4), AMP-activated protein kinase phosphorylation (pAMPK), and glycogen metabolism-related enzymes (glycogen phosphorylase, PYGM; glycogen debranching enzyme, AGL; glycogen branching enzyme, GBE1). shRNA-GS1 versus paired shRNA-Scr muscles had markedly lower GS1 abundance. IPEX versus Sed rats had lower glycogen and greater pAMPK, and neither of these IPEX-values differed for shRNA-GS1 versus paired shRNA-Scr muscles. IPEX versus Sed groups did not differ for abundance of metabolic proteins, regardless of GS1 knockdown. Glycogen in RF-rats was lower for shRNA-GS1 versus paired shRNA-Scr muscles at both 5hPEX and 9hPEX. HKII protein abundance was greater for 5hPEX versus Sed groups, regardless of GS1 knockdown or diet, and despite differing glycogen levels. At 9hPEX, shRNA-GS1 versus paired shRNA-Scr muscles had greater PDK4 and PGC1α abundance within each diet group. However, the magnitude of PDK4 or PGC1α changes was similar in each diet group regardless of GS1 knockdown although glycogen differed between paired muscles only in RF-rats. In summary, we established a novel genetic approach to investigate the relationship between muscle glycogen and other exercise effects. Our results suggest that exercise-effects on abundance of several metabolic proteins did not uniformly correspond to differences in postexercise glycogen.

Hydration, Hyperthermia, Glycogen, and Recovery: Crucial Factors in Exercise Performance-A Systematic Review and Meta-Analysis.

Hyperthermia accelerates dehydration and can lead to a glycolysis malfunction. Therefore, to deeply understand the relationship between dehydration and hyperthermia during exercise, as well as in the recovery time, there might be important factors to improve athletic performance. A systematic review was carried out in different databases using the words "hydration" OR "dehydration" AND "glycogen" OR "glycogenesis" OR "glycogenolysis" AND "muscle" OR "muscle metabolism" OR "cardiovascular system" and adding them to the "topic section" in Web of Science, to "Title/Abstract" in PubMed and to "Abstract" in SPORTDiscus. A total of 18 studies were included in the review and 13 in the meta-analysis. The free statistical software Jamovi was used to run the meta-analysis (version 1.6.15). A total sample of 158 people was included in the qualitative analysis, with a mean age of 23.5 years. Ten studies compared muscle glycogen content after hydration vs. remaining dehydrated (SMD -4.77 to 3.71, positive 80% of estimates, \hat{\mu} = 0.79 (95% CI: -0.54 to 2.12), z = 1.17, p = 0.24, Q-test (Q(9) = 66.38, p < 0.0001, tau2 = 4.14, I2 = 91.88%). Four studies examined the effect of temperature on postexercise muscle glycogen content (SMD -3.14 to -0.63, 100% of estimates being negative, \hat{\mu} = -1.52 (95% CI: -2.52 to -0.53), (z = -3.00, p = 0.003, Q-test (Q(3) = 8.40, p = 0.038, tau2 = 0.68, I2 = 66.81%). In conclusion, both hyperthermia and dehydration may contribute to elevated glycogenolysis during exercise and poor glycogen resynthesis during recovery. Although core and muscle hyperthermia are the key factors in glycogen impairments, they are also directly related to dehydration.

588-P: Probing the Role of Muscle Glycogen Resynthesis on Postexercise AMPK Activation and Metabolic Protein Abundance Using a Novel Genetic Model

Acute exercise can alter the abundance of key metabolic proteins in skeletal muscle. These effects are influenced by postexercise (PEX) refeeding. Muscle glycogen resynthesis is a putative mediator of these refeeding effects. However, it is challenging to test this idea, because glycogen resynthesis is only one of many outcomes with refeeding. Therefore, we devised a novel genetic model to modify muscle expression of glycogen synthase 1 (GS1) using injection of rat skeletal muscle with adeno-associated viral (AAV) vectors for short hairpin RNA targeting GS1 (shRNA-GS1). Contralateral muscles were injected with scrambled shRNA (shRNA-Scr). Rats were sedentary (SED) or exercised (120min swim-exercise). Muscles were collected immediately postexercise (IPEX) and 9-hours PEX (9hPEX), along with time-matched SED controls. The 9hPEX and their SED-control rats were either refed (RF) or not-refed (NRF). Muscles were analyzed for glycogen and phosphorylation and abundance of key metabolic proteins. Muscles injected with shRNA-GS1 vs shRNA-Scr had lower GS1 abundance in all groups. Regardless of genotype, in IPEX vs SED rats: glycogen fell to similarly low values and phosphorylation of AMPK Thr172 (pAMPK) and its substrate ACC Ser79 (pACC) were comparably increased. Muscle glycogen was increased in all groups of 9h-RF rats, but it was lower for shRNA-GS1 vs shRNA-Scr from RF-9hPEX rats. In the NRF-9hPEX rats, pAMPK and pACC were greater for shRNA-GS1 vs shRNA-Scr muscles. Muscle pyruvate dehydrogenase kinase-4 abundance from 9hPEX rats (both NRF and RF) was greater for shRNA-GS1 vs shRNA-Scr. Hexokinase II (HKII) abundance was greater for 9hPEX vs SED in NRF rats regardless of genotype. In RF-9hPEX rats, HKII abundance was greater for shRNA-GS1 vs shRNA-Scr. These results support the idea that some PEX effects on metabolic protein abundance are influenced by muscle GS1 abundance and the extent of glycogen resynthesis Disclosure S.Kwak: None. A.Zheng: None. E.B.Arias: None. H.Wang: None. X.Pan: None. D.Duan: None. Y.Yue: None. G.D.Cartee: None. Funding National Institutes of Health (R01DK071771); University of Michigan

Fenugreek and Its Effects on Muscle Performance: A Systematic Review.

Fenugreek extracts possess promising physiological and pharmacological properties in human and animal models. This review aims to provide a scientific and comprehensive analysis of the literature on the effects of fenugreek extracts on muscle performance. An extensive online search was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement guidelines. The main medical and scientific engines were searched for articles from May 1981 to May 2021 to capture all scientific studies focused on the effect of fenugreek on muscle and exercise or sport. Out of 81 studies acquired, six eligible randomized controlled trials (RCTs) were included in the qualitative analysis. Four RCTs observed that fenugreek supplementation had significantly improved muscle strength, repetitions to failure (muscle endurance), submaximal performance index, lean body mass, and reduced body fat. Among the remaining two trials, one reported the significant effect of fenugreek extracts on the rate of muscle glycogen resynthesis during post-exercise recovery; however, the other failed to do so. Those two trials were weak, with a minimal sample size (<10). Further, fenugreek glycoside supplementation with sapogenins and saponins reported substantial anabolic and androgenic activity, influencing testosterone levels and muscle performance. It was useful during eight weeks of resistance training without any clinical side effects. Fenugreek with creatine supplementation improved creatine uptake without the necessity of high carbohydrate intake. Hence, fenugreek extracts can be a helpful natural supplement and ergogenic aid for athletes. However, it is better to be aware of doping and liver and kidney damage before using the fenugreek supplement.

Energy expenditure, dietary intake and energy availability in female professional football players

ObjectivesTo quantify energy expenditure and intake in professional female footballers playing on a national and/or international level. Second, to determine the prevalence of low energy availability among these players, defined...

Insulin Sensitization Following a Single Exercise Bout Is Uncoupled to Glycogen in Human Skeletal Muscle: A Meta-analysis of 13 Single-Center Human Studies.

Exercise profoundly influences glycemic control by enhancing muscle insulin sensitivity, thus promoting glucometabolic health. While prior glycogen breakdown so far has been deemed integral for muscle insulin sensitivity to be potentiated by exercise, the mechanisms underlying this phenomenon remain enigmatic. We have combined original data from 13 of our studies that investigated insulin action in skeletal muscle either under rested conditions or following a bout of one-legged knee extensor exercise in healthy young male individuals (n = 106). Insulin-stimulated glucose uptake was potentiated and occurred substantially faster in the prior contracted muscles. In this otherwise homogenous group of individuals, a remarkable biological diversity in the glucometabolic responses to insulin is apparent both in skeletal muscle and at the whole-body level. In contrast to the prevailing concept, our analyses reveal that insulin-stimulated muscle glucose uptake and the potentiation thereof by exercise are not associated with muscle glycogen synthase activity, muscle glycogen content, or degree of glycogen utilization during the preceding exercise bout. Our data further suggest that the phenomenon of improved insulin sensitivity in prior contracted muscle is not regulated in a homeostatic feedback manner from glycogen. Instead, we put forward the idea that this phenomenon is regulated by cellular allostatic mechanisms that elevate the muscle glycogen storage set point and enhance insulin sensitivity to promote the uptake of glucose toward faster glycogen resynthesis without development of glucose overload/toxicity or feedback inhibition.

Exercise and emersion in air, and recovery in seawater in the green crab (Carcinus maenas): metabolic, acid-base, cardio-ventilatory and ionoregulatory responses.

In nature, the green crab exhibits emersion and terrestrial activity at low tide. Treadmill exercise in air (20-23°C) of crabs acclimated to 32ppt seawater (13°C) revealed an inverse relationship between velocity and duration: 2.0 body lengths (BL) s-1 was sustainable for several minutes, and 0.25BLs-1 was sustainable for long periods. Fatigue was not due to dehydration. Physiological responses over an 18h recovery in seawater after near-exhaustive exercise (0.25BLs-1, 1 h) in air were compared with responses after quiet emersion (1 h) in air. Exercising crabs exhibited transient scaphognathite slowing and progressive increases in heart rate, whereas emersed crabs exhibited persistent inhibition of ventilation and transient heart slowing. Upon return to seawater, all these rates increased above both control and treatment levels. Post-exercise disturbances were more marked and/or longer lasting (e.g. EPOC, hyperventilation, tachycardia, metabolic acidosis, lactate elevation, ionic disturbances) than those after simple air exposure. However, an increase in net acidic equivalent excretion to the environment occurred after emersion but not after exercise. Instead, post-exercise crabs relied on carapace buffering, signalled by elevated haemolymph Ca2+ and Mg2+. Prolonged lowering of haemolymph PCO2associated with hyperventilation also played a key role in acid-base recovery. EPOC after exercise was 3-fold greater than after emersion, sufficient to support resting ṀO2for >14 h. This reflected clearance of a large lactate load, likely by glycogen re-synthesis rather than oxidation. We conclude that the amphibious green crab uses a combination of aquatic and terrestrial strategies to support exercise in air, emersion in air and recovery in seawater.

Contrast With Compression Therapy Enhances Muscle Function Recovery and Attenuates Glycogen Disruption After Exercise.

Exercise-associated muscle damage (EAMD) temporally impairs muscle function and intramuscular glycogen storage. Contrast with compression (CwC) therapy provides localized EAMD treatment with minimal changes in core/tissue temperature that can impair glycogen resynthesis. CwC will enhance the recovery of strength, power, and joint mobility, reduce markers of EAMD, and attenuate the disruption of glycogen storage observed after damaging exercise. Randomized controlled trial with crossover design. Level 2. Ten men completed 2 bouts of eccentric elbow flexor exercise, separated by 1 week, using contralateral arms. After each bout, participants received either CwC therapy (at 0, 24, and 48 h postexercise) or no therapy with intervention order and limb randomly assigned. Prior to (pre-exercise) and 1, 24, 48, and 72 h after each exercise bout, muscular strength, muscular power, intramuscular glycogen, creatine kinase, muscle thickness, muscle soreness, pressure pain threshold, active elbow flexion, passive elbow extension, and dietary intake were assessed. Comparisons were made between conditions over time (interaction effects) using separate repeated-measures analyses of variance/multivariate analyses of variance and effect sizes (Cohen d) to describe treatment effect at each time point. Significant interaction effects were observed for muscular strength (d = 0.67-1.12), muscular power (d = 0.20-0.65), intramuscular glycogen (d = 0.29-0.81), creatine kinase (d = 0.01-0.96), muscle thickness (d = 0.35-0.70), muscle soreness (d = 0.18-0.85), and active elbow flexion (d = 0.65-1.17) indicating a beneficial effect of CwC over time (P ≤ 0.05). In contrast, no significant interaction effect was observed for pressure pain threshold or passive elbow extension (P > 0.05). These results support the use of CwC for the recovery of muscle function after damaging exercise in male patients and indicate that CwC attenuates, but does not remove, the disruption of intramuscular glycogen stores observed after intense eccentric exercise. Glycolysis-dependent athletes may benefit from CwC therapy after training/competition that causes EAMD.

The role of caffeine consumption on individuals' health and athletic performance: An overview

Caffeine is considered a very popular, extensively ingested substance among the general population and athletes or recreational exercisers. This narrative review seeks to present the most recent scientific literature on the role of caffeine consumption on individuals' health and athletic performance. There are favorable relations between coffee use and liver outcomes (e.g. cirrhosis, fibrosis, liver cancer, and chronic liver disease), and a wide range of other health outcomes, while, there are no decisive deleterious relations with any health outcomes, except for pregnancy. The ergogenic effects of caffeine are significant after consumption of doses 3 to 6 mg/kg/body weight, 15 to 60 min pre-exercise (it depends on the form), mainly due to the Central Nervous System. Caffeine may enhance the re-synthesis of glycogen during the recovery phase from exercise. Caffeine has beneficial effects in several features of exercise such as extended aerobic-type activities, fixed-term activities, brief duration activities, high-intensity prolonged exercise as in team sports, and strength/power activities. It does not cause harmful changes in urination, water loss, sweating rate, and fluid balance. In periods of sleep deprivation, it can improve vigilance and alertness. Among the most commonly incorporated side effects of caffeine, ingestion is anxiety and heart palpitations.

Interactions between insulin and exercise.

The interaction between insulin and exercise is an example of balancing and modifying the effects of two opposing metabolic regulatory forces under varying conditions. While insulin is secreted after food intake and is the primary hormone increasing glucose storage as glycogen and fatty acid storage as triglycerides, exercise is a condition where fuel stores need to be mobilized and oxidized. Thus, during physical activity the fuel storage effects of insulin need to be suppressed. This is done primarily by inhibiting insulin secretion during exercise as well as activating local and systemic fuel mobilizing processes. In contrast, following exercise there is a need for refilling the fuel depots mobilized during exercise, particularly the glycogen stores in muscle. This process is facilitated by an increase in insulin sensitivity of the muscles previously engaged in physical activity which directs glucose to glycogen resynthesis. In physically trained individuals, insulin sensitivity is also higher than in untrained individuals due to adaptations in the vasculature, skeletal muscle and adipose tissue. In this paper, we review the interactions between insulin and exercise during and after exercise, as well as the effects of regular exercise training on insulin action.

Salbutamol Increases Leg Glucose Uptake and Metabolic Rate but not Muscle Glycogen Resynthesis in Recovery From Exercise.

Exercise blunts the effect of beta2-agonists on peripheral glucose uptake and energy expenditure. Whether such attenuation extends into recovery is unknown. To examine the effect of a beta2-agonist on leg glucose uptake and metabolic rate in recovery from exercise. Using leg arteriovenous balance technique and analyses of thigh muscle biopsies, we investigated the effect of a beta2-agonist (24 mg of oral salbutamol) vs placebo on leg glucose, lactate, and oxygen exchange before and during quadriceps exercise, and 0.5 to 5 hours in recovery from quadriceps exercise, as well as on muscle glycogen resynthesis and activity in recovery. Twelve healthy, lean, young men participated. Before exercise, leg glucose uptake was 0.42 ± 0.12 and 0.20 ± 0.02 mmol × min-1 (mean ± SD) for salbutamol and placebo (P = .06), respectively, while leg oxygen consumption was around 2-fold higher (P < .01) for salbutamol than for placebo (25 ± 3 vs 14 ± 1 mL × min-1). No treatment differences were observed in leg glucose uptake, lactate release, and oxygen consumption during exercise. But in recovery, cumulated leg glucose uptake, lactate release, and oxygen consumption was 21 mmol (95% CI 18-24, P = .018), 19 mmol (95% CI 16-23, P < .01), and 1.8 L (95% CI 1.6-2.0, P < .01) higher for salbutamol than for placebo, respectively. Muscle glycogen content was around 30% lower (P < .01) for salbutamol than for placebo in recovery, whereas no treatment differences were observed in muscle glycogen resynthesis or glycogen synthase activity. Exercise blunts the effect of beta2-agonist salbutamol on leg glucose uptake, but this attenuation diminishes in recovery. Salbutamol increases leg lactate release in recovery, which may relate to glycolytic trafficking due to excessive myocellular glucose uptake.

Coffee Increases Post-Exercise Muscle Glycogen Recovery in Endurance Athletes: A Randomized Clinical Trial

Coffee is one of the most widely consumed beverages worldwide and caffeine is known to improve performance in physical exercise. Some substances in coffee have a positive effect on glucose metabolism and are promising for post-exercise muscle glycogen recovery. We investigated the effect of a coffee beverage after exhaustive exercise on muscle glycogen resynthesis, glycogen synthase activity and glycemic and insulinemic response in a double-blind, crossover, randomized clinical trial. Fourteen endurance-trained men performed an exhaustive cycle ergometer exercise to deplete muscle glycogen. The following morning, participants completed a second cycling protocol followed by a 4-h recovery, during which they received either test beverage (coffee + milk) or control (milk) and a breakfast meal, with a simple randomization. Blood samples and muscle biopsies were collected at the beginning and by the end of recovery. Eleven participants were included in data analysis (age: 39.0 ± 6.0 years; BMI: 24.0 ± 2.3 kg/m2; VO2max: 59.9 ± 8.3 mL·kg−1·min−1; PPO: 346 ± 39 W). The consumption of coffee + milk resulted in greater muscle glycogen recovery (102.56 ± 18.75 vs. 40.54 ± 18.74 mmol·kg dw−1; p = 0.01; d = 0.94) and greater glucose (p = 0.02; d = 0.83) and insulin (p = 0.03; d = 0.76) total area under the curve compared with control. The addition of coffee to a beverage with adequate amounts of carbohydrates increased muscle glycogen resynthesis and the glycemic and insulinemic response during the 4-h recovery after exhaustive cycling exercise.

Caffeine coingested with carbohydrate on performance recovery in national-level paddlers: a randomized, double-blind, crossover, placebo-controlled trial.

Caffeine enhances muscle glycogen resynthesis postexercise; however, the next-day effects on recovery are unknown. The present study aimed to examine the effects of carbohydrate (CHO) supplementation with or without caffeine (CAF) 24-h following exhaustive exercise on time trial performance in elite paddling athletes. Nine highly trained male paddlers (21±2 y) completed three experimental trials in a randomized, double-blind, crossover manner. Following an exhaustive exercise session (20-km timed paddle) participants ingested: 1) 0.6 g/kg of carbohydrate (CHO); 2) 0.6 g/kg of carbohydrate with 6 mg/kg of caffeine (CAF+CHO); or 3) placebo (PLA), at four time-points (immediately after, and 2, 6, and 12-h postexercise) in addition to their typical dietary intake. After 24 h, 5 attempts of on-water 500-m paddling time-trial was performed, and the average time was recorded. Blood samples were taken at rest and following both the 20-km and the 5×500 m exercise to determine changes in plasma cortisol, insulin, and glucose. There was a significant main effect of condition (P<0.001), with post-hoc analysis revealing that both CHO conditions (CHO: 98.7±2.8 s, P=0.0003; CAF+CHO: 97.9±2.3 s, P=0.0002) were significantly faster compared to PLA (101.0±3.1 s); however, CAF did not augment time trial performance compared to CHO (P=0.16). There was no significant condition by time interactions for glucose, cortisol, or insulin before and after the 20-km depleting exercise and 500-m time trial. In elite male paddlers, CHO, independent of caffeine, enhanced time trial performance 24 hours following exhaustive exercise.

Relationship between Skin Temperature Variation and Muscle Damage Markers after a Marathon Performed in a Hot Environmental Condition.

This study aimed to assess the effect of a marathon running at a hot environmental temperature on the baseline skin temperature (Tsk) of the posterior day and to analyze the relationship between Tsk response and muscle damage markers variation. The Tsk, creatine kinase, and lactate dehydrogenase of 16 marathon runners were assessed four times before (15 days and 45 min) and after (24 h and 6 days) a marathon in a hot environment (thermal stress index = 28.3 ± 3.3 °C and humidity ~81%). The Tsk of thirteen different body regions of both right and left lower limbs were analyzed. Higher values after the marathon were observed than 45 min before in creatine kinase (174.3 ± 136.4 UI/L < 1159.7 ± 699.7 UI/L, p < 0.01 and large effect size) and lactate dehydrogenase (362.6 ± 99.9 UI/L < 438 ± 115.5 UI/L, p = 0.02 and moderate effect size). Generally, Tsk was higher the day after the marathon than at the other three moments (e.g., rectus femoris region, 6 days before vs. the day after, 95% confidence interval of the difference (0.3, 1.6 °C), p = 0.04 and large effect size). No relationship or correlation was observed between the variation of Tsk and muscle damage markers (p > 0.05). In conclusion, performing a marathon in a hot environmental condition results in a higher Tsk the day after the marathon. This increase in Tsk could be because of the heat generated by the marathon and its subsequent physiological processes (e.g., increase in endothelial nitric oxide, glycogen resynthesis, or increase of systemic hormones), which would be reflected in the Tsk due to the peripheral vasodilation promoted by the hot environment. However, among these processes, muscle damage does not seem to be of great importance due to the lack of an observed relationship between Tsk and muscle damage markers.

Neither Peristaltic Pulse Dynamic Compressions nor Heat Therapy Accelerate Glycogen Resynthesis after Intermittent Running.

To investigate the effects of a single session of either peristaltic pulse dynamic leg compressions (PPDC) or local heat therapy (HT) after prolonged intermittent shuttle running on skeletal muscle glycogen content, muscle function, and the expression of factors involved in skeletal muscle remodeling. Twenty-six trained individuals were randomly allocated to either a PPDC (n = 13) or a HT (n = 13) group. After completing a 90-min session of intermittent shuttle running, participants consumed 0.3 g·kg-1 protein plus 1.0 g·kg-1 carbohydrate and received either PPDC or HT for 60 min in one randomly selected leg, while the opposite leg served as control. Muscle biopsies from both legs were obtained before and after exposure to the treatments. Muscle function and soreness were also evaluated before, immediately after, and 24 h after the exercise bout. The changes in glycogen content were similar (P > 0.05) between the thigh exposed to PPDC and the control thigh ~90 min (Control: 14.9 ± 34.3 vs PPDC: 29.6 ± 34 mmol·kg-1 wet wt) and ~210 min (Control: 45.8 ± 40.7 vs PPDC: 52 ± 25.3 mmol·kg-1 wet wt) after the treatment. There were also no differences in the change in glycogen content between thighs ~90 min (Control: 35.9 ± 26.1 vs HT: 38.7 ± 21.3 mmol·kg-1 wet wt) and ~210 min (Control: 61.4 ± 50.6 vs HT: 63.4 ± 17.5 mmol·kg-1 wet wt) after local HT. The changes in peak torque and fatigue resistance of the knee extensors, muscle soreness, and the mRNA expression and protein abundance of select factors were also similar (P > 0.05) in both thighs, irrespective of the treatment. A single 1-h session of either PPDC or local HT does not accelerate glycogen resynthesis and the recovery of muscle function after prolonged intermittent shuttle running.

Carbohydrate and Protein Supplements, an Effective Means for Maintaining Exercise-Induced Glucose Metabolism Homeostasis

This study aimed to verify the effects of an independently developed carbohydrate and protein (CHO+P) beverage (7.2% oligosaccharide and 1.6% soy-polypeptide) supplement on exerciseinduced glucose metabolism and associated gene expression. Mice received 1 mL/100 g body weight of normal saline (group C; n = 36) or CHO+P (group E; n = 36) at 30 min before an immediately after exercise. Mice without exercise and supplementation served as normal controls (group NC; n = 9). The expression levels related to glucose metabolism were measured at 0, 4, 12, and 24 h after exercise (n = 9 per group). The blood glucose, insulin, and liver glycogen contents in groups C and E were dramatically lower than group NC immediately after exercise. Those in group E were significantly higher than group C, with few differences between the two. Muscle glycogen was restored more quickly when the CHO+P beverage was consumed compared to normal saline. Furthermore, exercise-induced increase in glucose transporter-4 (GLUT-4) mRNA could be depressed by CHO+P supplementation but enhanced in GLUT-4 protein. Interleukin-6 (IL-6) showed a double peak curve in the recovery period, but IL-6 increased again in group E earlier than group C. These findings confirmed that the beverage has significantly improved time in maintaining blood glucose stability, reducing glycogen consumption, accelerating glycogen resynthesis, and repairing injury in rats. This study suggests the future application of this beverage in humans with experimental support and provides a scientific direction for promoting glycogen synthesis and recovery through nutrition.

Carbohydrate restriction following strenuous glycogen-depleting exercise does not potentiate the acute molecular response associated with mitochondrial biogenesis in human skeletal muscle

PurposeCarbohydrate (CHO) restriction could be a potent metabolic regulator of endurance exercise-induced muscle adaptations. Here, we determined whether post-exercise CHO restriction following strenuous exercise combining continuous cycling exercise (CCE) and sprint interval exercise could affect the gene expression related to mitochondrial biogenesis and oxidative metabolism in human skeletal muscle.MethodsIn a randomized cross-over design, 8 recreationally active males performed two cycling exercise sessions separated by 4 weeks. Each session consisted of 60-min CCE and six 30-s all-out sprints, which was followed by ingestion of either a CHO or placebo beverage in the post-exercise recovery period. Muscle glycogen concentration and the mRNA levels of several genes related to mitochondrial biogenesis and oxidative metabolism were determined before, immediately after, and at 3 h after exercise.ResultsCompared to pre-exercise, strenuous cycling led to a severe muscle glycogen depletion (> 90%) and induced a large increase in PGC1A and PDK4 mRNA levels (~ 20-fold and ~ 10-fold, respectively) during the acute recovery period in both trials. The abundance of the other transcripts was not changed or was only moderately increased during this period. CHO restriction during the 3-h post-exercise period blunted muscle glycogen resynthesis but did not increase the mRNA levels of genes associated with muscle adaptation to endurance exercise, as compared with abundant post-exercise CHO consumption.ConclusionCHO restriction after a glycogen-depleting and metabolically-demanding cycling session is not effective for increasing the acute mRNA levels of genes involved in mitochondrial biogenesis and oxidative metabolism in human skeletal muscle.