Sodium nitrate ingestion increases skeletal muscle nitrate content in humans.

Nitrate ([Formula: see text]) ingestion has been shown to have vasoactive and ergogenic effects that have been attributed to increased nitric oxide (NO) production. Recent observations in rodents suggest that skeletal muscle tissue serves as an endogenous [Formula: see text] "reservoir." The present study determined [Formula: see text] contents in human skeletal muscle tissue in a postabsorptive state and following ingestion of a sodium nitrate bolus (NaNO3). Seventeen male, type 2 diabetes patients (age 72 ± 1 yr; body mass index 26.5 ± 0.5 kg/m2; means ± SE) were randomized to ingest a dose of NaNO3 (NIT; 9.3 mg [Formula: see text]/kg body wt) or placebo (PLA; 8.8 mg NaCl/kg body wt). Blood and muscle biopsy samples were taken before and up to 7 h following [Formula: see text] or placebo ingestion to assess [Formula: see text] [and plasma nitrite ([Formula: see text])] concentrations. Additionally, basal plasma and muscle [Formula: see text] concentrations were assessed in 10 healthy young (CON-Y; age 21 ± 1 yr) and 10 healthy older (CON-O; age 75 ± 1 yr) control subjects. In all groups, baseline [Formula: see text] concentrations were higher in muscle (NIT, 57 ± 7; PLA, 61 ± 7; CON-Y, 80 ± 10; CON-O, 54 ± 6 µmol/l) than in plasma (NIT, 35 ± 3; PLA, 32 ± 3; CON-Y, 38 ± 3; CON-O, 33 ± 3 µmol/l; P ≤ 0.011). Ingestion of NaNO3 resulted in a sustained increase in plasma [Formula: see text], plasma [Formula: see text], and muscle [Formula: see text] concentrations (up to 185 ± 25 µmol/l) in the NIT group (time effect P < 0.001) compared with PLA (treatment effect P < 0.05). In conclusion, basal [Formula: see text] concentrations are substantially higher in human skeletal muscle tissue compared with plasma. Ingestion of a bolus of dietary [Formula: see text] increases both plasma and muscle [Formula: see text] contents in humans.NEW & NOTEWORTHY Literature of the pharmacokinetics following dietary nitrate ingestion is usually limited to the changes observed in plasma nitrate and nitrite concentrations. The present investigation assessed the skeletal muscle nitrate content in humans during the postabsorptive state, as well as following dietary nitrate ingestion. We show that basal nitrate content is higher in skeletal muscle tissue than in plasma and that ingestion of a dietary nitrate bolus strongly increases both plasma and muscle nitrate concentrations.

Fructose and Sucrose Intake Increase Exogenous Carbohydrate Oxidation during Exercise.

Peak exogenous carbohydrate oxidation rates typically reach ~1 g∙min-1 during exercise when ample glucose or glucose polymers are ingested. Fructose co-ingestion has been shown to further increase exogenous carbohydrate oxidation rates. The purpose of this study was to assess the impact of fructose co-ingestion provided either as a monosaccharide or as part of the disaccharide sucrose on exogenous carbohydrate oxidation rates during prolonged exercise in trained cyclists. Ten trained male cyclists (VO2peak: 65 ± 2 mL∙kg-1∙min-1) cycled on four different occasions for 180 min at 50% Wmax during which they consumed a carbohydrate solution providing 1.8 g∙min-1 of glucose (GLU), 1.2 g∙min-1 glucose + 0.6 g∙min-1 fructose (GLU + FRU), 0.6 g∙min-1 glucose + 1.2 g∙min-1 sucrose (GLU + SUC), or water (WAT). Peak exogenous carbohydrate oxidation rates did not differ between GLU + FRU and GLU + SUC (1.40 ± 0.06 vs. 1.29 ± 0.07 g∙min-1, respectively, p = 0.999), but were 46% ± 8% higher when compared to GLU (0.96 ± 0.06 g∙min-1: p < 0.05). In line, exogenous carbohydrate oxidation rates during the latter 120 min of exercise were 46% ± 8% higher in GLU + FRU or GLU + SUC compared with GLU (1.19 ± 0.12, 1.13 ± 0.21, and 0.82 ± 0.16 g∙min-1, respectively, p < 0.05). We conclude that fructose co-ingestion (0.6 g∙min-1) with glucose (1.2 g∙min-1) provided either as a monosaccharide or as sucrose strongly increases exogenous carbohydrate oxidation rates during prolonged exercise in trained cyclists.

Sodium nitrate co-ingestion with protein does not augment postprandial muscle protein synthesis rates in older, type 2 diabetes patients.

The age-related anabolic resistance to protein ingestion is suggested to be associated with impairments in insulin-mediated capillary recruitment and postprandial muscle tissue perfusion. The present study investigated whether dietary nitrate co-ingestion with protein improves muscle protein synthesis in older, type 2 diabetes patients. Twenty-four men with type 2 diabetes (72 ± 1 yr, 26.7 ± 1.4 m/kg(2) body mass index, 7.3 ± 0.4% HbA1C) received a primed continuous infusion of l-[ring-(2)H5]phenylalanine and l-[1-(13)C]leucine and ingested 20 g of intrinsically l-[1-(13)C]phenylalanine- and l-[1-(13)C]leucine-labeled protein with (PRONO3) or without (PRO) sodium nitrate (0.15 mmol/kg). Blood and muscle samples were collected to assess protein digestion and absorption kinetics and postprandial muscle protein synthesis rates. Upon protein ingestion, exogenous phenylalanine appearance rates increased in both groups (P < 0.001), resulting in 55 ± 2% and 53 ± 2% of dietary protein-derived amino acids becoming available in the circulation over the 5h postprandial period in the PRO and PRONO3 groups, respectively. Postprandial myofibrillar protein synthesis rates based on l-[ring-(2)H5]phenylalanine did not differ between groups (0.025 ± 0.004 and 0.021 ± 0.007%/h over 0-2 h and 0.032 ± 0.004 and 0.030 ± 0.003%/h over 2-5 h in PRO and PRONO3, respectively, P = 0.7). No differences in incorporation of dietary protein-derived l-[1-(13)C]phenylalanine into de novo myofibrillar protein were observed at 5 h (0.016 ± 0.002 and 0.014 ± 0.002 mole percent excess in PRO and PRONO3, respectively, P = 0.8). Dietary nitrate co-ingestion with protein does not modulate protein digestion and absorption kinetics, nor does it further increase postprandial muscle protein synthesis rates or the incorporation of dietary protein-derived amino acids into de novo myofibrillar protein in older, type 2 diabetes patients.

Sucrose ingestion after exhaustive exercise accelerates liver, but not muscle glycogen repletion compared with glucose ingestion in trained athletes.

The purpose of this study was to assess the effects of sucrose vs. glucose ingestion on postexercise liver and muscle glycogen repletion. Fifteen well-trained male cyclists completed two test days. Each test day started with glycogen-depleting exercise, followed by 5 h of recovery, during which subjects ingested 1.5 g·kg(-1)·h(-1) sucrose or glucose. Blood was sampled frequently and (13)C magnetic resonance spectroscopy and imaging were employed 0, 120, and 300 min postexercise to determine liver and muscle glycogen concentrations and liver volume. Results were as follows: Postexercise muscle glycogen concentrations increased significantly from 85 ± 27 (SD) vs. 86 ± 35 mmol/l to 140 ± 23 vs. 136 ± 26 mmol/l following sucrose and glucose ingestion, respectively (no differences between treatments: P = 0.673). Postexercise liver glycogen concentrations increased significantly from 183 ± 47 vs. 167 ± 65 mmol/l to 280 ± 72 vs. 234 ± 81 mmol/l following sucrose and glucose ingestion, respectively (time × treatment, P = 0.051). Liver volume increased significantly over the 300-min period after sucrose ingestion only (time × treatment, P = 0.001). As a result, total liver glycogen content increased during postexercise recovery to a greater extent in the sucrose treatment (from 53.6 ± 16.2 to 86.8 ± 29.0 g) compared with the glucose treatment (49.3 ± 25.5 to 65.7 ± 27.1 g; time × treatment, P < 0.001), equating to a 3.4 g/h (95% confidence interval: 1.6-5.1 g/h) greater repletion rate with sucrose vs. glucose ingestion. In conclusion, sucrose ingestion (1.5 g·kg(-1)·h(-1)) further accelerates postexercise liver, but not muscle glycogen repletion compared with glucose ingestion in trained athletes.

Fructose Coingestion Does Not Accelerate Postexercise Muscle Glycogen Repletion.

BACKGROUND: Postexercise muscle glycogen repletion is largely determined by the systemic availability of exogenous carbohydrate provided. PURPOSE: This study aimed to assess the effect of the combined ingestion of fructose and glucose on postexercise muscle glycogen repletion when optimal amounts of carbohydrate are ingested. METHODS: Fourteen male cyclists (age: 28 ± 6 yr; Wmax: 4.8 ± 0.4 W·kg⁻¹) were studied on three different occasions. Each test day started with a glycogen-depleting exercise session. This was followed by a 5-h recovery period, during which subjects ingested 1.5 g·kg⁻¹·h⁻¹ glucose (GLU), 1.2 g·kg⁻¹·h⁻¹ glucose + 0.3 g·kg⁻¹·h⁻¹ fructose (GLU + FRU), or 0.9 g·kg⁻¹·h⁻¹ glucose + 0.6 g·kg⁻¹·h⁻¹ sucrose (GLU + SUC). Blood samples and gastrointestinal distress questionnaires were collected frequently, and muscle biopsy samples were taken at 0, 120, and 300 min after cessation of exercise to measure muscle glycogen content. RESULTS: Plasma glucose responses did not differ between treatments (ANOVA, P = 0.096), but plasma insulin and lactate concentrations were elevated during GLU + FRU and GLU + SUC when compared with GLU (P < 0.01). Muscle glycogen content immediately after exercise averaged 207 ± 112, 219 ± 107, and 236 ± 118 mmol·kg⁻¹ dry weight in the GLU, GLU + FRU, and GLU + SUC treatments, respectively (P = 0.362). Carbohydrate ingestion increased muscle glycogen concentrations during 5 h of postexercise recovery to 261 ± 98, 289 ± 130, and 315 ± 103 mmol·kg⁻¹ dry weight in the GLU, GLU + FRU, and GLU + SUC treatments, respectively (P < 0.001), with no differences between treatments (time × treatment, P = 0.757). CONCLUSIONS: Combined ingestion of glucose plus fructose does not further accelerate postexercise muscle glycogen repletion in trained cyclists when ample carbohydrate is ingested. Combined ingestion of glucose (polymers) plus fructose or sucrose reduces gastrointestinal complaints when ingesting large amounts of carbohydrate.

Ingestion of glucose or sucrose prevents liver but not muscle glycogen depletion during prolonged endurance-type exercise in trained cyclists.

The purpose of this study was to define the effect of glucose ingestion compared with sucrose ingestion on liver and muscle glycogen depletion during prolonged endurance-type exercise. Fourteen cyclists completed two 3-h bouts of cycling at 50% of peak power output while ingesting either glucose or sucrose at a rate of 1.7 g/min (102 g/h). Four cyclists performed an additional third test for reference in which only water was consumed. We employed (13)C magnetic resonance spectroscopy to determine liver and muscle glycogen concentrations before and after exercise. Expired breath was sampled during exercise to estimate whole body substrate use. After glucose and sucrose ingestion, liver glycogen levels did not show a significant decline after exercise (from 325 ± 168 to 345 ± 205 and 321 ± 177 to 348 ± 170 mmol/l, respectively; P > 0.05), with no differences between treatments. Muscle glycogen concentrations declined (from 101 ± 49 to 60 ± 34 and 114 ± 48 to 67 ± 34 mmol/l, respectively; P < 0.05), with no differences between treatments. Whole body carbohydrate utilization was greater with sucrose (2.03 ± 0.43 g/min) vs. glucose (1.66 ± 0.36 g/min; P < 0.05) ingestion. Both liver (from 454 ± 33 to 283 ± 82 mmol/l; P < 0.05) and muscle (from 111 ± 46 to 67 ± 31 mmol/l; P < 0.01) glycogen concentrations declined during exercise when only water was ingested. Both glucose and sucrose ingestion prevent liver glycogen depletion during prolonged endurance-type exercise. Sucrose ingestion does not preserve liver glycogen concentrations more than glucose ingestion. However, sucrose ingestion does increase whole body carbohydrate utilization compared with glucose ingestion. This trial was registered at https://www.clinicaltrials.gov as NCT02110836.

A Sucrose Mouth Rinse Does Not Improve 1-hr Cycle Time Trial Performance When Performed in the Fasted or Fed State.

Carbohydrate mouth rinsing during exercise has been suggested to enhance performance of short (45-60 min) bouts of high-intensity (>75% VO2peak) exercise. Recent studies indicate that this performance enhancing effect may be dependent on the prandial state of the athlete. The purpose of this study was to define the impact of a carbohydrate mouth rinse on ~1-hr time trial performance in both the fasted and fed states. Using a double-blind, crossover design, 14 trained male cyclists (27 ± 6 years; 5.0 ± 0.5 W · kg(-1)) were selected to perform 4 time trials of ~1 hr (1,032 ± 127 kJ) on a cycle ergometer while rinsing their mouths with a 6.4% sucrose solution (SUC) or a noncaloric sweetened placebo (PLA) for 5 s at the start and at every 12.5% of their set amount of work completed. Two trials were performed in an overnight fasted state and two trials were performed 2 h after consuming a standardized breakfast. Performance time did not differ between any of the trials (fasted-PLA: 68.6 ± 7.2; fasted-SUC: 69.6 ± 7.5; fed-PLA: 67.6 ± 6.6; and fed-SUC: 69.0 ± 6.3 min; Prandial State × Mouth Rinse Solution p = .839; main effect prandial state p = .095; main effect mouth rinse solution p = .277). In line, mean power output and heart rate during exercise did not differ between trials. In conclusion, a sucrose mouth rinse does not improve ~1-hr time trial performance in well-trained cyclists when performed in either the fasted or the fed state.

Postprandial Protein Handling Is Not Impaired in Type 2 Diabetes Patients When Compared With Normoglycemic Controls.

CONTEXT: The progressive loss of muscle mass with aging is accelerated in type 2 diabetes patients. It has been suggested that this is attributed to a blunted muscle protein synthetic response to food intake. OBJECTIVE: The objective of the study was to test the hypothesis that the muscle protein synthetic response to protein ingestion is impaired in older type 2 diabetes patients when compared with healthy, normoglycemic controls. DESIGN: A clinical intervention study with two parallel groups was conducted between August 2011 and July 2012. SETTING: The study was conducted at the research unit of Maastricht University, The Netherlands. Intervention, Participants, and Main Outcome Measures: Eleven older type 2 diabetes males [diabetes; age 71 ± 1 y, body mass index (BMI) 26.2 ± 0.5 kg/m(2)] and 12 age- and BMI-matched normoglycemic controls (control; age 74 ± 1 y, BMI 24.8 ± 1.1 kg/m(2)) participated in an experiment in which they ingested 20 g intrinsically L-[1-(13)C]phenylalanine-labeled protein. Continuous iv L-[ring-(2)H5]phenylalanine infusion was applied, and blood and muscle samples were obtained to assess amino acid kinetics and muscle protein synthesis rates in the postabsorptive and postprandial state. RESULTS: Plasma insulin concentrations increased after protein ingestion in both groups, with a greater rise in the diabetes group. Postabsorptive and postprandial muscle protein synthesis rates did not differ between groups and averaged 0.029 ± 0.003 vs 0.029 ± 0.003%/h(1) and 0.031 ± 0.002 vs 0.033 ± 0.002%/h(1) in the diabetes versus control group, respectively. Postprandial L-[1-(13)C]phenylalanine incorporation into muscle protein did not differ between groups (0.018 ± 0.001 vs 0.019 ± 0.002 mole percent excess, respectively). CONCLUSIONS: Postabsorptive muscle protein synthesis and postprandial protein handling is not impaired in older individuals with type 2 diabetes when compared with age-matched, normoglycemic controls.

A single dose of sodium nitrate does not improve oral glucose tolerance in patients with type 2 diabetes mellitus.

Dietary nitrate (NO3(-)) supplementation has been proposed as an emerging treatment strategy for type 2 diabetes. We hypothesized that ingestion of a single bolus of dietary NO3(-) ingestion improves oral glucose tolerance in patients with type 2 diabetes. Seventeen men with type 2 diabetes (glycated hemoglobin, 7.3% ± 0.2%) participated in a randomized crossover experiment. The subjects ingested a glucose beverage 2.5 hours after consumption of either sodium NO3(-) (0.15 mmol NaNO3(-) · kg(-1)) or a placebo solution. Venous blood samples were collected before ingestion of the glucose beverage and every 30 minutes thereafter during a 2-hour period to assess postprandial plasma glucose and insulin concentrations. The results show that plasma NO3(-) and nitrite levels were increased after NaNO3(-) as opposed to placebo ingestion (treatment-effect, P = .001). Despite the elevated plasma NO3(-) and nitrite levels, ingestion of NaNO3(-) did not attenuate the postprandial rise in plasma glucose and insulin concentrations (time × treatment interaction, P = .41 for glucose, P = .93 for insulin). Despite the lack of effect on oral glucose tolerance, basal plasma glucose concentrations measured 2.5 hours after NaNO3(-) ingestion were lower when compared with the placebo treatment (7.5 ± 0.4 vs 8.3 ± 0.4 mmol/L, respectively; P = .04). We conclude that ingestion of a single dose of dietary NO3(-) does not improve subsequent oral glucose tolerance in patients with type 2 diabetes.

[Performance enhancement by carbohydrate intake during sport: effects of carbohydrates during and after high-intensity exercise]. / Koolhydraatinname tijdens en na intensieve inspanning.

Endogenous carbohydrate availability does not provide sufficient energy for prolonged moderate to high-intensity exercise. Carbohydrate ingestion during high-intensity exercise can therefore enhance performance.- For exercise lasting 1 to 2.5 hours, athletes are advised to ingest 30-60 g of carbohydrates per hour.- Well-trained endurance athletes competing for longer than 2.5 hours at high intensity can metabolise up to 90 g of carbohydrates per hour, provided that a mixture of glucose and fructose is ingested.- Athletes participating in intermittent or team sports are advised to follow the same strategies but the timing of carbohydrate intake depends on the type of sport.- If top performance is required again within 24 hours after strenuous exercise, the advice is to supplement endogenous carbohydrate supplies quickly within the first few hours post-exercise by ingesting large amounts of carbohydrate (1.2 g/kg/h) or a lower amount of carbohydrate (0.8 g/kg/h) with a small amount of protein (0.2-0.4 g/kg/h).

Dietary protein considerations to support active aging.

Given our rapidly aging world-wide population, the loss of skeletal muscle mass with healthy aging (sarcopenia) represents an important societal and public health concern. Maintaining or adopting an active lifestyle alleviates age-related muscle loss to a certain extent. Over time, even small losses of muscle tissue can hinder the ability to maintain an active lifestyle and, as such, contribute to the development of frailty and metabolic disease. Considerable research focus has addressed the application of dietary protein supplementation to support exercise-induced gains in muscle mass in younger individuals. In contrast, the role of dietary protein in supporting the maintenance (or gain) of skeletal muscle mass in active older persons has received less attention. Older individuals display a blunted muscle protein synthetic response to dietary protein ingestion. However, this reduced anabolic response can largely be overcome when physical activity is performed in close temporal proximity to protein consumption. Moreover, recent evidence has helped elucidate the optimal type and amount of dietary protein that should be ingested by the older adult throughout the day in order to maximize the skeletal muscle adaptive response to physical activity. Evidence demonstrates that when these principles are adhered to, muscle maintenance or hypertrophy over prolonged periods can be further augmented in active older persons. The present review outlines the current understanding of the role that dietary protein occupies in the lifestyle of active older adults as a means to increase skeletal muscle mass, strength and function, and thus support healthier aging.

The use of doubly labeled milk protein to measure postprandial muscle protein synthesis rates in vivo in humans.

We aimed to determine the impact of precursor pool dilution on the assessment of postprandial myofibrillar protein synthesis rates (MPS). A Holstein dairy cow was infused with large amounts of L-[1-(13)C]phenylalanine and L-[1-(13)C]leucine, and the milk was collected and fractionated. The enrichment levels in the casein were 38.7 and 9.3 mole percent excess, respectively. In a subsequent human experiment, 11 older men (age: 71 ± 1 y, body mass index: 26 ± 0.1 kg·m(-2)) received a primed constant infusion of L-[ring-(2)H5]phenylalanine and L-[1-(13)C]leucine. Blood and muscle samples were collected before and after the ingestion of 20-g doubly labeled casein to assess postprandial MPS based on the 1) constant tracer infusion of L-[ring-(2)H5]phenylalanine, 2) ingestion of intrinsically L-[1-(13)C]phenylalanine-labeled casein, and 3) constant infusion of L-[1-(13)C]leucine in combination with the ingestion of intrinsically L-[1-(13)C]leucine-labeled casein. Postprandial MPS was increased (P < 0.05) after protein ingestion (∼70% above postabsorptive values) based on the L-[1-(13)C]leucine tracer. There was no significant stimulation of postprandial MPS (∼27% above postabsorptive values) when the calculated fractional synthesis rate was based on the L-[ring-(2)H5]phenylalanine (P = 0.2). Comparisons of postprandial MPS based on the primed continuous infusion of L-[1-(13)C]leucine or the ingestion of intrinsically L-[1-(13)C]phenylalanine-labeled casein protein demonstrated differences compared with the primed continuous infusion of L-[ring-(2)H5]phenylalanine (P > 0.05). Our findings confirm that the postprandial MPS assessed using the primed continuous tracer infusion approach may differ if tracer steady-state conditions in the precursor pools are perturbed. The use of intrinsically doubly labeled protein provides a method to study the metabolic fate of the ingested protein and the subsequent postprandial MPS response.

The use of carbohydrates during exercise as an ergogenic aid.

Carbohydrate and fat are the two primary fuel sources oxidized by skeletal muscle tissue during prolonged (endurance-type) exercise. The relative contribution of these fuel sources largely depends on the exercise intensity and duration, with a greater contribution from carbohydrate as exercise intensity is increased. Consequently, endurance performance and endurance capacity are largely dictated by endogenous carbohydrate availability. As such, improving carbohydrate availability during prolonged exercise through carbohydrate ingestion has dominated the field of sports nutrition research. As a result, it has been well-established that carbohydrate ingestion during prolonged (>2 h) moderate-to-high intensity exercise can significantly improve endurance performance. Although the precise mechanism(s) responsible for the ergogenic effects are still unclear, they are likely related to the sparing of skeletal muscle glycogen, prevention of liver glycogen depletion and subsequent development of hypoglycemia, and/or allowing high rates of carbohydrate oxidation. Currently, for prolonged exercise lasting 2-3 h, athletes are advised to ingest carbohydrates at a rate of 60 g·h⁻¹ (~1.0-1.1 g·min⁻¹) to allow for maximal exogenous glucose oxidation rates. However, well-trained endurance athletes competing longer than 2.5 h can metabolize carbohydrate up to 90 g·h⁻¹ (~1.5-1.8 g·min⁻¹) provided that multiple transportable carbohydrates are ingested (e.g. 1.2 g·min⁻¹ glucose plus 0.6 g·min⁻¹ of fructose). Surprisingly, small amounts of carbohydrate ingestion during exercise may also enhance the performance of shorter (45-60 min), more intense (>75 % peak oxygen uptake; VO(2peak)) exercise bouts, despite the fact that endogenous carbohydrate stores are unlikely to be limiting. The mechanism(s) responsible for such ergogenic properties of carbohydrate ingestion during short, more intense exercise bouts has been suggested to reside in the central nervous system. Carbohydrate ingestion during exercise also benefits athletes involved in intermittent/team sports. These athletes are advised to follow similar carbohydrate feeding strategies as the endurance athletes, but need to modify exogenous carbohydrate intake based upon the intensity and duration of the game and the available endogenous carbohydrate stores. Ample carbohydrate intake is also important for those athletes who need to compete twice within 24 h, when rapid repletion of endogenous glycogen stores is required to prevent a decline in performance. To support rapid post-exercise glycogen repletion, large amounts of exogenous carbohydrate (1.2 g·kg⁻¹·h⁻¹) should be provided during the acute recovery phase from exhaustive exercise. For those athletes with a lower gastrointestinal threshold for carbohydrate ingestion immediately post-exercise, and/or to support muscle re-conditioning, co-ingesting a small amount of protein (0.2-0.4 g·kg⁻¹·h⁻¹) with less carbohydrate (0.8 g·kg⁻¹·h⁻¹) may provide a feasible option to achieve similar muscle glycogen repletion rates.

Astaxanthin supplementation does not augment fat use or improve endurance performance.

INTRODUCTION: Astaxanthin is a lipid-soluble carotenoid found in a variety of aquatic organisms. Prolonged astaxanthin supplementation has been reported to increase fat oxidative capacity and improve running time to exhaustion in mice. These data suggest that astaxanthin may be applied as a potent ergogenic aid in humans. PURPOSE: To assess the effect of 4 wk of astaxanthin supplementation on substrate use and subsequent time trial performance in well-trained cyclists. METHODS: Using a double-blind parallel design, 32 young, well-trained male cyclists or triathletes (age = 25 ± 1 yr, weight = 73 ± 1 kg, V˙O2peak = 60 ± 1 mL·kg·min, Wmax = 395 ± 7 W; mean ± SEM) were supplemented for 4 wk with 20 mg of astaxanthin per day (ASTA) or a placebo (PLA). Before and after the supplementation period, subjects performed 60 min of exercise (50% Wmax), followed by an time trial of approximately 1 h. RESULTS: Daily astaxanthin supplementation significantly increased basal plasma astaxanthin concentrations from nondetectable values to 187 ± 19 µg·kg (P < 0.05). This elevation was not reflected in greater total plasma antioxidant capacity (P = 0.90) or attenuated malondialdehyde levels (P = 0.63). Whole-body fat oxidation rates during submaximal exercise did not differ between groups and did not change over time (from 0.71 ± 0.04 to 0.68 ± 0.03 g·min and from 0.66 ± 0.04 to 0.61 ± 0.05 g·min in the PLA and ASTA groups, respectively; P = 0.73). No improvements in time trial performance were observed in either group (from 236 ± 9 to 239 ± 7 and from 238 ± 6 to 244 ± 6 W in the PLA and ASTA groups, respectively; P = 0.63). CONCLUSION: Prolonged astaxanthin supplementation does not augment antioxidant capacity, increase fat oxidative capacity, or improve time trial performance in trained cyclists.

Eccentric exercise increases satellite cell content in type II muscle fibers.

INTRODUCTION: Satellite cells (SCs) are of key importance in skeletal muscle tissue growth, repair, and regeneration. A single bout of high-force eccentric exercise has been demonstrated to increase mixed muscle SC content after 1-7 d of postexercise recovery. However, little is known about fiber type-specific changes in SC content and their activation status within 24 h of postexercise recovery. METHODS: Nine recreationally active young men (23 ± 1 yr) performed 300 eccentric actions of the knee extensors on an isokinetic dynamometer. Skeletal muscle biopsies from the vastus lateralis were collected preexercise and 24 h postexercise. Muscle fiber type-specific SC content and the number of activated SCs were determined by immunohistochemical analyses. RESULTS: There was no difference between Type I and Type II muscle fiber SC content before exercise. SC content significantly increased 24 h postexercise in Type II muscle fibers (from 0.085 ± 0.012 to 0.133 ± 0.016 SCs per fiber, respectively; P < 0.05), whereas there was no change in Type I fibers. In accordance, activation status increased from preexercise to 24 h postexercise as demonstrated by the increase in the number of DLK1+ SCs in Type II muscle fibers (from 0.027 ± 0.008 to 0.070 ± 0.017 SCs per muscle fiber P < 0.05). Although no significant changes were observed in the number of Ki-67+ SCs, we did observe an increase in the number of proliferating cell nuclear antigen-positive SCs after 24 h of postexercise recovery. CONCLUSION: A single bout of high-force eccentric exercise increases muscle fiber SC content and activation status in Type II but not Type I muscle fibers.

Protein supplementation augments the adaptive response of skeletal muscle to resistance-type exercise training: a meta-analysis.

BACKGROUND: Protein ingestion after a single bout of resistance-type exercise stimulates net muscle protein accretion during acute postexercise recovery. Consequently, it is generally accepted that protein supplementation is required to maximize the adaptive response of the skeletal muscle to prolonged resistance-type exercise training. However, there is much discrepancy in the literature regarding the proposed benefits of protein supplementation during prolonged resistance-type exercise training in younger and older populations. OBJECTIVE: The objective of the study was to define the efficacy of protein supplementation to augment the adaptive response of the skeletal muscle to prolonged resistance-type exercise training in younger and older populations. DESIGN: A systematic review of interventional evidence was performed through the use of a random-effects meta-analysis model. Data from the outcome variables fat-free mass (FFM), fat mass, type I and II muscle fiber cross-sectional area, and 1 repetition maximum (1-RM) leg press strength were collected from randomized controlled trials (RCTs) investigating the effect of dietary protein supplementation during prolonged (>6 wk) resistance-type exercise training. RESULTS: Data were included from 22 RCTs that included 680 subjects. Protein supplementation showed a positive effect for FFM (weighted mean difference: 0.69 kg; 95% CI: 0.47, 0.91 kg; P < 0.00001) and 1-RM leg press strength (weighted mean difference: 13.5 kg; 95% CI: 6.4, 20.7 kg; P < 0.005) compared with a placebo after prolonged resistance-type exercise training in younger and older subjects. CONCLUSION: Protein supplementation increases muscle mass and strength gains during prolonged resistance-type exercise training in both younger and older subjects.

No improvement in endurance performance after a single dose of beetroot juice.

INTRODUCTION: Dietary nitrate supplementation has received much attention in the literature due to its proposed ergogenic properties. Recently, the ingestion of a single bolus of nitrate-rich beetroot juice (500 ml, ~6.2 mmol NO3-) was reported to improve subsequent time-trial performance. However, this large volume of ingested beetroot juice does not represent a realistic dietary strategy for athletes to follow in a practical, performance-based setting. Therefore, we investigated the impact of ingesting a single bolus of concentrated nitrate-rich beetroot juice (140 ml, ~8.7 mmol NO3-) on subsequent 1-hr time-trial performance in well-trained cyclists. METHODS: Using a double-blind, repeated-measures crossover design (1-wk washout period), 20 trained male cyclists (26 ± 1 yr, VO(2peak) 60 ± 1 ml · kg(-1) · min(-1), Wmax 398 ± 7.7 W) ingested 140 ml of concentrated beetroot juice (8.7 mmol NO3-; BEET) or a placebo (nitrate-depleted beetroot juice; PLAC) with breakfast 2.5 hr before an ~1-hr cycling time trial (1,073 ± 21 kJ). Resting blood samples were collected every 30 min after BEET or PLAC ingestion and immediately after the time trial. RESULTS: Plasma nitrite concentration was higher in BEET than PLAC before the onset of the time trial (532 ± 32 vs. 271 ± 13 nM, respectively; p < .001), but subsequent time-trial performance (65.5 ± 1.1 vs. 65 ± 1.1 s), power output (275 ± 7 vs. 278 ± 7 W), and heart rate (170 ± 2 vs. 170 ± 2 beats/min) did not differ between BEET and PLAC treatments (all p > .05). CONCLUSION: Ingestion of a single bolus of concentrated (140 ml) beetroot juice (8.7 mmol NO3-) does not improve subsequent 1-hr time-trial performance in well-trained cyclists.

Diffusion tensor MRI to assess skeletal muscle disruption following eccentric exercise.

INTRODUCTION: Structural evidence of exercise-induced muscle disruption has traditionally involved histological analysis of muscle tissue obtained by needle biopsy, however, there are multiple limitations with this technique. Recently, diffusion tensor magnetic resonance imaging (DT-MRI) has been successfully demonstrated to noninvasively assess skeletal muscle abnormalities induced by traumatic injury. METHODS: To determine the potential for DT-MRI to detect musculoskeletal changes after a bout of eccentric exercise, 10 healthy men performed 300 eccentric actions on an isokinetic dynamometer. DT-MRI measurements and muscle biopsies from the vastus lateralis were obtained before and 24 h post-exercise. RESULTS: Z-band streaming was higher 24 h post-exercise compared with baseline (P < 0.05). The histological indices of damage coincided with changes in DT-MRI parameters of fractional anisotropy (FA) and apparent diffusion coefficient; reflecting altered skeletal muscle geometry (P < 0.05). Z-band streaming quantified per fiber correlated with FA (r = -0.512; P < 0.05). CONCLUSIONS: DT-MRI can detect changes in human skeletal muscle structure following eccentric exercise.