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 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.

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.

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.

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.

Muscle metabolism during exercise with carbohydrate or protein-carbohydrate ingestion.

INTRODUCTION: Ingesting protein (PRO) with CHO during prolonged exercise is purported to improve performance compared with CHO alone by altering the regulation of skeletal muscle energy provision. However, no study has directly investigated this issue. We tested the hypothesis that compared with CHO alone, coingestion of PRO would alter markers of metabolic control, including the magnitude of glycogen use and the net expansion of the tricarboxylic acid cycle intermediate pool, which has been linked to the capacity for oxidative energy delivery. METHODS: Eight trained men (mean +/- SE: age = 29 +/- 2 yr; VO2peak = 55 +/- 2 mL x kg(-1) x min(-1)) cycled at 69% +/- 1% VO2peak for 90 min on two occasions, and biopsy samples (vastus lateralis) were obtained before and after exercise. In a randomized, double-blind manner, subjects ingested one of two drinks during exercise that contained either 6% CHO or 6% CHO + 2% PRO (CHO + PRO) at a rate of 1 L x h(-1) to deliver 60 g x h(-1) CHO +/- 20 g x h(-1) PRO. RESULTS: CHO + PRO ingestion increased the plasma concentration of branched chain (561 +/- 46 vs 301 +/- 32 micromol x L(-1)) and essential amino acids (1071 +/- 98 vs 670 +/- 71 micromol x L(-1)) after exercise versus CHO (both P values

Divergent response of metabolite transport proteins in human skeletal muscle after sprint interval training and detraining.

Skeletal muscle primarily relies on carbohydrate (CHO) for energy provision during high-intensity exercise. We hypothesized that sprint interval training (SIT), or repeated sessions of high-intensity exercise, would induce rapid changes in transport proteins associated with CHO metabolism, whereas changes in skeletal muscle fatty acid transporters would occur more slowly. Eight active men (22 +/- 1 yr; peak oxygen uptake = 50 +/- 2 ml.kg(-1).min(-1)) performed 4-6 x 30 s all-out cycling efforts with 4-min recovery, 3 days/wk for 6 wk. Needle muscle biopsy samples (vastus lateralis) were obtained before training (Pre), after 1 and 6 wk of SIT, and after 1 and 6 wk of detraining. Muscle oxidative capacity, as reflected by the protein content of cytochrome c oxidase subunit 4 (COX4), increased by approximately 35% after 1 wk of SIT and remained higher compared with Pre, even after 6 wk of detraining (P < 0.05). Muscle GLUT4 content increased after 1 wk of SIT and remained approximately 20% higher compared with baseline during detraining (P < 0.05). The monocarboxylate tranporter (MCT) 4 was higher after 1 and 6 wk of SIT compared with Pre, whereas MCT1 increased after 6 wk of training and remained higher after 1 wk of detraining (P < 0.05). There was no effect of training or detraining on the muscle content of fatty acid translocase (FAT/CD36) or plasma membrane associated fatty acid binding protein (FABPpm) (P > 0.05). We conclude that short-term SIT induces rapid increases in skeletal muscle oxidative capacity but has divergent effects on proteins associated with glucose, lactate, and fatty acid transport.