Carbohydrate and fat are the main substrates utilized during prolonged endurance-type exercise. The relative contribution of each is determined primarily by the intensity and duration of exercise, along with individual training and nutritional status. During moderate- to high-intensity exercise, carbohydrate represents the main substrate source. Because endogenous carbohydrate stores (primarily in liver and muscle) are relatively small, endurance-type exercise performance/capacity is often limited by endogenous carbohydrate availability. Much exercise metabolism research to date has focused on muscle glycogen utilization, with little attention paid to the contribution of liver glycogen. (13)C magnetic resonance spectroscopy permits direct, noninvasive measurements of liver glycogen content and has increased understanding of the relevance of liver glycogen during exercise. In contrast to muscle, endurance-trained athletes do not exhibit elevated basal liver glycogen concentrations. However, there is evidence that liver glycogenolysis may be lower in endurance-trained athletes compared with untrained controls during moderate- to high-intensity exercise. Therefore, liver glycogen sparing in an endurance-trained state may account partly for training-induced performance/capacity adaptations during prolonged (>90 min) exercise. Ingestion of carbohydrate at a relatively high rate (>1.5 g/min) can prevent liver glycogen depletion during moderate-intensity exercise independent of the type of carbohydrate (e.g., glucose vs. sucrose) ingested. To minimize gastrointestinal discomfort, it is recommended to ingest specific combinations or types of carbohydrates (glucose plus fructose and/or sucrose). By coingesting glucose with either galactose or fructose, postexercise liver glycogen repletion rates can be doubled. There are currently no guidelines for carbohydrate ingestion to maximize liver glycogen repletion.

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.

Cermak NM, van Loon LJ. Ingestion of glucose or sucrose prevents liver but not muscle glycogen depletion during prolonged endurance-type exercise in trained cyclists. Am J Physiol Endocrinol Metab 309: E1032-E1039, 2015. First published October 20, 2015; doi:10.1152/ajpendo.00376.2015.-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 Ϯ 168 to 345 Ϯ 205 and 321 Ϯ 177 to 348 Ϯ 170 mmol/l, respectively; P Ͼ 0.05), with no differences between treatments. Muscle glycogen concentrations declined (from 101 Ϯ 49 to 60 Ϯ 34 and 114 Ϯ 48 to 67 Ϯ 34 mmol/l, respectively; P Ͻ 0.05), with no differences between treatments. Whole body carbohydrate utilization was greater with sucrose (2.03 Ϯ 0.43 g/min) vs. glucose (1.66 Ϯ 0.36 g/min; P Ͻ 0.05) ingestion. Both liver (from 454 Ϯ 33 to 283 Ϯ 82 mmol/l; P Ͻ 0.05) and muscle (from 111 Ϯ 46 to 67 Ϯ 31 mmol/l; P Ͻ 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.glucose; hepatic glycogen; metabolism; nutrition; sucrose CARBOHYDRATE AND FAT are the main substrates oxidized during moderate-intensity, endurance-type exercise (41). In the fasted state, muscle glycogen and plasma glucose are predominant sources of carbohydrate for oxidation (41), the latter continuously replenished by glycogenolysis and gluconeogenesis from the liver, with smaller contributions from the kidneys and intestine (30). Consequently, in the absence of carbohydrate consumption, liver and muscle glycogen concentrations decrease by 40 -60% within 90 min of exercise at a workload of 70% of peak oxygen uptake (V O 2 peak ) (6, 37). Given the importance of liver glycogen for metabolic regulation (16), and the close relationship between liver glycogen content and exercise tolerance (6), it is important to understand the impact of carbohydrate ingestion on liver glycogen depletion during exercise.Carbohydrate feeding during prolonged (Ͼ2 h) moderate-to high-intensity, endurance-type exercise e...

Background Dietary protein ingestion stimulates muscle protein synthesis by providing amino acids to the muscle. The magnitude and duration of the postprandial increase in muscle protein synthesis rates are largely determined by dietary protein digestion and amino acid absorption kinetics. Objective We assessed the impact of protein type, protein dose, and age on dietary protein digestion and amino acid absorption kinetics in vivo in humans. Methods We included data from 18 randomized controlled trials with a total of 602 participants [age: 53 ± 23 y; BMI (kg/m2): 24.8 ± 3.3] who consumed various quantities of intrinsically l-[1-13C]-phenylalanine–labeled whey (n = 137), casein (n = 393), or milk (n = 72) protein and received intravenous infusions of l-[ring-2H5]-phenylalanine, which allowed us to assess protein digestion and phenylalanine absorption kinetics and the postprandial release of dietary protein–derived phenylalanine into the circulation. The effect of aging on these processes was assessed in a subset of 82 young (aged 22 ± 3 y) and 83 older (aged 71 ± 5 y) individuals. Results A total of 50% ± 14% of dietary protein–derived phenylalanine appeared in the circulation over a 5-h postprandial period. Casein ingestion resulted in a smaller (45% ± 11%), whey protein ingestion in an intermediate (57% ± 10%), and milk protein ingestion in a greater (65% ± 13%) fraction of dietary protein–derived phenylalanine appearing in the circulation (P &lt; 0.001). The postprandial availability of dietary protein–derived phenylalanine in the circulation increased with the ingestion of greater protein doses (P &lt; 0.05). Protein digestion and phenylalanine absorption kinetics were attenuated in older when compared with young individuals, with 45% ± 10% vs. 51% ± 14% of dietary protein–derived phenylalanine appearing in the circulation, respectively (P = 0.001). Conclusions Protein type, protein dose, and age modulate dietary protein digestion and amino acid absorption kinetics and subsequent postprandial plasma amino acid availability in vivo in humans. These trials were registered at clinicaltrials.gov as NCT00557388, NCT00936039, NCT00991523, NCT01317511, NCT01473576, NCT01576848, NCT01578590, NCT01615276, NCT01680146, NCT01820975, NCT01986842, and NCT02596542, and at http://www.trialregister.nl as NTR3638, NTR3885, NTR4060, NTR4429, and NTR4492.