Postexercise Glucose–Fructose Coingestion Augments Cycling Capacity During Short-Term and Overnight Recovery From Exhaustive Exercise, Compared With Isocaloric Glucose

During short-term recovery, postexercise glucose–fructose coingestion can accelerate total glycogen repletion and augment recovery of running capacity. It is unknown if this advantage translates to cycling, or to a longer (e.g., overnight) recovery. Using two experiments, the present research investigated if postexercise glucose–fructose coingestion augments exercise capacity following 4-hr (short experiment; n = 8) and 15-hr (overnight experiment; n = 8) recoveries from exhaustive exercise in trained cyclists, compared with isocaloric glucose alone. In each experiment, a glycogen depleting exercise protocol was followed by a 4-hr recovery, with ingestion of 1.5 or 1.2 g·kg−1·hr−1 carbohydrate in the short experiment (double blind) and the overnight experiment (single blind), respectively. Treatments were provided in a randomized order using a crossover design. Four or fifteen hours after the glycogen depletion protocol, participants cycled to exhaustion at 70% Wmax or 65% Wmax in the short experiment and the overnight experiment, respectively. In both experiments there was no difference in substrate oxidation or blood glucose and lactate concentrations between treatments during the exercise capacity test (trial effect, p > .05). Nevertheless, cycling capacity was greater in glucose + fructose versus glucose only in the short experiment (28.0 ± 8.4 vs. 22.8 ± 7.3 min, d = 0.65, p = .039) and the overnight experiment (35.9 ± 10.7 vs. 30.6 ± 9.2 min, d = 0.53, p = .026). This is the first study to demonstrate that postexercise glucose–fructose coingestion enhances cycling capacity following short-term (4 hr) and overnight (15 hr) recovery durations. Therefore, if multistage endurance athletes are ingesting glucose for rapid postexercise recovery then fructose containing carbohydrates may be advisable.

Effects of β-hydroxybutyrate treatment on glycogen repletion and its related signaling cascades in epitrochlearis muscle during 120 min of postexercise recovery

We investigated the effects of β-hydroxybutyrate (β-HB), the most abundant type of ketone body in mammals, on postexercise glycogen recovery in skeletal muscle by using an in vitro experimental model. Male ICR mice swam for 60 min and then their epitrochlearis muscles were removed and incubated with either physiological levels of glucose (8 mmol/L) and insulin (60 μU/mL) or glucose and insulin plus 1, 2, or 4 mmol/L of sodium β-HB. Four millimoles per liter β-HB had a significant positive effect on glycogen repletion in epitrochlearis muscle at 120 min after exercise (p < 0.01), while 2 mmol/L of β-HB showed a tendency to increase the glycogen level (p < 0.09), and 1 mmol/L of β-HB had no significant effect. We further investigated the effect of 4 mmol/L β-HB treatment on the signaling cascade related to glycogen repletion in the epitrochlearis muscles throughout a 120-min recovery period. After incubating the muscles in 4 mmol/L of β-HB for 15 min postexercise, the Akt substrate of 160 kDa Thr642 (p < 0.05) and Akt Thr308 (p < 0.05) phosphorylations were significantly increased compared with the control treatment. At the same time point, 5′-AMP–activated protein kinase and acetyl-coenzyme A carboxylase phosphorylations were significantly lower (p < 0.05) in the epitrochlearis muscle incubated with 4 mmol/L of β-HB than in the control muscle. Our results demonstrate that postexercise 4 mmol/L β-HB administration enhanced glycogen repletion in epitrochlearis muscle. Four millimoles per liter β-HB treatment was associated with alternation of the phosphorylated status of several proteins involved in glucose uptake and metabolic/energy homeostasis at the early stage of postexercise.

Liver glycogen metabolism during and after prolonged endurance-type exercise

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. 13C 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.

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 13C 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.