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Exercising with low muscle glycogen content increases fat oxidation and decreases endogenous, but not exogenous carbohydrate oxidation.
Margolis, LM, Wilson, MA, Whitney, CC, Carrigan, CT, Murphy, NE, Hatch, AM, Montain, SJ, Pasiakos, SM
Metabolism: clinical and experimental. 2019;:1-8
Abstract
BACKGROUND Initiating aerobic exercise with low muscle glycogen content promotes greater fat and less endogenous carbohydrate oxidation during exercise. However, the extent exogenous carbohydrate oxidation increases when exercise is initiated with low muscle glycogen is unclear. PURPOSE Determine the effects of muscle glycogen content at the onset of exercise on whole-body and muscle substrate metabolism. METHODS Using a randomized, crossover design, 12 men (mean ± SD, age: 21 ± 4 y; body mass: 83 ± 11 kg; VO2peak: 44 ± 3 mL/kg/min) completed 2 cycle ergometry glycogen depletion trials separated by 7-d, followed by a 24-h refeeding to elicit low (LOW; 1.5 g/kg carbohydrate, 3.0 g/kg fat) or adequate (AD; 6.0 g/kg carbohydrate, 1.0 g/kg fat) glycogen stores. Participants then performed 80 min of steady-state cycle ergometry (64 ± 3% VO2peak) while consuming a carbohydrate drink (95 g glucose +51 g fructose; 1.8 g/min). Substrate oxidation (g/min) was determined by indirect calorimetry and 13C. Muscle glycogen (mmol/kg dry weight), pyruvate dehydrogenase (PDH) activity, and gene expression were assessed in muscle. RESULTS Initiating steady-state exercise with LOW (217 ± 103) or AD (396 ± 70; P < 0.05) muscle glycogen did not alter exogenous carbohydrate oxidation (LOW: 0.84 ± 0.14, AD: 0.87 ± 0.16; P > 0.05) during exercise. Endogenous carbohydrate oxidation was lower and fat oxidation was higher in LOW (0.75 ± 0.29 and 0.55 ± 0.10) than AD (1.17 ± 0.29 and 0.38 ± 0.13; all P < 0.05). Before and after exercise PDH activity was lower (P < 0.05) and transcriptional regulation of fat metabolism (FAT, FABP, CPT1a, HADHA) was higher (P < 0.05) in LOW than AD. CONCLUSION Initiating exercise with low muscle glycogen does not impair exogenous carbohydrate oxidative capacity, rather, to compensate for lower endogenous carbohydrate oxidation acute adaptations lead to increased whole-body and skeletal muscle fat oxidation.
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Repeated muscle glycogen supercompensation with four days' recovery between exhaustive exercise.
Doering, TM, Cox, GR, Areta, JL, Coffey, VG
Journal of science and medicine in sport. 2019;(8):907-911
Abstract
OBJECTIVES To determine if a 4 d period of high carbohydrate intake can supercompensate muscle glycogen and exercise work capacity on back-to-back occasions. DESIGN Seven trained cyclists (6 male, VO2peak: 57 ± 4 mL kg-1 min-1) completed a 9-d experimental period, consisting of three intermittent exhaustive cycling trials on days 1 (trial 1), 5 (trial 2) and 9 (trial 3). Following trial 1 cyclists were fed a high carbohydrate diet (˜10 g kg-1 day-1) for eight days to assess their capacity to repeatedly supercompensate muscle glycogen with 4 d recovery. METHODS A resting muscle biopsy was obtained prior to each trial consisting of 2 min work intervals (90-60% peak power output) interspersed with 2 min recovery (40% peak power output) repeated until exhaustion. Each 72-h period between trial days included two days of low volume cycling and a rest day. Resting muscle glycogen and total work completed was determined for each trial day. RESULTS Baseline muscle glycogen on day 1 (583.6 ± 111.0 mmol kg-1 dry mass) was supercompensated on day 5 (835.1 ± 112.8 mmol kg-1 dry mass; p = 0.04, d = 2.25) and again on day 9 (848.3 ± 111.4 mmol kg-1 dry mass; p = 0.01, d = 2.38). Total cycling work capacity increased from trial 1 to trial 2 (+8.7 ± 5.4 kJ kg-1; p = 0.01; d = 1.41); a large effect was observed in trial 3 compared to trial 1 (+6.4 ± 6.8 kJ kg-1; p = 0.10; d = 1.10). CONCLUSIONS A 4 d high carbohydrate feeding strategy is sufficient to repeatedly supercompensate muscle glycogen content following exhaustive exercise and results in enhanced work capacity.
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Ultrasound Does Not Detect Acute Changes in Glycogen in Vastus Lateralis of Man.
Routledge, HE, Bradley, WJ, Shepherd, SO, Cocks, M, Erskine, RM, Close, GL, Morton, JP
Medicine and science in sports and exercise. 2019;(11):2286-2293
Abstract
PURPOSE To examine the validity of ultrasound (via cloud-based software that measures pixilation intensity according to a scale of 0-100) to noninvasively assess muscle glycogen in human skeletal muscle. METHODS In study 1, 14 professional male rugby league players competed in an 80-min competitive rugby league game. In study 2 (in a randomized repeated measures design), 16 recreationally active males completed an exhaustive cycling protocol to deplete muscle glycogen followed by 36 h of HIGH or LOW carbohydrate intake (8 g·kg vs 3 g·kg body mass). In both studies, muscle biopsies and ultrasound scans were obtained from the vastus lateralis (at 50% of the muscle length) before and after match play in study 1 and at 36 h after glycogen depletion in study 2. RESULTS Despite match play reducing (P < 0.01) muscle glycogen concentration (pregame: 443 ± 65; postgame: 271 ± 94 mmol·kg dw, respectively) in study 1, there were no significant changes (P = 0.4) in ultrasound scores (pregame: 47 ± 6, postgame: 49 ± 7). In study 2, muscle glycogen concentration was significantly different (P < 0.01) between HIGH (531 ±129 mmol·kg dw) and LOW (252 ± 64 mmol·kg dw) yet there was no difference (P = 0.9) in corresponding ultrasound scores (HIGH: 56 ± 7, LOW: 54 ± 6). In both studies, no significant correlations (P > 0.05) were present between changes in muscle glycogen concentration and changes in ultrasound scores. CONCLUSIONS Data demonstrate that ultrasound (as based on measures of pixilation intensity) is not valid to measure muscle glycogen status within the physiological range (i.e., 200-500 mmol·kg dw) that is applicable to exercise-induced muscle glycogen utilization and postexercise muscle glycogen resynthesis.
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Structural basis of glycogen metabolism in bacteria.
Cifuente, JO, Comino, N, Trastoy, B, D'Angelo, C, Guerin, ME
The Biochemical journal. 2019;(14):2059-2092
Abstract
The evolution of metabolic pathways is a major force behind natural selection. In the spotlight of such process lies the structural evolution of the enzymatic machinery responsible for the central energy metabolism. Specifically, glycogen metabolism has emerged to allow organisms to save available environmental surplus of carbon and energy, using dedicated glucose polymers as a storage compartment that can be mobilized at future demand. The origins of such adaptive advantage rely on the acquisition of an enzymatic system for the biosynthesis and degradation of glycogen, along with mechanisms to balance the assembly and disassembly rate of this polysaccharide, in order to store and recover glucose according to cell energy needs. The first step in the classical bacterial glycogen biosynthetic pathway is carried out by the adenosine 5'-diphosphate (ADP)-glucose pyrophosphorylase. This allosteric enzyme synthesizes ADP-glucose and acts as a point of regulation. The second step is carried out by the glycogen synthase, an enzyme that generates linear α-(1→4)-linked glucose chains, whereas the third step catalyzed by the branching enzyme produces α-(1→6)-linked glucan branches in the polymer. Two enzymes facilitate glycogen degradation: glycogen phosphorylase, which functions as an α-(1→4)-depolymerizing enzyme, and the debranching enzyme that catalyzes the removal of α-(1→6)-linked ramifications. In this work, we rationalize the structural basis of glycogen metabolism in bacteria to the light of the current knowledge. We describe and discuss the remarkable progress made in the understanding of the molecular mechanisms of substrate recognition and product release, allosteric regulation and catalysis of all those enzymes.
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Carbohydrate dose influences liver and muscle glycogen oxidation and performance during prolonged exercise.
King, AJ, O'Hara, JP, Morrison, DJ, Preston, T, King, RFGJ
Physiological reports. 2018;(1)
Abstract
This study investigated the effect of carbohydrate (CHO) dose and composition on fuel selection during exercise, specifically exogenous and endogenous (liver and muscle) CHO oxidation. Ten trained males cycled in a double-blind randomized order on 5 occasions at 77% V˙O2max for 2 h, followed by a 30-min time-trial (TT) while ingesting either 60 g·h-1 (LG) or 75 g·h-113 C-glucose (HG), 90 g·h-1 (LGF) or 112.5 g·h-113 C-glucose-13 C-fructose ([2:1] HGF) or placebo. CHO doses met or exceed reported intestinal transporter saturation for glucose and fructose. Indirect calorimetry and stable mass isotope [13 C] tracer techniques were utilized to determine fuel use. TT performance was 93% "likely/probable" to be improved with LGF compared with the other CHO doses. Exogenous CHO oxidation was higher for LGF and HGF compared with LG and HG (ES > 1.34, P < 0.01), with the relative contribution of LGF (24.5 ± 5.3%) moderately higher than HGF (20.6 ± 6.2%, ES = 0.68). Increasing CHO dose beyond intestinal saturation increased absolute (29.2 ± 28.6 g·h-1 , ES = 1.28, P = 0.06) and relative muscle glycogen utilization (9.2 ± 6.9%, ES = 1.68, P = 0.014) for glucose-fructose ingestion. Absolute muscle glycogen oxidation between LG and HG was not significantly different, but was moderately higher for HG (ES = 0.60). Liver glycogen oxidation was not significantly different between conditions, but absolute and relative contributions were moderately attenuated for LGF (19.3 ± 9.4 g·h-1 , 6.8 ± 3.1%) compared with HGF (30.5 ± 17.7 g·h-1 , 10.1 ± 4.0%, ES = 0.79 & 0.98). Total fat oxidation was suppressed in HGF compared with all other CHO conditions (ES > 0.90, P = 0.024-0.17). In conclusion, there was no linear dose response for CHO ingestion, with 90 g·h-1 of glucose-fructose being optimal in terms of TT performance and fuel selection.
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Glycophagy: An emerging target in pathology.
Zhao, H, Tang, M, Liu, M, Chen, L
Clinica chimica acta; international journal of clinical chemistry. 2018;:298-303
Abstract
Autophagy, a highly conserved self-digestion process, is initially regarded as non-selectively sequestering and degradation cytoplasmic contents. Nowadays, many kinds of selective autophagy have been found in response to various physiological cues such as mitophagy, reticulophagy and glycophagy. Glycophagy, as a selective autophagy, plays a crucial role in maintaining glucose homeostasis in many tissues including heart, liver and skeletal muscles. Moreover, glycophagy is highly regulated by many signal pathways like the cyclic AMP protein kinase A/protein kinase A, PI3K-Akt/PKB-mTOR and Calcium. Latest studies have demonstrated that glycophagy is triggered by STBD1, which tethers glycogen to membranes via binding itself to the cognate autophagy protein GABARAPL1. More importantly, glycophagy might act as a protective role in coping with the accumulation of glycogen-rich lysosomes in infant patients with Pompe disease. However, glycophagy might aggravate diabetic cardiomyopathy via FoxO1 signal pathway. In this review, we focus on some findings about the occurrence and development, as well as the regulatory mechanism of glycophagy. We also analyze the role of glycophagy in Pompe disease and diabetic cardiomyopathy. Targeting glycophagy may open a new avenue of therapeutic intervention to these diseases.
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Do We Need a Cool-Down After Exercise? A Narrative Review of the Psychophysiological Effects and the Effects on Performance, Injuries and the Long-Term Adaptive Response.
Van Hooren, B, Peake, JM
Sports medicine (Auckland, N.Z.). 2018;(7):1575-1595
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Abstract
It is widely believed that an active cool-down is more effective for promoting post-exercise recovery than a passive cool-down involving no activity. However, research on this topic has never been synthesized and it therefore remains largely unknown whether this belief is correct. This review compares the effects of various types of active cool-downs with passive cool-downs on sports performance, injuries, long-term adaptive responses, and psychophysiological markers of post-exercise recovery. An active cool-down is largely ineffective with respect to enhancing same-day and next-day(s) sports performance, but some beneficial effects on next-day(s) performance have been reported. Active cool-downs do not appear to prevent injuries, and preliminary evidence suggests that performing an active cool-down on a regular basis does not attenuate the long-term adaptive response. Active cool-downs accelerate recovery of lactate in blood, but not necessarily in muscle tissue. Performing active cool-downs may partially prevent immune system depression and promote faster recovery of the cardiovascular and respiratory systems. However, it is unknown whether this reduces the likelihood of post-exercise illnesses, syncope, and cardiovascular complications. Most evidence indicates that active cool-downs do not significantly reduce muscle soreness, or improve the recovery of indirect markers of muscle damage, neuromuscular contractile properties, musculotendinous stiffness, range of motion, systemic hormonal concentrations, or measures of psychological recovery. It can also interfere with muscle glycogen resynthesis. In summary, based on the empirical evidence currently available, active cool-downs are largely ineffective for improving most psychophysiological markers of post-exercise recovery, but may nevertheless offer some benefits compared with a passive cool-down.
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Restoration of Muscle Glycogen and Functional Capacity: Role of Post-Exercise Carbohydrate and Protein Co-Ingestion.
Alghannam, AF, Gonzalez, JT, Betts, JA
Nutrients. 2018;(2)
Abstract
The importance of post-exercise recovery nutrition has been well described in recent years, leading to its incorporation as an integral part of training regimes in both athletes and active individuals. Muscle glycogen depletion during an initial prolonged exercise bout is a main factor in the onset of fatigue and so the replenishment of glycogen stores may be important for recovery of functional capacity. Nevertheless, nutritional considerations for optimal short-term (3-6 h) recovery remain incompletely elucidated, particularly surrounding the precise amount of specific types of nutrients required. Current nutritional guidelines to maximise muscle glycogen availability within limited recovery are provided under the assumption that similar fatigue mechanisms (i.e., muscle glycogen depletion) are involved during a repeated exercise bout. Indeed, recent data support the notion that muscle glycogen availability is a determinant of subsequent endurance capacity following limited recovery. Thus, carbohydrate ingestion can be utilised to influence the restoration of endurance capacity following exhaustive exercise. One strategy with the potential to accelerate muscle glycogen resynthesis and/or functional capacity beyond merely ingesting adequate carbohydrate is the co-ingestion of added protein. While numerous studies have been instigated, a consensus that is related to the influence of carbohydrate-protein ingestion in maximising muscle glycogen during short-term recovery and repeated exercise capacity has not been established. When considered collectively, carbohydrate intake during limited recovery appears to primarily determine muscle glycogen resynthesis and repeated exercise capacity. Thus, when the goal is to optimise repeated exercise capacity following short-term recovery, ingesting carbohydrate at an amount of ≥1.2 g kg body mass-1·h-1 can maximise muscle glycogen repletion. The addition of protein to carbohydrate during post-exercise recovery may be beneficial under circumstances when carbohydrate ingestion is sub-optimal (≤0.8 g kg body mass-1·h-1) for effective restoration of muscle glycogen and repeated exercise capacity.
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Insulin Regulates Glycogen Synthesis in Human Endometrial Glands Through Increased GYS2.
Flannery, CA, Choe, GH, Cooke, KM, Fleming, AG, Radford, CC, Kodaman, PH, Jurczak, MJ, Kibbey, RG, Taylor, HS
The Journal of clinical endocrinology and metabolism. 2018;(8):2843-2850
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Abstract
CONTEXT Glycogen synthesis is a critical metabolic function of the endometrium to prepare for successful implantation and sustain embryo development. Yet, regulation of endometrial carbohydrate metabolism is poorly characterized. Whereas glycogen synthesis is attributed to progesterone, we previously found that the metabolic B isoform of the insulin receptor is maximally expressed in secretory-phase endometrium, indicating a potential role of insulin in glucose metabolism. OBJECTIVE We sought to determine whether insulin or progesterone regulates glycogen synthesis in human endometrium. DESIGN, PARTICIPANTS, OUTCOME MEASUREMENTS Endometrial epithelial cells were isolated from 28 healthy women and treated with insulin, medroxyprogesterone (MPA), or vehicle. Intracellular glycogen and the activation of key enzymes were quantified. RESULTS In epithelia, insulin induced a 4.4-fold increase in glycogen, whereas MPA did not alter glycogen content. Insulin inactivated glycogen synthase (GS) kinase 3α/β (GSK3α/β), relieving inhibition of GS. In a regulatory mechanism, distinct from liver and muscle, insulin also increased GS by 3.7-fold through increased GS 2 (GYS2) gene expression. CONCLUSIONS We demonstrate that insulin, not progesterone, directly regulates glycogen synthesis through canonical acute inactivation of GSK3α/β and noncanonical stimulation of GYS2 transcription. Persistently elevated GS enables endometrium to synthesize glycogen constitutively, independent of short-term nutrient flux, during implantation and early pregnancy. This suggests that insulin plays a key, physiological role in endometrial glucose metabolism and underlines the need to delineate the effect of maternal obesity and hyperinsulinemia on fertility and fetal development.
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Fundamentals of glycogen metabolism for coaches and athletes.
Murray, B, Rosenbloom, C
Nutrition reviews. 2018;(4):243-259
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The ability of athletes to train day after day depends in large part on adequate restoration of muscle glycogen stores, a process that requires the consumption of sufficient dietary carbohydrates and ample time. Providing effective guidance to athletes and others wishing to enhance training adaptations and improve performance requires an understanding of the normal variations in muscle glycogen content in response to training and diet; the time required for adequate restoration of glycogen stores; the influence of the amount, type, and timing of carbohydrate intake on glycogen resynthesis; and the impact of other nutrients on glycogenesis. This review highlights the practical implications of the latest research related to glycogen metabolism in physically active individuals to help sports dietitians, coaches, personal trainers, and other sports health professionals gain a fundamental understanding of glycogen metabolism, as well as related practical applications for enhancing training adaptations and preparing for competition.