Dominic Stone
Glycogen is a form of glucose, a primary energy source for the body, which is stored in the liver and muscles. During exercise, skeletal muscles are the major tissue that uses glucose for energy, and glycogen is the main energy substrate during high-intensity exercise. Therefore, muscle glycogen storage will deplete without sufficient carbohydrate intake. Certain hormones play a role in glycogen storage and energy metabolism, including insulin and glucagon. Insulin increases glucose uptake in muscles, while glucagon triggers the conversion of glycogen to glucose in the liver and increases blood sugar levels. Additionally, growth hormone increases protein retention, and hormones like glucagon, epinephrine, and glucocorticoids mobilize energy reserves to help the body cope with adverse situations. Furthermore, exercise-induced peroxisome proliferator-activated γ-receptor co-activator 1α (PGC-1α) activity may spare muscle glycogen, potentially improving exercise performance.
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What You'll Learn
Insulin stimulates glucose uptake in skeletal muscles
Insulin is a hormone that plays a crucial role in regulating blood glucose levels in the body. When blood glucose levels are high, the pancreas releases insulin to bring these levels back into the normal range. Insulin stimulates glucose uptake in skeletal muscles, which is essential for maintaining overall blood glucose control.
Skeletal muscle is the principal tissue for insulin-stimulated glucose disposal, making it a key player in whole-body glycemic control. In fact, skeletal muscle is responsible for over 80% of glucose uptake from an oral glucose load. This process is facilitated by glucose transporters, specifically GLUT4, GLUT1, and GLUT3 (with GLUT3 only being expressed in fetal and neonatal muscle).
GLUT4 is the most abundant and well-known insulin-regulated glucose transporter in skeletal muscle. It is an intracellular protein that requires a stimulus, such as insulin or exercise, to translocate to the plasma membrane and facilitate glucose uptake. When insulin is released by the pancreas, it stimulates the translocation of GLUT4 to the cell surface, allowing glucose to enter the cell.
However, in some cases, skeletal muscle can develop insulin resistance, which is a key defect in Type 2 Diabetes. Insulin resistance occurs when the muscle becomes desensitized to insulin, resulting in impaired glucose uptake and elevated blood glucose levels. This can be influenced by various factors, including chronic hyperinsulinemia, which can reduce insulin-stimulated glucose disposal and total-body glucose uptake. Additionally, O-GlcNAc, which is increased in the skeletal muscle of obese and Type 2 Diabetic individuals, can inhibit components of the insulin-stimulated glucose uptake pathway, contributing to insulin resistance.
In summary, insulin stimulates glucose uptake in skeletal muscles by activating glucose transporters, particularly GLUT4, which translocate to the cell surface in response to insulin. This process is vital for maintaining blood glucose homeostasis, and disruptions in this mechanism can lead to insulin resistance and metabolic disorders such as Type 2 Diabetes.
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Glucagon triggers glycogenolysis
Glucagon is a hormone that is produced by the alpha cells in the islets of Langerhans, which are located in the endocrine portion of the pancreas. It is released in response to low blood glucose levels (hypoglycemia). When blood glucose levels are high, the pancreas releases insulin, which decreases blood sugar levels. Together, glucagon and insulin work to regulate blood glucose levels.
Additionally, glucagon inhibits the liver from taking in and storing glucose, ensuring that more glucose remains in the bloodstream. This process is particularly important during fasting, exercise, or hypoglycemia, when the body needs to maintain stable energy levels. During prolonged fasting, glucagon also triggers the formation of glucose from non-carbohydrate sources, such as lipids, amino acids, and proteins, through a process called gluconeogenesis.
Overall, glucagon plays a crucial role in regulating blood glucose levels and ensuring the body has sufficient energy by triggering glycogenolysis and other metabolic processes.
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Muscle glycogen content and exercise type
Glycogen is a form of glucose, a main source of energy that is stored in the liver and muscles. During exercise, the body uses glycogen to maintain blood glucose levels as the working muscles use it for energy.
The amount of glycogen content in the muscles depends on body composition. The more muscle mass one has, the more glycogen can be stored. It is important to note that the glycogen content in the muscles being actively used during exercise is what matters, rather than the total glycogen content in the body. For example, the glycogen content in the triceps is relevant when doing push-ups, but not when running.
Exercise type also plays a role in muscle glycogen content. Intense and prolonged exercise can substantially reduce glycogen content in active muscle cells, but it generally does not fall below 10% of initial values. Glycogen depletion negatively affects endurance exercise performance. However, recent research suggests that endurance training with low glycogen availability can lead to similar or even better adaptations and performance compared to training with replenished glycogen stores.
To improve performance and speed up recovery, it is recommended to consume a diet rich in carbohydrates and ingest carbohydrates during and after exercise. Post-exercise carbohydrate ingestion improves exercise recovery by increasing glycogen resynthesis. Additionally, consuming carbohydrates before exercise ensures that the body begins the activity with ample muscle glycogen stores, which contribute to improved exercise performance.
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Glycogenesis and glycogenolysis
Glycogenolysis is the breakdown of glycogen into glucose. When the amount of glucose in the blood decreases and the body needs glucose, the stored glycogen in the liver and muscles is broken down to form glucose. This process is carried out by the enzyme glycogen phosphorylase. The liver then releases the glucose into the bloodstream, so it can be used by cells throughout the body for energy. This process of liberating glucose from glycogen is called glycogenolysis.
The pancreas releases the hormone glucagon to trigger glycogenolysis. Glucagon increases blood sugar levels to prevent them from falling too low (hypoglycemia). It does this by stimulating the liver to convert stored glycogen into glucose and preventing the liver from taking in and storing more glucose. The pancreas also releases insulin, which brings blood sugar levels back down when they get too high. Together, glucagon and insulin are the primary hormones that regulate blood glucose levels.
Exercise can affect glycogen availability. For example, endurance training with low glycogen availability can lead to better performance compared to training with replenished glycogen stores. Enhanced activity of PGC-1α and increased mitochondrial volume improve oxidative capacity through increased fatty acid β-oxidation and mitigating glycogenolysis. As a result, muscle glycogen can be spared, delaying the onset of muscle fatigue and enhancing oxidative exercise performance.
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Growth hormone and muscle glycogen
Insulin and glucagon are the primary hormones that regulate the body's blood glucose levels. Glucagon is a hormone that triggers glycogen to convert back into glucose and enter the bloodstream for energy. Insulin, on the other hand, is released when blood glucose levels are high to bring them back into range.
Growth hormone (GH) is a peptide hormone predominantly secreted by somatotrophs in the anterior pituitary. It is considered the primary anabolic hormone during stress and fasting. During these states, GH stimulates the release and oxidation of free fatty acids (FFA), which leads to decreased glucose oxidation and preservation of glycogen stores. This is particularly important for the preservation of lean body mass (LBM) and glycogen reserves.
In well-nourished individuals, GH-induced stimulation of insulin and insulin-like growth factor 1 (IGF-I) is crucial for the anabolic storage and growth of LBM, adipose tissue, and glycogen reserves. GH also increases insulin secretion and glucose uptake, with short-term exposure inhibiting insulin-stimulated glucose disposal and blunting glycogen synthase activity in skeletal muscle.
Research has shown that growth hormone replacement therapy can induce insulin resistance by activating the glucose-fatty acid cycle. This ability of GH to induce insulin resistance is significant in preventing hypoglycemia and may play a role in the development of "stress" diabetes during fasting and inflammatory illness.
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Frequently asked questions
Glycogen is a form of glucose, a main source of energy that your body stores primarily in your liver and muscles.
Insulin and glucagon are the primary hormones that regulate your body’s blood glucose levels and spare muscle glycogen. Insulin increases the movement of glucose into peripheral tissues, including muscle and fat. Glucagon triggers glycogen in your liver to convert back to glucose so it can enter your bloodstream and be used for energy.
When your body doesn't need glucose right away, it stores it as glycogen in your liver and muscles.
