Victor Forge
Glycogen is a fuel source stored in the cytosol of cells, occupying 2% of the volume of cardiac cells, 1-2% of the volume of skeletal muscle cells, and 5-6% of the volume of liver cells. The accumulation of glycogen in the fetal heart helps the heart deal with increased energy demands. Studies have shown that glycogen deposits are present within the nuclei of normal human cardiac muscle cells. However, some studies have also shown a lack of glycogen in cardiac muscle cells. So, does cardiac muscle store glycogen?
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What You'll Learn
Cardiac muscle glycogen may increase during fasting
Fasting involves a significant change in cellular physiology and metabolism. While blood glucose typically provides the body with sufficient energy through glycolysis, during fasting, the body's maintenance of blood glucose levels relies on glycogen stores in the liver and skeletal muscle.
Cardiac muscle does store glycogen, and it is possible that cardiac muscle glycogen may increase during fasting. The heart converts chemical energy, in the form of substrates and oxygen, to mechanical energy (cardiac work) and heat (calories). Cardiac muscle cells contain large amounts of monoparticulate glycogen, which is a metabolic reserve that is readily mobilized in times of need.
During fasting, the body shifts its energy source from carbohydrates to triglycerides. This shift is triggered by a glycogen shortage in the liver, which activates a liver-brain-adipose-tissue neurocircuit. This neurocircuit signals the switch in fuel source from liver glycogen to triglycerides in fat cells. The liver has a crucial role in maintaining blood glucose levels during fasting, and when its glycogen stores are depleted, the body begins to use adipose tissue and protein for energy.
While fasting, the body's dependence on glucose gradually decreases as ketone bodies become more readily available for metabolism. The process of gluconeogenesis, which produces glucose from amino acids, also occurs during fasting. However, the rate of glucose production through gluconeogenesis is limited and may not be sufficient to maintain blood glucose levels during exercise or other periods of increased energy demand.
Fasting practices, such as intermittent fasting or religious observances like Ramadan, can result in metabolic responses that are contrary to maintaining high muscle glycogen concentrations, especially if physical activity continues during the fast. However, the impact of fasting on muscle glycogen concentration is minimal for resting individuals, as muscle glycogen is not a major fuel source in this state.
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Glycogen is a repository of glucose in mammalian tissues
Glycogen is a form of glucose, a main source of energy for the body. It is stored primarily in the liver and muscles, with small amounts in the kidneys, red and white blood cells, glial cells in the brain, and the uterus during pregnancy. The body creates glycogen from glucose through a process called glycogenesis and breaks it down through glycogenolysis. This process is regulated by the hormones insulin and glucagon, which promote anabolism and catabolism, respectively.
Glycogen is a branched biopolymer consisting of linear chains of glucose residues with an average chain length of approximately 8–12 glucose units and 2,000–60,000 residues per molecule of glycogen. It is composed of two major bonds, alpha-1,4 and alpha-1,6 glycosidic bonds, which give rise to linear chains and branching points, respectively. The branching of glycogen allows for increased water solubility and provides several sites for breakdown, facilitating quick and easy utilisation when needed.
In the liver, glycogen can make up 5–6% of the organ's fresh weight, while in skeletal muscle, it is found in lower concentrations of 1–2%. The accumulation of glycogen (metabolic reserve) in the fetal heart is a mechanism to meet the increased energy demands of the developing heart. Cardiac muscle cells contain large amounts of monoparticulate glycogen, as revealed by electron microscopic studies.
Overall, glycogen serves as a repository of glucose in mammalian tissues, providing a readily available source of energy for the body's needs.
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Absence of heart glycogen can cause abnormal cardiac development
The absence of glycogen in the heart has been linked to abnormal cardiac development and function. This has been demonstrated in mice models where a disruption of the GYS1 gene, which encodes an isoform of glycogen synthase, has resulted in a lack of heart glycogen. These GYS1-deficient mice exhibit smaller heart sizes, dilated atria, thin ventricular walls, and abnormal formation of the ventricular septum. The hearts of these mice also show impaired function, with pooled blood in the atria and blood vessels, indicating poor cardiac performance.
The role of glycogen in cardiac development is crucial, as it serves as a repository of glucose in mammalian tissues. The accumulation of glycogen in the fetal heart helps meet the increased energy demands during this critical period of growth and maturation. This is particularly important for developing cardiomyocytes to proliferate and support adequate circulation in embryos.
In the case of GYS1-null mice, the absence of glycogen leads to smaller hearts, reduced proliferative activity, and impaired cardiac function. This suggests that glycogen is an essential energy source for the developing heart. Interestingly, it has been observed that a small percentage of embryos can pass through this critical stage without cardiac glycogen, which may be due to other genetic factors or differences in species.
The study of abnormal cardiac development in the absence of heart glycogen has provided valuable insights into the potential causes of congenital heart defects in humans. Congenital heart disease is one of the most common birth defects, affecting up to 1 in 50 live births. By understanding the role of glycogen in cardiac development, researchers can explore new avenues for prevention and treatment, potentially reducing the incidence of these defects.
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Glycogen deposits found in human cardiac muscle cells
The presence of glycogen deposits within the nuclei of hypertrophied and normal human cardiac muscle cells has been observed in multiple studies. These intranuclear glycogen deposits were discovered through ultrastructural and cytochemical studies of myocardial biopsies.
In one study, electron microscopy revealed large, rounded, or polygonal cells containing large amounts of monoparticulate glycogen. These cells, known as cardiac rhabdomyomas, are likely hamartomas. Another study observed glycogen deposits in the form of rosettes in the cardiac muscle cells of patients with aortic valvular disease and idiopathic hypertrophic subaortic stenosis. These rosettes were identified as a pathologic alteration of glycogen metabolism in hypertrophied and degenerated cardiac muscle cells.
The accumulation of glycogen in the fetal heart serves as a mechanism to meet increased energy demands. This process is regulated by the GYS1 gene, which encodes GS, promoting glycogen synthesis. Abnormal cardiac development and function can occur when this gene is disrupted.
The discovery of glycogen deposits in human cardiac muscle cells provides valuable insights into cardiac metabolism and its potential implications for cardiac function and various cardiac diseases.
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Glycogen storage is essential for glucose homeostasis
Glycogen is a form of glucose, a primary source of energy for the body. Carbohydrates from food are essential for the body to form glucose and glycogen. The body creates glycogen from glucose through a process called glycogenesis and breaks down glycogen for use through glycogenolysis.
Glycogen is stored in the liver and skeletal muscles, with the highest concentrations in the liver. Glycogen functions as the body's short-term storage of glucose, while triglycerides in adipose tissues serve as long-term storage. The liver plays a crucial role in regulating blood glucose levels. Glycogen in the liver serves as a store of glucose for use throughout the body, especially in the central nervous system. The brain consumes about 60% of blood glucose in fasted, sedentary individuals.
The breakdown of glycogen is controlled by the peptide hormones insulin and glucagon, which are produced in the pancreas. Insulin decreases blood glucose levels, while glucagon increases them. Insulin is responsible for adding glucose to glycogen under energy-rich conditions, thus lowering blood glucose levels. Glucagon, on the other hand, stimulates the breakdown of glycogen, increasing blood glucose levels.
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Frequently asked questions
Yes, cardiac muscle stores glycogen. Ultrastructural and cytochemical studies of myocardial biopsies have shown the presence of glycogen deposits within nuclei of hypertrophied and normal cardiac muscle cells.
Glycogen serves as a repository of glucose in many mammalian tissues, including the heart. It is a fuel source stored in the cytosol of cells, occupying 2% of the volume of cardiac cells. The ability to synthesize glycogen in cardiac muscle is critical for normal heart development, and its impairment could be a significant contributor to congenital heart defects.
A lack of glycogen in the cardiac muscle can lead to abnormal cardiac development and function. In mice, the disruption of the GYS1 gene, which encodes an isoform of glycogen synthase, resulted in impaired cardiac function and smaller heart size. Similarly, in humans, a homozygous stop mutation in the muscle glycogen synthase gene caused profound muscle and heart glycogen deficiency, leading to sudden cardiac arrest in one case.
Interestingly, cardiac muscle glycogen may be increased during fasting as gluconeogenic substrates such as amino acids and glycerol are converted to glucose and stored as glycogen to ensure the heart has adequate energy reserves.
