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Hardgainer
A hardgainer is a person who practices bodybuilding but finds it challenging to develop musculature regardless of the amount of effort put in. The opposite of a hardgainer is an easygainer. Difficulty building muscle is often associated with the ectomorph body somatotype, however other common reasons also include a lack of proper nutrition, suitable physical activity level or not allowing enough recovery time for the stressed muscles to regain their previous state and then grow bigger (overtraining). For the true hardgainer, the issue lies deeper beneath any of the required elements of muscle gain listed above. Those are typically either diseases that affect muscles and/or protein synthesis, or there might be a genetic disorder that hinders protein synthesis and/or limits the maximum amount of muscles the body can hold to a relatively small amount for that person. Muscular dystrophy is a group of inherited diseases that are characterized by weakness and wasting away of muscle t ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Bodybuilding
Bodybuilding is the use of progressive resistance exercise to control and develop one's muscles (muscle building) by muscle hypertrophy for aesthetic purposes. It is distinct from similar activities such as powerlifting because it focuses on physical appearance instead of strength. An individual who engages in this activity is referred to as a bodybuilder. In professional bodybuilding, competitors appear in lineups and perform specified poses (and later individual posing routines) for a panel of judges who rank them based on symmetry, muscularity, size, conditioning, posing, and stage presentation. Bodybuilders prepare for competitions through the elimination of nonessential body fat, enhanced at the last stage by a combination of extracellular dehydration and carbo-loading, to achieve maximum muscular definition and vascularity; they also tan and shave to accentuate the contrast of their skin under the spotlights. Bodybuilding takes a great amount of effort and time to r ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Metabolic Diseases
Inborn errors of metabolism form a large class of genetic diseases involving congenital disorders of enzyme activities. The majority are due to defects of single genes that code for enzymes that facilitate conversion of various substances (substrate (biochemistry), substrates) into others (Product (chemistry), products). In most of the disorders, problems arise due to accumulation of substances which are toxic or interfere with normal function, or due to the effects of reduced ability to synthesize essential compounds. Inborn errors of metabolism are now often referred to as congenital metabolic diseases or inherited metabolic disorders. To this concept it's possible to include the new term of Enzymopathy. This term was created following the study of Biochemical Processes, Biodynamic Enzymology, a science based on the study of the enzymes and their derivated products. Finally, ''inborn errors of metabolism'' were studied for the first time by British physician Archibald Garrod (1857â ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Phosphoglycerate Kinase Deficiency
Phosphoglycerate kinase () (PGK 1) is an enzyme that catalyzes the Reversible reaction, reversible transfer of a phosphate group from 1,3-bisphosphoglycerate (1,3-BPG) to Adenosine diphosphate, ADP producing 3-phosphoglycerate (3-PG) and Adenosine triphosphate, ATP : :1,3-bisphosphoglycerate + ADP glycerate 3-phosphate + ATP Like all kinases it is a transferase. PGK is a major enzyme used in glycolysis, in the first ATP-generating step of the glycolytic pathway. In gluconeogenesis, the reaction catalyzed by PGK proceeds in the opposite direction, generating ADP and 1,3-BPG. In humans, two isozymes of PGK have been so far identified, PGK1 and PGK2. The isozymes have 87-88% identical amino acid sequence identity and though they are structurally and functionally similar, they have different localizations: PGK2, encoded by an autosomal gene, is unique to meiotic and postmeiotic spermatogenic cells, while PGK1, encoded on the X-chromosome, is ubiquitously expressed in all cells. ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Phosphofructokinase Deficiency
Phosphofructokinase deficiency is a rare muscular metabolic disorder, with an autosomal recessive inheritance pattern. It may affect humans as well as other mammals (especially dogs). It was named after the Japanese physician Seiichiro Tarui (b. 1927), who first observed the condition in 1965. Presentation In humans Human PFK deficiency is categorized into four types: classic, late-onset, infantile and hemolytic. These types are differentiated by age at which symptoms are observed and which symptoms present. Classic form Classic phosphofructokinase deficiency is the most common type of this disorder. This type presents with exercise-induced muscle cramps and weakness (sometimes rhabdomyolysis), myoglobinuria, as well as with haemolytic anaemia causing dark urine a few hours later. Hyperuricemia is common, due to the kidneys' inability to process uric acid following damage resulting from processing myoglobin. Nausea and vomiting following strenuous exercise is another common ind ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Glycogen Storage Disease Type V
Glycogen storage disease type V (GSD5, GSD-V), also known as McArdle's disease, is a metabolic disorder, one of the metabolic myopathies, more specifically a muscle glycogen storage disease, caused by a deficiency of myophosphorylase. Its incidence is reported as one in 100,000, roughly the same as glycogen storage disease type I. The disease was first reported in 1951 by Dr. Brian McArdle of Guy's Hospital, London. Signs and symptoms The onset of this disease is usually noticed in childhood, but often not diagnosed until the third or fourth decade of life. Symptoms include exercise intolerance with muscle pain, early fatigue, painful cramps, inappropriate rapid heart rate response to exercise, and may include myoglobin in the urine (often provoked by a bout of exercise).Lucia A, Martinuzzi A, Nogales-Gadea G, Quinlivan R, Reason S; International Association for Muscle Glycogen Storage Disease study group. Clinical practice guidelines for glycogen storage disease V & VII (McA ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Myoadenylate Deaminase Deficiency
Adenosine monophosphate deaminase deficiency type 1 or AMPD1, is a human metabolic disorder in which the body consistently lacks the enzyme AMP deaminase, in sufficient quantities. This may result in exercise intolerance, muscle pain and muscle cramping. The disease was formerly known as myoadenylate deaminase deficiency. In virtually all cases, the deficiency has been caused by an SNP mutation, known as ''rs17602729'' or ''C34T''. While it was initially regarded as a recessive (or purely homozygous) disorder, some researchers have reported the existence of similarly deleterious effects from the heterozygous form of the SNP. In the homozygous form of the mutation, a single genetic base (character) has been changed from cytosine ("C") to thymine ("T") on both strands of Chromosome 1 – in other words, "C;C" has been replaced by "T;T". A rarer but analogous condition, in which two guanine bases ("G;G") bases (in the unmutated form) have been changed to adenine ("A;A") has also been ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Mitochondrial Myopathy
Mitochondrial myopathies are types of myopathies associated with mitochondrial disease. On biopsy, the muscle tissue of patients with these diseases usually demonstrate "ragged red" muscle fibers. These ragged-red fibers contain mild accumulations of glycogen and neutral lipids, and may show an increased reactivity for succinate dehydrogenase and a decreased reactivity for cytochrome c oxidase. Inheritance was believed to be maternal ( non-Mendelian extranuclear). It is now known that certain nuclear DNA deletions can also cause mitochondrial myopathy such as the OPA1 gene deletion. There are several subcategories of mitochondrial myopathies. Signs and symptoms Signs and symptoms include (for each of the following causes): * Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like syndrome (MELAS) ** Varying degrees of cognitive impairment and dementia ** Lactic acidosis ** Strokes ** Transient ischemic attacks ** Hearing loss ** Weight loss * Myoclonic epilepsy and ra ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Lactate Dehydrogenase Deficiency
Lactate dehydrogenase (LDH or LD) is an enzyme found in nearly all living cells. LDH catalyzes the conversion of lactate to pyruvate and back, as it converts NAD+ to NADH and back. A dehydrogenase is an enzyme that transfers a hydride from one molecule to another. LDH exists in four distinct enzyme classes. This article is specifically about the NAD(P)-dependent L-lactate dehydrogenase. Other LDHs act on D-lactate and/or are dependent on cytochrome c: D-lactate dehydrogenase (cytochrome) and L-lactate dehydrogenase (cytochrome). LDH is expressed extensively in body tissues, such as blood cells and heart muscle. Because it is released during tissue damage, it is a marker of common injuries and disease such as heart failure. Reaction Lactate dehydrogenase catalyzes the interconversion of pyruvate and lactate with concomitant interconversion of NADH and NAD+. It converts pyruvate, the final product of glycolysis, to lactate when oxygen is absent or in short supply ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Debrancher Enzyme Deficiency
Glycogen storage disease type III (GSD III) is an autosomal recessive metabolic disorder and inborn error of metabolism (specifically of carbohydrates) characterized by a deficiency in glycogen debranching enzymes. It is also known as Cori's disease in honor of the 1947 Nobel laureates Carl Cori and Gerty Cori. Other names include Forbes disease in honor of clinician Gilbert Burnett Forbes (1915–2003), an American physician who further described the features of the disorder, or limit dextrinosis, due to the limit dextrin-like structures in cytosol. Limit dextrin is the remaining polymer produced after hydrolysis of glycogen. Without glycogen debranching enzymes to further convert these branched glycogen polymers to glucose, limit dextrinosis abnormally accumulates in the cytoplasm. Glycogen is a molecule the body uses to store carbohydrate energy. Symptoms of GSD-III are caused by a deficiency of the enzyme amylo-1,6 glucosidase, or debrancher enzyme. This causes excess amount ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Carnitine Palmitoyltransferase II Deficiency
Carnitine palmitoyltransferase II deficiency is an autosomal recessively inherited genetic metabolic disorder characterized by an enzymatic defect that prevents long-chain fatty acids from being transported into the mitochondria for utilization as an energy source. The disorder presents in one of three clinical forms: lethal neonatal, severe infantile hepatocardiomuscular and myopathic. First characterized in 1973 by DiMauro and DiMauro the adult myopathic form of this disease is triggered by physically strenuous activities and/or extended periods without food and leads to immense muscle fatigue and pain. It is the most common inherited disorder of lipid metabolism affecting the skeletal muscle of adults, primarily affecting males. CPT II deficiency is also the most frequent cause of hereditary myoglobinuria. Signs and symptoms The three main types of carnitine palmitoyltransferase II deficiency classified on the basis of tissue-specific symptomatology and age of onset. Among t ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Carnitine Deficiency
Systemic primary carnitine deficiency (SPCD)Systemic primary carnitine deficiency Orphanet is an inborn error of fatty acid transport caused by a defect in the transporter responsible for moving across the . Carnitine is an important amino acid for fatty acid metabolism. When carnitine cannot be transported into tissues, ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Acid Maltase Deficiency
Glycogen storage disease type II, also called Pompe disease, is an autosomal recessive metabolic disorder which damages muscle and nerve cells throughout the body. It is caused by an accumulation of glycogen in the lysosome due to deficiency of the lysosomal acid alpha-glucosidase enzyme. It is the only glycogen storage disease with a defect in lysosomal metabolism, and the first glycogen storage disease to be identified, in 1932 by the Dutch pathologist J. C. Pompe. The build-up of glycogen causes progressive muscle weakness (myopathy) throughout the body and affects various body tissues, particularly in the heart, skeletal muscles, liver and the nervous system. Signs and symptoms Newborn The infantile form usually comes to medical attention within the first few months of life. The usual presenting features are cardiomegaly (92%), hypotonia (88%), cardiomyopathy (88%), respiratory distress (78%), muscle weakness (63%), feeding difficulties (57%) and failure to thrive (50%). ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
