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Amino acid metabolism
Nitrogen and urea cycle
Citric acid cycle
Electron transport chain and oxidative phosphorylation
Pentose phosphate pathway
Physiological changes during exercise
Fatty acid oxidation
Fatty acid synthesis
Ketone body metabolism
Maple syrup urine disease
Ornithine transcarbamylase deficiency
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Hereditary fructose intolerance
Pyruvate dehydrogenase deficiency
Glycogen storage disease type I
Glycogen storage disease type II (NORD)
Glycogen storage disease type III
Glycogen storage disease type IV
Glycogen storage disease type V
Mucopolysaccharide storage disease type 1 (Hurler syndrome) (NORD)
Mucopolysaccharide storage disease type 2 (Hunter syndrome) (NORD)
Fabry disease (NORD)
Gaucher disease (NORD)
Metachromatic leukodystrophy (NORD)
Niemann-Pick disease type C
Niemann-Pick disease types A and B (NORD)
Tay-Sachs disease (NORD)
Disorders of amino acid metabolism: Pathology review
Disorders of carbohydrate metabolism: Pathology review
Disorders of fatty acid metabolism: Pathology review
Dyslipidemias: Pathology review
Glycogen storage disorders: Pathology review
Lysosomal storage disorders: Pathology review
During physical exercise, our organs and tissues are working hard to keep us moving; or, technically speaking, for our musculoskeletal system to do its job.
Now it’s fairly obvious that during exercise, skeletal muscles work, or contract, harder and faster than when we’re at rest, so they use a lot of energy in a short time, so they need a lot more blood and oxygen to keep going.
So organ systems like the cardiovascular and respiratory system have to make some quick physiological adjustments, to meet the skeletal muscles demand.
Moreover, the endocrine system also kicks things into high gear, by secreting hormones like cortisol and adrenaline, that speed up intracellular processes to keep us going.
But before we delve into the specifics of that, let’s remember how muscle contraction works on a microscopic level.
So, skeletal muscles are made up of muscle fibers which are actually the skeletal muscle cells.
We just call them “fibers” because they are long, multinucleated cells, meaning they have more than one nucleus.
Their structure also differs from other cells because their cytoplasm, sometimes also called sarcoplasm, is filled with stacks of long filaments called myofibrils, which are made up of contractile units called sarcomeres.
And finally, sarcomeres are made up of the thick myosin filaments, and thin actin filaments, which can slide over one another, shortening the sarcomeres.
So when all the sarcomeres in a muscle fiber do that in sync, that results in shortening of the muscle as a whole, or muscle contraction.
And this process is powered by energy in the shape of ATP molecules, where adenosine-triphosphate.
The three phosphates in the molecule are linked in a chain, and between two adjacent phosphate molecules, there are high-energy phosphate bonds.
ATP molecules attach to a part of the myosin filament called the myosin head.
The myosin head is actually an ATPase, or an enzyme that can cleave an ATP molecule into ADP and phosphate ion, releasing the energy stored in the bonds.
After the energy is released, ADP detaches from the myosin head, so myosin can bind to actin filaments, forming cross-bridges that result in shortening of the muscle fiber.
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