Hypertrophy training is training with the goal of increasing the volume of the muscles. In humans, such an increase is not achieved by an increase in the number of cells (hyperplasia), but only by an increase in the size of the individual cells (hypertrophy).
Like other cells, muscle cells need an incentive to grow. This can be, for example, a growth messenger (for example, testosterone) or increased stress.
Muscle training leads to hypertrophy in two ways: on the one hand, more energy is consumed by high levels of stress than can be replenished by the metabolism of the cell.
There is a lack of energy and the rise of metabolites that are formed under stress, such as lactate.
These substances trigger a signaling pathway that, in particular, expands the elements responsible for supplying energy and allows the cell to burn more oxygen.
This increases the endurance of the muscles, less the maximum strength and the muscle cross section.
For an increase in the muscle cross-section, the direct mechanical load plays a greater role.
Muscle fibers are interconnected via adhesive elements to prevent the muscle from tearing apart. If these adhesive elements are heavily stressed or even injured (microtrauma), a signal pathway is triggered which leads to increased protein production.
In the process, other cells (satellite cells) in the vicinity of the muscle are integrated into the muscle fibers in order to enable higher protein production. The principle of hypertrophy training is based on exploiting these mechanisms.
First, a training stimulus is set, which exceeds the load capacity of the muscles. It comes to a degeneration, ie a violation of the muscles, then to the regeneration, in which the injured structures are repaired.
The mechanical stimulus leads to supercompensation. In this phase, a training stimulus can start the process again.
The man's prostate is a gland below the urinary bladder that produces some of the sperm's fluid. Not only the vas deferens, but also the beginning of the urethra pass through the prostate. The prostate is also in a tight capsule. If there is an increase in the size of the organ, therefore, the urethra is compressed and makes urinating more difficult. The increase in size of the prostate occurs in almost all men in later life. The cells of the prostate become both larger (hypertrophy) and more numerous (hyperplasia). Benign prostate hyperplasia is commonly referred to as the increase in size of the prostate gland (benign meaning that it is a harmless cell gain - as opposed to prostate cancer).
Symptoms of prostatic hypertrophy include delayed onset of urination, decreased urinary stream, residual urinary alert, and constant urinary urgency without proper drainage. In an advanced stage, incomplete bladder emptying with the risk of inflammation and even later a urinary blockage in the kidneys, which can lead to kidney damage and kidney failure. (
Hypertrophy can arise through different mechanisms. Messengers (hormones) can cause hypertrophy. There are a number of growth factors, such as growth hormone, that are released in childhood growth stages, leading to the growth of bones, muscles, and other organs. Sex hormones not only lead to the formation and growth of primary and secondary sexual characteristics, but also to muscle growth in the case of male sex hormones. The long-term impact of sex hormones lead to the condition prostate hyperplasia, which is very common among older men.
However, hypertrophy can also be caused by metabolic and mechanical stimuli. Thus, increased mechanical stress with damage to the cells leads to hypertrophy of the muscles, while endurance exercise leads to hypertrophy of the heart. However, hypertrophy can also be pathological. Some heart disease is associated with hypertrophy as compensation, and excessive sports hypertrophy of the heart can also lead to pathological changes in the heart. Another example is the hypertrophy of the thyroid gland in the disease Graves' disease, in which the thyroid is greatly stimulated by a malfunction of the immune system and hypertrophied.