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28. 5. 2012.

Hormones in human body - general info


Hormones are involved in most physiological processes, so their actions are relevant to many aspects of exercise and sport performance. A discussion of hormonal control is included cause hormones significantly affect metabolism. However, hormones play key roles in almost every system of the body. Here will be described general mechanisms by which hormones act and their chemical nature.

Chemical classification of hormones

Hormones can be categorized as two basic types: steroid hormones and nonsteroid hormones. Steroid hormones have a chemical structure similar to cholesterol, since most are derived from cholesterol. For this reason, they are soluble in lipids and diffuse rather easily through cell membranes. This group includes the hormones secreted by:
  • The adrenal cortex(such as cortisol and aldosterone);
  • The ovaries(estrogen and progesterone);
  • The testes(testosterone), and
  • The placenta(estrogen and progesterone).

Nonsteroid hormones are not lipid soluble, so they cannot easily cross cell membranes. The nonsteroid hormone group can be subdivided into two groups: protein or peptide chormones and amino acid-derived hormones. The two hormones from the thyroid gland(thyroxine and triiodothyronine) and the two from the adrenal medulla(epinephrine and norepinephrine) are amino acid hormones. All other nonsteroid hormones are protein or peptide hormones. 



Hormone actions

Because hormones travel in the blood, they contact virtually all body tissues. How, then, do they limit their effects to specific targets? This ability is attributable to the specific hormone receptors possessed by the target tissues. The interaction between the hormone and its specific receptor has been compared with a lock(receptor) and key(hormone) arrangement, in which only the correct key can unlock a given action within the cells. The combination of a hormone bound to its receptor is referred to as a hormone-receptor complex.
Each cell typically has from 2,000 to 10,000 receptors. Receptors for nonsteroid hormones are located  on the cell membrane, whereas those for steroid hormones are found either in the cell’s cytoplasm or in its nucleus. Each hormone is usually highly specific for a single type of receptor and binds only with its specific receptors, thus affecting only tissues that contain those specific receptors. Numerous mechanisms allow hormones to control the actions of cells.



As mentioned earlier, steroid hormones are lipid soluble and thus pass easily through the cell membrane. Their mechanism of action is illustrated below. Once inside the cell, a steroid hormone binds to its specific receptors. The hormone-receptor complex then enters the nucleus, binds to part of the cell’s DNA, and activates certain genes. This process is referred to as direct gene activation. In response to this activation, mRNA is synthesized within the nucleus. The mRNA then enters the cytoplasm and promotes protein synthesis. These proteins may be:
  • Enzymes that can have numerous effects on cellular processes;
  • Structural proteins to be used for tissue growth and repair;
  • Regulatory proteins that can alter enzyme function.

Because nonsteroid hormones cannot cross the cell membrane, they react with specific receptors outside the cell, on the cell membrane. A nonsteroid hormone molecule binds to its receptor and triggers a series of enzymatic reactions that lead to the formation of an intracellular second messenger. A widely distributed second messenger that mediates a specific hormone-receptor response is cyclic adenosine monophosphate(cyclic AMP, or cAMP). This mechanism is illustrated in the picture below.



In this case, attachment of the hormone to the appropriate membrane receptor activates an enzyme, adenylate cyclase, situated within the cell membrane. This enzyme catalyzes the formation of cAMP from cellular ATP. Cyclic AMP then can produce specific physiological responses, which can include:
  • Activation of cellular enzymes
  • Change in membrane permeability
  • Change in cellular metabolism
  • Stimulation of cellular secretions.

Thus, nonsteroid hormones typically activate the cAMP system of the cell, which then alters intracellular functions.
Hormones are not secreted uniformly, but rather are released in relatively brief bursts, so plasma concentrations of specific hormones fluctuate over short periods such as an hour or less. But these concentrations also fluctuate over longer periods of time, showing daily or even monthly cycles(such as monthly menstrual cycles). How do endocrine glands know when to release their hormones?
Most hormone secretion is regulated by a negative feedback system. Secretion of a hormone causes some change in the body, and this change in turn inhibits further hormone secretion. Consider how a home thermostat works. When the room temperature decreases below some preset level, the thermostat signals the furnace to produce heat. When the room temperature increases to the preset level, the thermostat’s signal ends, and the furnace stops producing heat. When the temperature again falls below the preset level, the cycle begins anew. In the body, secretion of a specific hormone is similary turned on or off(or up or down) by specific physiological changes.
Negative feedback is the primary mechanism through which the endocrine system maintains homeostasis. Using the example of plasma glucose concentrations and the hormone insulin, when the plasma glucose concentration is high, the pancrease releases insulin. Insulin increases cellular uptake of glucose, lowering plasma concentration of glucose. When plasma glucose concentration returns to normal, insulin release is inhibited until the plasma glucose level increases again.

Hormone receptors

The plasma concentration of a specific hormone is not always the best indicator of that hormone’s activity because the number of receptors on target cells can be altered to increase or decrease that cell’s sensitivity to the hormone. Most commonly, an increased amount of a specific hormone decreases the number of cell receptors available to it. When this happens, the cell becomes less sensitive to that hormone, because with fewer receptors, fewer hormone molecules can bind. This is reffered to as downregulation, or desensitization. In some people with obesity, for example, the number of insulin receptors on their cells appears to be reduced. Their bodies respond by increasing insulin secretion from the pancreas, so their plasma insulin concentrations increase. To obtain the same degree of plasma glucose control as normal, healthy people, these individuals must release much more insulin.
In a few instances, a cell may respond to the prolonged presence of large amounts of a hormone by increasing its number of available receptors. When this happens, the cell becomes more sensitive to that hormone because more can be bound at one time. This is reffered to as upregulation. In addition, one hormone occasionally can regulate the receptors for another hormone.

Prostaglandins

Prostaglandins, although technically not hormones, are often considered to be  a third class of hormones. These substances are derived from a fatty acid, arachidonic acid, and they are associated with the plasma membranes of almost all body cells. Prostaglandins typically act as local hormones, exerting their effects in the immediate area where they are produced. But some also survive long enough to circulate through the blood to affect distant tissues. Prostaglandin release can be triggered by many stimuli, such as other hormones or a local injury. Their functions are quite numerous because there are several different types of prostaglandins. They often mediate the effects of other hormones. They are also known to act directly on blood vessels, increasing vascular permeability(which promotes swelling) and vasodilatation. In this capacity, they are important mediators of the inflammatory response. They also sensitize the nerve endings of pain fibers; thus, they promote both inflammation and pain.

“Physiology of sport and exercise”, fourth edition; Jack H. Wilmore, David L. Costill, W. Larry Kenney

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