During prenatal development, infancy, and childhood, GH and IGF-1 levels are low, but progressively increase and reach a peak at puberty, with a 1.5- to 3-fold increase in pulsatile GH secretion and a 3-fold or greater increase in serum IGF-1 levels being capable of occurring at this time. In late adolescence and early adulthood, GH and IGF-1 levels significantly decrease, and continue to decrease throughout the rest of life. It has been found that both estrogen and GH are essential for breast development at puberty – in the absence of either, no development will take place. Moreover, most of the role of GH in breast development has been found to be mediated by its induction of IGF-1 production and secretion, as IGF-1 administration rescues breast development in the absence of GH. GH induction of IGF-1 production and secretion occurs in almost all types of tissue in the body, but especially in the liver, which is the source of approximately 80% of circulating IGF-1, as well as locally in the breasts. Although IGF-1 is responsible for most of the role of GH in mediating breast development, GH itself has been found to play a direct, augmenting role as well, as it increases estrogen receptor (ER) expression in breast stromal (connective) tissue, while IGF-1, in contrast, has been found to not do this.
There is little to no compensatory increase in heart rate or blood pressure when standing for up to 10 minutes. This is often due to an underlying disorder or medication use and is accompanied by other hypoadrenergic signs. Central nervous system ischemia
The central ischemic response is triggered by an inadequate supply of oxygenated blood in the brain. Common examples include strokes and transient ischemic attacks. While these conditions often impair consciousness they rarely meet the medical definition of syncope. Vertebrobasilar transient ischemic attacks may produce true syncope as a symptom.The respiratory system may compensate for dropping oxygen levels through hyperventilation, though a sudden ischemic episode may also proceed faster than the respiratory system can respond. These processes cause the typical symptoms of fainting: pale skin, rapid breathing, nausea, and weakness of the limbs, particularly of the legs. If the ischemia is intense or prolonged, limb weakness progresses to collapse. The weakness of the legs causes most people to sit or lie down if there is time to do so. This may avert a complete collapse, but whether the patient sits down or falls down, the result of an ischaemic episode is a posture in which less blood pressure is required to achieve adequate blood flow. An individual with very little skin pigmentation may appear to have all color drained from his or her face at the onset of an episode. This effect combined with the following collapse can make a strong and dramatic impression on bystanders.