Damage to the CNS as a result of stroke or spinal cord injury, alter the [net inhibition] of peripheral nerves in the affected region. This change in input to bodily structures tends to favor excitation and therefore increase nerve excitability. CNS damage also causes nerve cell membranes to rest in a more [depolarized] state. The combination of decreased inhibition and an increased depolarized state of cell membranes, decreases action potential threshold for nerve signal conduction, and thus increases activity of structures innervated by the affected nerves (spasticity). Muscles affected in this way have many other potential features of altered performance in addition to spasticity, including muscle weakness; decreased movement control; clonus (a series of involuntary rapid muscle contractions often symptomatic of muscle over-exertion and/or muscle fatigue); exaggerated deep tendon reflexes; and decreased endurance. Spasticity and clonus
Clonus (i.e. involuntary, rhythmic, muscular contractions and relaxations) tends to co-exist with spasticity in many cases of stroke and spinal cord injury likely due to their common physiological origins. Some consider clonus as simply an extended outcome of spasticity. Although closely linked, clonus is not seen in all patients with spasticity. Clonus tends to not be present with spasticity in patients with significantly increased muscle tone, as the muscles are constantly active and therefore not engaging in the characteristic on/off cycle of clonus. Clonus results due to an increased motor neuron excitation (decreased action potential threshold) and is common in muscles with long conduction delays, such as the long reflex tracts found in distal muscle groups.
When an ovum is released from the ovary, the structure that remains develops into the corpus luteum. The corpus luteum emits the hormone progesterone during the 10–16 days of the luteal phase. Without experiencing regular, ovulatory menstrual cycles, the female is not secreting the hormone progesterone during the luteal phase of her cycle. Progesterone directly stimulates osteoblasts to make new bone. Therefore if the woman is not ovulating, she is not creating progesterone, and misses out on this opportunity to stimulate new bone growth. Causes
Gymnastics, figure skating, ballet, diving, swimming, and long distance running are examples of sports which emphasize low body weight. The triad is seen more often in aesthetic sports such as these versus ball game sports. Women taking part in these sports may be at an increased risk for developing RED-S.Athletes at greatest risk for low energy availability are those who restrict dietary energy intake, who exercise for prolonged periods, who are vegetarian, and who limit the types of food they will eat. Many factors appear to contribute to disordered eating behaviors and clinical eating disorders. Dieting is a common entry point and interest has focused on the contribution of environmental and social factors, psychological predisposition, low self-esteem, family dysfunction, abuse, biological factors, and genetics. Additional factors for athletes include early start of sport-specific training and dieting, injury, and a sudden increase in training volume. Surveys show more negative eating attitude scores in athletic disciplines favoring leanness. Disordered eating behaviors are risk factors for eating disorders.