The fight, fright, or flight response to stressors involves the catecholamines, substances that prepare the body for a call to immediate action and response, by causing short-term hyperglycemia. This rapid catabolism of blood glucose is the result of liver-glycogen storage breakdown and an increased rate of gluconeogenesis. Catecholamines can also liberate rapid stores of energy by catabolizing fat from adipose tissue stores. The stress adaptation phase primarily involves glucocorticoids, released by the adrenal cortex, that have a profound effect on energy metabolism and biologic functions. These substances raise blood-sugar levels, increase muscle-protein breakdown and hepatic gluconeogenesis, and mobilize fatty acids.11
Following normal diurnal patterns for the release of serum cortisol, glucocorticoid levels are at their lowest point at approximately midnight to 1 am. Peak levels occur between 6 am and 8 am. Research has shown that elevation or suppression of daily cortisol levels indicates imbalanced hypothalamus-pituitary-axis (HPA) activity.12 This may be interpreted as hyper-function or hypofunction, depending on a patient's levels of cortisol and his or her clinical presentation. Sustained activation of the sympathetic nervous system marks the compensation stage, also known as the adrenal hyperfunction stage, with a secondary influence on the HPA axis. The pituitary gland responds to the influence of sympathetic nervous system activity by releasing adrenocorticotropic hormone (ACTH). In turn, the adrenal glands respond to the pituitary release of ACTH by producing excess cortisol and androgen hormones. In an attempt to compensate for this faulty hyperfunction, the HPA becomes less sensitive to the influence of cortisol's feedback inhibition. As serum cortisol levels rise, glucose utilization declines and insulin resistance increases, gluconeogenesis in the liver increases, and blood glucose levels increase rapidly. In addition, the body responds to increased cortisol by increasing the degradation of protein stores to supply amino acids for gluconeogenesis in an attempt to mobilize energy rapidly. Adrenal hyperfunction can be marked by a tendency toward insulin resistance, hypertension, mild obesity, and elevated serum lipid and triglyceride levels. What is more, high cortisol and lowered DHEA have been shown to suppress the immune system.13 Histologic studies have revealed lowered production of secretory immunoglobulin A (sIgA) in the mucus membranes of competition swimmers under the influence of chronic levels of physiologic and psychologic stressors. At this phase of the stress response, athletes and other individuals will often complain of a decrease in performance or work production and a generalized feeling of lassitude. The final stage of the stress response is the adrenal hypofunction stage or the fatigue stage. The body's ability to synthesize Cortisol and other corticosteroid hormones is greatly diminished. The resulting excessive fatigue, changes in a person's ability to concentrate, inability to tolerate alcohol, intractable headaches, lowered blood pressure, menstrual irregularities, reactive hypoglycemia, and carbohydrate sensitivity may follow.14 With this compromised ability to control inflammation, the body goes into a pro-inflammatory state. The absence of cortisol leads to an increase in endogenous inflammatory eicosanoids and cytokines and leads to eventual tissue damage and degenerative disease.15
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