Circulating Beta-endorphin Levels Research Articles

Beta-endorphin response to exercise. An update.

beta-Endorphin, a 31-amino-acid peptide, is primarily synthesised in the anterior pituitary gland and cleaved from pro-opiomelanocortin, its larger precursor molecule. beta-Endorphin can be released into the circulation from the pituitary gland or can project into areas of the brain through nerve fibres. Exercise of sufficient intensity and duration has been demonstrated to increase circulating beta-endorphin levels. Previous reviews have presented the background of opioids and exercise and discussed the changes in beta-endorphin levels in response to aerobic and anaerobic exercise. The present review is to update the response of beta-endorphin to exercise. This review suggests that exercise-induced beta-endorphin alterations are related to type of exercise and special populations tested, and may differ in individuals with health problems. Additionally, some of the possible mechanisms which may induce beta-endorphin changes in the circulation include analgesia, lactate or base excess, and metabolic factors. Based on the type of exercise, different mechanisms may be involved in the regulation of beta-endorphin release during exercise.

Endogenous beta-endorphins in hypertension: Correlation with 24-hour ambulatory blood pressure

The aims of this study were to determine whether hypertensive patients showed increased endogenous opioid tone and to find a possible correlation between beta-endorphin levels and 24-h ambulatory blood pressure. We also investigated whether circulating beta-endorphin levels were associated with pain perception at rest. Experimental studies suggest an involvement of the endogenous opioid system in cardiovascular control mechanisms. We determined baseline beta-endorphin plasma levels by radioimmunoassay in 81 consecutive subjects (48 hypertensive, 33 normotensive) after a 30-min rest and before 24-h ambulatory blood pressure monitoring. In 72 of 81 subjects with a dental formula suitable for the pulpar test (graded increase of test current -0 to 0.03 mA applied to three healthy teeth), pain perception was also investigated. Hypertensive patients showed higher beta-endorphin plasma levels than normotensive subjects (p < 0.002). Circulating endogenous opioid levels correlated with 24-h diastolic blood pressure (p < 0.01), whereas the relation with systolic pressure did not reach statistical significance. When 24-h blood pressure recordings were divided into daytime and nighttime values, and blood pressure loads (percent of measurements > or = 140 mm Hg for systolic blood pressure and > or = 90 mm Hg for diastolic pressure) were calculated, a significant correlation was found between beta-endorphin levels and diastolic pressures and load. Similarly, presampling diastolic blood pressure was significantly correlated with beta-endorphin levels. Of the 72 subjects tested, hypertensive patients showed a lower pain sensitivity than normotensive subjects. A positive correlation was found between pain threshold and circulating beta-endorphin levels (p < 0.05). Sustained arterial pressure is probably involved in the tonic activation of cardiovascular mechanisms linked to endogenous opioid tone. Circulating plasma endorphins may account, at least in part, for the pain perception pattern relating to blood pressure levels at rest.

Analgesic effect and beta-endorphin and substance P levels in plasma after short-term administration of a ketoprofen-lysine salt or acetylsalicylic acid in patients with osteoarthrosis

Osteoarthrosis is a chronic degenerative disease that involves a high disability rate and creates serious social problems. This study compared the analgesic effect after short-term administration of a keto-profen-lysine salt and acetylsalicylic acid (ASA) as well as the behavior of plasma-circulating beta-endorphin and substance P levels, which appear to be related to the analgesic response in some pathologic conditions. The ketoprofen-lysine salt significantly increased circulating beta-endorphin levels from 30 minutes until 12 hours after administration and reduced substance P levels until 18 hours. Modifications in plasma beta-endorphin and substance P induced by administration of ASA generally were not significant.

Is Fetal Blood Sampling Associated with Increased Beta-Endorphin Release into the Fetal Circulation?

This study was conducted to determine whether fetal blood sampling during the second trimester is associated with changes in circulating fetal beta-endorphin (BE) concentrations. We measured BE concentrations in 68 paired fetal and maternal blood samples obtained between 18 and 28 weeks' gestation. Patients were divided into a control group (n = 50), if the fetal blood samples were obtained by a single umbilical cord puncture, or multiple insertion group (n = 18), if multiple cord punctures were required to obtain a sample. The mean (+/- SE) fetal BE value for the multiple insertion group was significantly higher than BE levels from the control group (771.2 +/- 79.2 pg/ml versus 107.1 +/- 11.7 pg/ml; p < 0.001]. This elevation did not appear to be related to acidosis, since no differences in fetal umbilical pH were observed between the two groups. Fetal BE levels from the control but not from the multiple insertion group significantly correlated with maternal values (Spearman rank r = 0.59; p < 0.001 vs r = -0.08; p > 0.5). In neither group did fetal BE levels correlate with gestational age. These findings indicate that multiple cord punctures at the time of fetal blood sampling are associated with significant increases in BE release. Furthermore, although a maternal or placental contribution to steady state circulating fetal BE cannot be excluded, it would seem that the fetus itself is the primary source of elevated circulating BE levels following multiple cord punctures.

The effects of glucose ingestion and fasting on plasma immunoreactive beta-endorphin, adrenocorticotropic hormone and cortisol in obese subjects.

It has been demonstrated that opioid peptides are involved in the stimulation of food intake in rats and that the circulating beta-endorphin levels are increased in genetically obese rodents. Therefore, to assess whether the changes in food intake may influence circulating beta-endorphin levels in obese subjects, plasma beta-endorphin, ACTH and cortisol concentrations were determined in obese patients after an oral glucose load and during a 7-day total starvation. Baseline plasma beta-endorphin concentrations were significantly higher in obese patients than in control normal-weight subjects, while ACTH and cortisol levels were similar in both groups. Plasma beta-endorphin, ACTH and cortisol concentrations were not affected by the ingestion of 75 g glucose, neither were plasma beta-endorphin concentrations modified during prolonged starvation. Moreover, the lack of nycthemeral variations in beta-endorphin levels, documented before and during starvation while plasma ACTH and cortisol were significantly reduced in the evening, suggests that some extra anterior pituitary sources or some obesity-related changes in beta-endorphin metabolism may contribute to the pool of circulating beta-endorphin in obese subjects. On the other hand, even the extreme changes in nutritional conditions, such as total food deprivation or glucose ingestion, are devoid of any detectable influence on circulating beta-endorphin levels.

Naltrexone potentiates glycemic responses during stress and epinephrine challenge in genetically obese mice.

The genetically obese mouse (C57BL/6J ob/ob) is a commonly used animal model of non-insulin-dependent diabetes mellitus. These mice show exaggerated glycemic responses during behavioral stress and adrenergic stimulation, but the precise glucoregulatory mechanisms are not well characterized. The ob/ob mice have multiple endocrine abnormalities, including elevated pituitary and circulating beta-endorphin levels; and a relationship between hyperglycemia and altered opioid function has been suspected. We now report that opiate antagonism with naltrexone potentiates hyperglycemic responses during stress and epinephrine challenge in obese mice. This effect of opioid blockade suggests that endogenous opioids inhibit stress- and epinephrine-induced hyperglycemia in the genetically obese mouse.

α‐θ Brainwave Training and β‐Endorphin Levels in Alcoholics

An alpha-theta brainwave biofeedfack training program was applied as a novel treatment technique for chronic alcoholics. Following a temperature biofeedback pretraining phase, experimental subjects completed 15 30-min sessions of alpha-theta biofeedback training. Compared to a nonalcoholic control group and a traditionally treated alcoholic control group, alcoholics receiving brainwave training (BWT) showed significant increases in percentages of EEG record in alpha and theta rhythms, and increased alpha rhythm amplitudes. Alcoholics receiving BWT showed a gradual increase in alpha and theta brain rhythms across the 15 experimental sessions. These experimentally treated alcoholics showed sharp reductions in self-assessed depression (Beck's Depression Inventory) compared to the control groups. Alcoholics receiving standard medical treatment (abstinence, group psychotherapy, antidepressants) showed a significant elevation in serum beta-endorphin levels at the conclusion of the experiment. This neuropeptide is an index of stress and a stimulant of caloric (e.g., ethanol) intake. Application of brainwave treatment, a relaxation therapy, appears to counteract the increase in circulating beta-endorphin levels seen in the control group of alcoholics. 13-month follow-up data indicate sustained prevention of relapse in alcoholics that completed alpha-theta brainwave training.