Allan H. Goldfarb

β-Endorphin Response to Exercise

Summaryβ-Endorphin, a 31-amino-acid peptide, is primarily synthesised in the anterior pituitary gland and cleaved from pro-opiomelanocortin, its larger precursor molecule. β-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 β-endorphin levels. Previous reviews have presented the background of opioids and exercise and discussed the changes in β-endorphin levels in response to aerobic and anaerobic exercise. The present review is to update the response of β-endorphin to exercise. This review suggests that exercise-induced β-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 β-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 β-endorphin release during exercise.

Resistance exercise effects on blood glutathione status and plasma protein carbonyls: Influence of partial vascular occlusion

Seven weight-trained males performed both light resistance with partial occlusion (LRO: 30% 1xa0RM) and moderate resistance (MR: 70% 1xa0RM) to failure to ascertain whether blood protein carbonyls (PC) and glutathione status was altered compared to partial occlusion (PO) in a counterbalanced fashion. PO was identical in duration to the LRO session and all sessions were on separate days. PC did not differ for the three conditions at PRE (0.05xa0nMxa0mgxa0protein−1). PC significantly increased for PO and MR over time and was greater than the LRO treatment at POST (0.13xa0nMxa0mgxa0protein−1). The GSSG/TGSH ratio at PRE did not differ across treatments (8%) whereas the ratio at POST was significantly elevated for PO and MR treatments (17%). In contrast, no change occurred for the LRO session at any time. These results indicate that MR to failure and PO can significantly increase blood oxidative stress but LRO did not elicit oxidative stress.

Beta-endorphin infusion alters pancreatic hormone and glucose levels during exercise in rats

Abstractβ-Endorphin (BE) infusion at rest can influence insulin and glucagon levels and thus may affect glucose availability during exercise. To clarify the effect of BE on levels of insulin, glucagon and glucose during exercise, 72 untrained male Sprague-Dawley rats were infused i.v. with either: (1) BE (bolus 0.05u2009mgu2009·u2009kg−1 +0.05u2009mgu2009·u2009kg−1u2009·u2009h−1, nu2009=u200924); (2) naloxone (N, bolus 0.8u2009mgu2009·u2009kg−1u2009+u20090.4u2009mgu2009·u2009kg−1, nu2009=u200924); or (3) volume-matched saline (S, nu2009=u200924). Six rats from each group were killed after 0, 60, 90 or 120 min of running at 22u2009mu2009·u2009min−1, at 0% gradient. BE infusion resulted in higher plasma glucose levels at 60u2009min [5.93 (0.32)u2009mM] and 90u2009min [4.16 (0.29)u2009mM] of exercise compared to S [4.62 (0.27) and 3.41 (0.26u2009mM] and N [4.97 (0.38) and 3.44 (0.25)u2009mM]. Insulin levels decreased to a greater extent with BE [21.5 (0.9) and 18.3 (0.6) uIUu2009·u2009ml−1] at 60 and 90u2009min compared to S [24.5 (0.5) and 20.6 (0.6)u2009uIUu2009·u2009ml−1] and N [24.5 (0.4) and 21.6 (0.7)u2009uIUu2009· ml−1] groups. Plasma C-peptide declined to a greater extent at 60 and 90u2009min of exercise with BE infusion compared to both S and N. BE infusion increased glucagon at all times during exercise compared to S and N. These data suggest that BE infusion during exercise influences plasma glucose by augmenting glucagon levels and attenuating insulin release.

Low carbohydrate diet induces changes in central and peripheral beta-endorphins

Abstract Sprague-Dawley male rats (n=21) weighing 175 ± 10 g, after one week of control diet feeding, were assigned to one of two treatments for another week: a) control diet group (CD) which was fed a diet consisting of 65% carbohydrate (n=10), and b) low carbohydrate diet group (LCD) which was fed an isocaloric diet consisting of 5% carbohydrate (n=11). Rats were killed by decapitation under pentobarbital anesthesia after a 12 hour fast. Brain tissue and mixed arteriovenous blood were collected. Body weight, weight gain and food intake were unaffected by diet (159.2 ± 9.8 g vs 158.5 ± 7.5 g, 52.5 g vs 51.0 g, and 14.3 ± 1.7 g vs 14.5 ± 1.8 g for CD and LCD, respectively. Hypothalamic and plasma B-Endorphin (B-EP) were significantly elevated in the LCD compared to the CD (376.7 ± 17.5 pmol/g vs 153.0 ± 14.7 pmol/g, and 8.7 ± 1.2 pg/ml vs 4.7± 1.4 pg/ml, p

Vitamin E reduces peroxisomal fatty acid oxidation and indicators of oxidative stress in untrained, exercised rats treated with dehydroepiandrosterone (DHEA)

Abstract The protective effect of vitamin E (Vit E) on oxidative stress induced by dehydroepiandrosterone (DHEA) treatment in untrained, exercised, male Sprague-Dawley rats was investigated. Thirty-two rats were treated with DHEA (0 or 100 mg/kg body weight/d i.p) and/or Vit E (0 or 1 g/kg diet) for 5 weeks. Untrained rats were exercised for 1 hr on a motorized rodent treadmill immediately prior to being killed. DHEA treatment decreased (P

Exercise and Endogenous Opiates

Endogenous opiates, endorphins and enkephalins, influence numerous processes within the body including pain, cardiac function, cellular growth, immunity, and blood glucose regulation. Both opiates are released in the brain and stay within the brain compartment. Beta-endorphins (βE) released into the blood arise primarily from the anterior pituitary gland but are also released from immune cells. Generally, acute aerobic exercise of sufficient intensity (>60 % VO2 max) can also increase circulating βE, with higher exercise intensity increasing βE to a greater extent. Exercise duration may also influence βE blood concentration. High-intensity anaerobic exercise can increase circulating βE. Resistance exercise depending on total work volume and relative intensity level can elevate blood βE. Aerobically trained individuals need to work at a greater absolute workload to manifest similar blood βE increases compared to untrained individuals. Circulating βE levels at rest are unaffected in both men and women after aerobic training with both genders being comparable. Resistance training does not appear to influence resting βE blood levels. However, it should be noted that most resistance studies utilized trained subjects. The elevation in βE appears to help modify the immune response, alter blood pressure, pain, and assists with blood glucose regulation during exercise. Limited research on enkephalins and exercise has been reported and the results are equivocal. A limited number of studies have reported an increased enkephalin level within certain regions of the brain. There are discrepancies with the enkephalin response to endurance training. Clearly more research is needed in the area of endogenous opioids and exercise especially within the CNS compartment.