Resistance exercise decreases beta-endorphin immunoreactivity.

Previous research investigating the response of plasma beta-endorphins (beta-EP) to resistance exercise has resulted in equivocal findings. To examine further the effects of resistance exercise on beta-EP immunoreactivity, 10 male and 10 female college-age students participated in a series of controlled isotonic resistance exercises. The session consisted of three sets of eight repetitions at 80% of one repetition maximum (1-RM) for each of the following exercises: (1) bench press; (2) lateral pull-downs; (3) seated arm curls; and (4) military press. Blood plasma was sampled both before and after the lifting routine and beta-endorphin levels were determined by radioimmunoassay. A Students t test for paired samples indicated that mean(s.e.) plasma beta-endorphin levels after exercise (10.5(1.3) pg beta-EP ml-1) were significantly decreased as compared with pre-exercise (control) levels (16.5(1.2), P < 0.05). While the mechanism(s) contributing to the decrease in immunoreactivity is unclear, it may be the result of the synergistic effect of beta-EP clearance during rest intervals and changes in psychological states between sampling.

Beta-endorphin response to endurance exercise: relationship to exercise dependence.

Considerable research has shown significant increases in beta-endorphin levels after aerobic activity. These increases and their accompanying euphoric effect have been suggested as a possible psychophysiological mechanism underlying the exercise-dependence syndrome. The relationship between plasma beta-endorphin levels and a tendency towards exercise dependence, however, has not been established. To examine this relationship, 8 women trained in aerobic dance completed an exercise-dependence assessment prior to participation in a 45-min. session of continuous aerobic dance. Plasma beta-endorphin concentration was measured both prior to and following the aerobics routine. A Student t test for paired observations indicated that mean plasma beta-endorphin levels (+/- SE) were significantly higher after the aerobics routine (11.96 +/- 1.3 pg beta-EP.ml-1) than preexercise levels (8.62 +/- 1.4). However, beta-endorphin difference values (% change) were not significantly correlated with scores on the exercise-dependence survey. Those data suggest that scores on exercise dependence are not related to changes in plasma beta-endorphin levels after aerobic exercise.

Plasma beta-endorphin immunoreactivity: response to resistance exercise.

Previous research investigating the response of plasma beta-endorphins (beta-EP) to resistance exercise has resulted in equivocal findings. To further examine the effects of resistance exercise on beta-endorphin immunoreactivity, six resistance-trained athletes participated in a three-set series of eight repetitions of isotonic exercise. All exercises were performed at 80% maximal effort. Blood was sampled from the group by venepuncture, both prior to and following the exercise bout, and beta-endorphin concentration was determined by radioimmunoassay. The results indicated that mean (+/- S.E.) plasma levels of beta-endorphins following exercise (18.04 +/- 3.4 pg beta-EP ml-1) were not significantly changed from pre-exercise (control) levels (19.59 +/- 2.4 pg beta-EP ml-1), although there was considerable inter-individual variability. Our results support previous research which has reported no significant changes in beta-endorphin immunoreactivity following resistance exercise, as well as reported findings of considerable variability in the beta-endorphin response to exercise.

Morphine-induced modulation of calcitonin gene-related peptide levels.

Calcitonin gene-related peptide (CGRP) is a novel calcium-modulatory product of the gene that encodes for calcitonin. Acute administration of morphine decreases levels of CGRP in rat corpus striatum. Tolerance to morphine did not alter the levels of CGRP in any brain region or in the spinal cord of the rat. CGRP did not alter the tolerance to the antinociceptive effects of morphine. Chronic naltrexone increased the levels of CGRP in the hypothalamus. Concurrent chronic administration of naltrexone plus morphine raised the levels of CGRP in the medulla, midbrain, and spinal cord. CGRP enhances naloxone-precipitated withdrawal jumping in mice. In rats, during withdrawal the levels of CGRP were tripled in the corpus striatum and significantly reduced in the hippocampus and hypothalamus. In the corpus striatum, CGRP enhances forskolin-stimulated cyclic adenosine monophosphate (cAMP) accumulation when such accumulation is suppressed (as with the chronic opiate administration), but conversely depresses forskolin-stimulated cAMP accumulation under normal conditions (as with chronic vehicle administration). These data are consistent with the hypothesis that CGRP acts as a modulatory peptide in opiate-sensitive systems and tonic opioid control of CGRP levels exists in brain.

Salmon calcitonin-induced modulation of free intracellular calcium.

Salmon calcitonin (sCT), a hormone shown to modulate calcium in the periphery modulated free, intracellular calcium, ([Ca++]i), in mouse brain synaptosomes as measured by changes in fura-2-mediated fluorescence. A 5-min incubation of synaptosomes with sCT produced an increase in the basal levels of [Ca++]i and an increase in KCl-stimulated levels of [Ca++]i. A 5-min pretreatment of mice with intraventricularly administered sCT antagonized morphine-induced antinociception in the tail-flick test, and facilitated naloxone antagonism of morphine. Conversely, pretreatment of synaptosomes for 1 h with salmon CT produced a decrease in depolarization-stimulated levels of [Ca++]i. The sCT-induced decrease in the stimulated rise in [Ca++]i at 1 h correlated temporally to sCT-induced antinociception in vivo. The effects of sCT in the electrically stimulated guinea pig ileum bioassay appeared to correlate to sCT effects in vivo. The data indicate that calcitonin may function as a neuromodulator via modulation of Ca++ within the central nervous system.

Effects of hyperbaric simulation of scuba diving pressure on plasma beta-endorphin.

In contrast to our previous studies on the submersion of scuba divers in a state of neutral buoyancy, neither plasma beta-endorphin-like immunoreactivity (beta-EIR) nor affective feelings were significantly changes in scuba divers by mimicking diving pressures of 2 feet (0.6 m) and 50 feet (15.2 m) for 20 min in a hyperbaric chamber. It is concluded that the submersion-induced increase in plasma beta-EIR and accompanying changes in affect reported previously are not due solely to changes in pressure.

Opiate tolerance-induced modulation of free intracellular calcium in synaptosomes.

Synaptosomes were prepared from morphine-tolerant and non-tolerant mice. Significantly higher levels of basal free intracellular calcium were observed in the synaptosomes from the opiate-tolerant mice compared to synaptosomes from non-tolerant mice (468 nM versus 328 nM, respectively). In addition, morphine (1 microM) failed to attenuate KCl-induced rises in intracellular calcium in the synaptosomes from the tolerant mice. Conversely, morphine produced a concentration-related, naloxone-reversible attenuation of 50 mM KCl-induced rises in intracellular calcium in the synaptosomes from the non-tolerant mice. Omega conotoxin, which blocks both "L" and "N" type calcium channels, attenuated KCl-stimulated rises in intracellular calcium only in synaptosomes from non-tolerant mice. BAY-K 8644, an "L-type" calcium channel agonist, produced nifedipine-reversible increases in intracellular calcium in the synaptosomes from the tolerant animals only. These data suggest that chronic exposure to morphine results in an alteration in either the number of the activation state of calcium channels in the membrane. Changes in intracellular free calcium may be the final common pathway through which neurons adapt to the chronic exposure to morphine.

The effects of dynorphin A (1-13) and U50, 488H on free intracellular calcium in guinea pig cerebellar synaptosomes.

The effects of the kappa-selective ligands dynorphin A (1-13) (DYN) and U50, 488H (U50) on free intracellular calcium were evaluated using synaptosomes prepared from the cerebellum of the guinea pig, an area with a high density of kappa receptors. DYN (10 microM) produced small nonsignificant decreases in basal free intracellular calcium (5-7%). U50 (10 microM) produced significant 15-20% decreases in basal free intracellular calcium which were reversed by nor-BNI (1 microM). When intracellular calcium levels were increased 8-10% by the administration of c-AMP or forskolin, DYN (10 microM) produced significant decreases in intracellular calcium of 10%. The effects of U50, 488H were not enhanced by increasing the synaptosomal levels of c-AMP. Neither DYN nor U50 (1 microM) significantly blocked the rise in free intracellular calcium induced by 50 mM KCI. When intracellular calcium concentrations were increased by the administration of 50 mM KCI prior to the administration of DYN or U50 (10 microM), the kappa ligands decreased intracellular calcium concentrations. These data indicate that DYN and U50 interact with kappa receptors resulting in a decrease in free intracellular calcium possibly via an enhancement of the efflux of calcium. The modulation of intracellular free calcium by the kappa opioids may be a mechanism by which these opioids produce their biological effects.