β-Endorphin and corticotropin release is dependent on a threshold intensity of running exercise in male endurance athletes

Rahkila, Paavo; Hakala, Elina; Alén, Markku; Salminen, K.; Laatikainen, Timo

doi:10.1016/0024-3205(88)90158-0

Cited by 69 publications

(36 citation statements)

References 17 publications

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“…E level started to increase at 92% and its increase peaked at 98% VO 2 max-along with the elevation of serum lactate level. Therefore, the anaerobic component has a great impact, whereas exercise with a negligible only aerobic component does not increase E level (Rahkila et al 1988). A study conducted on Nordic cross-country skiers revealed the simultaneous elevation of E, cortisol, and lactate levels, with no change in met-enkephalin concentration.…”

Section: Exercise and E Levelsmentioning

confidence: 99%

The effect of physical therapy on beta-endorphin levels

Bender¹,

Nagy²,

Barna

et al. 2007

Eur J Appl Physiol

112

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Beta-endorphin (betaE) is an important reliever of pain. Various stressors and certain modalities of physiotherapy are potent inducers of the release of endogenous betaE to the blood stream. Most forms of exercise also increase blood betaE level, especially when exercise intensity involves reaching the anaerobic threshold and is associated with the elevation of serum lactate level. Age, gender, and mental activity during exercise also may influence betaE levels. Publications on the potential stimulating effect of manual therapy and massage on betaE release are controversial. Sauna, mud bath, and thermal water increase betaE levels through conveying heat to the tissues. The majority of the techniques for electrical stimulation have a similar effect, which is exerted both centrally and--to a lesser extent--peripherally. However, the parameters of electrotherapy have not yet been standardised. The efficacy of analgesia and the improvement of general well-being do not necessarily correlate with betaE level. Although in addition to blood, increased brain and cerebrospinal fluid betaE levels are also associated with pain, the majority of studies have concerned blood betaE levels. In general, various modalities of physical therapy might influence endorphin levels in the serum or in the cerebrospinal fluid--this is usually manifested by elevation with potential mitigation of pain. However, a causal relationship between the elevation of blood, cerebrospinal fluid or brain betaE levels and the onset of the analgesic action cannot be demonstrated with certainty.

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Section: Exercise and E Levelsmentioning

confidence: 99%

The effect of physical therapy on beta-endorphin levels

Bender¹,

Nagy²,

Barna

et al. 2007

Eur J Appl Physiol

112

View full text Add to dashboard Cite

show abstract

“…We do not know whether the induction of endogenous ␤-endorphin expression in the myenteric plexus is induced locally by lymphocytes present in the plexus or via a systemic effect. In that regard, it is important to point out that the lowest stimulatory concentration of ␤-endorphin in the present study was 10 Ϫ10 M, which is physiologically relevant (20,21).…”

mentioning

confidence: 57%

Lymphocyte-mediated regulation of β-endorphin in the myenteric plexus

Verma-Gandhu¹,

Verdú²,

Cohen-Lyons³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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Verma-Gandhu M, Verdu EF, Cohen-Lyons D, Collins SM. Lymphocyte-mediated regulation of ␤-endorphin in the myenteric plexus. Am J Physiol Gastrointest Liver Physiol 292: G344 -G348, 2007. First published September 7, 2006; doi:10.1152/ajpgi.00318.2006.-Lymphocytes are antinociceptive and can modulate visceral pain perception in mice. Previously, we have shown that adoptive transfer of CD4 ϩ T cells to severe combined immune-deficient (SCID) mice normalized immunodeficiency-related visceral hyperalgesia. Pain attenuation was associated with an increase in ␤-endorphin release by T cells and an upregulation of ␤-endorphin in the enteric nervous system. In this study, we investigated the relationship between T cells and opioid expression in the myenteric plexus. We examined opioid peptide and receptor expression in the myenteric plexus in the presence and absence of mucosal T cells. We found a positive association between T cells and ␤-endorphin expression; this was accompanied by a downregulation of the -opioid receptor (MOR). In vitro, T helper (Th) type 1 and type 2 cytokine stimulation of CD4 ϩ T cells or isolation of T cells from in vivo Th-polarized mice did not increase T cell release of ␤-endorphin or the induction of ␤-endorphin expression in the myenteric plexus. However, exogenous ␤-endorphin did upregulate ␤-endorphin expression, and both cycloheximide and naloxone methiodide inhibited peptide upregulation. Therefore, our results suggest that nonpolarized CD4 ϩ T cells release ␤-endorphin, which, through an interaction with MOR, stimulates an upregulation of ␤-endorphin expression in the myenteric plexus. Thus, we propose that the mechanism underlying lymphocyte modulation of visceral pain involves T cell modulation of opioid expression in the enteric nervous system. enteric nervous system; opioid; CD4 ϩ T cells MECHANISMS INVOLVED in the homeostatic regulation of visceral pain are not well understood. Visceral pain is traditionally examined in the context of inflammation; noxious inflammatory stimuli are commonly used to evaluate the effect of acute inflammation on visceral sensitivity. Several mediators released by acute inflammatory cells either directly or indirectly stimulate sensory afferent neurons in the gut and are thus are pronociceptive. Pronociceptive mediators are also released in a healthy gut; the intestine exists in a state of controlled inflammation due to continuous immune surveillance of luminal antigens (9), and the sensory apparatus is constantly exposed to inflammatory mediators, but in the absence of pain. An antinociceptive influence originating from the periphery is a plausible explanation for the absence of hyperalgesia or allodynia in a healthy gut. We consider the immune system to be a source of this antinociception. Recently, we have provided evidence for antinociception derived from mucosal T lymphocytes. We demonstrated increased visceral sensitivity in severe combined immune-deficient (SCID) mice compared with immunocompetent wildtype mice (22). Our results demonstrated a n...

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“…The rise in plasma P-endorphin concentration has been suggested to be related to exercise intensity so that light to moderate aerobic exercise does not exert any influence on circulating P-endorphin whereas exercise intensities greater than 75-80% of an individual's V02 max quickly elevates these levels (McMurray et al, 1987;Rahkila et al, 1988 3-endorphin has been demonstrated to reduce left ventricular systolic and diastolic pressure in the rat isolated heart preparation (Lee et al, 1984) probably by its action on pre-synaptic inhibitory ,u-receptors located on excitatory non-adrenergic, non-cholinergic (NANC) nerves present in the mammalian heart Rubino et al, 1990). Although the NANC were not inhibited in our study, since no effect in heart rate was seen with the administration of naloxone, it would appear that an insufficient concentration of this opioid antagonfist was given to induce a local effect on the heart.…”

Section: Discussionmentioning

confidence: 99%

“…It is well established that circulatory levels of opioids increase with exercise (Brooks et al, 1988;McMurray et al, 1987;Rahkila et al, 1988). Opioid antagonism with naloxone further increases these levels (Bramnert, 1988;Staessen et al, 1988) but has not been found to alter heart rate in the presence of intact neural innervation.…”

Section: Introductionmentioning

confidence: 99%