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Abstract

Endogenous opioid peptides rose to prominence with the discovery of the enkephalins in 1975. Since then, a vast amount of research has been directed toward understanding their role in normal and pathophysiological situations. Although the place of endogenous opioids in psychiatry remains uncertain, there is good evidence that a variety of tumors may secrete endorphins or enkephalins, and these may contribute to the non-metastatic complications of malignant disease. In addition, changes in cerebrospinal fluid met-enkephalin and beta-endorphin after acupuncture may be involved in the effectiveness of this therapy in the treatment of heroin withdrawal and severe pain. The hormonal effects of opiate agonists and antagonists are now well characterized; exercise-induced changes in circulating catecholamines are markedly enhanced by the opiate antagonist naloxone. It is possible that the opiate inhibition of catecholamine release during exercise is a reflection of endogenous opioid modulation of effort perception.

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... It was demonstrated that endogenous opioid peptides appeared to cover a wide range of activities. Stress, pain, and various physical dysfunctions such as depression and schizophrenia have all now been shown to be associated with increased endogenous opiate activity (3,13,52,99,131). Furthermore, a role has been determined for endorphins and analogues in a number of endocrinological pathologies as, for example, acromegaly (52,80) and hyperprolactinemia (51,52,80,107,108). ...
... Stress, pain, and various physical dysfunctions such as depression and schizophrenia have all now been shown to be associated with increased endogenous opiate activity (3,13,52,99,131). Furthermore, a role has been determined for endorphins and analogues in a number of endocrinological pathologies as, for example, acromegaly (52,80) and hyperprolactinemia (51,52,80,107,108). It has also been suggested that the ancient Chinese method of acupuncture achieves its well-known analgesic activity by means of endogenous opiate activation (3,14,52). ...
... Stress, pain, and various physical dysfunctions such as depression and schizophrenia have all now been shown to be associated with increased endogenous opiate activity (3,13,52,99,131). Furthermore, a role has been determined for endorphins and analogues in a number of endocrinological pathologies as, for example, acromegaly (52,80) and hyperprolactinemia (51,52,80,107,108). It has also been suggested that the ancient Chinese method of acupuncture achieves its well-known analgesic activity by means of endogenous opiate activation (3,14,52). ...
Article
It is well known that women athletes engaged in strenuous physical exercise and endurance training may develop “athletic menstrual irregularities” (AMI). Although many studies have appeared dealing with the immediate endocrinological and physiological changes in these women, the underlying mechanisms have remained unknown to date. A number of hypotheses have been put forward, the most well-known among them, for example, defending the existence of a critical percent of body fat necessary to trigger or maintain normal menstruation. All these theories have, however, their own, sometimes numerous, methodological in-acurracies and a teleological way of investigation. Spectacular, and perhaps promising new developments concern the possible involvement of endogenous opioid peptides and catecholestrogens in these processes. In basal circumstances ß-endorphin, the most well-known endogenous substance with opiate-like activity, may decrease LH levels by suppressing hypothalamic GnRH. This phenomenon is, however, only observed during the estrogen-dominant late-follicular and mid-luteal phases. As for catecholestrogens, it appears essential to differentiate between, for example, the 2- and 4-hydroxy derivatives of both estrone and estradiol. While some of these catecholestrogens obviously seem to suppress LH levels, others seem to potentiate and induce the LH surge. In any case, similar to ß-endorphin, these activities of catecholestrogens appear to depend upon the essential presence of a sufficiently estrogenic environment. In addition, both endogenous opioid peptides and some of the catecholestrogens appear to be able to suppress prolactin release, probably by interfering with its inhibiting factor dopamine. Other effects of catecholestrogens may include the control of the lutcolysis-potent prostaglandin F2α. Although a number of studies have investigated the behaviour of ß-endorphin during and post-exercise, similar studies investigating catecholestrogens as to their relation to physical exercise are almost nonexistent. This, in association with the numerous methodological inaccuracies of various studies, makes it difficult to draw any firm conclusion. As to formulate new hypotheses, the only reasonable suggestion considers the possible existence of a complex feedback system including catecholestrogens and endogenous opioid peptides. Furthermore, recommendations made in this survey may be helpful in designing new, perhaps more firmly supported and appropriate future studies.
... Especially during the 1980s, there was a large interest in ␤-endorphins in relation to prolonged exercise as there appeared to be an association between the exercise-induced increase of circulating ␤-endorphins and changes in mood, perception of pain and sometimes also performance (Willer et al., 1981;Carr et al., 1981;Shyu et al., 1982;Jungkunz et al., 1983;Surbey et al., 1984;Harber and Sutton, 1984;McMurray et al., 1984;Grossman et al., 1984;Morgan, 1985;Wildmann et al., 1986;Paulev et al., 1989). The euphoria and joy occasionally experienced during or after prolonged exercise (the so-called "runners high") was ascribed to the release of endogenous opioids (Janal et al., 1984) and endorphins have been referred to as "opiates for the masses" (Grossman, 1985). Recently, Sgherza et al. (2002) reported that perceived exertion was enhanced and the exercise capacity reduced during incremental cycling when naloxone, a competitive opioid antagonist, was administered intravenously prior to the start of exercise. ...
Article
This review addresses cerebral metabolic and neurohumoral alterations during prolonged exercise in humans with special focus on associations with fatigue. Global energy turnover in the brain is unaltered by the transition from rest to moderately intense exercise, apparently because exercise-induced activation of some brain regions including cortical motor areas is compensated for by reduced activity in other regions of the brain. However, strenuous exercise is associated with cerebral metabolic and neurohumoral alterations that may relate to central fatigue. Fatigue should be acknowledged as a complex phenomenon influenced by both peripheral and central factors. However, failure to drive the motorneurons adequately as a consequence of neurophysiological alterations seems to play a dominant role under some circumstances. During exercise with hyperthermia excessive accumulation of heat in the brain due to impeded heat removal by the cerebral circulation may elevate the brain temperature to >40 degrees C and impair the ability to sustain maximal motor activation. Also, when prolonged exercise results in hypoglycaemia, perceived exertion increases at the same time as the cerebral glucose uptake becomes low, and centrally mediated fatigue appears to arise as the cerebral energy turnover becomes restricted by the availability of substrates for the brain. Changes in serotonergic activity, inhibitory feed-back from the exercising muscles, elevated ammonia levels, and alterations in regional dopaminergic activity may also contribute to the impaired voluntary activation of the motorneurons after prolonged and strenuous exercise. Furthermore, central fatigue may involve depletion of cerebral glycogen stores, as signified by the observation that following exhaustive exercise the cerebral glucose uptake increases out of proportion to that of oxygen. In summary, prolonged exercise may induce homeostatic disturbances within the central nervous system (CNS) that subsequently attenuates motor activation. Therefore, strenuous exercise is a challenge not only to the cardiorespiratory and locomotive systems but also to the brain.
... Enormous research activity has demonstrated a functional role of the EO systems in pain modulation, some kinds of stress, learning, memory and reward, tolerance and dependence, gastrointestinal and hepatic functions, intake of food and drink, and the modulation of mood, blood pressure, heart rate, and the respiratory function (for reviews, see Holaday, 1983;Akil et al., 1984;Grossman, 1985;Szilagyi, 1989; for annual reviews, see, e.g., Olson et al., 1998). However, much less is known about the way (phasic or tonic) that the EO systems influence a function under physiological conditions. ...
Article
This study examined the possibility that a tonic activity in the endogenous opioid systems (EO systems) exists in animals under normal conditions. In a first set of experiments, concurrent changes in behavioral responses and in the numbers of c-Fos-like immunoreactive (Fos-LI) neurons in 58 structures of the brain and lumbosacral spinal cord were analyzed in rats after systemic administration of the opioid antagonist naloxone (NAL; 2 mg/kg). Possible roles of the EO systems were inferred from changes in the numbers of Fos-LI neurons between normal rats that received either NAL or the same volume of saline. Free-floating sections were processed immunohistochemically for c-Fos protein using standard avidin-biotin complex methods. After NAL, the numbers of Fos-LI neurons were significantly increased in the area postrema; in the caudal, intermediate, and rostral parts of the nucleus tractus solitarii; in the rostral ventrolateral medulla; in the Kölliker-Fuse nucleus; in the supramammillary nucleus; and in the central nucleus of the amygdala. In a second set of experiments examining changes in c-Fos expression in the latter structures, similar increases were found after NAL but not after an equimolar dose of NAL-methiodide, a preferential, peripherally acting opioid receptor antagonist. Therefore, Fos-LI was likely triggered after blockade of central opioid receptors, but not peripheral opioid receptors, releasing neurons from EO system-mediated inhibition. The results of this study suggest the existence of a tonic activity of the EO systems exerted on a restricted number of brain regions in normal rats. This tonic activity of the EO systems may control part of the neural networks involved in cardiorespiratory functions and in emotional and learning processes.
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In the United States today, as many as one third of the population suffers from chronic pain conditions. These syndromes cost an estimated $80 billion and are a major source of burden to the healthcare system as well as to the suffering patients. According to a study by Harvard Medical School in 1997, visits to alternative medicine providers had reached 629 million, mostly for these pain conditions. The action of acupuncture as an analgesic, although widely accepted, remains somewhat of an enigma. In reviewing the literature it became evident that many investigators have had conflicting data; however, with regard to acupuncture in pain management, quite a few results were found to be positive. Many now believe that acupuncture should be considered a valuable asset in the specialty of pain, and that it can be of value in comprehensive pain clinics as well as physical therapy practice. Acupuncture is certainly not a cure-all; however, researchers and experienced clinicians both attest to its benefits. This article is a review of the literature with regard to acupuncture as a modality for pain management.
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Although exercise in the form of stretching, strength maintenance, and aerobic conditioning is generally considered beneficial to patients with fibromyalgia (FM), there is no reliable evidence to explain why exercise should help alleviate the primary symptom of FM, namely pain. Study results are varied and do not provide a uniform consensus that exercise is beneficial or what type, intensity, or duration of exercise is best. Patients who suffer from exercise-induced pain often do not follow through with recommendations. Evidence-based prescriptions are usually inadequate because most are based on methods designed for persons without FM and, therefore, lack individualization. A mismatch between exercise intensity and level of conditioning may trigger a classic neuroendocrine stress reaction. This review considers the adverse and beneficial effects of exercise. It also provides a patient guide to exercise that takes into account the risks and benefits of exercise for persons with FM.
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The growing size of world cities and ever more competitive working conditions are thought to cause subjective stress, anxiety and depression, with a resulting decrease in the quality of life, sleep disturbances, drug and alcohol abuse and poor productivity. Acute stress may suppress immune function, leading to an increased incidence of infections, and chronic stress may predispose to a number of ailments, including digestive disturbances, hypertension, ischaemic heart disease and neoplasia; jointly, these factors cause a substantial shortening of life expectancy. The control of stress thus makes an important contribution to health. Stress-levels can be reduced by anxiolytic drugs, or by a variety of psychological techniques; however, an appropriate programme of physical activity may be the preferred option, since exercise has many positive effects on health that are unrelated to stress. If exercise is to be effective in inducing relaxation, it must be noncompetitive, moderate in intensity, and pursued in pleasant surroundings.
Article
The purpose of this study was to examine the effect of aerobic and strength conditioning on pain tolerance, pain appraisal and mood as a function of upper and lower limb pain location. Unfit males (n = 48) were randomly assigned to one of four groups: aerobic training, strength training, combined aerobic and strength training, and a 'no training' (control) group. The fitness regimens consisted of exercising at least three times per week for 12 weeks. Pain tolerance and appraisal and mood were ascertained before the treatment (baseline), and after 6 and 12 weeks. Statistical analyses using MANOVA indicated that the presence of aerobic training increased upper limb pain tolerance but was also linked to a more severe pain appraisal compared with the absence of aerobic training. Aerobic work also improved vigour while decreasing fatigue, tension and depression. Strength training had no influence on pain tolerance and positive mood states, but increased depression. Lower limb pain tolerance was unaffected by the treatments.
Article
The present study was designed to evaluate whether pain perception and pain tolerance are altered by submaximal aerobic exercise. Sixty male volunteers were randomly assigned to one of two control or experimental groups in the first of two sessions. In session 1, baseline measures of pain tolerance and pain perception were obtained for half of the subjects in each of the experimental and control groups, respectively. In addition, all subjects completed the Reactivity Scale, followed by estimation of their maximum aerobic power (VO2 max) using the Canadian Home Fitness Test. In session 2, the subjects in the two experimental groups exercised for 12 min by climbing a double step to pre-recorded musical cadences, working on average at 63% VO2 max, whereas the subjects in the two control groups spent approximately 12 min completing two short unrelated questionnaires. Measures of pain tolerance and pain perception were obtained from all subjects after exercising or completing questionnaires. Pain tolerance was assessed by the amount of time (up to 10 min) that subjects could voluntarily endure a 2300 g pressure to the index finger of their dominant hand. Pain perception was defined by participants' intensity ratings on an 11-point scale, made at 30 and 60 s. The results showed that reactivity and exercise were significant predictors of pain tolerance, together accounting for approximately 22% of the variance. The finding that submaximal workloads produce analgesia supports the potential usefulness of exercise in therapeutic intervention.
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The present article reviews a wide range of studies which suggest that energy balance mechanisms are affected by food restriction and exercise training. Specifically, food restriction produces adaptive decreases in basal metabolic rate, a decrease in the energy utilized in the performance of a specific task, and an increase in the efficiency of food utilization following resumption of pre-restriction feeding patterns. Exercise training produces an adaptive decrease in the energy required to perform a specific task and in the hormonal output to a standard work task. Conflicting evidence exists on the combined effects of exercise and dieting on energy conservation. This energy balance information is used as the basis for the development of a sympathetic arousal hypothesis of exercise dependence. We propose that exercise dependence is mediated by adaptive reductions in sympathetic output to exercise tasks as a result of training, requiring the individual to engage in heightened levels of activity to produce pre-training levels of physiological arousal.
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The remarkable morphinic capacities of endogenous opioid peptides give these agents particular and interesting properties. They can be found on different locations throughout the human body, where they bind to specific receptors. By means of various agonists and antagonists it was shown that endogenous opioids possibly play a prominent role in the control of hypophyseal secretions. The menstrual cycle is thought to represent one of the most important phenomena in which these agents are involved. In the presence of a steroid-sufficient environment (that is to say, in the luteal phase) beta-endorphin exerts a tonic inhibition on the secretion of GnRH and thereby on the LH-release. Moreover, the regulation of prolactin is probably under the control of endorphins interfering via dopamine (PIF). It becomes possible to explain a number of menstrual dysfunctions in this manner. The increased plasma concentrations of beta-endorphin, which are found after physical exercise, give rise to speculations as to their involvement in the frequently appearing menstrual irregularity in women athletes. The hypothesis proposing prolactin as being entirely responsible for these phenomena is unconvincing. We believe that endogenous opioid peptides could have a possible inhibitory effect on the GnRH-LH-axis. At this moment, methodological inaccuracies and differences of various studies make it very difficult to arrive at any firm conclusion.
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beta-Endorphin has a role in the regulation of the normal menstrual cycle and possibly in the onset of puberty. We have reviewed the evidence pointing to an alteration in this neuropeptide that may contribute to the pathogenesis of various reproductive dysfunctions. Elevated or high levels of beta-endorphin have been associated with exercise-associated amenorrhea, stress-associated amenorrhea, and polycystic ovarian syndrome. Depressed or low levels of beta-endorphin have been associated with PMS and menopause. Alterations in the levels of beta-endorphin may change the pulsatile release of GnRH via noradrenergic and/or dopaminergic pathways. We have primarily focused on beta-endorphin as representative of the endogenous opioid peptides, but other opioid peptides may also contribute to the pathogenesis of various types of reproductive dysfunction. Perhaps it will become possible to characterize and hone our understanding of the function of beta-endorphin and the other substances composing the endogenous opioid peptides. A better understanding of their role in physiological as well as pathophysiological processes may allow for the development of rational approaches to the treatment of specific disorders pertaining to reproduction. Many questions remain unanswered. Among the most relevant are: what is the precise mechanism of action by which beta-endorphin exerts its influence on pulsatile GnRH release? Is there a functional relationship between CNS and peripheral (serum) levels of beta-endorphin? Are the detected changes in beta-endorphin levels merely associated, or are they a cause of a particular disorder? Since it took almost 40 years between the time prostaglandins were first discovered and eventual realization of their clinical application, it may take some time before the beta-endorphin story is complete.
Chapter
One difficulty in conducting animal experiments and attempting to assess the effect of treatment on various physiological, biochemical and immunological functions is the frequently unavoidable imposition of stress factors (known or unknown) on the results of the measurements. One of these factors, which is especially a problem when working with larger animals, is the stress of restraint. Restraint usually is necessary for obtaining serial blood or other body fluid specimens and for monitoring bodily functions under relatively controlled conditions. Restraint related stress has been shown to influence a number of biological phenomena,1–3 including those related to immune function4 or in utero development,5 which in turn could be related to changes in endocrine or neuroendocrine organ activity.6,7
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Research has indicated that low-to-moderate dosages of caffeine supplementation are ergogenic for sustained endurance efforts as well as high-intensity exercise. The effects of caffeine supplementation on strength-power performance are equivocal, with some studies indicating a benefit and others demonstrating no change in performance. The majority of research that has examined the effects of caffeine supplementation on strength-power performance has been carried out in both trained and untrained men. Therefore, the purpose of this study was to determine the acute effects of caffeine supplementation on strength and muscular endurance in resistance-trained women. In a randomized manner, 15 women consumed caffeine (6 mg/kg) or placebo (PL) seven days apart. Sixty min following supplementation, participants performed a one-repetition maximum (1RM) barbell bench press test and repetitions to failure at 60% of 1RM. Heart rate (HR) and blood pressure (BP) were assessed at rest, 60 minutes post-consumption, and immediately following completion of repetitions to failure. Repeated measures ANOVA indicated a significantly greater bench press maximum with caffeine (p </= 0.05) (52.9 +/- 11.1 kg vs. 52.1 +/- 11.7 kg) with no significant differences between conditions in 60% 1RM repetitions (p = 0.81). Systolic blood pressure was significantly greater post-exercise, with caffeine (p < 0.05) (116.8 +/- 5.3 mmHg vs. 112.9 +/- 4.9 mmHg). These findings indicate a moderate dose of caffeine may be sufficient for enhancing strength performance in resistance-trained women.
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Forty-two patients with primary fibromyalgia were randomized into a 20-week program consisting of either cardiovascular fitness (CVR) training or simple flexibility exercises (FLEX) that did not lead to enhanced cardiovascular fitness. Patients were supervised by the same medical fitness instructors. Patients in neither group had contact with members of the other group, and were blinded as to the exercise taught to the alternative group. Groups met for 60 minutes 3 times each week. The compliance rate was 90%. Thirty-eight patients completed the study (18 with CVR training and 20 with FLEX). Blind assessments (standardized in preliminary trials to achieve acceptable inter-rater agreement) were performed by the same 2 examiners. After 20 weeks, patients receiving CVR training showed significantly improved cardiovascular fitness scores compared with those receiving FLEX training (t[35] = -4.22, P less than 0.003). Logistic regression analysis showed clinically and statistically significant improvements in pain threshold scores, which were measured directly over fibrositic tender points, in patients undergoing CVR (t[35] = 2.21, P less than 0.04). There was also a trend toward improvement in pain scores (visual analog scale) in the CVR group, but this did not reach statistical significance. There was no improvement in the percentage of body area affected by fibrositic symptoms or the number of nights per week or hours per night of disturbed sleep (self-report inventories). However, compared with the FLEX group, the CVR-trained patients improved significantly in both patient and physician global assessment scores.(ABSTRACT TRUNCATED AT 250 WORDS)
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This is a qualitative study exploring the meaning of exercise for individuals who could be labelled as ‘addicted’. Sixty people originally volunteered to participate of whom twelve scored above the midpoint on the Exercise Dependence Questionnaire (Ogden, J., Veale, D. and Summers, Z., 1997). Ten people were subsequently interviewed. A grounded theory approach was employed to analyse the data (Strauss, A. and Corbin, J., 1990). Themes that emerged were centred around control, the body, the positive and negative consequences of high frequency exercise and whether exercise is a means to an end or an end in itself. The discussion concentrates on how addiction diminished in relevance and importance for the participants when exploring meanings behind their exercising.
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Theories regarding how exercise can become addictive, and studies of withdrawal from exercise are reviewed. Several physiological mechanisms, including endogenous opioids, catecholamines, and dopamine pathways, have been implicated in exercise dependence. The higher levels of endogenous opioids found following strenuous exercise, has prompted researchers to suggest that a form of autoaddiction to these hormones might be responsible for continued excessive exercising in humans. As well, investigators have suggested that, exercise dependence could be the result of a dependence on the exercise stimulated release of catecholamines, resulting in an overarousal of the sympathetic nervous system. Moreover, the increased stimulation of dopaminergic brain structures by exercise, and the likely involvement of these structures in behavioural and pharmacological addictions, could provide another explanation for exercise-dependent behaviour. Finally, reports of withdrawal symptoms following cessation of regular exercise, has led investigators to propose that exercise can, like pharmacological and other behavioural stimuli, become addictive. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Conference Paper
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A medical device to deliver skin stimulation was developed in Russia in the early 1980s and several studies were done on the device. These studies indicated a high degree of success in the treatment of a variety of disorders. The device and method of use were based loosely on the practice of acupuncture. These, however, does not help to explain the phenomenon within Western scientific paradigm. Aside from metaphysical explanations about energy flow through the channels-meridians, there have been few theories proposed. The present paper reviews the development and the early Russian studies, as well as results of the pilot research program conducted in the Community Wholistic Health Center, Carrboro, NC. The paper then discusses two of the theories applicable to the results.
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Exercise-induced increases in the peripheral β-endorphin concentration are mainly associated both with changes in pain perception and mood state and are possibly of importance in substrate metabolism. A more precise understanding of opioid function during exercise can be achieved by investigating the changes in β-endorphin concentrations dependent upon intensity and duration of physical exercise and in comparison to other stress hormones. Published studies reveal that incremental graded and short term anaerobic exercise lead to an increase in β-endorphin levels, the extent correlating with the lactate concentration. During incremental graded exercise β-endorphin levels increase when the anaerobic threshold has been exceeded or at the point of an overproportionate increase in lactate. In endurance exercise performed at a steady-state between lactate production and elimination, blood β-endorphin levels do not increase until exercise duration exceeds approximately 1 hour, with the increase being exponential thereafter. β-Endorphin and ACTH are secreted simultaneously during exercise, followed by a delayed release of Cortisol. It is not yet clear whether a relationship exists between the catecholamines and β-endorphin. These results support a possible role of β-endorphin in changes of mood state and pain perception during endurance sports. In predominantly anaerobic exercise the behaviour of β-endorphin depends on the degree of metabolic demand, suggesting an influence of endogenous opioids on anaerobic capacity or acidosis tolerance. Further investigations are necessary to determine the role of β-endorphin in exercise-mediated physiological and psychological events.
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Physical exercise induces a significant increase in plasma β-endorphin levels and presumably also stimulates central opioid activity in humans. However, the physiological role of opioid peptides released into the blood flow or at the central nervous system level still remains to be clarified. Data from the literature and personal results in this field show that endogenous opioid peptides are likely to play a significant role in the adaptations of major physiological functions to exercise and physical training. First, complex interactions have been demonstrated between opioid peptides and the autonomic nervous system. Endogenous opioids seem to partially inhibit the release of catecholamines in response to exercise. Such an effect must be kept in mind in the study of physiological actions of the opioid peptides, since it might have substantial repercussions on cardio-respiratory and metabolic adaptation to exercise. Thus, the opioid peptides, like morphine and other opiates, could be responsible for a limited inhibition of cardio-vascular and respiratory functions during exercise and in trained individuals. These effects are likely to be the result of the concurrent decrease in peripheral catecholamine activity. Prolonged exercise also has been shown to induce a significant increase in pain threshold, as well as positive mood changes and reduction in anxiety. The role of endogenous opioid peptides in these behavioral changes is likely and match the well known pharmacological effects of morphine derivatives. In other respects, a number of studies have demonstrated that opiate agonists and antagonists have various effects on glucose metabolism and pancreatic hormones. It seems to be established that central or peripheral injection of β-endorphin is responsible for a simultaneous increase in circulating plasma glucose and glucagon concentrations in humans and other mammal species. However, such pharmacological actions are not clearly observed in the physiological situation of exercise-induced activation of the opioid system. Rather, from the few studies published at this time, it appears that opioid peptides could have a stimulating effect on insulin secretion at least in the post-exercise period. The precise role of endogenous opioids in modulating glucose metabolism during muscular exercise yet remains to be clarified. Finally, the endogenous opioids have been implicated in the pathophysiology of pubertal retardation and amenorrhea sometimes observed in highly trained young athletes. An increase in hypothalamic β-endorphinergic neurons activity has been proposed to explain dysfunctions in the pituitary-gonadal axis associated with sports training. Interesting hypothesis have been made to reconcile the various effects of the endogenous opioid peptides on the physiological adaptations to exercise. The effects on pain, mood and cardio-respiratory function suggest that opioids could help in improving subjects' physical performance. In other respects, their metabolic and hormonal effects might play a role in the fine tuning of the balance between energy needs and consumption, particularly on glucose metabolism.
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Caffeine, nicotine, ethanol and tetrahydrocannabinol (THC) are among the most prevalent and culturally accepted drugs in western society. For example, in Europe and North America up to 90% of the adult population drinks coffee daily and, although less prevalent, the other drugs are also used extensively by the population. Smoked tobacco, excessive alcohol consumption and marijuana (cannabis) smoking are addictive and exhibit adverse health effects. These drugs are not only common in the general population, but have also made their way into elite sports because of their purported performance-altering potential. Only one of the drugs (i.e., caffeine) has enough scientific evidence indicating an ergogenic effect. There is some preliminary evidence for nicotine as an ergogenic aid, but further study is required; cannabis and alcohol can exhibit ergogenic potential under specific circumstances but are in general believed to be ergolytic for sports performance. These drugs are currently (THC, ethanol) or have been (caffeine) on the prohibited list of the World Anti-Doping Agency or are being monitored (nicotine) due to their potential ergogenic or ergolytic effects. The aim of this brief review is to evaluate the effects of caffeine, nicotine, ethanol and THC by: 1) examining evidence supporting the ergogenic or ergolytic effects; 2) providing an overview of the mechanism(s) of action and physiological effects; and 3) where appropriate, reviewing their impact as performance-altering aids used in recreational and elite sports.
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The authors introduce the concepts of cardiorespiratory tests, the adaptive mechanism of oxygen transportation during exercise, oxygen consumption and maximal oxygen consumption. They also review the literature looking for studies evaluating the tolerance for exercise and cardiovascular conditioning in SLE patients.
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Position Statement: The position of The Society regarding caffeine supplementation and sport performance is summarized by the following seven points: 1.) Caffeine is effective for enhancing sport performance in trained athletes when consumed in low-to-moderate dosages (~3-6 mg/kg) and overall does not result in further enhancement in performance when consumed in higher dosages (>/= 9 mg/kg). 2.) Caffeine exerts a greater ergogenic effect when consumed in an anhydrous state as compared to coffee. 3.) It has been shown that caffeine can enhance vigilance during bouts of extended exhaustive exercise, as well as periods of sustained sleep deprivation. 4.) Caffeine is ergogenic for sustained maximal endurance exercise, and has been shown to be highly effective for time-trial performance. 5.) Caffeine supplementation is beneficial for high-intensity exercise, including team sports such as soccer and rugby, both of which are categorized by intermittent activity within a period of prolonged duration. 6.) The literature is equivocal when considering the effects of caffeine supplementation on strength-power performance, and additional research in this area is warranted. 7.) The scientific literature does not support caffeine-induced diuresis during exercise, or any harmful change in fluid balance that would negatively affect performance.
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