Effect of the enhancement of the cholinergic tone by pyridostigmine on the exercise-induced growth hormone release in man

Cappa, Marco; Grossi, Armando; Benedetti, Sabina; Drago, Fabrizio; Loche, Sandro; Ghigo, Ezio

doi:10.1007/bf03348871

Cited by 22 publications

(7 citation statements)

References 21 publications

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“…For instance, the age‐related decline in stimulated GH secretion is reversed by pyridostigmine (31, 32). Exercise‐induced stimulation of GH release is also blunted with aging and can be reversed by administration of pyridostigmine (31, 33). The low levels of GH found in persons who are morbidly obese are increased by pyridostigmine (34).…”

Section: Discussionmentioning

confidence: 99%

Impaired growth hormone secretion in fibromyalgia patients: Evidence for augmented hypothalamic somatostatin tone

Paiva¹,

Deodhar²,

Jones³

et al. 2002

Arthritis & Rheumatism

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Objective. To determine whether female fibromyalgia (FM) patients exhibit a normal growth hormone (GH) response to an acute exercise stressor, and to assess the importance of somatostatin tone in the generation of this GH response.Methods. Twenty female FM patients were compared with 10 healthy female controls. All subjects exercised to volitional exhaustion on a treadmill. A standard metabolic cart was used to monitor pulse, blood pressure, electrocardiography, oxygen uptake, carbon dioxide output, anaerobic threshold, and maximal workload. Blood was drawn for GH and cortisol measurements 1 hour before exercise, immediately before exercise, immediately after exercise, and 1 hour after exercise. One month later, testing that was exactly similar was performed, except all subjects were given pyridostigmine bromide (Mestinon; 30 mg orally) 1 hour before exercise.Results. Compared with controls, FM patients failed to exhibit a GH or cortisol response to acute exercise (P ‫؍‬ 0.003). After administration of pyridostigmine, 1 hour before exercise, the GH levels of FM patients increased 8-fold (P ‫؍‬ 0.001), to a value comparable with that of controls. Pyridostigmine did not increase the cortisol response to exercise in FM patients. Pyridostigmine alone did not stimulate GH secretion in FM patients, nor did it improve exerciseinduced GH secretion in controls. FM patients with normal insulin-like growth factor 1 (IGF-1) levels had an impaired GH response to exercise. Conclusion.Three new findings are reported: 1) FM patients have a reduced GH response to exercise, 2) pyridostigmine reverses this impaired response, and 3) defective GH secretion in FM can occur in patients with normal IGF-1 levels. Because pyridostigmine is known to reduce somatostatin tone, it is surmised that the defective GH response to exercise in FM patients probably results from increased levels of somatostatin, a hypothalamic hormone that inhibits GH secretion.Fibromyalgia (FM) is a common clinical syndrome characterized by widespread musculoskeletal pain, with a high prevalence both in the general population and among patients attending rheumatology clinics (1-4). Increasing evidence implicates a perturbation in the central mechanisms of sensory processing as being relevant to understanding the pain component of FM (5-7). Fibromyalgia is more than a state of chronic musculoskeletal pain, however, because most FM patients also experience fatigue, poor sleep, visceral pain (e.g., irritable bowel or bladder), exercise intolerance, and neurologic symptoms (e.g., dizziness, numbness, tingling) (8).A theoretical model explaining the complexity of FM symptoms has been proposed, which links dysregulation of neuroendocrine/stress/pain mechanisms to disordered sleep-wake physiology (5). This evolving paradigm promotes the notion that FM is a stress-related syndrome, in which a disordered hypothalamicpituitary-adrenal (HPA) axis acts as a final common pathway linking FM to other stress-related somatic and psychiatric syndromes (7,9,10). The HPA and the HPgro...

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Section: Discussionmentioning

confidence: 99%

Impaired growth hormone secretion in fibromyalgia patients: Evidence for augmented hypothalamic somatostatin tone

Paiva¹,

Deodhar²,

Jones³

et al. 2002

Arthritis & Rheumatism

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“…Although not addressed by the present study, cholinergic, opiatergic, and other pathways can also modulate GH release. Cappa et al (3) reported that pyri-dostigmine (an indirect cholinergic agonist) and exercise stimulated GH release additively. We corroborated that oral pyridostigmine, alone or in combination with the opiate receptor antagonist naltrexone, can potentiate exercise-induced GH release (33).…”

Section: Discussionmentioning

confidence: 99%

Exercise-dependent growth hormone release is linked to markers of heightened central adrenergic outflow

Weltman¹,

Pritzlaff²,

Wideman³

et al. 2000

Journal of Applied Physiology

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To test the hypothesis that heightened sympathetic outflow precedes and predicts the magnitude of the growth hormone (GH) response to acute exercise (Ex), we studied 10 men [age 26.1 +/- 1.7 (SE) yr] six times in randomly assigned order (control and 5 Ex intensities). During exercise, subjects exercised for 30 min (0900-0930) on each occasion at a single intensity: 25 and 75% of the difference between lactate threshold (LT) and rest (0.25LT, 0.75LT), at LT, and at 25 and 75% of the difference between LT and peak (1.25LT, 1.75LT). Mean values for peak plasma epinephrine (Epi), plasma norepinephrine (NE), and serum GH concentrations were determined [Epi: 328 +/- 93 (SE), 513 +/- 76, 584 +/- 109, 660 +/- 72, and 2,614 +/- 579 pmol/l; NE: 2. 3 +/- 0.2, 3.9 +/- 0.4, 6.9 +/- 1.0, 10.7 +/- 1.6, and 23.9 +/- 3.9 nmol/l; GH: 3.6 +/- 1.5, 6.6 +/- 2.0, 7.0 +/- 2.0, 10.7 +/- 2.4, and 13.7 +/- 2.2 microg/l for 0.25, 0.75, 1.0, 1.25, and 1.75LT, respectively]. In all instances, the time of peak plasma Epi and NE preceded peak GH release. Plasma concentrations of Epi and NE always peaked at 20 min after the onset of Ex, whereas times to peak for GH were 54 +/- 6 (SE), 44 +/- 5, 38 +/- 4, 38 +/- 4, and 37 +/- 2 min after the onset of Ex for 0.25-1.75LT, respectively. ANOVA revealed that intensity of exercise did not affect the foregoing time delay between peak NE or Epi and peak GH (range 17-24 min), with the exception of 0.25LT (P < 0.05). Within-subject linear regression analysis disclosed that, with increasing exercise intensity, change in (Delta) GH was proportionate to both DeltaNE (P = 0.002) and DeltaEpi (P = 0.014). Furthermore, within-subject multiple-regression analysis indicated that the significant GH increment associated with an antecedent rise in NE (P = 0.02) could not be explained by changes in Epi alone (P = 0.77). Our results suggest that exercise intensity and GH release in the human may be coupled mechanistically by central adrenergic activation.

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“…In particular, naloxone, an opiate receptor antagonist, blocks GH secretion [12]. Pyridostigmine, a cholinergic muscarine agonist, enhances the GH induced by physical exercise [4]. The mechanism by which GH is enhanced by cholinergic muscarine suggests that physical exercise and cholinergic activation act through different mechanism/s of action.…”

Section: Introductionmentioning

confidence: 99%

Neuroregulation of Growth Hormone During Exercise in Children

Cappa¹,

Bizzarri²,

Martinez³

et al. 2000

Int J Sports Med

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Physical exercise is an important physiological stimulus to growth hormone (GH) release in man. Many neurotransmitters are involved in GH regulation. We studied the effect of the cholinergic pathway on GH secretion induced by physical exercise. Particularly, we studied the effect of a cholinergic muscarinic agonist on GH-induced physical exercise, both in children and adults. Moreover, we investigated the refractoriness of GH secretion after a second physical exercise stimulus. Three different protocols were performed: 1) GH response to physical exercise in children and adults; 2) effect of pyridostigmine on exercise-induced GH secretion in children and adults; 3) GH response to two consecutive exercises in children and adults. Our data show that in children GH peak after physical exercise is higher than in adults. Pyridostigmine enhances GH release in children and in adults. Exercise stimulus was able to release GH in the second test only in children, while the refractory phase did not permit a new GH release in adults. The shift to a modality of neural control of GH secretion peculiar of adults is likely due to neuroregulatory mechanisms which may be partly dependent on long-term variation in hormonal milieu.

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Effect of the enhancement of the cholinergic tone by pyridostigmine on the exercise-induced growth hormone release in man

Cited by 22 publications

References 21 publications

Impaired growth hormone secretion in fibromyalgia patients: Evidence for augmented hypothalamic somatostatin tone

Impaired growth hormone secretion in fibromyalgia patients: Evidence for augmented hypothalamic somatostatin tone

Exercise-dependent growth hormone release is linked to markers of heightened central adrenergic outflow

Neuroregulation of Growth Hormone During Exercise in Children

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