Influence of rest and exercise at a simulated altitude of 4,000 m on appetite, energy intake, and plasma concentrations of acylated ghrelin and peptide YY

The reason for high altitude anorexia is unclear but could involve alterations in the appetite hormones ghrelin and peptide YY (PYY). This study examined the effect of resting and exercising in hypoxia (12.7% O(2); ～4,000 m) on appetite, energy intake, and plasma concentrations of acylated ghrelin and PYY. Ten healthy males completed four, 7-h trials in an environmental chamber in a random order. The four trials were control-normoxia, control-hypoxia, exercise-normoxia, and exercise-hypoxia. During exercise trials, participants ran for 60 min at 70% of altitude-specific maximal oxygen consumption (Vo(2max)) and then rested. Participants rested throughout control trials. A standardized meal was consumed at 2 h and an ad libitum buffet meal at 5.5 h. Area under the curve values for hunger (assessed using visual analog scales) tended to be lower during hypoxic trials than normoxic trials (repeated-measures ANOVA, P = 0.07). Ad libitum energy intake was lower (P = 0.001) in hypoxia (5,291 ± 2,189 kJ) than normoxia (7,718 ± 2,356 kJ; means ± SD). Mean plasma acylated ghrelin concentrations were lower in hypoxia than normoxia (82 ± 66 vs. 100 ± 69 pg/ml; P = 0.005) while PYY concentrations tended to be higher in normoxia (32 ± 4 vs. 30 ± 3 pmol/l; P = 0.059). Exercise suppressed hunger and acylated ghrelin and increased PYY but did not influence ad libitum energy intake. These findings confirm that hypoxia suppresses hunger and food intake. Further research is required to determine if decreased concentrations of acylated ghrelin orchestrate this suppression.     

Growth hormone, ghrelin and peptide YY secretion after oral glucose administration in healthy and obese women

The mechanism of the altered GH secretion in obesity is unclear. There is evidence that oral glucose (OG) administration initially decreases and subsequently stimulates GH secretion. Ghrelin is a peptide that displays strong growth hormone-releasing activity. Its physiological importance on GH regulation is unclear. Our aim was to study fasting GH concentrations and their response to OG administration in relation with ghrelin secretion in obese and healthy women, in order to elucidate the hypothetical participation of ghrelin on post-oral glucose GH secretion. 36 women were included in the study. After an overnight fast, 75?g of oral glucose was administered; glucose, insulin, ghrelin, and PYY (1-36) were obtained at baseline and during 300?min. The area under the curve between 0 and 300?min (AUC) of GH μ/l·min) was lower in obese patients than in controls; 262.5±57.5 vs. 534.9±95.6, p=0.01, for obese and controls respectively. GH peak (μg/l) was lower in obese patients than in controls; 3.7±0.7 vs. 7.1±1.0, p=0.012, for obese and controls, respectively. The AUC of total ghrelin (pg/ml·min) was lower in obese patients than in controls; 233,032±12,641 vs. 333,697±29,877, p=0.004, for the obese patients and controls respectively. PYY (1-36) was similar in obese and healthy women after OG. There were significant correlations between the different indices of post-oral glucose GH and ghrelin secretion. These data suggest that ghrelin is a physiological regulator of GH in the post-oral glucose state, and the decreased ghrelin secretion could be one of the mechanisms responsible for the altered GH secretion in obesity.     

24-Hour profiles of circulating ghrelin and peptide YY are inversely associated in normal weight premenopausal women

Peptide YY (PYY) and ghrelin (GHR) may modulate one another's actions within the hypothalamus. Peripheral infusion of PYY in humans acutely suppresses circulating concentrations of GHR. Whether an association between PYY and GHR exists in the peripheral circulation of humans over 24 h is unknown. The purpose of this study was to determine if circulating concentrations of PYY and GHR were significantly associated over 24 h in humans. Participants (n = 13) were normal weight, moderately active, women ages 18–24 yr. Blood samples were obtained q10 min for 24 h and assayed using RIA for total PYY and total GHR hourly from 0800 to 1000 h and 2000 to 0800 h and q20 min from 1000 to 2000 h. Dietary intake during the 24 h procedure was comprised of 55% carbohydrates, 30% fat, and 15% protein (three meals and a snack). Statistical analyses included linear mixed-effects modeling to test whether PYY predicted GHR concentrations over 24 h. Participants weighed 57.0 ± 1.5 kg and had 26.1 ± 1.5% body fat (15.0 ± 1.1 kg), 42.1 ± 1.1 kg fat free mass, a BMI of 21.3 ± 0.5 kg/m² and RMR of 1072 ± 28 kcal/24 h. Visually, PYY and GHR exhibited an inverse association over nearly the entire 24 h period. Statistically, circulating concentrations of 24 h PYY predicted 24 h GHR (ghrelin = 1860.51–2.14*PYY; p = 0.04). Circulating concentrations of PYY are inversely associated with GHR over 24 h. These data provide evidence that PYY may contribute to the modulation of the secretion of GHR in normal weight, premenopausal women over a 24 h period and supports similar inferences from experimental studies in animals and humans.     

Central effects of a novel acylated peptide, ghrelin, on growth hormone release in rats

Ghrelin, a novel growth-hormone-releasing acylated peptide, was recently isolated from rat stomach by the search of an endogenous ligand to an "orphan" G-protein-coupled-receptor. Ghrelin neuron is present in the arcuate nucleus of rat hypothalamus, but its central effect on growth hormone (GH) release has yet to be clarified. We determined the plasma GH concentration and GH mRNA level in the pituitary in response to central administration of ghrelin. A single intracerebroventricular (ICV) administration of ghrelin to rats increased the plasma GH concentration dose-dependently. A continuous ICV administration of ghrelin via osmotic pump for 12 days increased the plasma GH concentration on day 6, but did not keep the high GH concentration on day 12. The GH mRNA levels in both groups of single and continuous administration of ghrelin were not significantly different from those of controls. A single administration of growth-hormone secretagogue also did not stimulate GH synthesis. Central ghrelin stimulated GH release but did not augment GH synthesis. In addition to gastric ghrelin, hypothalamic ghrelin functions to regulate GH release.     

Meal-related changes in ghrelin, peptide YY, and appetite in normal weight and overweight children

Objective: Ghrelin and peptide YY (PYY) are two gut hormones that have effects on appetite. Our objectives were to characterize the patterns of secretion of these hormones in response to feeding in school‐age children and determine whether there were differences between normal weight (NW) and overweight (OW) subjects. Methods and Procedures: This was a cross‐sectional study at one tertiary care center. Subjects were 7‐ to 11‐year‐old healthy NW and OW volunteers recruited from local advertisements. Following an overnight fast, the subjects were given a standardized breakfast and lunch and had nine hourly blood samples for total ghrelin and total PYY. We assessed whether ghrelin and PYY levels changed from the preprandial to postprandial state and corresponded to reported hunger/satiety. Results: Hunger ratings were similar between the two groups throughout the study period. Ghrelin was not suppressed after eating, did not rise prior to the next meal, and did not correspond to hunger ratings in either group. PYY increased postprandially and decreased preprandially in the NW group, but OW children exhibited this pattern for only part of the day. PYY levels incompletely corresponded to reported satiety in the OW group. Discussion: Mixed meal consumption had little effect on ghrelin secretion and a variable effect on PYY secretion in young children in our study. Differences that were observed between the groups do not suggest that an abnormality in their secretion contributes to the development of obesity.     

Serum acylated ghrelin, adiponectin and leptin levels in normal-weight and obese premenopausal women.

Ghrelin, leptin, and adiponectin play an important role in the regulation of energetic homeostasis, but physiological relationships between these hormones have not been elucidated. This study was therefore designed to characterize the association between serum acylated ghrelin, leptin, and adiponectin levels, as well as insulin resistance evaluated by homeostasis model of assessment in 32 normal-weight and 60 age-matched metabolically healthy obese women. In normal-weight, but not in obese women, we found a positive linear correlation between leptin and ghrelin (r=0.375; p=0.034). In the multiply regression analysis we observed the change of direction of leptin influence on acylated ghrelin level from positive in normal-weight (p=0.001) to negative in obese women without insulin-resistance (p=0.033); in obese women with insulin resistance leptin was not significantly associated with ghrelin. In neither group was any linear correlation found between ghrelin and adiponectin. However, by multivariate analysis adiponectin was positively associated with ghrelin, but only in obese women without insulin resistance (p=0.01). In conclusion, in normal-weight women leptin is positively correlated with acylated ghrelin. In obese women without insulin resistance different interactions between both hormones might reflect a physiological mechanism of adaptation to a positive energy balance.     

Changes of ghrelin and brain natriuretic peptide levels in systemic vascular resistance after cardiopulmonary bypass

The application of cardiopulmonary bypass (CPB) using a heart-lung machine in open heart surgery is associated with numerous pathophysiological changes in the vascular system and the neurohormonal environment. In this study our purpose was to investigate whether the hormones brain natriuretic peptide (BNP) and ghrelin are involved in changes in the systemic vascular resistance index (SVRI) after CPB, using data from 20 patients who had undergone coronary artery by pass grafting accompanied by CPB. Hemodynamic measurements were obtained using a thermodilution catheter and included cardiac index and systemic vascular resistance index. Blood samples were taken before CPB, after CPB, and at 0 and 24 h postoperatively. The blood levels of total and acylated ghrelin were quantified by radioimmunoassay. Blood levels of BNP were measured by a fluorescence immunoassay kit. The SVRI was significantly higher at the end of CPB and at 0 h postoperatively than before CPB (end of CPB: 4282±1035 dyne·s·cm^?5·m^?2, 0 h postoperatively: 3239±635 dyne·s·cm^?5·m^?2 vs. before CPB: 2289±330 dyne·s·cm^?5·m^?2, p<0.05). Total and acylated ghrelin levels decreased until 0 h postoperatively but the change was not statistically significant. However, at 24 h after surgery, they showed a statistically significant increase over the initial ghrelin values (total before CPB: 1413.71±287.93 pg/ml vs. 24 h postoperatively: 1736.85±236.89 pg/ml; acylated ghrelin before CPB: 55.85±25.53 pg/ml vs. 24 h postoperatively: 106.28±30.86 pg/ml; p<0.05 for both). BNP values were markedly lower after than before CPB (before CPB: 69.07±48 pg/ml vs. after CPB: 21.96±13 pg/ml, p<0.05) and reached a maximum value 24 h postoperatively (before CPB: 56.3±42 vs. after CPB: 454.7±229 pg/ml, p<0.05). There was a weak negative correlation between the changes in SVRI and total and acylated ghrelin levels after the CPB period, but this was not statistically significant. However, there was a statistically significant negative correlation between SVRI and BNP after CPB and at 24 h postoperatively (r:?0.709, p<0.01 and r:?0.649, p<0.03, respectively). Taken together, our results show that the observed initial increases in ghrelin and/or BNP in the postoperative period (at 24 h) might be causally related to the decrease in the SVRI in the same period. However, further investigations are needed to clarify the significance of this observation with respect to that of SVRI.     

Early life overfeeding decreases acylated ghrelin circulating levels and upregulates GHSR1a signaling pathway in white adipose tissue of obese young mice

Ghrelin is a hormone synthesized by the stomach that acts in different tissues via a specific receptor (GHS-R1a), including hypothalamus and adipose tissue. For instance, recent reports have shown that ghrelin has a direct action on hypothalamic regulation of food intake mainly inducing an orexigenic effect. On the other hand, ghrelin also modulates energy stores and expenditure in the adipocytes. This dual action has suggested that this hormone may act as a link between the central nervous system and peripheral mechanisms. Furthermore, concerning nutritional disorders, it has been suggested that obesity may be considered an impairment of the above cited link. Therefore, considering that neonatal overfeeding induces obesity in adulthood by unknown mechanisms, in this study we examined the effects of early life overnutrition on the development of obesity and in particular on adipose tissue ghrelin signaling in young mice. Our data demonstrated that overnutrition during early life induces a significant increase in body weight of young mice, starting at 10 days, and this increase in weight persisted until adulthood (90 days of age). In these animals, blood glucose, liver weight and visceral fat weight were found higher at 21 days when compared to the control group. Acylated ghrelin circulating levels were found lower in the young obese pups. In addition, in white adipose tissue ghrelin receptor (GHS-R1a) expression increased and was associated to positive modulation of content and phosphorylation of proteins involved in cell energy store and use as AKT, PI3K, AMPK, GLUT-4, and CPT1. However, PPARγ content decreased in obese group. Basically, we showed that adipose tissue metabolism is altered in early life acquired obesity and probably due to such modification a new pattern of ghrelin signaling pathway takes place.     

The impact of weight loss on the 24-h profile of circulating peptide YY and its association with 24-h ghrelin in normal weight premenopausal women

Peptide YY (PYY) and ghrelin exhibit a reciprocal association and antagonistic physiological effects in the peripheral circulation. Research has yet to clarify the effect of weight loss on the 24 h profile of PYY or its association to 24 h ghrelin. We sought to determine if diet- and exercise-induced weight loss affects the 24 h profile of PYY and its association with 24 h ghrelin in normal weight, premenopausal women. Participants (n = 13) were assessed at baseline (BL) and after a 3-month diet and exercise intervention (post). Blood samples obtained q10 min for 24 h were assayed for total PYY and total ghrelin q60 min from 0800 to 1000 h and 2000 to 0800 h and q20 min from 1000 to 2000 h. The ghrelin/PYY ratio was used as an index of hormonal exposure. Statistical analyses included paired t-tests and linear mixed effects modeling. Body weight (−1.85 ± 0.67 kg; p = 0.02), and body fat (−2.53 ± 0.83%; p = 0.01) decreased from BL to post. Ghrelin AUC (5252 ± 2177 pg/ml/24 h; p = 0.03), 24 h mean (216 ± 90 pg/ml; p = 0.03) and peak (300 ± 134 pg/ml; p = 0.047) increased from BL to post. No change occurred in PYY AUC (88.2 ± 163.7 pg/ml; p = 0.60), 24 h mean (4.8 ± 6.9 pg/ml; p = 0.50) or peak (3.6 ± 6.4 pg/ml; p = 0.58). The 24 h association between PYY and ghrelin at baseline (p = 0.04) was weakened at post (p = 0.14); however, the ghrelin/PYY lunch ratio increased (p = 0.01) indicating the potential for ghrelin predominance over PYY in the circulation. PYY and ghrelin are reciprocally associated during a period of weight stability, but not following weight loss. An “uncoupling” may have occurred, particularly at lunch, due to factors that modulate ghrelin in response to weight loss.     

Energy cost of moderate-duration resistance and aerobic exercise

The purpose of this study was to compare energy expenditure of resistance and aerobic exercise matched for total time and relative intensity. Ten trained men (24.3 +/- 3.8 years) performed 30 minutes of intermittent free-weight squatting at 70% of 1 repetition maximum and continuous cycling at 70% of Vo(2)max, in a crossover design. Vo(2), kilocalories (kcal), work, respiratory exchange ratio (RER), V(E), heart rate (HR), and rating of perceived exertion (RPE) data were recorded. Cycling resulted in greater total Vo(2) (87 +/- 3 vs. 53 +/- 3 L, mean +/- SEM), kcal expenditure (441 +/- 17 vs. 269 +/- 13), and work (335 +/- 11 vs. 128 +/- 11 kJ) than squatting did. The mean RER was greater during squatting (1.03 +/- 0.01 vs. 0.94 +/- 0.01), and the V(E) values were greater during cycling (82 +/- 3 vs. 70 +/- 3 L.min(-1)). The HR response was nearly identical between exercise modes (160 +/- 5 vs. 160 +/- 4 bpm), whereas the RPE was greater during squatting (16.96 +/- 0.41 vs. 14.88 +/- 0.42). These data suggest that although lower than similarly matched aerobic exercise, resistance exercise resulted in an energy cost that would meet the recommendations for kcal expenditure as suggested by the American College of Sports Medicine, if performed 4-5 days per week. These findings should be considered by coaches and trainers working with individuals mutually interested in muscular development and weight management, because programs of structured resistance exercise may assist with both.     

Obestatin, acylated and total ghrelin concentrations in the perinatal rat pancreas

BACKGROUND: Ghrelin and obestatin are encoded by the preproghrelin gene and originate from posttranslational processing of the preproghrelin peptide. The fetal rat pancreas contains acylated and desacylated ghrelin peptides, as well as growth hormone secretagogue receptor -1a mRNA. Acylated ghrelin inhibits insulin secretion. We investigated the plasma and tissue ontogeny of ghrelin and obestatin in the rat. METHODS: We measured obestatin and acylated and total ghrelin concentrations in plasma, pancreas and stomach from rat fetuses (F20) and neonates at postnatal day (PN) 1, 6, 12 and 21). RESULTS: Overall, obestatin concentrations were markedly lower than total ghrelin concentrations. In plasma, total ghrelin concentrations decreased abruptly after birth (p < 0.05), contrasting with a 3 times increase in the concentration of acylated ghrelin between F20 and PN1 (p < 0.05). In pancreas, total ghrelin and obestatin concentrations decreased progressively from PN1 to PN21 but acylated ghrelin concentrations increased 6-7 times from F20 (18 [6] pg/ml) to PN6 (122 [59] pg/ml). The percent of acylated ghrelin increased from 1.8 (0.6) at F20 to 39.7 (13.0) % of total ghrelin immunoreactivity at PN12 (p < 0.05). There were significant positive correlations between postnatal obestatin, acylated or total ghrelin and insulin concentrations in the pancreas (all p < 0.02, r(2) > 0.21) and between postnatal total ghrelin and obestatin (in pancreas, r(2) = 0.37) or acylated ghrelin (in stomach, r(2) = 0.27) (p < 0.001). CONCLUSION: Ghrelin and obestatin are present in the perinatal pancreas where they could potentially affect insulin secretion.     

Plasma ghrelin levels and hunger scores in humans initiating meals voluntarily without time- and food-related cues

Ghrelin is an orexigenic hormone that is implicated in meal initiation, in part because circulating levels rise before meals. Because previous human studies have examined subjects fed on known schedules, the observed preprandial ghrelin increases could have been a secondary consequence of meal anticipation. A causal role for ghrelin in meal initiation would be better supported if preprandial increases occurred before spontaneously initiated meals not prompted by external cues. We measured plasma ghrelin levels among human subjects initiating meals voluntarily without cues related to time or food. Samples were drawn every 5 min between a scheduled lunch and a freely requested dinner, and hunger scores were obtained using visual analog scales. Insulin, glucose, fatty acids, leptin, and triglycerides were also measured. Ghrelin levels decreased shortly after the first meal in all subjects. A subsequent preprandial increase occurred over a wide range of intermeal intervals (IMI; 320-425 min) in all but one subject. Hunger scores and ghrelin levels showed similar temporal profiles and similar relative differences in magnitude between lunch and dinner. One subject displayed no preprandial ghrelin increase and was also the only individual whose insulin levels did not return to baseline between meals. This finding, along with a correlation between area-under-the-curve values of ghrelin and insulin, suggests a role for insulin in ghrelin regulation. The preprandial increase of ghrelin levels that we observed among humans initiating meals voluntarily, without time- or food-related cues, and the overlap between these levels and hunger scores are consistent with a role for ghrelin in meal initiation.     

Influence of acute maximal exercise on lecithin:cholesterol acyltransferase activity in healthy adults of differing aerobic performance

To document the possible influence of a single episode of maximal aerobic stress on the serum lecithin:cholesterol acyltransferase (LCAT) activity in subjects with differing histories of training, two groups of healthy male adults [controls (C), n = 18, 28.6 years, SD 5.2, 50.1 ml.kg-1.min-1 maximal O2 uptake (VO2max), SD 5.3; endurance trained athletes (T), n = 18, 31.4 years, SD 8.8, 65.0 ml.kg-1.min-1 VO2max, SD 2.8] were examined in a maximal aerobic stress test. In addition to the routine assessment of lipid status, LCAT activity was measured immediately before and after exercise. At rest nearly identical LCAT activity values were found in both groups: C 64.4 nmol.ml-1.h-1, SD 16.7 vs T 65.0 nmol.ml-1.h-1, SD 20.9. The post-exercise LCAT values induced by the maximal stress test increased significantly to (C) 95.7 nmol.ml-1.h-1, SD 23.5, +48.6%, P less than 0.001; (T) 83.5 nmol.ml-1.h-1, SD 24.3, +29.1%, P less than 0.01. Neither the pre nor the postexercise individual LCAT activity values showed any significant correlation to the corresponding data on physical performance.     

Effects of aerobic exercise on serum leptin levels in obese women

It has been demonstrated that leptin concentrations in obese patients may be altered by weight loss. We examined the effects of a 9-week aerobic exercise program on serum leptin concentrations in overweight women (20-50% above ideal body mass) under conditions of weight stability. Sixteen overweight women, mean (SE) age 42.75 (1.64) years, comprised the exercise group which adhered to a supervised aerobic exercise program. A graded exercise treadmill test was conducted before and after the exercise program to determine maximal oxygen uptake (VO2max) using open-circuit spirometry. The women demonstrated improved aerobic fitness (VO2max increased 12.29%), however, body fat and the body mass index did not change significantly [42.27 (1.35)-41.87 (1.33)%]. Fourteen women, age 40.57 (2.80) years, did not exercise over the same time period and served as a control group. Serum leptin levels were not significantly altered for either the exercise [28.00 (2.13)-31.04 (2.71) ng x ml(-1)] or the control group [33.24 (3.78)-34.69 (3.14) ng x mg(-1)]. The data indicate that 9 weeks of aerobic exercise improves aerobic fitness, but does not affect leptin concentrations in overweight women.     

Effect of moderate-intensity exercise session on preprandial and postprandial responses of circulating ghrelin and appetite.

Responses of plasma total ghrelin and appetite were investigated during preprandial and postprandial stages of recovery from a moderate-intensity cycling session. Healthy recreationally active men underwent one exercise and one control trial. In the exercise trial, subjects exercised for approximately 60 minutes, while in the control trial they rested quietly for the same duration. After the intervention, subjects rested for 120 minutes and then consumed a test meal. Measurements were obtained immediately and 120 minutes after the intervention and then during 180 minutes of the postprandial period. The post-intervention concentration of total ghrelin was lower (p<0.05) in the exercise than in the control trial. The modulating effect of exercise was related to the reduction in the postprandial rather than preprandial concentration. Post-intervention scores of appetite were not different between the two trials, but when preprandial and postprandial responses were considered separately, postprandial hunger and desire to eat was higher (p<0.05) in the exercise trial. In summary, during recovery from moderate-intensity exercise, total ghrelin does not respond in a compensatory manner to disturbances in energy balance. Thus, an exercise-induced increase in appetite during the later stages of recovery coinciding with the postprandial state cannot be explained by changes in the plasma concentration of total ghrelin.     

Effect of aerobic exercise on acquired gefitinib resistance in lung adenocarcinoma

Lung adenocarcinoma patients with epidermal growth factor receptor (EGFR)-activating mutations respond well to tyrosine kinase inhibitors but typically develop resistance. Current therapies mainly target differentiated cells, not cancer stem cells (CSCs), but CSCs affect the occurrence, invasion, metastasis and treatment sensitivity of malignant tumours. Recently, aerobic exercise has emerged as adjuvant therapy for cancer. Aerobic exercise can accelerate blood circulation, improve tissue oxygen supply, reduce the stress level of patients, improve the antioxidant capacity of the body, and facilitate the degradation of hypoxia-inducible factor-1 (HIF-1) in tumour tissues, thus weakening its maintenance effect on CSCs. In this study, we successfully established lung adenocarcinoma cell lines with gefitinib resistance. Long-term gefitinib induction could increase the level of oxidative stress in lung adenocarcinoma cells and reduce the antioxidant capacity, resulting in the high expression of HIF-1 and ALDH1 and leading to the enrichment of CSCs, and a decreased response to gefitinib. This may be one of the important reasons for gefitinib-acquired resistance in lung adenocarcinoma. In the case of drug resistance, effective aerobic exercise could reduce ROS, activate SOD, inhibit HIF-1 and ALDH1, and cause a reduction in CSCs to sensitise cells to gefitinib again and ultimately inhibit the malignant proliferation of tumours. Therefore, in the treatment of lung adenocarcinoma, the inhibitory effect of aerobic exercise on oxidative stress can enhance the response of drug-resistant cells to gefitinib and can be used as an effective adjunct measure in the treatment of lung adenocarcinoma.     

Influence of altitude and caffeine during rest and exercise on plasma levels of proenkephalin peptide F

The purpose of this study was to examine the resting and exercise response patterns of plasma Peptide F immunoreactivity (ir) to altitude exposure (4300 m) and caffeine ingestion (4 mg.kg b.w.-1). Nine healthy male subjects performed exercise tests to exhaustion (80-85% VO2max) at sea level (50 m), during an acute altitude exposure (1 hr, hypobaric chamber, 4300 m) and after a chronic (17-day sojourn, 4300 m) altitude exposure. Using a randomized, double-blind/placebo experimental design, a placebo or caffeine drink was ingested 1 hour prior to exercise. Exercise (without caffeine) significantly (p less than 0.05) increased plasma Peptide F ir values during exercise at chronic altitude only. Caffeine ingestion significantly increased plasma Peptide F ir concentrations during exercise and in the postexercise period at sea level. Conversely caffeine ingestion at altitude resulted in significant reductions in the postexercise plasma Peptide F ir values. The results of this study demonstrate that the exercise and recovery response patterns of plasma Peptide F ir may be significantly altered by altitude exposure and caffeine ingestion. These data support further study examining relationships between Peptide F (and other enkephalin-containing polypeptides) and epinephrine release in response to these types of physiological stresses.     

Plasma ghrelin levels during exercise - effects of intensity and duration

Ghrelin, a recently discovered hormone of gastric origin has been shown to stimulate appetite and food intake. In man it is considered to play a role in energy homeostasis and regulation of somatropic function. As exercise affects hunger/satiety sensations and food intake, at least under some experimental conditions, we investigated the effect of exercise intensity and duration on ghrelin release and subsequent ad libitum food intake in normal weight subjects. Bicycle exercise on an ergometer for 30 min at 50 W which was below the aerob-anaerobic threshold led to an increase of ghrelin which remained unchanged during the higher intensity at 100 W. Respective hunger/satiety ratings and subsequent food intake and postprandial ghrelin suppression were identical and not different from controls. In a second group 7 subjects cycled at 50 W for 30, 60 and 120 min, respectively. Ghrelin concentrations rose significantly by 50-70 pg/ml above baseline for the respective period of exercise. While postexercise premeal ghrelin levels were not significantly different subsequent food intake after 120 min of cycling was significantly greater compared to control, 30 min and 60 min exercise, respectively. The present data suggest that low rather than high-intensity exercise stimulates ghrelin levels independent of exercise duration. Stimulation of food intake during prolonged exercise is most likely not due to changes of ghrelin.