Appetite-regulatory hormone responses on the day following a prolonged bout of moderate-intensity exercise
TL;DR: It is indicated that short-term energy deficits induced by exercise initially prompt a compensatory response by chronic but not acute hormonal regulators of appetite and energy balance within this 24h time-frame however there is no conscious recognition of the perturbation to energy balance.
About: This article is published in Physiology & Behavior.The article was published on 2015-03-15 and is currently open access. It has received 27 citations till now. The article focuses on the topics: Appetite.
Summary (3 min read)
Jump to: [Introduction] – [Participants] – [Pre-assessment and Study Familiarisation] – [Main Experimental Trials] – [Food Provision & Test Meals] – [Blood Biochemistry] – [Statistical Analysis] – [Appetite Hormone Responses] – [Appetite Responses] and [Discussion]
Introduction
- The relationship between exercise and appetite regulation has important implications regarding the role of exercise in weight management (33) .
- The body's appetite regulatory system includes several peptides of gastro-intestinal, pancreatic and adipose tissue origin, which communicate acute nutrient status and chronic energy availability to the central nervous system (28) .
- Notably however, these alterations appear to be transient.
- Circulating levels of acylated ghrelin are distinctly suppressed during exercise of moderate intensity or higher (10, 29, 31) .
Participants
- Participants were weight stable (< 2 kg change in body mass in the last three months), non-smokers, free of cardiometabolic disease, had a BMI within the healthy range (18.5 -24.9 kgm 2 ) and were not taking any medications or supplements.
- Participants were recreationally active i.e. typically games players, but were not accustomed to undertaking endurance exercise regularly.
Pre-assessment and Study Familiarisation
- Before main trials, participants attended the laboratory where they were familiarised with the study procedures and underwent necessary pre-assessments.
- Participants completed questionnaires assessing health status and physical activity habits after which measurements of height, weight and waist circumference were taken.
- Participants then completed two treadmill running tests; 1) a progressive 16 min submaximal test to determine the relationship between treadmill running speed and oxygen consumption; 2) a maximum oxygen uptake test ( 2 O V max).
- These tests have been described in depth previously (10) .
Main Experimental Trials
- In subsequent weeks participants completed two main experimental trials (exercise and control) separated by a washout period of at least seven days.
- Each main trial was composed of an intervention phase (day one) and a data collection phase (day two).
- During main trials participants were provided with all of their food which was consumed at set times that were standardised across trials.
- Herein, participants ran on a motorised treadmill (Technogym Excite Med, Cesena, Italy) for 90 min at a speed predicted to elicit 70% of their maximum oxygen uptake.
- After lunch participants went home where they remained until returning to the laboratory the following morning.
Food Provision & Test Meals
- On day one of main trials participants received all of their food pre-packaged from the study team with the food provided being identical in the exercise and control trial.
- The amount of food each participant received was calculated as 1.4x their estimated basal metabolic rate (42) .
- On day one breakfast consisted of white bread and chocolate spread (carbohydrate 64%, fat 25%, protein 11% -20% of daily energy provision).
- Each participant received the exact same meal i.e. the meal was not normalised to participants' daily energy requirements.
- To keep hydrated participants drank 250 mL of water one hour after each test meal (1 h and 5 h).
Blood Biochemistry
- During day two of main trials venous blood samples were collected via a 21G cannula (Venflon, Becton Dickinson, Helsingborg, Sweden) that was kept patent throughout by flushing with isotonic saline (0.9% w/v sodium chloride).
- To preserve the integrity of the acylated ghrelin sample, monovettes for this peptide were pre-treated with a serine protease inhibitor as described previously (10) .
- Samples for total PYY were collected into ice-cooled syringes containing 10µL/mL di-peptidyl peptidase-4 inhibitor (Millipore, Watford, UK) and after mixing were immediately dispensed into EDTA tubes containing aprotinin (Nordic Pharma Ltd, Reading, UK) (500 KIU/mL).
- Plasma was obtained after spinning whole blood samples at 1600 g for 10 min in a refrigerated centrifuge (4 o C) and was stored at -80 o C until analysis.
- Concentrations of plasma acylated ghrelin (SPI BIO, Montigney le Bretonneux, France), total PYY (Millipore, Watford, UK), leptin (R and D Systems Europe Ltd., Abingdon, UK) & insulin (Mercodia, Uppsala, Sweden) were determined using enzyme-linked immunosorbant assay kits.
Statistical Analysis
- Data were analysed using the Statistical Package for the Social Sciences (SPSS) software version 21.0 for Windows.
- Two-way repeated measures ANOVA were used to examine responses over time for appetite regulatory hormones and appetite perceptions.
- Where significant differences were found these were explored using post hoc analysis using the Bonferroni correction for multiple comparisons.
- Statistical significance was accepted at the 5% level.
- The sample size for this investigation was determined using data derived from the authors' previous research which detected compensatory acylated ghrelin responses to food restriction (31) .
Appetite Hormone Responses
- On the morning of day two plasma acylated ghrelin concentrations were no different between the exercise and control trial (P = 0.56) (Figure 2 upper panel).
- Two-way repeated measures ANOVA (trial x time) revealed significant time (P < 0.001) and interaction (P = 0.009) main effects for acylated ghrelin indicating divergent changes over time between trials.
- After correction for multiple comparisons using the Bonferroni method no differences were found at individual time points between trials.
- The plasma leptin AUC showed significantly reduced circulating levels across the entirety of day two (Table 1 ).
- At baseline on day two fasting plasma concentration of insulin were no different between the exercise and control trial (Figure 3 upper panel).
Appetite Responses
- There were no significant differences in fasting appetite perceptions on day two (hunger, fullness, satisfaction and PFC) between the exercise and control trial (all P > 0.05) (Figure 4 ).
- For each appetite perception two-way repeated measures ANOVA (trial x time) revealed a main effect of time (all P < 0.001) representing changes in response to test meals.
Discussion
- Several studies have shown that there are no acute compensatory changes in appetite or appetite regulatory hormones on the day during which an acute bout of exercise is performed (6, 10, 31) .
- Paradoxically, circulating levels of acylated ghrelin were actually lower following a lunch time meal consumed 24 h after the end of exercise.
- A more long term influence of PYY on energy homeostasis has also been suggested by associations that have been found between PYY, substrate oxidation and resting metabolic rate (25, 48) .
- Notably, the consensus arising from previous work, and supported here, are that substantial reductions in circulating leptin occur after exercise when associated with sufficiently high energy expenditure (> 3348 kJ) and following a latency period of ~24-48 h (17, 45, 53) .
- In the present investigation the authors sought to explore this relationship further within a controlled laboratory setting by assessing changes in subjective appetite parameters on the day after exercise.
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TL;DR: The authors showed that post-prandial elevation of PYY3-36 may act through the arcuate nucleus Y2R to inhibit feeding in a gut-hypothalamic pathway.
Abstract: Food intake is regulated by the hypothalamus, including the melanocortin and neuropeptide Y (NPY) systems in the arcuate nucleus. The NPY Y2 receptor (Y2R), a putative inhibitory presynaptic receptor, is highly expressed on NPY neurons in the arcuate nucleus, which is accessible to peripheral hormones. Peptide YY3-36 (PYY3-36), a Y2R agonist, is released from the gastrointestinal tract postprandially in proportion to the calorie content of a meal. Here we show that peripheral injection of PYY3-36 in rats inhibits food intake and reduces weight gain. PYY3-36 also inhibits food intake in mice but not in Y2r-null mice, which suggests that the anorectic effect requires the Y2R. Peripheral administration of PYY3-36 increases c-Fos immunoreactivity in the arcuate nucleus and decreases hypothalamic Npy messenger RNA. Intra-arcuate injection of PYY3-36 inhibits food intake. PYY3-36 also inhibits electrical activity of NPY nerve terminals, thus activating adjacent pro-opiomelanocortin (POMC) neurons. In humans, infusion of normal postprandial concentrations of PYY3-36 significantly decreases appetite and reduces food intake by 33% over 24 h. Thus, postprandial elevation of PYY3-36 may act through the arcuate nucleus Y2R to inhibit feeding in a gut–hypothalamic pathway.
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TL;DR: Blood redistribution during exercise may be important for suppressing ghrelin, while other mechanisms involving cytokine release, changes in plasma glucose and insulin concentrations, SNS activity, and muscle metabolism likely mediate changes in the anorexigenic signals PYY and GLP-1.
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TL;DR: The balance of evidence suggests that adiposity and sex do not modify appetite or energy intake responses to acute or chronic exercise interventions, but individuals with higher habitual physical activity levels may better adjust energy intake in response to energy balance perturbations.
Abstract: Exercise facilitates weight control, partly through effects on appetite regulation. Single bouts of exercise induce a short-term energy deficit without stimulating compensatory effects on appetite, whilst limited evidence suggests that exercise training may modify subjective and homeostatic mediators of appetite in directions associated with enhanced meal-induced satiety. However, a large variability in responses exists between individuals. This article reviews the evidence relating to how adiposity, sex, and habitual physical activity modulate exercise-induced appetite, energy intake, and appetite-related hormone responses. The balance of evidence suggests that adiposity and sex do not modify appetite or energy intake responses to acute or chronic exercise interventions, but individuals with higher habitual physical activity levels may better adjust energy intake in response to energy balance perturbations. The effect of these individual characteristics and behaviours on appetite-related hormone responses to exercise remains equivocal. These findings support the continued promotion of exercise as a strategy for inducing short-term energy deficits irrespective of adiposity and sex, as well as the ability of exercise to positively influence energy balance over the longer term. Future well-controlled studies are required to further ascertain the potential mediators of appetite responses to exercise.
127 citations
TL;DR: How iron deficiency may interact with each component of the female athlete triad, that is, energy status, reproductive function, and bone health, is described.
Abstract: Despite the severity and prevalence of iron deficiency in exercising women, few published reports have explored how iron deficiency interacts with another prevalent and severe condition in exercising women: the ‘female athlete triad.’ This review aims to describe how iron deficiency may interact with each component of the female athlete triad, that is, energy status, reproductive function, and bone health. The effects of iron deficiency on energy status are discussed in regards to thyroid function, metabolic fuel availability, eating behaviors, and energy expenditure. The interactions between iron deficiency and reproductive function are explored by discussing the potentially impaired fertility and hyperprolactinemia due to iron deficiency and the alterations in iron metabolism due to menstrual blood loss and estrogen exposure. The interaction of iron deficiency with bone health may occur via dysregulation of the growth hormone/insulin-like growth factor-1 axis, hypoxia, and hypothyroidism. Based on these discussions, several future directions for research are presented.
64 citations
Cites background from "Appetite-regulatory hormone respons..."
...On the other hand, an energy deficiency achieved via increased exercise energy expenditure suppresses ghrelin and increases PYY, GLP-1, and PP serum concentrations in the hours following exercise [98–100] and even suppresses serum ghrelin concentrations the day after exercise [101]....
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TL;DR: The concept of dynamic energy balance is reviewed, including two mathematical models developed to improve weight-loss predictions based on changes in diet and exercise and these models are now available on the Internet.
Abstract: Weight management for athletes and active individuals is unique because of their high daily energy expenditure; thus, the emphasis is usually placed on changing the diet side of the energy balance equation. When dieting for weight loss, active individuals also want to preserve lean tissue, which means that energy restriction cannot be too severe or lean tissue is lost. First, this brief review addresses the issues of weight management in athletes and active individuals and factors to consider when determining a weight-loss goal. Second, the concept of dynamic energy balance is reviewed, including two mathematical models developed to improve weight-loss predictions based on changes in diet and exercise. These models are now available on the Internet. Finally, dietary strategies for weight loss/maintenance that can be successfully used with active individuals are given. Emphasis is placed on teaching the benefits of consuming a low-ED diet (e.g., high-fiber, high-water, low-fat foods), which allows for the consumption of a greater volume of food to increase satiety while reducing energy intake. Health professionals and sport dietitians need to understand dynamic energy balance and be prepared with effective and evidence-based dietary approaches to help athletes and active individuals achieve their body-weight goals.
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References
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TL;DR: It is demonstrated that plasma acylated ghrelin concentration and hunger are suppressed during running.
Abstract: Ghrelin is an orexigenic hormone secreted from endocrine cells in the stomach and other tissues. Acylation of ghrelin is essential for appetite regulation. Vigorous exercise induces appetite suppre...
291 citations
TL;DR: It is demonstrated that in obese individuals, insulin resistance and hyperinsulinemia are inversely associated with ghrelin concentrations, suggesting that insulin resistance or related metabolic abnormalities may constitute part of a feedback mechanism by which body weight is regulated in humans.
Abstract: Ghrelin, an orexigenic hormone that may play a role in body weight regulation, is reduced in states of obesity. Because obesity is associated with insulin resistance and compensatory hyperinsulinemia, we determined whether these metabolic characteristics were independently associated with suppressed ghrelin concentrations. To investigate this hypothesis, using steady-state plasma glucose concentrations, we identified 20 insulin-resistant (IR) and 20 insulin-sensitive (IS) individuals who were equally obese. The mean body mass indexes were 32.5 +/- 0.4 and 32.0 +/- 0.4 kg/m(2) for the IR and IS groups, respectively. Fasting insulin concentrations were 19.5 and 7.4 micro U/ml (P < 0.001), respectively. Ghrelin concentrations were suppressed in the IR group (252 +/- 19 pg/ml) relative to the IS group (412 +/- 35 pg/ml; P < 0.001). Ghrelin correlated inversely with both insulin resistance (r = -0.64; P < 0.001) and fasting insulin concentration (r = -0.58; P < 0.001). Multivariate analysis confirmed that both insulin resistance and hyperinsulinemia independently predicted low ghrelin concentrations. Our results demonstrate that in obese individuals, insulin resistance and hyperinsulinemia are inversely associated with ghrelin concentrations. Thus, insulin resistance or related metabolic abnormalities may constitute part of a feedback mechanism by which body weight is regulated in humans.
273 citations
"Appetite-regulatory hormone respons..." refers background in this paper
...discovered between appetite hormones with insulin resistance [48,49], we chose to look closer at the relationships between these factors....
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TL;DR: Hormones of the endocrine pancreas are collectively at the crossroads of many aspects of energy homeostasis, and glucagon and amylin act in the short term to reduce meal size, and insulin sensitizes the brain to short-term meal-generated satiety signals; and insulin and perhaps amyl in as well act over longer intervals to modulate the amount of fat maintained and defended by the brain.
Abstract: The control of food intake and body weight by the brain relies upon the detection and integration of signals reflecting energy stores and fluxes, and their interaction with many different inputs related to food palatability and gastrointestinal handling as well as social, emotional, circadian, habitual and other situational factors. This review focuses upon the role of hormones secreted by the endocrine pancreas: hormones, which individually and collectively influence food intake, with an emphasis upon insulin, glucagon and amylin. Insulin and amylin are co-secreted by B-cells and provide a signal that reflects both circulating energy in the form of glucose and stored energy in the form of visceral adipose tissue. Insulin acts directly at the liver to suppress the synthesis and secretion of glucose, and some plasma insulin is transported into the brain and especially the mediobasal hypothalamus where it elicits a net catabolic response, particularly reduced food intake and loss of body weight. Amylin reduces meal size by stimulating neurons in the hindbrain, and there is evidence that amylin additionally functions as an adiposity signal controlling body weight as well as meal size. Glucagon is secreted from A-cells and increases glucose secretion from the liver. Glucagon acts in the liver to reduce meal size, the signal being relayed to the brain via the vagus nerves. To summarize, hormones of the endocrine pancreas are collectively at the crossroads of many aspects of energy homeostasis. Glucagon and amylin act in the short term to reduce meal size, and insulin sensitizes the brain to short-term meal-generated satiety signals; and insulin and perhaps amylin as well act over longer intervals to modulate the amount of fat maintained and defended by the brain. Hormones of the endocrine pancreas interact with receptors at many points along the gut-brain axis, from the liver to the sensory vagus nerve to the hindbrain to the hypothalamus; and their signals are conveyed both neurally and humorally. Finally, their actions include gastrointestinal and metabolic as well as behavioural effects.
253 citations
"Appetite-regulatory hormone respons..." refers background in this paper
...In concert with leptin, insulin also functions as a chronic regulator of energy homeostasis, providing information to the central nervous system regarding stored energy within adipose tissue [47]....
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TL;DR: Increasing evidence indicates that insulin, in concert with permissive effects of cortisol, can increase serum leptin over this time frame and likely contributes to meal-induced increases in serum leptin.
Abstract: Serum levels of the adipocyte hormone leptin are increased in proportion to body fat stores as a result of increased production in enlarged fat cells from obese subjects. In vitro studies indicate that insulin and glucocorticoids work directly on adipose tissue to upregulate in a synergistic manner leptin mRNA levels and rates of leptin secretion in human adipose tissue over the long term. Thus, the increased leptin expression observed in obesity could result from the chronic hyperinsulinemia and increased cortisol turnover. Superimposed upon the long-term regulation, nutritional status can influence serum leptin over the short term, independent of adiposity. Fasting leads to a gradual decline in serum leptin that is probably attributable to the decline in insulin and the ability of catecholamines to decrease leptin expression, as observed in both in vivo and in vitro studies. In addition, increases in serum leptin occur approximately 4-7 h after meals. Increasing evidence indicates that insulin, in concert with permissive effects of cortisol, can increase serum leptin over this time frame and likely contributes to meal-induced increases in serum leptin. Further research is required to elucidate the cellular and molecular mechanisms underlying short- and long-term nutritional and hormonal regulation of leptin production and secretion.
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TL;DR: Peptide YY (PYY)(3-36) has been shown to produce dramatic reductions in energy intake (EI), but no human data exist regarding energy expenditure (EE), glucose and fat metabolism, and nothing is known regarding PYY1-36.
Abstract: Peptide YY (PYY)3–36 has been shown to produce dramatic reductions in energy intake (EI), but no human data exist regarding energy expenditure (EE), glucose and fat metabolism. Nothing is known reg...
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"Appetite-regulatory hormone respons..." refers background in this paper
...A more long term influence of PYY on energy 331 homeostasis has also been suggested by associations that have been found 332 between PYY, substrate oxidation and resting metabolic rate (25, 48)....
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