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Journal ArticleDOI

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)

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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Citations
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Journal Article
01 Jan 2004-Nature
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.

1,960 citations

Journal ArticleDOI
01 Mar 2016-Appetite
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.

131 citations

Journal ArticleDOI
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

Journal ArticleDOI
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]....

    [...]

Journal ArticleDOI
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.

62 citations

References
More filters
Journal ArticleDOI
TL;DR: It is found that obese subjects were not resistant to the anorectic effects of PYY, and endogenous PYY levels were low in obese subjects, suggesting that PYY deficiency may contribute to the pathogenesis of obesity.
Abstract: Background: The gut hormone fragment peptide YY3-36 (PYY) reduces appetite and food intake when infused into subjects of normal weight. In common with the adipocyte hormone leptin, PYY reduces food intake by modulating appetite circuits in the hypothalamus. However, in obesity there is a marked resistance to the action of leptin, which greatly limits its therapeutic effectiveness. We investigated whether obese subjects were also resistant to the anorectic effects of PYY.Methods: We compared the effects of PYY infusion on appetite and food intake in 12 obese and 12 lean subjects in a double-blind, placebo-controlled, crossover study. The plasma levels of PYY, ghrelin, leptin, and insulin were also determined.Results: Caloric intake during a buffet lunch offered two hours after the infusion of PYY was decreased by 30 percent in the obese subjects (P<0.001) and 31 percent in the lean subjects (P<0.001). PYY infusion also caused a significant decrease in the cumulative 24-hour caloric intake in both obese and lean subjects. PYY infusion reduced plasma levels of the appetite-stimulatory hormone ghrelin. Endogenous fasting and postprandial levels of PYY were significantly lower in obese subjects (the mean [+/-SE] fasting PYY levels were 10.2+/-0.7 pmol per liter in the obese group and 16.9+/-0.8 pmol per liter in the lean group, P<0.001). Furthermore, the fasting PYY levels correlated negatively with the body-mass index (r=-0.84, P<0.001).Conclusions: We found that obese subjects were not resistant to the anorectic effects of PYY. Endogenous PYY levels were low in the obese subjects, suggesting that PYY deficiency may contribute to the pathogenesis of obesity.

1,614 citations


"Appetite-regulatory hormone respons..." refers background in this paper

  • ...PYY is an anorectic peptide secreted primarily by the distal intestine in response to nutrient intake [9,35]....

    [...]

Journal ArticleDOI
TL;DR: Results showed that perceived pedal resistance followed a positively accelerating function with an exponent of 1.6, and a model for inter-individunl comparisons using subjective range as a frame is proposed.
Abstract: Early studies of subjective force estimates for short-time work on a bicycle ergometer are reviewed. Results showed that perceived pedal resistance followed a positively accelerating function with an exponent of 1.6. A model for inter-individunl comparisons using subjective range as a frame

1,232 citations


"Appetite-regulatory hormone respons..." refers methods in this paper

  • ...Ratings of perceived exertion were also assessed using the Borg scale [24]....

    [...]

Journal ArticleDOI
TL;DR: The known potent biologic actions of PYY, its high concentrations in gut endocrine cells, and its release into the circulation after a normal meal suggest that this peptide may function physiologically as a circulating gut hormone.

1,119 citations

Journal ArticleDOI
TL;DR: It is suggested that modulating the release of endogenous satiety factors, such as PYY, through alteration of specific diet constituents could provide a rational therapy for obesity.

584 citations

Journal ArticleDOI
TL;DR: Obese subjects have a PYY deficiency that would reduce satiety and could thus reinforce their obesity, and fasting and postprandial endogenous plasma PYY levels were attenuated in obese humans and rodents.
Abstract: The responses of the gut hormone peptide YY (PYY) to food were investigated in 20 normal-weight and 20 obese humans in response to six test meals of varying calorie content. Human volunteers had a graded rise in plasma PYY (R2 = 0.96; P < 0.001) during increasing calorific meals, but the obese subjects had a lower endogenous PYY response at each meal size (P < 0.05 at all levels). The ratio of plasma PYY1–36 to PYY3–36 was similar in normal-weight and obese subjects. The effect on food intake and satiety of graded doses of exogenous PYY3–36 was also evaluated in 12 human volunteers. Stepwise increasing doses of exogenous PYY3–36 in humans caused a graded reduction in food intake (R2 = 0.38; P < 0.001). In high-fat-fed (HF) mice that became obese and low-fat-fed mice that remained normal weight, we measured plasma PYY, tissue PYY, and PYY mRNA levels and assessed the effect of exogenous administered PYY3–36 on food intake in HF mice. HF mice remained sensitive to the anorectic effects of exogenous ip PYY3–...

549 citations

Trending Questions (1)
How do appetite hormones respond after exercising?

After a single bout of exercise, levels of leptin were reduced on the day after exercise, but no compensatory changes were seen for other appetite hormones.