Appetite and gut peptide responses to exercise and calorie restriction. The effect of modest energy deficits

Highlights

• Acute food restriction of 682 kJ at breakfast and 796 kJ at lunch increased appetite.

• A government-recommended exercise bout expending ~1469 kJ did not increase appetite.

• Divergent appetite responses to diet and exercise occur with modest energy deficits.

• Plasma acylated ghrelin concentrations were not related to changes in appetite.

• Plasma peptide YY₃₋₃₆ concentrations were inversely related to changes in appetite.

Abstract

Weight loss is the result of a sustained negative energy balance, which is typically achieved by decreasing food intake and/or increasing physical activity. Current evidence suggests that acute energy deficits of ~4820 kJ elicit contrasting homeostatic responses when induced by exercise and food restriction but the response to government-recommended energy deficits is unknown. Twelve healthy men (mean(SD): age 24(5) years, body mass index 23.8(2.7) kg⋅m⁻², maximum oxygen uptake 55.4(9.1) mL⋅kg⁻¹⋅min⁻¹) completed three 8 h trials (control (Con), exercise-induced energy deficit (Ex-Def) and food restriction (Food-Def)) separated by 1 week. Thirty minutes of cycling at 64.5(3.2)% of maximum oxygen uptake was performed in Ex-Def from 0 to 0.5 h, which induced an energy deficit of 1469(256) kJ. An equivalent energy deficit was induced in Food-Def (1478(275) kJ) by reducing the energy content of standardised test meals at 1 h and 4 h. Appetite ratings, acylated ghrelin and peptide YY_3–36 concentrations were measured throughout each trial. An ad libitum meal was provided at 7 h. Appetite was higher in Food-Def than Ex-Def from 4 to 8 h (P = 0.033) and tended to be higher across the entire 8 h trial (P = 0.059). However, energy intake at the ad libitum meal did not differ between trials (P = 0.634; Con 4376 (1634); Food-Def 4481 (1846); Ex-Def 4217 (1850) kJ). Acylated ghrelin was not related to changes in appetite but plasma PYY_3–36 concentrations were higher in Ex-Def than Food-Def (P < 0.05) and negatively correlated with changes in appetite across the entire 8 h trial (P = 0.037). An energy deficit of ~1475 kJ stimulated compensatory increases in appetite when induced via calorie restriction but not when achieved by an acute bout of exercise. Appetite responses were associated with changes in plasma PYY_3–36 but not acylated ghrelin concentrations and did not influence subsequent energy intake.

Introduction

Obesity is characterised by an excess accumulation of body fat and is associated with an increased prevalence of chronic diseases including type 2 diabetes, osteoarthritis, cardiovascular disease and some forms of cancer (Bray, 2004). Consequently, overweight and obesity has recently been classified as one of the top five global risk factors for mortality and one of the top 10 risk factors for morbidity (World Health Organization, 2009). However, weight loss as little as 3% has been associated with favourable changes in chronic disease risk factors and therefore represents a major public health priority (Donnelly et al., 2009).

For weight loss to occur, a sustained negative energy balance is required and is typically achieved by decreasing energy intake (i.e. dieting) and/or increasing energy expenditure (i.e. exercising). Although both interventions induce a negative energy balance, current research suggests that exercise and caloric restriction elicit contrasting homeostatic responses. In this regard, acute caloric restriction appears to stimulate rapid compensatory increases in appetite and energy intake that do not occur in response to equivalent energy deficits induced by exercise (Hubert et al, 1998, King et al, 2011a). Furthermore, King et al. (2011a) reported immediate decreases in circulating concentrations of the anorectic gut hormone PYY_3–36 and increases in the orexigenic gut hormone acylated ghrelin in response to food restriction but no compensatory changes in response to exercise. Such findings suggest that these appetite-regulating gut hormones have a mediating role in the immediate appetite and energy intake responses to acute energy deficits but this requires further investigation.

Although these studies have provided interesting information regarding energy homeostasis and the regulation of appetite, large and abrupt methods of energy restriction have been employed as calorie intake was reduced by ~1820 kJ at a single meal (Hubert et al., 1998) and ~4820 kJ across two meals (King et al., 2011a). Such substantial decreases in energy intake at individual meals increases the likelihood that compensatory increases in appetite will occur and does not represent a practical strategy for energy restriction. In this regard, research has demonstrated that compensatory changes in gastrointestinal hormones and increases in appetite persist for at least 1 year after weight loss induced by a very low energy diet, despite increases in body weight (Sumithran et al., 2011).

The current UK government and American College of Sports Medicine (ACSM) guidelines recommend a minimum of 150 min per week of moderate intensity physical activity, spread over most days of the week (British Heart Foundation, 2009, Donnelly et al, 2009). This may be interpreted as five 30 min exercise bouts performed on separate days of the week and is considered to be sufficient to reduce chronic disease risk, prevent significant weight gain, and elicit modest weight loss in overweight and obese populations (Donnelly et al., 2009). The appetite and energy intake response to such a practical energy deficit achieved via exercise and food restriction is unknown. This requires further investigation as compensatory increases in appetite contribute to the difficulty of maintaining an energy deficit in current society where energy dense, highly palatable foods are abundant and easily accessible. Furthermore, increases in appetite are commonly cited as a reason for unsuccessful dieting (Ikeda, Lyons, Schwartzman, & Mitchell, 2004) and are inversely related to exercise-induced weight loss (King, Hopkins, Caudwell, Stubbs, & Blundell, 2008).

The purpose of this study was to investigate the appetite, acylated ghrelin, PYY_3–36 and energy intake responses to a 30 min bout of moderate intensity cycling compared with an equivalent energy deficit achieved via caloric restriction. This study also enables further investigation into the sensitivity of the appetite-regulating system and the role of acylated ghrelin and PYY_3–36 in energy homeostasis via the utilisation of small, yet practical, energy deficits. It was hypothesised that appetite and acylated ghrelin would increase, and that PYY_3–36 would decrease in response to food restriction but that these variables would remain unaffected by exercise, resulting in a higher energy intake in the food restriction trial.