Effect of food intake on exercise fatigue in trained and untrained subjects

Summary The effects of carbohydrate and fat intake on exercise-induced fatigue was investigated in 30 untrained — ( of 40.6±2.7 ml · kg⁻¹ · min⁻¹) and 24 trained-subjects ( of 52.3±2.7 ml · kg⁻¹ · min⁻¹) performing a 34 km march with a 25 kg backpack. Marching time was 8 1/2 h and 6 1/3 h in the untrained and trained-subjects respectively. The subjects were divided into 3 dietary groups. One group had free access to sugar cubes, the second group was offered almonds and the third one served as a control. Triglyceride levels decreased by 65 mg · dl⁻¹ in untrained, and by 115 mg · dl⁻¹ in trained subjects, while blood glucose remained at normal levels. In the untrained subjects, ingestion of almonds delayed the subjective sensation of exhaustion, while 50% of the controls and the sugar consuming subjects complained of exhaustion. The data suggest that ingestion of food containing fat delays exercise induced exhaustion or fatigue to a greater extent than does carbohydrate ingestion.     

Energy balance and food intake: the role of PPARgamma gene polymorphisms

Mechanisms regulating energy balance involve complex interactions between genetic, environmental and behavioural (learnt and intrinsic) factors. Genotype may drive the partitioning of energy metabolism and predispose to site-specific adiposity, culminating in a state of energy imbalance. One candidate gene with a direct link to adiposity is the peroxisome proliferator-activated receptor gamma (PPARG) gene. PPARG is a cell nuclear receptor expressed almost exclusively in adipose tissue that regulates adipocyte differentiation, lipid metabolism and insulin sensitivity. PPARgamma appears to be a key regulator of energy balance, with polymorphisms on the PPARG gene linked to obesity and effects on body composition. Our research has confirmed an association between the pro12ala allele and reduced incidence of obesity in pre-pubertal children and there are strong associations between genetic variation at the PPARG locus and percentage body fat. Moreover, our evidence suggests that PPARG C-681G and pro12ala polymorphisms display opposing effects in terms of growth phenotype, with pro12Ala associated with deficient energy utilisation, leading to reduced growth and the G-681 variant associated with accelerated growth compared with wildtypes. Common differences in this gene have also been associated with variations in body weight in response to dietary macronutrients. Preliminary evidence suggests that PPARG variants may even be involved in the control of short term energy compensation. Taken together these data suggest that the role of PPARG is varied and complex, influencing fat deposition and growth velocity early in life, with potential impact in the control of energy intake and appetite regulation, and could provide a key target for future research and anti-obesity agents.     

Effects of a combination fiber system on appetite and energy intake in overweight humans

Appetite management may aid energy balance through moderation of the size (satiation) and/or frequency (satiety) of eating occasions. This double-blind, randomized, cross-over design study explored the effects of the addition of alginate and guar gum to a breakfast bar on appetite and food intake. Following baseline evaluations of health, appetite and diet, participants were randomized to receive the fiber containing bar or control bar. They reported to the laboratory after an overnight fast, rated their appetite and consumed the relevant 55 g bar within 10 min in place of their normal breakfast meal. Appetite ratings were again made immediately after consuming the bar and at 30 minute intervals for 5 h. This was repeated for 5 consecutive days (Monday–Friday) followed by a 9-day washout period and a similar 5-day treatment period with the alternate bar. Gastrointestinal tolerance was rated daily. Sensory ratings of the bars were obtained on the first and fifth study days. Twenty-four-hour diet recalls were conducted on three random days during baseline and each intervention period. No significant treatment effects were observed in self-reported appetitive sensations over each 5-hour post-loading period. There also was no evidence of a cumulative effect over the five treatment days. Daily energy intake was not different on the two treatments. Although these data do not support the efficacy of including guar and an alginate fiber combination in a solid food matrix for moderation of appetite and acute food intake, further testing of the concept under different conditions and with different forms of guar and alginate may prove worthwhile.     

48-h glucose infusion in humans: effect on hormonal responses, hunger and food intake

Experimentally-induced hyperglycemia by prolonged glucose infusion allows investigation of the effects of sustained stimulation of the pancreatic β-cell on insulin secretion and sensitivity. Hormonal responses to a meal following prolonged glucose infusions have not been investigated. To determine if a 48-h glucose infusion alters hormonal responses to a test meal as well as food intake and hunger in normal weight individuals, 16 subjects (8 men, 8 women, age 18–30 years, mean BMI = 21.7 ± 1.6 kg/m²) were infused for 48 h with either saline (50 ml/h) or 15% glucose (200 mg/m²/min). Subjects ingested a 600 kcal mixed nutrient meal 3 h after infusion termination. Blood samples were taken during the 48 h and for 4 h following food ingestion. The 48-h glucose infusion elicited a metabolic profile of a glucose intolerant obese subjects, with increased plasma glucose, insulin and leptin (all P < 0.01) and increased HOMA-IR (P < 0.001). During meal ingestion, early insulin secretion was increased (P < 0.05) but post-prandial glucose (P < 0.01) and insulin (P < 0.01) excursions were lower following the glucose infusion. Post-prandial plasma triglyceride concentrations were increased after glucose compared with saline. Food intake and hunger ratings were not different between the two conditions. Plasma leptin levels were inversely correlated with hunger (P < 0.03) in both conditions and with food intake (P < 0.003) during the glucose condition only. Thus, a 48-h glucose infusion does not impair post-prandial hormonal responses, alter food intake or hunger in normal weight subjects. The glucose-induced increases in plasma leptin result in a stronger inverse relationship between plasma leptin and hunger as well as food intake. These data are the first to demonstrate a relationship between leptin and hunger in normal weight, non-calorically restricted human subjects.     

Effects of electroconvulsive shock on food and water intake in the rat

Forty-two male rats were habituated to laboratory conditions for four weeks under constant light conditions. Food and water intakes were recorded daily. Following the habituation period half of the animals were given electroconvulsive shock (ECS) and half Sham-ECS (SECS). ECS treatments produced significant decrements in both food and eater intakes which returned to baseline levels after three days.     

Energy density, diet composition and palatability: influences on overall food energy intake in humans

This paper considers the role of energy density (ED), diet composition and palatability in the control of energy intake (EI) in humans through several related considerations: (i) the relationship between ED and diet composition, (ii) the relationship between ED, diet composition and EI, (iii) the relationship between palatability and EI, (iv) the relationship between ED, palatability and EI, (v) the importance of postingestive factors in influencing palatability in the longer term, (vi) the contribution of sensory and nutritional factors to dietary hyperphagia and (vii) the implications these considerations have for people living their normal lives in their natural environment. The main factors influencing ED are the fat and water content of foods. Energy density does elevate EI, especially in short-term studies where it can account for >40% of the variance in EI. In real life, ED accounts for only approximately 7% of the variance in EI. This is because the determinants of EI are multifactorial and also because the short-term effects of ED on EI do not translate into the longer term. We argue that part of the longer term amelioration of short-term effects of ED on EI is due to learned compensation, based on the postingestive consequences of consuming familiar food that differ in ED. More energy-dense foods tend to be more palatable but we learn to consume them in smaller portion sizes. In the longer term, the perceived palatability of a food is strongly influenced by the postingestive consequences of eating it. This effect can override sensory factors alone. This implies that nutrient mimetics, if used continuously, would not be as efficacious as initially supposed and that their ad hoc use may undermine the stability of learned appetites and satieties for foods with different EDs and contribute to the poor weight control capability exhibited by consumers at large.     

Prostaglandins and food intake of rats: A component of energy balance regulation?

Modulation of food intake by signals arising in adipose tissue has been an important component of theories concerning energy balance regulation. Our experiments tested the effects of some prostaglandins (PG) which are produced in adipose tissue, on food and water intakes in rats. Rats were injected intrahypothalamically with 1 μg of either PGE₁ or PGB₁ in 1 μl bilaterally prior to a 2-hr daily meal. PGE₁, but not PGB₁, reduced food intake of the rats in groups with lateral hypothalamic (LH) and anterior commissure (AC) cannulas, but did not reduce food intake in groups with perifornical hypothalamic (PFH) or mammillary body (MB) cannulas. Water intake was reduced in all groups injected with PGE₁ except the LH and MB groups. Anterior and medial hypothalamic groups showed a sustained 2°C rise in rectal temperature following injections of PGE₁. Subcutaneous injections of PGE₁ reduced food intake of three different groups of rats at different levels of adiposity. We hypothesize that some PG's may be components of a signal relating fat depots and energy balance regulation.     

Effects of palatability and learned satiety on energy density influences on breakfast intake in humans

The present report explored firstly how palatability modified the effects of energy density (ED) on short-term food intake and changes in rated appetite within a single test meal, and secondly how repeated consumption altered these relationships. Experiment 1 contrasted disguised high (HED) and low (LED) versions of a food presented in bland and palatable forms. Mass consumed varied as an interaction of palatability and ED, with subjects eating least of the bland/HED version, suggesting some un-learned satiating effects. No such compensation for ED was seen in the palatable/HED condition, and overall energy intake increased with ED. Palatability had the expected stimulatory effect on appetite, but rated hunger decreased more rapidly as a function of energy consumed in the HED conditions. Experiment 2 introduced novel distinctive flavours to examine whether repeated experience of palatable HED and LED versions resulted in learned satiety. Participants ate the same mass of LED and HED versions on first exposure, but after two training days with each food, where they consumed a fixed amount, they subsequently ate a greater mass of the LED version, consistent with learned satiety. Increased intake was accompanied by a slower rate of decline in hunger in the LED condition. Despite these changes, energy intake remained higher with the HED version. Liking for the LED version was greater than the HED version at the end, possibly due to mild aversive qualities of eating a fixed portion of the HED food during training. Together these data suggest that energy density is the major determinant of short-term energy intake in the absence of orosensory cues predictive of energy differences, but that learning of flavour-energy associations can, to some extent, allow short-term energy consumption to be regulated.     

TRH decreases food intake and increases water intake and body temperature in rats

Thyrotropin-releasing hormone (TRH) is a key regulator of the hypothalamus-pituitary-thyroid axis, which plays an important role in energy homeostasis and is involved in the regulation of feeding behavior. In the present study, we investigated the effects of acute and chronic TRH treatment on water intake, body temperature and feeding behavior in rats. TRH (0, 4, 16 and 64 mg/kg) was injected subcutaneously twice a day (06:00 and 18:00 h) in rats fed ad libitum. TRH decreased food and water intake in the first few hours (P < .05). There was a small reduction in food intake over the 24-h period, but body weight was not affected (P < .05). When TRH was injected at a dose of 32 mg/kg twice a day (06:00 and 18:00 h) for 5 days, T(3) and T(4) concentrations were increased (P < .05). TRH increased body temperature for 2 h after injection. Water intake was markedly increased (P < .05), but there was no effect on food intake or body weight. These results show that whereas a single injection of TRH decreases short-term food and water intake in rats, repeated daily treatments stimulate water intake but not food intake, and, thus, the increase in water consumption is mediated independently of food intake under these conditions.     

Imprecise control of energy intake: absence of a reduction in food intake following overfeeding in young adults

The objective was to examine the extent to which overfeeding reduces spontaneous food intake in humans. Twelve normal-weight adults participated in the three stage study. During the 14 day baseline period and 21 day recovery period, food intake was consumed ad libitum, beyond a minimum 5 MJ (1200 kcal) basal diet. During the 13 day period of overfeeding, each subject consumed 35% more energy than they consumed at baseline. Overfeeding resulted in a weight gain of 2.3+/-0.37 kg, (p<0.0001), approximately half the weight gain was determined to be fat (1.2+/-0.19 kg, p<0.0001) by underwater densitometry. Following overfeeding, mean daily caloric intake was not significantly suppressed returning immediately to baseline values. Despite normal energy intake, participants lost 1.3+/-0.24 kg of body weight (p<0.0001), of which 0.75+/-0.15 kg (p<0.0001) was fat. These results indicated that (1) the physiological control of eating behavior in humans is not the major mechanism responsible for the recovery of body weight following a period of overfeeding and (2) an increase in energy expenditure of 1.28 MJ (307 kcal)/day or about 14% was required to account for the weight loss following overfeeding.     

The effects of caerulein on food intake in the cat

The effects of physiological doses of caerulein, a pure cholecystokinin analog, was measured on food intake of cats. Food intake was increased by caerulein when infused at 400 ng/kg/hr. However, at the lowest dose, a slight decrease of intake was observed suggesting that low levels of caerulein may inhibit food intake in this species. Slow infusion of caerulein as compared to bolus injection may have opposite effects on food intake, that is, stimulation with infusion and inhibition with injection.     

Increase of food intake induced by glucagon in the rat

The effect of intraperitoneal administration of saline, glucose (25 mg/100 g b.w.), insulin (0.025 U/100 g b.w.) and glucagon (50 micrograms/kg b.w.) on glycemia, liver glycogen concentration and food intake was studied on 104 male adult Wistar rats. When saline was injected the amount of food ingested was similar to that expected at the metabolic moment selected for the tests. Glucose administration did not reduce food intake but both insulin and glucagon provoked a threefold increase during the 60 minutes ensuing the injection. The overall ingestion of food during the 24 hours after the injection of the hormones was significantly higher (about 10%) than the control values during the preceding or the succeeding 24 hours. A hyperphagic, rather than a hypophagic effect of glucagon administration is possibly related to the small dose used in the experiments. The mechanisms involved in the increase of food intake due to glucagon are discussed in terms of acceleration of the metabolic reactions that normally prevent large drops of glycemia as glucose utilization proceeds during the inter-meal periods and that in physiological conditions build up until the need for food arises.     

Stress and the relative reinforcing value of food in female binge eaters

The purpose of this study was to examine the independent and interactive effects of stress reactivity and binge eating (BE) status on changes in the relative reinforcing value of snack foods. The relative reinforcing value of snack foods was assessed in binge eaters and non-binge eaters across a stress-induction session (after 3-minutes of anticipation of giving a speech) or a control day (after 3-minutes of reading magazines), with order of conditions counterbalanced. Subjects were divided into four groups based on scores on the Binge Eating Scale (BES) and changes in perceived stress: Binge eaters/low stress reactivity (n=12), binge eaters/high stress reactivity (n=10), non-binge eaters/low stress reactivity (n=6), non-binge eaters/high stress reactivity (n=9). Dietary restraint, hunger, disinhibition, and hedonics were measured by self-report. Body composition was estimated by body mass index (BMI=weight in kilograms divided by height in metres squared). The relative reinforcing value of snack food was influenced differently by binge status and stress reactivity in the stress and control conditions (p<0.05). Binge eaters who reacted to stress earned more snack food points (p<0.001) in stress condition, but non-binge eaters who showed high stress reactivity earned less points for snack food in stress condition (p<0.05). This same pattern of results remained after statistically controlling for body mass index (BMI) and dietary restraint. Findings suggest that reactivity to interpersonal or ego-related stress increases the relative reinforcing value of food in binge eaters but decreases the relative reinforcing value of snack food in non-binge eaters, and these findings appear to be independent of dietary restraint and BMI.     

Effects of gastric acidity on food intake in rats

Intragastric infusion of hydrochloric acid lowered rats' intragastric pH, but failed to produce any increase or decrease in food intake. Conversely, infusions of base (aluminum and magnesium hydroxide) increased pH without altering food intake.     

Dose-dependent effects of alcohol on appetite and food intake

To examine the potential dose-response effect of alcohol on appetite and food intake, 12 males attended the laboratory on three occasions. On each occasion, they were given a standard breakfast, then lunch 3 h later, and dinner, 4 h after that. Thirty minutes before lunch, Ss received 330 ml of no-alcohol lager (263 kJ: no-alcohol condition), the same amount of lager spiked with 1 unit (1 UA: 8 g ethyl alcohol, 498.2 kJ) or 4 units of alcohol (4 UA: 32 g ethyl alcohol, 1203.8 kJ). Visual analogue scale (VAS) ratings of appetite and mood were recorded before and after preloads and lunch, then hourly across the day. Intake at lunch (excluding energy from the preload) was significantly higher following 4 UA (5786+/-991 kJ) compared to 1 UA (4928+/-1245 kJ). Participants consumed more high-fat salty food items at lunch following 4 UA compared to the other preloads. Hunger was rated higher following 4 UA across the day in comparison to the other preloads, but fullness ratings failed to reflect any difference by condition. Energy intake at dinner was similar in all conditions and total energy intake across the day was significantly higher after 4 UA (14,615+/-1540 kJ) than after 1 UA (13,204+/-2156 kJ). In conclusion, above a certain threshold, alcohol appears to stimulate appetite in part, due to elevated levels of subjective hunger. When this occurs, energy intake is not reduced at subsequent meals. Thus, alcohol may contribute to positive energy balance via its additive effects to total energy intake and by short-term appetite stimulation.     

Gut peptides in the control of food intake: 30 years of ideas

The demonstration of the ability of exogenous cholecystokinin (CCK) to inhibit food intake began a series of investigations into whether and how gut and brain peptides affected ingestive behavior. In that original demonstration, Gerry Smith and colleagues both established criteria for evaluating roles for gut peptides in food intake and shifted the focus of feeding controls to factors that contribute to limiting meal size. Although new gut peptides with novel mechanisms and durations of action have been identified in the past few years, Smith's criteria and his distinction between direct and indirect controls of meal size continue to provide a framework for understanding how such peptides may contribute to overall feeding control.     

The effects of liver denervation on food and water intake in the rat

In Experiment 1, liver denervations or sham operations were performed on rats in two separate trials. Food and water intakes and body weights of denervated rats did not deviate significantly from their sham operated controls. Male and female rats responded similarly. In Experiment 2, in addition to daily food and water intakes, initial daily meal size was investigated in two groups of liver denervated and sham operated rats. Initial daily meal size was determined during a one hour test at the start of the dark period of the light:dark cycle. In one group of rats a chow diet was used for testing, while a liquid diet was utilized in the second group. According to the “liver glucoreceptor preabsorptive satiety and general food intake control hypothesis” the denervated rats should have experienced a depression of daily food intake and preabsorptive satiety. No differences were found in either preabsorptive satiety or daily food and water intakes and body weights when denervated rats were compared to sham operated control animals. The results question whether liver glucoreceptors have any detectable influence on the control of feeding behavior. Certainly the data does not support the role of liver glucoreceptors as a major controller of feeding behavior in the rat.     

Sexually dimorphic effects of forced exercise on food intake and body weight in the rat

The food intake (FI), body weight (BWt) and water intake (WI) of adult male and female rats were compared during a seven day period of forced exercise in a treadmill. Work loads for the exercised groups were gradually increased across the seven-day test period, whereas work loads for the sedentary controls were maintained at the same level used during a previous three-day training period. Relative to their respective control groups, male rats showed a decrease in FI and BWt in response to the exercise challenge, but female rats showed an increase in FI sufficient to maintain their BWt at control levels. Both male and female rats showed a reliable increase in WI during the period of forced exercise. These sexually dimorphic changes in FI and BWt in response to forced exercise indicate that female rats are capable of demonstrating a more vigorous defense of BWt than are male rats and suggest that there is a sex difference in the long-term control of feeding behavior in the rat.     

Effect of short-term energy intake level and exercise on oxygen consumption in men

Summary The influence of short-term energy intake and cycle exercise on oxygen consumption in response to a 1.5 MJ test meal was investigated in ten young, adult men. On the morning after a previous day's low-energy intake (LE regimen) of 4.5 MJ, the mean resting oxygen consumption increased by 0.7 ml · kg^–1 · min^–1 after the test meal (P<0.025). After a high-energy intake (HE regimen) of 18.1 MJ, the resting measurement was unchanged (+0.4 ml · kg^–1 · min^–1) after the meal (n.s.). These trends are the reverse of what would be expected if oxygen consumption in response to feeding is a factor in the acute control of body weight. The mean fasting oxygen consumption during cycle exercise at 56% of (constant work) for both LE and HE prior intakes was not different at 31.1 ml · kg^–1 · min^–1. Oxygen consumption during exercise increased after feeding by 0.5 ml · kg^–1 · min^–1 on the LE regimen (n.s.) and decreased by 1.2 ml · kg^–1 · min^–1 on the HE regimen (n.s.). These results are also the reverse of what would be expected if oxygen consumption in response to exercise is related to short-term energy intake.