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Changes in Respiratory Quotient With Overfeeding 

Changes in Respiratory Quotient With Overfeeding 

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Relatively little is known about the influence of age on energy regulation during energy imbalance. We compared the effects of overfeeding on changes in energy expenditure, substrate oxidation, and energy deposition between young men (age 23.7 +/- 1.1 [SEM] years) and older men (age 70.0 +/- 7.0) of normal body weight who were leading unrestricted...

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... inter- action between session and time approached significance (p = .08). Table 5 shows information on changes over time in respiratory quotient (RQ) in the young and older subjects (the mean food quotient was 0.866). There was a significant effect of age-group on the fasting RQ (values for young men were lower), and the increase in RQ following consumption of the test meals was significantly lower in the older group. ...

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... Most studies in which post-overfeeding food intake has been quantified have been of short duration and the data suggest an incomplete compensation for the excess energy [2,10]. One study reported that food intake was significantly suppressed following 21 days of overfeeding in young men, however changes of dietary conditions during the recovery phase might have confounded these data [19]. ...
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Body weight is under physiological regulation. When body fat mass decreases, a series of responses are triggered to promote weight regain by increasing food intake and decreasing energy expenditure. Analogous, in response to experimental overfeeding, excessive weight gain is counteracted by a reduction in food intake and possibly by an increase in energy expenditure. While low blood leptin and other hormones defend against weight loss, the signals that oppose overfeeding-induced fat mass expansion are still unknown. In this article, we discuss insights gained from overfeeding interventions in humans and intragastric overfeeding studies in rodents. We summarize the knowledge on the relative contributions of energy intake, energy expenditure and energy excretion to the physiological defence against overfeeding-induced weight gain. Furthermore, we explore literature supporting the existence of unidentified endocrine and non-endocrine pathways that defend against weight gain. Finally, we discuss the physiological drivers of constitutional thinness and suggest that overfeeding of individuals with constitutional thinness represents a gateway to understand the physiology of weight gain resistance in humans. Experimental overfeeding, combined with modern multi-omics techniques, has the potential to unveil the long-sought signalling pathways that protect against weight gain. Discovering these mechanisms could give rise to new treatments for obesity. This article is part of a discussion meeting issue ‘Causes of obesity: theories, conjectures and evidence (Part I)’.
... More recently, Rodriguez and colleagues [78] observed both absolute and FFM-adjusted increases in RMR among 20 resistancetrained men completing a supervised resistance training program in conjunction with an estimated 11% energy surplus and daily total intake comprising 18% protein. However, whether there may remain some residual effect of high food intake-specifically of protein-on conventionally fasted RMR in the context of overfeeding is a question in need of further investigation, especially as FFM-related differences in protein turnover rates may partially explain variable responses to overfeeding [79]. ...
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... These findings corroborate with studies evidencing the association of sarcopenia with general loss of mass in the elderly, not being selective only for loss of muscle mass. [32][33][34] What is already known on this topic Therefore, some studies suggest that older people have greater energy dysregulation, which predisposes them to BMI, body mass index; IRR, incidence rate ratio; * P = < 0.05 malnutrition, leading to morphological and functional alterations that arise as a reflex of the physiological and metabolic alterations, and consequent progressive reductions in body weight. 33,34 When compared to the condition of sarcopenia, it has been observed that this marked weight loss is stronger mainly in sarcopenic elderly. ...
... [32][33][34] What is already known on this topic Therefore, some studies suggest that older people have greater energy dysregulation, which predisposes them to BMI, body mass index; IRR, incidence rate ratio; * P = < 0.05 malnutrition, leading to morphological and functional alterations that arise as a reflex of the physiological and metabolic alterations, and consequent progressive reductions in body weight. 33,34 When compared to the condition of sarcopenia, it has been observed that this marked weight loss is stronger mainly in sarcopenic elderly. 32 Regarding nutritional factors, the following parameters can be considered as the main indicators of malnutrition in the elderly: body mass index (BMI) less than 22 kg/m 2 , total serum cholesterol level below 160 mg/dL, muscle circumference of the lower arm below the 10th percentile (<26.8 cm in the present study) and triceps cutaneous fold below the 10th percentile (<6.0 mm in the present study) or above the 95th. ...
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... Multiple genetic, social, economic, and personal life-style factors play a significant role in the pathogenesis of obesity [5]. In healthy individuals, energy intake is adjusted to energy expenditure and vice versa [6]. ...
... J o u r n a l P r e -p r o o f 6 ...
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... All studies, except four [26,45,46,50], reported inclusion and/or exclusion criteria, and stated that the participants met these criteria. Of the studies measuring energy intake (49 studies), 18 studies matched the younger and older participants for body weight [23,26,27,29,30,35,40,45,51,52,54,58,63,69,70,72,76,80] and 13 studies for BMI [26,27,33,[40][41][42]45,[47][48][49]58,68,76] and 11 studies considered gender as a confounder [31,39,43,46,47,52,56,71,75,78,79]. No studies considered confounders for hunger or fullness. ...
... All studies, except four [26,45,46,50], reported inclusion and/or exclusion criteria, and stated that the participants met these criteria. Of the studies measuring energy intake (49 studies), 18 studies matched the younger and older participants for body weight [23,26,27,29,30,35,40,45,51,52,54,58,63,69,70,72,76,80] and 13 studies for BMI [26,27,33,[40][41][42]45,[47][48][49]58,68,76] and 11 studies considered gender as a confounder [31,39,43,46,47,52,56,71,75,78,79]. No studies considered confounders for hunger or fullness. ...
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... Hence this will also increase the release of free fatty acids to the blood in the elderly. Age is associated with decline in fat oxidation during activity, after meal and in resting condition (Robert et al., 1996). In principle, the capacity of metabolically active tissues such as the muscles to oxidize fat represents a combination of the tissue mass and oxidative capacity of the tissue. ...
... The increase of body fat in elderly individuals might be explained by the release of high amounts of free fatty acids from adipose tissue, the reduced capacity of respiring tissues (e.g. muscles) to oxidise free fatty acids at rest [34], following a meal [35] and during exercise [36] or even both. However, there is a lack of expert knowledge on the exact causes and development of A + symbolizes that the intake should be increased in comparison to younger adults; − means that the substance is not required in higher doses in the elderly Source: D-A-CH reference values [8] these metabolic processes. ...
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Basically, our lifespan is determined genetically. However, several other parameters such as the environment, lifestyle and diet have a high impact on living in the best of health. Many older persons suffer from various diseases, which often cannot be avoided; however, their development can be postponed and symptoms can be mitigated by a balanced diet, moderate physical activity as well as a healthy lifestyle. These diseases are, for example, sarcopenia (degenerative loss of muscle mass), osteoporosis (decomposition of bone structure), digestive restrictions, sensory impairment, water imbalance or a compromised immune system. Psychological modifications, obesity and loss of weight also commonly occur in older adults. To define an adequate diet for elderly between the ages 50 and 80 is difficult, even impossible, because the nutritional requirements differ between the dynamic quinquagenarian and the frailer eighty-year-old. However, several studies have shown that sufficient consumption of high-quality proteins, calcium, vitamin D, anti-oxidative food compounds, water as well as adapted energy values and nourishment with high-nutrient density in combination with physical activity especially help one to remain healthy to a great age. The cornerstone of healthy ageing is the maintenance of normal bodyweight in order to prevent the development of diseases such as osteoporosis, coronary heart disease or diabetes type 2. This publication will review the physiological changes that occur with advanced age and consequential nutritional recommendations for elderly persons. KeywordsAgeing-Physiological changes-Nutrition-Nutrient requirements-Elderly
... As will be discussed below, we believe that differences in the hormonal milieu in the fasted and postprandial states in older and younger adults contribute to differences in fuel availability and substrate oxidation. Although two previous studies reported a lower postprandial fat oxidation in older men (23) and women (17), this was only observed when subjects were overfed; there were no differences in postprandial fat oxidation after consumption of smaller meals. ...
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... Elevated levels of body fat in the elderly may, in part, be due to a decrease in fat mobilisation (Lonnqvist et al. 1990) and oxidation (Calles-Escandon et al. 1995). Aging is associated with reduced fat oxidation at rest (Nagy et al. 1996), following a meal (Roberts et al. 1996), and during exercise (Sial et al. 1996). For example, Sial et al. (1996) showed that during 60 min of sub-maximal exercise at 50% of maximal oxygen consumption ð _ VO 2 max Þ; the rate of appearance of free fatty acids in blood as well as fat oxidation was lower in older compared to younger individuals and that carbohydrate (CHO) oxidation was higher. ...
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Advancing age is associated with changes in fat and carbohydrate (CHO) metabolism, which is considered a risk factor for cardiovascular disease and diabetes. The effects of exercise intensity and duration on fat and CHO metabolism in elderly male subjects were investigated in the present study. Seven trained (63.7 ± 4.7 years) and six untrained (63.5 ± 4.5 years) healthy males performed three 30 min trials on a cycle ergometer at 50, 60 and 70% \( \ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{{2\max }} \) and two other trials at 60 and 70% \( \ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{{2\max }} \) in which the total energy expenditure was equal to that for 30 min at 50% \( \ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{{2\max }} . \) Respiratory measures were undertaken throughout the exercise and blood samples taken before and immediately after each trial. Statistical analyses revealed a significant effect of exercise intensity on fat oxidation when the exercise durations were equated as well as when the energy expenditure was held constant for the three trials, though no training effect was noted. Total carbohydrate oxidation increased significantly with exercise intensity (P < 0.05) and with training. Significantly higher levels of non-esterified free fatty acid (NEFA) and glycerol were observed for trained compared with untrained though not for B-hydroxybutyrate (3-OH) or insulin. No differences in NEFA, glycerol, 3-OH were evident for increases in exercise intensity. Carbohydrate and fat oxidation are significantly affected by exercise intensity in elderly males, although only CHO oxidation is influenced by training. Furthermore, training-induced increases in the availability of NEFA and glycerol are not associated with an increase in fat oxidation, rather an increase in CHO oxidation.
... Even in elderly individuals, where total body weight (and subcutaneous fat) declines toward the end of life, visceral adiposity continues to increase, pointing to a fundamental age-related defect in energy balance [1,3,5]. Elderly humans exhibit defects in both the normal reduction in energy expenditure caused by overfeeding [39], and the normal increase in perceived hunger caused by underfeeding [40]. Defects in compensatory hyperphagia similar to what we observed in our Pomcablation or double-ablation mice have also been described in studies of young (3-mo-old), middle-aged (12-mo-old), and elderly (24-mo-old) rats from Matsumoto and colleagues [6,41]. ...
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Normal aging in humans and rodents is accompanied by a progressive increase in adiposity. To investigate the role of hypothalamic neuronal circuits in this process, we used a Cre-lox strategy to create mice with specific and progressive degeneration of hypothalamic neurons that express agouti-related protein (Agrp) or proopiomelanocortin (Pomc), neuropeptides that promote positive or negative energy balance, respectively, through their opposing effects on melanocortin receptor signaling. In previous studies, Pomc mutant mice became obese, but Agrp mutant mice were surprisingly normal, suggesting potential compensation by neuronal circuits or genetic redundancy. Here we find that Pomc-ablation mice develop obesity similar to that described for Pomc knockout mice, but also exhibit defects in compensatory hyperphagia similar to what occurs during normal aging. Agrp-ablation female mice exhibit reduced adiposity with normal compensatory hyperphagia, while animals ablated for both Pomc and Agrp neurons exhibit an additive interaction phenotype. These findings provide new insight into the roles of hypothalamic neurons in energy balance regulation, and provide a model for understanding defects in human energy balance associated with neurodegeneration and aging.