BACKGROUND: Associations between body composition and the energy expended on basal metabolism and activity are complex and age dependent. OBJECTIVE: The objective was to examine associations between ...body composition and daily (DEE), basal (BEE), and activity energy expenditure (AEE) throughout the adult life span. DESIGN: A cross-sectional study was conducted in 529 adults aged 18-96 y. DEE was measured by using doubly labeled water, BEE by using respirometry, and body composition by isotope dilution. AEE was calculated as DEE - BEE, and physical activity level (PAL) was calculated as DEE/BEE. RESULTS: Up to age 52 y, fat-free mass (FFM) and fat mass (FM) were positively associated with age in men, but no significant effect was observed in women. No effects of age on DEE and AEE were observed. The average DEE in men (14.1 MJ/d) was 27% greater than that in women (10.7 MJ/d). PAL averaged 1.84 in men and 1.75 in women. Above and including the age of 52 y, FFM, FM, DEE, BEE, and AEE were all negatively associated with greater age. The effect of age on AEE was greater than on BEE; consequently, PAL by the age of 95 y was only 1.36. PAL and AEE were both unrelated to FFM (both age adjusted). CONCLUSIONS: PAL and AEE were not associated with age in subjects aged <52 y. AEE, BEE, and PAL were all negatively associated with age in subjects aged ≥52 y. An absence of a relation between age-adjusted PAL and FFM suggested that greater physical activity was not associated with higher FFM in the elderly.
The “thrifty gene hypothesis” suggests we evolved genes for efficient food collection and fat deposition to survive periods of famine and that now that food is continuously available, these genes are ...disadvantageous because they make us obese in preparation for a famine that never comes. However, famines are relatively infrequent modern phenomena that involve insufficient mortality for thrifty genes to propagate. I suggest here that early hominids would have been subjected to stabilizing selection for body fatness, with obesity selected against by the risk of predation. Around two million years ago predation was removed as a significant factor by the development of social behavior, weapons, and fire. The absence of predation led to a change in the population distribution of body fatness due to random mutations and drift. Because this novel hypothesis involves random drift, rather than directed selection, it explains why, even in Western society, most people are not obese.
Obesity represents one of the most serious global health issues with ∼310 million people presently affected. It develops because of a mismatch between energy intake and expenditure that results from ...behavior (feeding behavior and time spent active) and physiology (resting metabolism and expenditure when active). Both of these traits are affected by environmental and genetic factors. The dramatic increase in the numbers of obese people in Western societies reflects mostly changing environmental factors and is linked to reduced activity and perhaps also increased food intake. However, in all societies and subpopulations, there are both obese and nonobese subjects. These differences are primarily a consequence of genetic factors as is revealed by the high heritability for body mass index. Most researchers agree that energy balance and, hence, body weight are regulated phenomena. There is some disagreement about exactly how this regulation occurs. However, a common model is the “lipostatic” regulation system, whereby our energy stores generate signals that are compared with targets encoded in the brain, and differences between these drive our food intake levels, activity patterns, and resting and active metabolisms. Considerable advances were made in the last decade in understanding the molecular basis of this lipostatic system. Some obese people have high body weight because they have broken lipostats, but these are a rare minority. This suggests that for the majority of obese people, the lipostat is set at an inappropriately high level. When combined with exposure to an environment where there is ready availability of food at low energy costs to obtain it, obesity develops. The evolutionary background to how such a system might have evolved involves the evolution of social behavior, the harnessing of fire, and the development of weapons that effectively freed humans from the risks of predation. The lipostatic model not only explains why some people become obese whereas others do not, but also allows us to understand why energy-controlled diets do not work. Drug-based solutions to the obesity problem that work with the lipostat, rather than against it, are presently under development and will probably be in regular use within 5–10 y. However, several lines of evidence including genetic mapping studies of quantitative trait loci associated with obesity suggest that our present understanding of the regulatory system is still rudimentary. In particular, we know nothing about how the target body weight in the brain is encoded. As our understanding in this field advances, new drug targets are likely to emerge and allow us to treat this crippling disorder.
The obesity epidemic in the United States has been mirrored by an increase in calories consumed outside of the home and by expansions in the numbers of, and portion sizes at, both fast-food ...restaurants (FFRs) and full-service restaurants (FSRs), leading some to blame the epidemic on the restaurant industry. If this were indeed true, one would predict that greater per capita densities of FFRs and FSRs would lead to greater obesity prevalence.
We evaluated the population-level association between both FSRs and FFRs and the prevalence of obesity and calculated the proportion of calories consumed in these establishments.
In this ecological cross-sectional study, we used county-level data (aggregate-level data) for obesity prevalence across the mainland United States in 2012 and matched these data to county-level per capita densities of FFRs and FSRs in the same year. Multiple linear regression was used to determine the relation between the prevalence of obesity and the densities of FFRs and FSRs after adjustment for confounding factors.
Contrary to expectations, obesity prevalence was highly significantly negatively related to the densities of both FFRs and FSRs (combined-effect R2 = 0.195). This was principally because greater numbers of both FFRs and FSRs were located in areas in which individuals were on average wealthier and more educated. When we normalized for these factors (and additional socioeconomic variables), the associations between restaurant densities and obesity effectively disappeared (pooled R2 = 0.008). Our calculations showed that the percentage of total calories consumed in FFRs and FSRs is a mean of only 15.9% of the total intake (maximum: 22.6%).
Variations in the densities of FFRs and FSRs are not linked to the prevalence of obesity in the United States, and food consumed in these establishments is responsible for <20% of total energy intake. This finding has implications for policy decisions regarding how we aim to tackle the obesity epidemic.
Resistance exercise increases muscle mass and function in older adults, but responses are attenuated compared with younger people. Data suggest that long-chain n-3 polyunsaturated fatty acids (PUFAs) ...may enhance adaptations to resistance exercise in older women. To our knowledge, this possibility has not been investigated in men.
We sought to determine the effects of long-chain n-3 PUFA supplementation on resistance exercise training-induced increases in muscle mass and function and whether these effects differ between older men and women.
Fifty men and women men: n = 27, mean ± SD age: 70.6 ± 4.5 y, mean ± SD body mass index (BMI; in kg/m
): 25.6 ± 4.2; women: n = 23, mean ± SD age: 70.7 ± 3.3 y, mean ± SD BMI: 25.3 ± 4.7 were randomly assigned to either long-chain n-3 PUFA (n = 23; 3 g fish oil/d) or placebo (n = 27; 3 g safflower oil/d) and participated in lower-limb resistance exercise training twice weekly for 18 wk. Muscle size, strength, and quality (strength per unit muscle area), functional abilities, and circulating metabolic and inflammatory markers were measured before and after the intervention.
Maximal isometric torque increased after exercise training to a greater (P < 0.05) extent in the long-chain n-3 PUFA group than in the placebo group in women, with no differences (P > 0.05) between groups in men. In both sexes, the effect of exercise training on maximal isokinetic torque at 30, 90, and 240° s
, 4-m walk time, chair-rise time, muscle anatomic cross-sectional area, and muscle fat did not differ (P > 0.05) between groups. There was a greater (P < 0.05) increase in muscle quality in women after exercise training in the long-chain n-3 PUFA group than in the placebo group, with no such differences in men (P > 0.05). Long-chain n-3 PUFAs resulted in a greater decrease (P < 0.05) than the placebo in plasma triglyceride concentrations in both sexes, with no differences (P > 0.05) in glucose, insulin, or inflammatory markers.
Long-chain n-3 PUFA supplementation augments increases in muscle function and quality in older women but not in older men after resistance exercise training. This trial was registered at clinicaltrials.gov as NCT02843009.
The idea that resources are limited and animals can maximise fitness by trading costly activities off against one another forms the basis of life-history theory. Although investment in reproduction ...or growth negatively affects survival, the mechanisms underlying such trade-offs remain obscure. One plausible mechanism is oxidative damage to proteins, lipids, and nucleic acids caused by reactive oxygen species (ROS). Here, we critically evaluate the premise that ROS-induced oxidative damage shapes life history, focussing on birds and mammals, and highlight the importance of ecological studies examining free-living animals within this experimental framework. We conclude by emphasising the value of using multiple assays to determine oxidative protection and damage. We also highlight the importance of using standardised and appropriate protocols, and discuss future research directions.
Cold exposure imposes a metabolic challenge to mammals that is met by a coordinated response in different tissues to prevent hypothermia. This study reports a transcriptomic analysis in brown adipose ...tissue (BAT), white adipose (WAT) and liver of mice in response to 24 h cold exposure at 8°C. Expression of 1895 genes were significantly (P<0.05) up- or down-regulated more than two fold by cold exposure in all tissues but only 5 of these genes were shared by all three tissues, and only 19, 14 and 134 genes were common between WAT and BAT, WAT and liver, and BAT and liver, respectively. We confirmed using qRT-PCR, the increased expression of a number of characteristic BAT genes during cold exposure. In both BAT and the liver, the most common direction of change in gene expression was suppression (496 genes in BAT and 590 genes in liver). Gene ontology analysis revealed for the first time significant (P<0.05) down regulation in response to cold, of genes involved in oxidoreductase activity, lipid metabolic processes and protease inhibitor activity, in both BAT and liver, but not WAT. The results reveal an unexpected importance of down regulation of cytochrome P450 gene expression and apolipoprotein, in both BAT and liver, but not WAT, in response to cold exposure. Pathway analysis suggests a model in which down regulation of the nuclear transcription factors HNF4α and PPARα in both BAT and liver may orchestrate the down regulation of genes involved in lipoprotein and steroid metabolism as well as Phase I enzymes belonging to the cytochrome P450 group in response to cold stress in mice. We propose that the response to cold stress involves decreased gene expression in a range of cellular processes in order to maximise pathways involved in heat production.
Excised fat tissue has a lower thermal conductivity than excised lean tissue. In theory then subcutaneous fat might serve as a barrier to heat loss and influence thermoregulatory abilities. In some ...aquatic mammals and animals from severely cold habitats subcutaneous adipose tissue has evolved into a continuous sheet that envelopes the organs and acts as a thermal insulation layer. This layer can comprise more than half of the cross-sectional area of the body. In most mammals however, the distribution of fat is less continuous. It has been suggested that in tropical animals this distribution may in fact allow animals to still store energy while not impeding heat loss. Studies of humans immersed in cool water convincingly demonstrate that obesity in humans also serves an insulation function. Humans with obesity cool less rapidly and have to elevate their metabolism less significantly than lean individuals when immersed in water. Although obesity provides an advantage in cold conditions it conversely impedes heat loss and makes obese people susceptible to heat stress more than lean individuals. In small mammals like mice the role of subcutaneous (or intradermal) fat for providing thermal insulation is less clear. In theory variations in thermoregulatory capacity may allow individuals different capabilities to burn off excess consumption. Hence, thermoregulatory variations may cause obesity differences. Thermoregulatory capacity is related to ambient temperature. Yet, levels of obesity are only weakly related to ambient temperature and this effect disappears when confounding factors like poverty and race are taken into account. Hence we conclude that obesity may have a significant impact on thermoregulatory physiology, but the converse is much less likely.
Physical activity impacts energy balance because of its contribution to total energy expenditure. Measuring physical activity energy expenditure (PAEE) is often performed by subtracting the estimated ...24 h expenditure on basal metabolism (called basal energy expenditure or BEE) from the total energy expenditure (TEE) measured by doubly labelled water minus an estimate of the thermic effect of food (TEF). Alternatively it can be measured as the ratio of TEE/BEE, which is commonly called the physical activity level (PAL).
PAEE and PAL are widely used in the literature but their shortcomings are seldom addressed. In this review, we outline some of the issues with their use.
TEE and BEE are both measured with error. The estimate of PAEE by difference magnifies these errors and consequently the precision of estimated PAEE is about 3× worse than TEE and 25-35× worse than BEE. A second problem is that the component called PAEE is actually any component of TEE that is not BEE. We highlight how the diurnal variation of BEE, thermoregulatory expenditure and elevations of RMR because of stress will all be part of what is called PAEE and will contribute to a disconnect between what is measured and what energy expenditure is a consequence of physical activity. We emphasize caution should be exerted when interpreting these measurements of PAEE and PAL.
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