No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Genetic effect in resting and exercise metabolic rates
Abstract
Two studies dealing with the contribution of the genotype in individual differences for resting metabolic rate (RMR), thermic effect of a 4.2 MJ carbohydrate meal (TEM), and energy cost of submaximal exercise are reported. The genetic effect for RMR and TEM was studied in 31 pairs of parent-child, 21 pairs of dizygotic (DZ) twins, and 37 pairs of monozygotic (MZ) twins, whereas the heritability of the energy cost of submaximal exercise was determined from data on 22 pairs of DZ twins and 31 pairs of MZ twins. The heritability of RMR reached approximately 40% of the variance remaining after adjustment for age, gender, and fat-free mass, (FFM). The genetic effect for TEM was equivalent to at least 40% to 50% of the variation in the energy expended during four hours after the meal test. A highly significant genetic effect was found for fasting plasma glucose (greater than .72), but the results for fasting plasma insulin are unclear. No significant genetic variance was seen for the glucose and insulin response to the carbohydrate meal. Finally, heritability for the metabolic rate during cycle exercise was high (greater than or equal to .46) at low power output, but it became nonsignificant when the energy cost reached about 6 times the RMR.
... Genetic differences likely play an important role because several physical and performance traits, including maximal oxygen uptake (Bouchard et al. 1998), lean body mass (LBM), muscle strength (Arden and Spector 1997) and skeletal muscle fiber-type proportion (Simoneau and Bouchard 1995) have significant genetic components. Studies investigating the respiratory exchange ratio (RER) at rest and during exercise have demonstrated that the relative use of fatty acids in both conditions show familial resemblance (Bouchard et al. 1989;Toubro et al. 1998). However, to our knowledge, no researcher has studied the absolute fat oxidation rates at rest and during exercise among monozygotic (MZ) twins. ...
... This study's major finding is that hereditary factors influence fat oxidation capacity. The finding supports those of Toubro et al. (1998) and Bouchard et al. (1989), who reported that RER at rest and during low-intensity cycling showed significant familial resemblance. In a study involving male MZ twin pairs (Bouchard et al. 1989), the ICCs of RER ranged from 0.63 to 0.54 during cycling at low intensities (50 W and 100 W, respectively). ...
... The finding supports those of Toubro et al. (1998) and Bouchard et al. (1989), who reported that RER at rest and during low-intensity cycling showed significant familial resemblance. In a study involving male MZ twin pairs (Bouchard et al. 1989), the ICCs of RER ranged from 0.63 to 0.54 during cycling at low intensities (50 W and 100 W, respectively). As the researchers also investigated the substrate use of dizygotic twins, they were able to control their analysis for the common environmental effect. ...
Purpose
We aimed to investigate if hereditary factors, leisure-time physical activity (LTPA) and metabolic health interact with resting fat oxidation (RFO) and peak fat oxidation (PFO) during ergometer cycling.
Methods
We recruited 23 male monozygotic twin pairs (aged 32–37 years) and determined their RFO and PFO with indirect calorimetry for 21 and 19 twin pairs and for 43 and 41 twin individuals, respectively. Using physical activity interviews and the Baecke questionnaire, we identified 10 twin pairs as LTPA discordant for the past 3 years. Of the twin pairs, 8 pairs participated in both RFO and PFO measurements, and 2 pairs participated in either of the measurements. We quantified the participants’ metabolic health with a 2-h oral glucose tolerance test.
Results
Fat oxidation within co-twins was correlated at rest [intraclass correlation coefficient (ICC) = 0.54, 95% confidence interval (CI) 0.15–0.78] and during exercise (ICC = 0.67, 95% CI 0.33–0.86). The LTPA-discordant pairs had no pairwise differences in RFO or PFO. In the twin individual-based analysis, PFO was positively correlated with the past 12-month LTPA (r = 0.26, p = 0.034) and the Baecke score (r = 0.40, p = 0.022) and negatively correlated with the area under the curve of insulin (r = − 0.42, p = 0.015) and glucose (r = − 0.31, p = 0.050) during the oral glucose tolerance test.
Conclusions
Hereditary factors were more important than LTPA for determining fat oxidation at rest and during exercise. Additionally, PFO, but not RFO, was associated with better metabolic health.
... Etiology of the Obesity Epidemic Bray (1998) has succinctly summarized the etiology of obesity: "Genes load the gun, the environment pulls the trigger." Genes are currently thought to explain 25%-40% of the variance in BMI (Bouchard, 1994;Price, 2002) and contribute to differences among people in resting metabolic rate, in weight gain in response to overfeeding, and in where excess fat is stored (i.e., body fat distribution; Bouchard, 1994;Bouchard et al., 1989Bouchard et al., , 1990J. A. Levine, Eberhardt, & Jensen, 1999). Thus, some individuals appear to be born with a genetic predisposition to obesity that is readily nurtured by our nation's lifestyle, as discussed later. ...
Obesity has reached epidemic proportions in the United States and other developed nations. In the United States, 27% of adults are obese and an additional 34% are overweight. Research in the past decade has shown that genetic influences clearly predispose some individuals to obesity. The marked increase in prevalence, however, appears to be attributable to a toxic environment that implicitly discourages physical activity while explicitly encouraging the consumption of supersized portions of high-fat, high-sugar foods. Management of the obesity epidemic will require a two-pronged approach. First, better treatments, including behavioral, pharmacologic, and surgical interventions, are needed for individuals who are already obese. The second and potentially more promising approach is to prevent the development of obesity by tackling the toxic environment. This will require bold public policy initiatives such as regulating food advertising directed at children. The authors call not for the adoption of a specific policy initiative, but instead propose that policy research, based on viewing obesity as a public health problem, become a central focus of research.
... We have consider several different possible explanations. Other heritable genetic factors have been implicated in determining energy expenditure; REE and TEE are similar within families [21] and energy expenditure interclass correlations are greater among monozygotic versus dizygotic twins [22]. It is possible that these factors are different between the subjects with an LC-FAOD and the control population compared here; subjects with an LC-FAOD expressing other genetics factors associated with lower energy expenditure and controls expressing genetic factors associated with higher energy expenditure. ...
The basis of medical nutrition therapy for patients with LC-FAODs is to provide adequate energy to maintain anabolism and prevent catabolism. In practice, energy needs are estimated based on formulas derived from normal populations but it is unknown if energy expenditure among patients with LC-FAODs is similar to the normal population. We measured resting energy expenditure (REE), total energy expenditure (TEE) and body composition in 31 subjects with LC-FAODs ranging in age from 7 to 64 years. Measured REE was lower than estimated REE by various prediction equations and measured TEE was lower than estimated TEE. It is possible that the lower energy expenditure based on prediction formulas from the normal population is due to differences in body composition; we compared body composition to normal data from the 2017-18 National Health and Nutrition Examination Survey (NHANES). Fat free mass and fat mass was similar between subjects with an LC-FAOD and NHANES normal data suggesting no difference in body composition. We then compared measured REE and TEE to normal published data from the Dietary Reference Intakes (DRI). Measured REE and TEE were significantly lower among subjects with LC-FAODs compared to normal published energy expenditure data. Our results suggests patients with a LC-FAOD exhibit a lower REE and therefore actually have a slightly lower TEE than estimated. Current prediction equations may overestimate energy expenditure of patients with a LC-FAOD.
... fitness, lean mass, and leisure-time physical activity [4e7]. Genetic pleiotropy contributes to the associations, and higher PFO does not result solely from an active lifestyle [28,49]. Still, 12-week endurance-focused training increased fat oxidation during exercise but not at rest in postmenopausal women [50], showing that fat oxidation capacity can be improved in E2 deficiency. ...
Background and aims:
Menopause may reduce fat oxidation. We investigated whether sex hormone profile explains resting fat oxidation (RFO) or peak fat oxidation (PFO) during incremental cycling in middle-aged women. Secondarily, we studied associations of RFO and PFO with glucose regulation.
Method and results:
We measured RFO and PFO of 42 women (age 52-58 years) with indirect calorimetry. Seven participants were pre- or perimenopausal, 26 were postmenopausal, and nine were postmenopausal hormone therapy users. Serum estradiol (E2), follicle-stimulating hormone, progesterone, and testosterone levels were quantified with immunoassays. Insulin sensitivity (Matsuda index) and glucose tolerance (area under the curve) were determined by glucose tolerance testing. Body composition was assessed with dual-energy X-ray absorptiometry; physical activity with self-report and accelerometry; and diet, with food diaries. Menopausal status or sex hormone levels were not associated with the fat oxidation outcomes. RFO determinants were fat mass (β = 0.44, P = 0.006) and preceding energy intake (β = -0.40, P = 0.019). Cardiorespiratory fitness (β = 0.59, P = 0.002), lean mass (β = 0.49, P = 0.002) and physical activity (self-reported β = 0.37, P = 0.020; accelerometer-measured β = 0.35, P = 0.024) explained PFO. RFO and PFO were not related to insulin sensitivity. Higher RFO was associated with poorer glucose tolerance (β = 0.52, P = 0.002).
Conclusion:
Among studied middle-aged women, sex hormone profile did not explain RFO or PFO, and higher fat oxidation capacity did not indicate better glucose control.
... In general, total daily energy expenditure consists of three main components [3], and resting metabolic rate (RMR) accounts for the largest share of total daily energy requirements (approximately 60 to 75%). Numerous factors affect the level of RMR, including age, sex, race, size, body composition, and hormonal status [4][5][6][7][8]. Studies have shown that RMR is an important determinant of meal size and energy intake per day and reflects the physiological need for food intake [9,10], and is posited as a predictor of fasting hunger, affecting the overall hunger profile [11]. ...
Objective
Low resting metabolic rate (RMR), as a risk factor for weight gain and obesity, can be influenced by many factors. Empirical research has confirmed the role of appetite and related hormones in obesity and energy intake. This study aimed to investigate the relationship between appetite and related hormones in overweight or obese Iranian women with normal and hypo RMR.
Methods
This case–control study was conducted on 42 Iranian adult women (21 cases, and 21 controls), aged 18–48 years. An impedance body analyzer was used to obtain the body composition and an indirect calorimeter was used to assess the RMR. The Flint questionnaire was used to assess appetite, dietary intake, and physical activity were assessed by FFQ and IPAQ questionnaires respectively, and ELISA kits were used to assess leptin, ghrelin, and insulin hormones.
Results
The results of the study demonstrated a negative association between ghrelin hormone level (β = -0.34, 95%CI = -61.70,-3.86, P-value = 0.027) and RMR, and a positive association between insulin hormone level (β = 0.48, 95%CI = 9.38–34.35, P-value = 0.001) and RMR. Also, results of the appetite questionnaire showed that, in general, both appetite (β = 0.32, 95%CI = -0.10–2.99 P-value = 0.044) and hunger variable (β = 0.30, 95%CI = 0.04–5.87, P-value = 0.047) have a positive association with RMR. There was no significant association between leptin levels and RMR.
Conclusion
It is evident that appetite and related hormones have a potential role in promoting a normal RMR.
... Muscle cells play the biggest roles in energy expenditure in the body [3,6]. If basal metabolic rate, which is variable between people due to genetic diversities [1,26,27], is low, the risk of body weight gain can rise [1,2]. We observed that DT sap administration suppressed the increase in body weight ( Figure 1). ...
Dendropanax trifidus (DT) is a medicinal herb native to East Asia, which has been used extensively for its therapeutic properties in traditional medicine. In this study, we examined the effects of DT sap on the regulation of body weight and muscle metabolism in mice. Obese model db/db mice were administered daily with DT sap or vehicle control over a 6-week period. The effects of DT sap on muscle metabolism were studied in C2C12 muscle cells, where glycolytic and mitochondrial respiration rates were monitored. As AMP-activated protein kinase (AMPK) is a master regulator of metabolism and plays an important function as an energy sensor in muscle tissue, signaling pathways related with AMPK were also examined. We found that DT sap inhibited body weight increase in db/db, db/+, and +/+ mice over a 6-week period, while DT sap-treated muscle cells showed increased muscle metabolism and also increased phosphorylation of AMPK and Acetyl-CoA Carboxylase (ACC). Finally, we found that DT sap, which is enriched in estrogen in our previous study, significantly activates estrogen alpha receptor in a concentration-dependent manner, which can drive the activation of AMPK signaling and may be related to the muscle metabolism and weight changes observed here.
... Both genes and environment can influence behaviors and physiology and they are involved in the regulation of energy intake and energy expenditure [5]. A low basal metabolic rate is partly heritable (about 40%) [9,10] and is a risk factor for weight gain [11]. Appetite traits are also partly heritable (50-85%) in infancy and childhood [12][13][14] and are related to weight gain [15]. ...
Background
Many genes and molecular pathways are associated with obesity, but the mechanisms from genes to obesity are less well known. Eating behaviors represent a plausible pathway, but because the relationships of eating behaviors and obesity may be bi-directional, it remains challenging to resolve the underlying pathways. A longitudinal approach is needed to assess the contribution of genetic risk during the development of obesity in childhood. In this study we aim to examine the relationships between the polygenic risk score for body mass index (PRS-BMI), parental concern of overeating and obesity indices during childhood.
Methods
The IDEFICS/I.Family study is a school-based multicenter pan-European cohort of children observed for 6 years (mean ± SD follow-up 5.8 ± 0.4). Children examined in 2007/2008 (wave 1) (mean ± SD age: 4.4 ± 1.1, range: 2–9 years), in 2009/2010 (wave 2) and in 2013/2014 (wave 3) were included. A total of 5112 children (49% girls) participated at waves 1, 2 and 3. For 2656 children with genome-wide data we constructed a PRS based on 2.1 million single nucleotide polymorphisms. Z-score BMI and z-score waist circumference (WC) were assessed and eating behaviors and relevant confounders were reported by parents via questionnaires. Parental concern of overeating was derived from principal component analyses from an eating behavior questionnaire.
Results
In cross-lagged models, the prospective associations between z-score obesity indices and parental concern of overeating were bi-directional. In mediation models, the association between the PRS-BMI and parental concern of overeating at wave 3 was mediated by baseline z-BMI ( β = 0.16, 95% CI: 0.10, 0.21) and baseline z-WC ( β = 0.17, 95% CI: 0.11, 0.23). To a lesser extent, baseline parental concern of overeating also mediated the association between the PRS-BMI and z-BMI at wave 3 ( β = 0.10, 95% CI: 0.07, 0.13) and z-WC at wave 3 ( β = 0.09, 95% CI: 0.07, 0.12).
Conclusions
The findings suggest that the prospective associations between obesity indices and parental concern of overeating are likely bi-directional, but obesity indices have a stronger association with future parental concern of overeating than vice versa. The findings suggest parental concern of overeating as a possible mediator in the genetic susceptibility to obesity and further highlight that other pathways are also involved. A better understanding of the genetic pathways that lead to childhood obesity can help to prevent weight gain.
Trial registration
Registry number: ISRCTN62310987 Retrospectively registered 17 September 2018.
... OPRM1 SNP rs1799971 was also associated with norepinephrine and lactate changes during exercise. However, the study concluded that the physiological responses to aerobic exercise involve a complex interaction of metabolic functions, thus these genes and SNPs are likely to explain only a small portion of the variability in individual differences in response to aerobic exercise [153,154]. ...
AIM: The outstanding performance of elite athletes is a product of a complex interaction between genetic and environmental factors. The aims of this study was to compare differences in genetic and metabolic profiles among different classes of elite athletes and to identify genetically-influenced metabolic profiles (metabotypes) underlying these differences. METHODS: Genome-wide association study (GWAS) was conducted in 1259 elite athlete samples using Drug core BeadChip arrays, followed by non-targeted metabolomics of 692 serum samples. Genotype distribution, differences in metabolic levels and genetically-influenced metabotypes were compared between high and moderate endurance and power sports as well as among sports with different cardiovascular demands (CVD). RESULTS: Out of 341385 SNPs, two novel associations are reported for endurance status including rs56330321 in ATP2B2 (p=1.47E-7) and rs2635438 in SYNE1 (p=2.54E-7). A meta-analysis confirmed the association of rs56330321 and rs2635438 with endurance athlete status at GWAS level of significance. Metabolomics analysis of 740 metabolites was performed in in 191 (discovery cohort) and 500 (replication cohort) elite athletes. These studies revealed changes in various metabolites involved in steroid biosynthesis, fatty acid oxidation, oxidative stress response, xenobiotics and various mediators of cell signaling among different groups of endurance, power and CVD athletes. By combining GWAS with metabolomics profiling data (mGWAS), 19 common variant metabolic quantitative trait loci (mQTLs) were identified, of which 5 were novel. When focusing on metabolites associated with endurance, power and CVD, 4 common variant mQTLs were found, of which one novel mQTL linking 4-androsten-3alpha,17alpha-diol monosulfate and SULT2A1 involved in steroid sulfation was identified in association with endurance. CONCLUSIONS: GWAS, metabolomics and mGWAS of elite athletes identified novel markers associated with elite athletic performance with a potential application in biomarker discovery in relation to elite athletic performance.
... Human obesity is heritable and understanding its genetic determinants requires studying the genetic basis of energy intake and energy expenditure (EE), the two physiological factors contributing to daily energy balance and ultimately determining body weight change (1,2). Several studies conducted in twins (3)(4)(5) and in isolated American Indian populations (6,7) to minimize the effect of environmental factors, have consistently demonstrated that EE is a familial trait and the inter-individual variability in EE after controlling for differences in body size and composition among individuals has a substantial genetic component (8)(9)(10)(11). We recently conducted a genome-wide association study (GWAS) of human EE, as assessed by accurate measurement over 24 hours inside a whole-room indirect calorimeter and representing a metabolic determinant of weight change (6,12), in American Indians from different nuclear families using a custom, population-specific genotyping array (13). ...
Background
Obesity and energy expenditure (EE) are heritable and genetic variants influencing EE may contribute to the development of obesity. We sought to identify genetic variants that affect EE in American Indians, an ethnic group with high prevalence of obesity.
Methods
Whole-exome sequencing was performed in 373 healthy Pima Indians informative for 24-h EE during energy balance. Genetic association analyses of all high-quality exonic variants (≥5 carriers) was performed, and those predicted to be damaging were prioritized.
Results
Rs752074397 introduces a premature stop codon (Cys264Ter) in DAO and demonstrated the strongest association for 24-h EE, where the Ter allele associated with substantially lower 24-h EE (mean lower by 268 kcal/day) and sleeping EE (by 135 kcal/day). The Ter allele has a frequency=0.5% in Pima Indians, while is extremely rare in most other ethnic groups (frequency&0.01%). In vitro functional analysis showed reduced protein levels for the truncated form of DAO consistent with increased protein degradation. DAO encodes D-amino acid oxidase, which is involved in dopamine synthesis which might explain its role in modulating EE.
Conclusion
Our results indicate that a nonsense mutation in DAO may influence EE in American Indians. Identification of variants that influence energy metabolism may lead to new pathways to treat human obesity.
... С возрастом скорость основного обмена снижается. Исследования с участием близнецов свидетельствуют, что генетический фактор определяет примерно 40% основного обмена [9]. На сегодняшний день продолжительный положительный энергетический баланс, который возникает при потреблении пищи в количестве, превышающем расход энергии, либо снижении расхода энергии, считается одним из основных механизмов развития ожирения [6]. ...
... Many of the fundamental physiological effects of exercise are, however, poorly understood, let alone how these effects vary across individuals (5). One reason for this gap in our understanding is the factors, such as genetic background and environment, that are difficult or impossible to control in human-based exercise research (6), but that can more easily be controlled when working with model organisms. In fact, controlling for these factors is one of the primary advantages of model system-based research (7,8). ...
... Both these results support other studies that have found significant genetic variance in MR after controlling for body size (e.g. Bouchard et al., 1989;Dohm et al., 2001;Yashchenko et al., 2016;Pettersen et al., 2018), or have found a G×E interaction in the allometric intercept (e.g. Arnqvist et al., 2010;Niitepold, 2010). ...
Metabolic rate (MR) often scales with body mass (BM) following a power function of the form MR=aBM
b
, where log(a) is the allometric intercept and b is the allometric exponent (i.e. slope on a log-log scale). The variational properties of b have been debated, but very few studies have tested for genetic variance in b, and none have tested for a genotype-by-environment (G×E) interaction in b Consequently, the short-term evolutionary potentials of both b and its phenotypic plasticity remain unknown. Using 10 clones of a population of Daphnia magna, we estimated the genetic variance in b and assessed whether a G×E interaction affected b We measured MR on juveniles of different sizes reared and measured at three temperatures (17, 22 and 28°C). Overall, b decreased with increasing temperature. We found no evidence of genetic variance in b at any temperature, and thus no G×E interaction in b However, we found a significant G×E interaction in size-specific MR. Using simulations, we show how this G×E interaction can generate genetic variation in the ontogenetic allometric slope of animals experiencing directional changes in temperature during growth. This suggests that b can evolve despite having limited genetic variation at constant temperatures.
... Hereditability plays a role as well. Twin studies have shown that genetics account for approximately 40% of RMR [29]. Several studies identified low RMR as a risk factor for weight gain [30,31]. ...
Body fat mass increases when energy intake exceeds energy expenditure. In the long term, a positive energy balance will result in obesity. The worldwide prevalence of obesity has increased dramatically, posing a serious threat to human health. Therefore, insight in the pathogenesis of obesity is important to identify novel prevention and treatment strategies. This review describes the physiology of energy expenditure and energy intake in the context of body weight gain in humans. We focus on the components of energy expenditure and the regulation of energy intake. Finally, we describe rare monogenetic causes leading to an impairment in central regulation of food intake and obesity.
... With respect to energy metabolism this was indeed the case in the 1980s and early 1990s and particularly so in studies which aimed to establish energy requirements or test their applicability in different conditions. Now, however, many investigators are concentrating on the sources of individual variability in intake and expenditure, from differences at a whole-body level (Hill et al. 1995;Stubbs et al. 1995;Lissner, 1996) to differences at the tissue and molecular levels (Ravussin & Bogardus, 1987;Bouchard et al. 1989;Ravussin & Swinburn, 1993;Astrup et al. 1994;Schneiter et al. 1995). ...
Dr Widdowson and Professor McCance always expressed a great deal of interest in the inter-individual variability in their scientific data considering that extreme values often provided the most revealing results. Their interest developed as a result of Dr Widdowson’s studies of the individual diets of men, women and children conducted in the 1930s; she later used the phrase ‘nutritional individuality’ to describe between-individual variability in intake and expenditure (Widdowson, 1962). This paper continues Dr Widdowson’s theme of individual variability. It focuses on recent data which describe between-individual differences in daily energy expenditure, particularly the extremes, and also on the insights these have given into the measurements of energy intake (EI).
... Since fat-free mass (FFM), especially organ tissue, is very metabolically active, any change in FFM can dramatically influence RMR. There are number of ways that exercise might indirectly or directly change RMR (27). First, exercise may increase RMR indirectly by increasing an individual's FFM, which is strong determinant of RMR (28). ...
Nutritional science is increasingly seen in sports practice as an instrument capable of influencing the performance, recovery and gene expression of the athlete. Vice versa, the performance itself is able to modify human metabolism and the use of substrates for energy purposes. Since even small changes are important for the athlete,
nutritional science must be considered a precision medicine in which standardized protocols apply to the needs of the
individual athlete (based on the type of sport, the frequency of training and its intensity, the goals in terms of weight and muscle mass) in order to minimize measurement errors. The study of the baseline composition of the athlete’s body is essential to build up a nutritional plan that follows the athlete before, during and after competition, with the aim of optimizing performance and preventing the onset of fatigue. The purpose of this review is to sum up the most recent
guidelines, underlining the key points of the current state of art on the best strategies to achieve specific goals in terms of changes or maintenance of body weight, preparing adequately the athlete for competition and encouraging recovery, with a brief mention to the psycho-behavioral dimension that nutrition acquires in sports practice.
... One possibility is that this is due to genetic differences. A substantial portion of the variability in REE has been attributed to genetic influences independent of body composition, age, and gender (30,31). European ancestry admixture in African Americans has been shown to be strongly associated with higher REE (32). ...
... Low but significant narrow-sense heritabilities of basal oxygen consumption have been reported for domestic house mice (references in Lynch 1994), and significant realized heritabilities for oxygen consumption have been reported for chickens (e.g., MacLaury and Johnson 1972). Resting metabolic rate may also be heritable in humans (e.g., Bouchard et al. 1989). Twin studies suggest that VOzmax (the maximal rate of oxygen consumption during exercise) is heritable in humans (Bouchard et al. 1986), and full-sib analyses suggest genetic variation for VOzmax in garter snakes (Thamnophis sirtalis; Garland and Bennett 1990). ...
One of the most important events in vertebrate evolution was the acquisition of endothermy, the ability to use metabolic heat production to elevate body temperature above environmental temperature. Several verbal models have been proposed to explain the selective factors leading to the evolution of endothermy. Of these, the aerobic capacity model has received the most attention in recent years. The aerobic capacity model postulates that selection acted mainly to increase maximal aerobic capacity (or associated behavioral abilities) and that elevated resting metabolic rate evolved as a correlated response. Here we evaluate the implicit evolutionary and genetic assumptions of the aerobic capacity model. In light of this evaluation, we assess the utility of phenotypic and genetic correlations for testing the aerobic capacity model. Collectively, the available intraspecific data for terrestrial vertebrates support the notion of a positive phenotypic correlation between resting and maximal rates of oxygen consumption within species. Interspecific analyses provide mixed support for this phenotypic correlation. We argue, however, that assessments of phenotypic or genetic correlations within species and evolutionary correlations among species (from comparative data) are of limited utility, because they may not be able to distinguish between the aerobic capacity model and plausible alternatives, such as selection acting directly on aspects of thermoregulatory abilities. We suggest six sources of information that may help shed light on the selective factors important during the evolution of high aerobic metabolic rates and, ultimately, the attainment of endothermy. Of particular interest will be attempts to determine, using a combination of mechanistic physiological and quantitative-genetic approaches, whether a positive genetic correlation between resting and maximal rates of oxygen consumption is an ineluctable feature of vertebrate physiology.
... Several studies have demonstrated the heritability of RMR (h 2 ≈ 0.30) [1,8,9]. It has also been shown that RMR is lower in African than in European Americans, even in childhood [3,[10][11][12][13]. ...
Background:
Resting metabolic rates (RMR) vary across individuals. Understanding the determinants of RMR could provide biological insight into obesity and its metabolic consequences such as type 2 diabetes and cardiovascular diseases.
Methods:
The present study measured RMR using reference standard indirect calorimetry and evaluated genetic variations from an exome array in a sample of children and adults (N = 262) predominantly of African and European ancestry with a wide range of ages (10 - 67 years old) and body mass indices (BMI; 16.9 - 56.3 kg/m(2) for adults, 15.1 - 40.6 kg/m2 for children).
Results:
Single variant analysis for RMR identified suggestive loci on chromosomes 15 (rs74010762, TRPM1, p-value = 2.7 × 10-6), 1 (rs2358728 and rs2358729, SH3D21, p-values < 5.8x10-5), 17 (AX-82990792, DHX33, 5.5 × 10-5) and 5 (rs115795863 and rs35433829, C5orf33 and RANBP3L, p-values < 8.2 × 10-5). To evaluate the effect of low frequency variations with RMR, we performed gene-based association tests. Our most significant locus was SH3D21 (p-value 2.01 × 10-4), which also contained suggestive results from single-variant analyses. A further investigation of all variants within the reported genes for all obesity-related loci from the GWAS catalog found nominal evidence for association of body mass index (BMI- kg/m(2))-associated loci with RMR, with the most significant p-value at rs35433754 (TNKS, p-value = 0.0017).
Conclusions:
These nominal associations were robust to adjustment for BMI. The most significant variants were also evaluated using phenome-wide association to evaluate pleiotropy, and genetically predicted gene expression using the summary statistics implicated loci related to in obesity and body composition. These results merit further examination in larger cohorts of children and adults.
... 13 This strongly implicates a critical role of familial predisposition in energy expenditure regulation as a predictor for obesity, consistent with the notion of genetic factors accounting for~40% of the variance in RMR. 14,15 It should, however, be noted that studies on the relationship between RMR and obesity are quite confusing, with RMR reported to be negatively, positively or not at all associated with obesity. All of these may well be true as RMR-obesity is a dynamic relationship that changes depending on when and how the data are collected. ...
Obesity is a physiological condition of chronic positive energy balance. While the regulation of energy metabolism varies widely among individuals, identifying those who are metabolically prone to weight gain and intervening accordingly is a key challenge for reversing the course of the obesity epidemic. Indirect calorimetry is the most commonly used method to measure energy expenditure in the research setting. By measuring oxygen consumption and carbon dioxide production, indirect calorimetry provides minute-by-minute energy expenditure data that makes it the most valuable tool to distinguish the various components of energy expenditure, that is, sleeping and resting metabolic rate, thermic effect of food and the energy cost of activity. Importantly, such measures also provide information on energy substrate utilization. Here we summarized some of the research that revealed resting metabolic rate, spontaneous physical activity and respiratory quotient as key metabolic predictors of weight gain and obesity. Recent studies using indirect calorimetry in response to mid-term fasting or overfeeding have identified 'thrifty' and 'spendthrift' phenotypes in people who differ in propensity to weight gain. We propose the use of indirect calorimetry data as a basis for personalized interventions that may be efficacious in slowing down the rise of global obesity.European Journal of Clinical Nutrition advance online publication, 16 November 2016; doi:10.1038/ejcn.2016.220.
... Many other factors such as genetic and sex differences interact with exercise to influence its impact on obesity; yet the impact of sex and genetic variation on the physiological effects of exercise is poorly understood [10]. Experiments in humans demonstrate that genetic background influences the effects of exercise on metabolism [11][12][13], and studies in mice have shown the same for body composition [14]. Moreover, exercise resistance is an exciting new field focused on, individuals who may be programmed-genetically or epigenetically-to have a weak or absent metabolic response to exercise [15]. ...
Obesity is one of the dramatic health issues affecting developed and developing nations, and exercise is a well-established intervention strategy. While exercise-by-genotype interactions have been shown in humans, overall little is known. Using the natural negative geotaxis of Drosophila melanogaster, an important model organism for the study of genetic interactions, a novel exercise machine, the TreadWheel, can be used to shed light on this interaction. The mechanism for inducing exercise with the TreadWheel is inherently gentle, thus minimizing possible confounding effects of other stressors. Using this machine, we were able to assess large cohorts of adult flies from eight genetic lines for their response to exercise after one week of training. We measured their triglyceride, glycerol, protein, glycogen, glucose content, and body weight, as well as their climbing ability and feeding behavior in response to exercise. Exercised flies showed decreased stored triglycerides, glycogen, and body weight, and increased stored protein and climbing ability. In addition to demonstrating an overall effect of TreadWheel exercise on flies, we found significant interactions of exercise with genotype, sex, or genotype-by-sex effects for most of the measured phenotypes. We also observed interaction effects between exercise, genotype, and tissue (abdomen or thorax) for metabolite profiles, and those differences can be partially linked to innate differences in the flies' persistence in maintaining activity during exercise bouts. In addition, we assessed gene expression levels for a panel of 13 genes known to be associated with respiratory fitness and found that many responded to exercise. With this study, we have established the TreadWheel as a useful tool to study the effect of exercise in flies, shown significant genotype-specific and sex-specific impacts of exercise, and have laid the ground work for more extensive studies of how genetics, sex, environment, and aging interact with exercise to influence metabolic fitness in Drosophila.
... Other factors like age, 10e12 sex, 13 growth, 14 hormones, genotype, 15 physiological stress, 4 pregnancy 16 and hypothermia 17 can also influence RMR and they are presented in Fig. 1. ...
The energy used in post-prandial state during rest and physical activity is derived predominantly from the oxidation of carbohydrate (CHO) and fat. Although protein can also serve as a source of energy, amino acids oxidation is usually tightly adjusted to amino acids intake and their contribution to total energy expenditure is rather insignificant in healthy subjects. Blood glucose, glycogen, plasma fatty acids and intramuscular triglycerides, on the other hand, present major sources for energy production.
The amount of energy stored in the form of fat is large, representing 92–98% of all endogenously stored energy with CHO contributing only about 2–8%. Fat is at the bottom of an oxidative hierarchy that determines fuel selection, and its oxidation is governed by the presence or absence of the other macronutrients. In addition, the rate at which it can be oxidized depends on intensity of energy expenditure. In contrast, CHO elicit strong auto-regulatory adjustments in their oxidation.
This review aims at summarizing the current state of knowledge on CHO and fat body storage, hierarchy of fuel utilization during resting state, anaerobic and aerobic pathways for energy production during exercise, and the effects of exercise mode, intensity, duration, and training on CHO and fat utilization.
... However, the contribution of a low RMR to the etiology of obesity is controversial [29]. Some studies have reported that RMR has a strong genetic factor [30,31], and a prospective study in Pima Indians demonstrated that RMR for a given body composition, specifically RMR adjusted for fat-free mass (FFM) and fat mass (FM), is a predictor of subsequent weight change [32]. The authors reported that a relatively low RMR was considered as a risk factor for body weight gain. ...
Background: Metabolic abnormalities are usually linked with obesity; however, all obese people may not be affected by this condition. It has been indicated that obese people with higher resting metabolic rate (RMR) had an overall better metabolic profile than observed in those with low RMR. This study aimed to compare the RMR status of metabolically healthy (MHO) and unhealthy obese (MUHO).
Design: Cross-sectional sample of 226 obese women (BMI > 30 kg/m2) aged 17–69 years participated in the study. Participants were classified as MHO and MUHO. Metabolic health status was defined using Karelis definition. Metabolic profile, RMR, and body composition were examined.
Result: MHO participants showed more favorable lipid profile, had reduced insulin resistance and lower total fat percentage and fat mass. RMR per BMI was 25% higher in the MHO group compared to the MUHO subjects. Interestingly by adding RMR/kg in the binary regression model for finding the modulatory role of RMR on the Karelis criteria, no significant difference was observed anymore regarding the Homeostasis Model Assessment (HOMA) between the MHO and MUHO participants.
Conclusion: In this study we did not observe any major effects of RMR on metabolic health criteria except for the HOMA. Further studies are needed to investigate the effects of RMR on glucose abnormalities that may lead to modify cardio-metabolic criteria.
... Between RMR and the mitochondrial function there is a close relationship [6]. RMR is mainly influenced by the muscle mass, but it also varies with age, gender, some genetic traits [7], fat mass, disease status, and level of circulating hormones [8]. A low RMR was indicated as a risk factor for weight gain [9,10]. ...
Background and Aims: Resting metabolic rate (RMR) is important to estimate energy requirements. Our aim was to investigate the RMR in newly diagnosed type 2 diabetic (T2DM) patients with metabolic syndrome (MS) in relation with obesity, gender, some adipokines and insulin resistance parameters. Material and Methods: 138 newly diagnosed T2DM adults were evaluated for anthropometric, clinical, biochemical parameters, and RMR. The group was subdivided according to body mass index and MS presence. Results: Determined RMR (RMRd), predicted RMR (RMRp), oxygen consumption and carbon dioxide production at rest were significantly lower for subjects with BMI<30 kg/m2 compared to subjects with BMI≥30 kg/m2 (p<0.001). RMRd positively correlated with fat-free mass (p < 0.001), waist (p < 0.001), BMI (p < 0.001), insulinemia (p = 0.021) and negatively with age (p < 0.001) and adiponectin (p = 0.027). The percent of determined from predicted RMR in subjects with MS was lower than in those without MS, but only for men (p<0.005). Conclusions: Subjects with T2DM and MS have significantly lower than predicted RMR, compared to those without MS, indicating that they may have an energy sparing metabolism. Gender influences the energy metabolism and may play a particular role in energy the metabolism of people with T2DM and MS.
Chronic diseases are major killers in the modern era. Physical inactivity is a primary cause of most chronic diseases. The initial third of the article considers: activity and prevention definitions; historical evidence showing physical inactivity is detrimental to health and normal organ functional capacities; cause versus treatment; physical activity and inactivity mechanisms differ; gene‐environment interaction (including aerobic training adaptations, personalized medicine, and co‐twin physical activity); and specificity of adaptations to type of training. Next, physical activity/exercise is examined as primary prevention against 35 chronic conditions [accelerated biological aging/premature death, low cardiorespiratory fitness (V o 2 max), sarcopenia, metabolic syndrome, obesity, insulin resistance, prediabetes, type 2 diabetes, nonalcoholic fatty liver disease, coronary heart disease, peripheral artery disease, hypertension, stroke, congestive heart failure, endothelial dysfunction, arterial dyslipidemia, hemostasis, deep vein thrombosis, cognitive dysfunction, depression and anxiety, osteoporosis, osteoarthritis, balance, bone fracture/falls, rheumatoid arthritis, colon cancer, breast cancer, endometrial cancer, gestational diabetes, pre‐eclampsia, polycystic ovary syndrome, erectile dysfunction, pain, diverticulitis, constipation, and gallbladder diseases]. The article ends with consideration of deterioration of risk factors in longer‐term sedentary groups; clinical consequences of inactive childhood/adolescence; and public policy. In summary, the body rapidly maladapts to insufficient physical activity, and if continued, results in substantial decreases in both total and quality years of life. Taken together, conclusive evidence exists that physical inactivity is one important cause of most chronic diseases. In addition, physical activity primarily prevents, or delays, chronic diseases, implying that chronic disease need not be an inevitable outcome during life. © 2012 American Physiological Society. Compr Physiol 2:1143‐1211, 2012.
\"Egzersiz ve Beslenme\" adlı kitap, Dr. Akan Bayrakdar ve Prof. Dr. Erdal Zorba tarafından kaleme alınmıştır. Kitap, doğru beslenmenin vücut ağırlığı yönetimi ve fonksiyonlarının sürdürülmesi için önemini vurgulamaktadır. Besinlerle yeterli enerji almanın aktiflik ve kas kütlesi koruması sağladığı belirtilmektedir. Sporcu beslenmesi ise sporcuların antrenman ve müsabaka performanslarını geliştirmek için hazırlanan özel bir beslenme programıdır. Kitap, besin ögelerinin sağlık ve sporcu performansı üzerindeki etkilerinin yanı sıra kan gruplarına göre beslenme, alkali beslenme ve yeme bozuklukları gibi konuları ele almaktadır. Kitap, 300'den fazla kaynaktan yararlanılarak hazırlanmış olup, üniversitelerin Spor Bilimleri fakülteleri ve Beden Eğitimi ve Spor Yüksekokulları'nda kullanılabilecek düzeydedir. Kan gruplarına göre beslenme konusu, Mehmet Ali Bulut ve Peter J. D'Adamo'nun kitaplarından alıntılarla işlenmiştir. Alkali beslenme konusu ise Dr. Ayşegül Çoruhlu'nun kitaplarından faydalanılarak ele alınmıştır. Kitap ayrıca anoreksiya nevroza, bulimia nevroza ve ortoreksiya nevroza gibi yeme bozukluklarına da değinmektedir. The book titled \"Exercise and Nutrition\" is written by Dr. Akan Bayrakdar and Prof. Dr. Erdal Zorba. The book emphasizes the importance of proper nutrition for managing body weight and maintaining bodily functions. It states that consuming sufficient energy through food provides benefits such as maintaining activity levels and preserving muscle mass. Sports nutrition, on the other hand, is a specialized nutrition program designed to improve athletes' training and competition performance. The book covers topics such as the effects of nutrients on health and athletic performance, as well as subjects like nutrition based on blood types, alkaline nutrition, and eating disorders. The book is based on over 300 sources and is suitable for use in universities' faculties of Sports Sciences and Physical Education and Sports Schools. The topic of nutrition based on blood types is discussed with excerpts from the books of Mehmet Ali Bulut and Peter J. D'Adamo. The topic of alkaline nutrition is approached by benefiting from the books of Dr. Ayşegül Çoruhlu. The book also addresses eating disorders such as anorexia nervosa, bulimia nervosa, and orthorexia nervosa.
A person's metabolic rate corresponds to the whole-body level sum of all oxidative reactions occurring on the cellular level. The energy expenditure (EE) can be categorized into various essential and facultative processes. In sedentary adults, basal metabolic rate is the largest contributor to total daily EE, and interindividual variability can be significant. Additional EE to support facultative processes corresponds to digesting and metabolizing food; thermoregulatory adaptation to cold; and to supporting exercise and non-exercise body movements. Interindividual variability also exists for facultative EE processes, even after controlling for known factors. The complex mechanisms of interindividual variability in EE can have genetic and environmental origins and require further investigation. Exploration of interindividual variability in EE and its underlying factors holds importance to metabolic health, as it may predict disease risk, and be useful in the personalisation of preventative and treatment strategies.
At usual weight, energy intake and expenditure are coupled and covary to maintain body weight (energy stores). A change in energy balance, especially weight loss, invokes discoordinated effects on energy intake and output that favor return to previous weight. These regulatory systems reflect physiological changes in systems regulating energy intake and expenditure rather than a lack of resolve. The biological and behavioral physiology of dynamic weight change are distinct from those of attempts at static weight maintenance of an altered body weight. This suggests that optimal therapeutic approaches to losing or gaining vs. sustaining weight changes are different for most individuals.
Le bypass Roux-en-Y (RYGB) permet d’induire une perte de poids massive et durable chez des patients atteints d’obésité sévère, ainsi qu’une rémission du diabète de type 2 (DT2) chez environ 50% des patients, bien que cette proportion diminue avec le temps. Notre équipe et d’autres ont décrit des modifications de la composition du microbiote intestinal (MI) à court et long terme après RYGB. Nous faisons l’hypothèse donc que ces modifications du MI participent à l’amélioration métabolique, et/ou la réaggravation du DT2 après quelques années. Grace à la description d’une cohorte de 175 patients DT2 ayant eu un RYGB et ayant été caractérisés au cours des 5 années post-RYGB, et montrons que plusieurs paramètres cliniques sont associés à la probabilité de rémission du T2D, ce qui nous a permis de développer un score de prédiction de la rémission du DT2 à 5 ans, le 5y-Ad-DiaRem. Nous avons ensuite réalisé des séquençages métagénomiques par MinION du MI de 100 de ces patients à 5 ans postopératoire. Par clustering hiérarchique, nous avons mis en évidence 2 groupes de sévérité du DT2. Nous montrons que ces groupes présentent des différences notoires de composition du MI. Afin d’apprécier la causalité liant amélioration métabolique post-RYGB et MI, nous avons réalisé une étude de transferts de matières fécales, qui a montré une modulation métabolique notable (tolérance au glucose, résistance à l’insuline) chez les animaux receveurs en lien direct avec l’état métabolique des donneurs. Nos résultats démontrent donc la contribution partielle du MI à l’amélioration métabolique post-RYGB, ce qui offre des perspectives prédictives, mécanistiques et thérapeutiques très précieuses.
Purpose
Low Resting Metabolic Rate (RMR), as a risk factor for obesity, can be affected by many factors. Indeed, genetic and environmental factors are variables taken into account when predicting RMR, and may contribute to a high inter-individual variance. Besides the well-known causes of obesity, researchers have demonstrated the contribution of gut microflora in obesity and energy expenditure. Therefore, the goal of the current study was to compare the Firmicutes/Bacteroidetes ratio and the relative abundance of, Prevotellaceae, Faecalibacterium prausnitzii, bifidobactrium spp, lactobacillus spp, Akkermansia muciniphila, Bacteroides fragilis, and Escherichia coli in two groups of people with normal and low RMR in overweigh/obese women in Iran.
Results
The abundance of F. prausnitzii (p>0.001), B. fragilis (P= 0.02), and Firmicutes phylum (P= 0.02) were significantly higher in the controls compared to the cases, and showed significant positive association with RMR, (β = 1.29 ×10⁻⁵, P=0.01), (β = 4.13 ×10⁻⁶, p= 0.04), and (β = 7.76 ×10⁻¹, p= 0.01), respectively. Regarding Lactobacilus, the results showed a significant positive association with RMR (β = 1.73 ×10⁻⁴, p= 0.01).
Conclusion
Intestinal microbiota may be associated with host metabolism. Therefore, future work should investigate, using clinical trials, the impact of manipulating gut microflora to positively influence energy expenditure.
Objective: Low resting metabolic rate (RMR) as a risk factor for weight gain and obesity can be influenced by many factors. Researchers have pointed out the role of appetite and related hormones in obesity and energy intake. The aim of this study was to investigate the relationship between appetite and related hormones in the two groups with normal and impaired resting metabolic rate in overweight or obese Iranian women.
Methods: In this case-control study, 42 healthy female volunteers aged 18-50 years (21 cases,and 21 controls) participated and were evaluated for RMR by indirect calorimetry. Body composition was determined by a body composition analyzer. The Filint questionnaire was used to assess appetite. We also used ELISA kits to assess appetite-related hormones. Finally, the data were analyzed using SPSS software version 25.
Results: The results of the study showed that there is a negative relationship between ghrelin hormone level (p-value = 0.024) and RMR, and there is a positive relationship between insulin hormone level (p-value = 0.001) and RMR. Also, result of the appetite questionnaire showed that in general, both appetite (p-value = 0.044) and hunger index (p-value = 0.043) have a positive relationship with RMR. There was no significant relationship between leptin levels and RMR.
Conclusion: As the results of this study show, it seems that appetite and related hormones have a possible role in promoting RMR.
Doğru beslenme; enerji dengesini sağlayarak, vücut ağırlığı yönetimini ve vücudun en uygun şekilde fonksiyonlarını sürdürmesini sağlar. Besinlerle yeterli enerji alırsanız daha aktif olabilir, yeterli protein alırsanız kas kütlenizi koruyabilirsiniz. Beslenme; aktif kişiler ve sporcuların egzersiz için yaptığı hazırlığın önemli bir parçasıdır. Sporcu beslenmesi, sporcuların yaptıkları spor dalına göre hem antrenmanlarını hem de müsabaka sırasındaki atletik performanslarının geliştirilmesi için hazırlanan özel bir beslenme programıdır. İster yürüyüş yapın, ister pilates yapın, ister fitnes yapın, isterseniz maraton koşun. Hangi sporu yaparsanız yapın, spor yapanların sağlığın korunması, dayanıklılığın artması, konsantrasyon ve dikkat yeteneğinin iyi olması ve spordan maksimum faydayı sağlamak için sağlıklı beslenmelisiniz. Son yıllarda beslenmenin sağlık ve sporcu performansı üzerinde etkilerini belirten birçok çalışma yapılmıştır. Bu kitapta besin ögelerinin sağlık ve sporcu performansı üzerindeki etkilerinin yanısıra, kan gruplarına göre beslenme, alkali beslenme ve yeme bozuklukları gibi konularda işlenmiştir. Kitap hazırlanırken 300’den fazla eski ve yeni kaynaktan yararlanılmıştır. Bu kaynakların çoğunluğunu yabancı literatür oluşturmaktadır. Kitap üniversitelerin Spor Bilimleri fakülteleri ve Beden Eğitimi ve Spor Yüksekokulları’nın Sporcu Beslenmesi, Egzersiz ve Beslenme derslerinde işlenebilecek düzeydedir. Kan gruplarına göre beslenme konusu Mehmet Ali Bulut ve Peter J. D’Adamo isimli yazarların kitaplarından işlenmiştir. Kan gruplarına göre beslen-me konusu bilimsel geçerliliği henüz net olarak tespit edilmese de, birçok kişinin uyguladığı ve kendilerini daha hissettiklerini belirten bir yöntemdir. Alkali beslenme konusu hazırlanırken birçok kaynaktan faydalanılmıştır. Ayrıca kitapta anoreksiya nevroza, bulimia nevroza ve ortoreksiya nevroza yeme bozukluklarındanda bahsedilmiştir. Son olarak kitabın yazılmasındaki her aşamada katkı sağlayan Dr. Rıdvan Kır’a teşekkür ederiz.
Constructing Norms of Body Composition and Resting Metabolic Rate amongst the Fourth Basic Grades in Governmental Schools in Palestine
Journal of An-Najah for Research (Humaneties ), in Press, accepted in 6/5/2019.
An-najah National University
The purpose of this study was to construct norms of Body Composition (PC) and Resting Metabolic Rate (RMR) amongst the fourth basic grades in governmental schools in Palestine. Furthermore, to determine the differences in (PC) , (RMR), Body Mass Index (BMI), and Body Surface Area (BSA) according to the class and gender variables. Also, to determine the contribution of (BMI) in predicting Fat Percent (% Fat) and (RMR) . The sample consisted of (2200) male and female students from (11) educational governorate in West-Bank. Tanita DC-360 Bioelectrical impedance analyzer (BIA) was used to determine (PC), WHO equation to determine (RMR), and (BMI) equation were used for data collection. The results revealed that the means of Height (Ht), Body Mass (BM), Lean Body Mass (LBM), % Fat, Body Water Mass (BWM), (BMI), BSA and RMR for male were respectively: (126.38 cm, 26.99 kg, 20.50 kg, 18.38%, 15.92 kg, 16.67 kg/m2, 0.97 m2, and 1107.22 kcal/day), and for female were respectively: (125.25 cm, 26.48 kg, 19.61 kg, 20.60%, 15.15 kg, 16.65 kg/m2, 0.95 m2 and 1092.22 kcal/day ).Furthermore, the results indicated a significant differences in all variables between male and female in favor of male except % Fat in favor of female, and according to the class in all variables except % Fat in favor of the higher one. Also, the results of Regression (R2) contribute in developing four equations for the prediction of % Fat and RMR, using BMI as independent variable, the equations were as follow:
Male:
(%BF) = (-11.795) + ((BMI) × (1.810)). (R2 =0.804).
(RMR) kcal/day = (266.487) + ((BMI) × (716.466)). (R2 =0.766).
Female:
(%BF) = (-15.413) + ((BMI) × (2.163)). (R2 =0.873).
(RMR) kcal/day = (257.375) + ((BMI) × (50.126)). (R2 =0.741).
Based on the findings of the study the researchers recommended using the norms as critical values for follow up development, nutrition, obesity and health among students.
Key words: Body Composition, Resting Metabolic Rate, Fourth Basic Grades, Palestine.
The doubly labeled water method was used to measure average daily total energy expenditure (EE) in 23 healthy normal-weight women classified as restrained or unrestrained eaters. Although the relative weight of restrained eaters was found to be higher (BMI 21.1 +/- 1.3 vs 20.0 +/- 1.3 kg/m2, p less than 0.03), the self-reported energy consumption of the restrained eaters, when adjusted for body composition and height, totaled approximately 410 kcal/d less energy than that of the unrestrained group (p less than 0.002). Correspondingly, the adjusted EE was found to be lower by 620 kcal/d in restrained eaters (p less than 0.005). In both groups metabolic indices of starvation (beta-hydroxybutyric acid and triiodothyronine) were in the normal range. Neither these nor weight changed from the beginning to the end of the 14-d observation period. Thus, the lower EE of the restrained group reflects diminished caloric requirements and is not an adaptive response to a temporary decrease in food intake.
The aim of this study was to clarify heritability estimates for endurance-related phenotypes and the underlying factors affecting these estimates. A systematic literature search was conducted for studies reporting heritability estimates of endurance-related phenotypes using the PubMed database (up to September 30, 2016). Studies that estimated the heritability of maximal oxygen uptake (VO2 max), submaximal endurance phenotypes, and endurance performance were selected. The weighted mean heritability for endurance-related phenotypes was calculated using a random-effects model. A total of 15 studies were selected via a systematic review. Meta-analysis revealed that the weighted means of the heritability of VO2 max absolute values and those adjusted for body weight and for fat-free mass were 0.68 (95% CI: 0.59-0.77), 0.56 (95% CI: 0.47-0.65), and 0.44 (95% CI: 0.13-0.75), respectively. There was a significant difference in the weighted means of the heritability of VO2 max across these different adjustment methods (P < 0.05). Moreover, there was evidence of statistical heterogeneity in the heritability estimates among studies. Meta-regression analysis revealed that sex could partially explain the heterogeneity in the VO2 max heritability estimates adjusted by body weight. For submaximal endurance phenotypes and endurance performance, the weighted mean heritabilities were 0.49 (95% CI: 0.33-0.65) and 0.53 (95% CI: 0.27-0.78), respectively. There was statistically significant heterogeneity in the heritability estimates reported among the studies, and we could not identify the specific factors explaining the heterogeneity. Although existing studies indicate that genetic factors account for 44% to 68% of the variability in endurance-related phenotypes, further studies are necessary to clarify these values. This article is protected by copyright. All rights reserved.
Pima Indians living in Arizona suffer from a high prevalence of obesity, and we have previously shown that a relatively lower energy expenditure (EE) predicts weight and fat mass gain in this population. Energy expenditure (EE) is a familial trait (heritability=0.52); therefore, in the current study, we aimed to identify genetic variants that affect EE and thereby influence BMI and body fatness in Pima Indians.
Genotypic data from 491,265 variants were analyzed for association with resting metabolic rate (RMR) and 24-h EE assessed in a whole-room calorimeter in 507 and 419 Pima Indians, respectively. Variants associated with both measures of EE were analyzed for association with maximum BMI and percent body fat (PFAT) in 5870 and 912 Pima Indians, respectively.
Rs11014566 nominally associated with both measures of EE and both measures of adiposity in Pima Indians, where the G-allele (frequency: Pima Indians=0.60, Europeans<0.01) associated with lower 24-h EE (β=−33 kcal/day per copy), lower RMR (β=−31 kcal/day), higher BMI (β=+0.6 kg/m²) and higher PFAT (β=+0.9%). However, the association of rs11014566 with BMI did not directionally replicate when assessed in other ethnic groups. Rs11014566 tags rs144895904, which affected promoter function in an in vitro luciferase assay. These variants map to GPR158, which is highly expressed in the brain and interacts with two other genes (RGS7 and CACNA1B) known to affect obesity in knock-out mice.
Our results suggest that common ethnic-specific variation in GPR158 may influence EE; however, its role in weight gain remains controversial since it either had no association with BMI, or associated with BMI but in the opposite direction, in other ethnic groups.
Mammals have evolved complex mechanisms to obtain energy from food; store excess energy in the forms of glycogen, fat, and protein; and utilize energy efficiently for vital functions. Obesity develops when energy intake exceeds energy expenditure. While obesity treatment is mostly focused on reducing food intake, studies suggest that increasing energy expenditure through physical activity and adaptive thermogenesis is an important strategy for weight loss and maintenance of health. This chapter will describe fundamental concepts of bioenergetics and provide a framework for understanding the pathogenesis and treatment of metabolic syndrome.
Body weight is regulated by a complex interaction of biological, behavioral, and cultural factors. The population as a whole is at risk for obesity because of increased intake of dietary fat, the consumption of calories in fewer meals per day, striking accessibility to palatable foods, and decreased physical activity. This risk may become a reality in individuals with certain biological predispositions (genetic tendency, low metabolic rate, increased fat cell number), specific eating patterns, and susceptibility to the extreme cultural pressure to be lean. These factors must be considered in establishing goals for treatment, which fall into medical and psychosocial categories. This includes defining a “reasonable” as opposed to “ideal” weight. A three-stage process is proposed for identifying the best treatment for an individual. This involves a classification decision, a stepped care decision, and then a matching decision. Criteria are provided for a comprehensive assessment of the overweight individual, and treatment options are reviewed for programs of varying intensity, cost, and risk.
Physical fitness including muscle strength and endurance capacity varies substantially among individuals. Physical activity level and exercise behavior also vary among individuals. Many family studies and studies on twins have reported that genetic factors are responsible for heterogeneity in fitness-related traits. However, there is much dispersion in heritability, as previously reported. A systematic review was performed to determine the extent of heritability in physical fitness. A literature search was conducted through PubMed using the following keywords: (heredity or heritability) and (“muscle strength” or “muscle contraction” or endurance or athlete* or fitness or exercise) and (twin* or family). Finally, 43 articles that included 137 phenotypes met the criteria. Only one article focused on the heritability of athletic status. With respect to muscle strength, 23 articles and 54 phenotypes were collected, and showed a range of heritability of 0%-98% (mean: 55±22%). This heterogeneity was partly explained by the ages of subjects. With respect to endurance capacity, 13 articles and 28 phenotypes showed heritability of 0%-93% (mean: 54±25%). The considerable degree of variability in heritability of fitness-related traits may depend on age, sex, race, and environmental factors. Therefore it is necessary to investigate the interaction between genetic factor and factors other than genetic factor. On the other hand, with respect to exercise behavior or physical activity level which is important for improving the physical fitness or health status, the heritability of 0%-85% has also been reported. That is, the genetic factor plays a role in not only physiological phenotypes but also behavioral phenotypes. Understanding of these genetic factors and their mechanisms will lead to improvement in physical fitness or encouragement of physical activity/exercise behavior.
Although most forms of NIDDM in humans do not exhibit simple Mendelian inheritance, the large contribution of heredity is well recognized (1-5). Progress toward an understanding of the genetic basis of NIDDM has been largely restricted to a few distinct monogenic syndromes with predictable modes of inheritance. For example, one form of autosomal-dominant maturity-onset diabetes of the young (MODY) is caused by mutations in the glucokinase (M0DY2) gene (6,7) autosomal-recessive syndromes of extreme insulin resistance are the result of mutations in the insulin receptor gene (8) and maternally inherited diabetes and deafness (MIDD) is the result of mutations in mitochondrial DNA (9). These rare subphenotypes of diabetes are examples in which single gene defects have a major influence on the phenotype and for which environmental influences on expression of the phenotype are negligible.
Die Adipositas ist weit verbreitet und ist auslösender Faktor für Typ-2-Diabetes, Hypertonie, kardiovaskuläre Erkrankungen und degenerative Gelenkerkrankungen, besonders wenn das viszerale Fettgewebe übermäßig vermehrt ist. Die Ursachen der Adipositas liegen in einer übermäßigen Nahrungsaufnahme und zum Teil auch in einem verminderten Energieverbrauch. Der Energieverbrauch ist individuell verschieden und genetisch determiniert.
Mammals have evolved complex mechanisms to obtain energy from food; store excess energy in the forms of glycogen, fat, and protein; and utilize energy efficiently for vital functions. Obesity develops when energy intake exceeds energy expenditure. While obesity treatment is mostly focused on reducing food intake, studies suggest that increasing energy expenditure through physical activity and adaptive thermogenesis is an important strategy for weight loss and maintenance of health. This chapter will describe fundamental concepts of bioenergetics and provide a framework for understanding the pathogenesis and treatment of metabolic syndrome.
The high, and increasing, prevalence of obesity in affluent societies has become a major health problem. Obesity commonly occurs as part of a metabolic syndrome that may show one or more manifestations, such as hyperlipidaemia, non-insulin-dependent (type II) diabetes mellitus, hypertension and atherosclerosis, either alone or in concert, causing ischaemic heart disease, stroke and premature mortality. Despite a wide range of efforts to prevent obesity, the prevalence of both moderate overweight and obesity is still increasing. An improved understanding of the mechanisms causing obesity seems necessary if efforts to prevent and treat overweight and obesity are to be successful. This review will deal with three genetically determined traits predisposing to weight gain: low relative resting energy expenditure expressed when sympathetic activity is suppressed by a low dietary carbohydrate content; low fat oxidation, which becomes significant when the fat content of the diet is high; and a taste preference for high-fat food items. In concert, these risk factors favour a positive fat balance and, over time, lead to obesity.
This chapter describes the current methods for assessing usual energy needs of an individual, and summarizes national recommendations on energy intake using extracts from the Dietary Reference Intakes (DRI) publication on energy and macronutrients. Energy requirement of an individual is defined in the Dietary Reference Intakes (DRI) publication of the Food and Nutrition Board as "the dietary energy intake that is predicted to maintain energy balance in a healthy adult of a defined age, gender, weight, height, and level of physical activity consistent with good health." Thus, energy requirements are equal to total energy expenditure (TEE) in weight-maintaining individuals. TEE is the sum of energy expended for different metabolic processes and activity, with three main components being typically defined: basal metabolic rate (BMR), energy expenditure for physical activity and arousal (EEPA), and thermic effect of feeding (TEF). The alternative approach to estimating energy requirements of summarizing measurements of TEE determined using the doubly labeled water method for groups of individuals of normal body weight. Equations developed from statistical modeling of measurements of TEE in healthy individuals now exist for predicting the energy requirements of groups and individuals from age, weight, height, and estimated level of physical activity. Other factors such as genetic inheritance, racial origin, and climate also exert some influence on energy requirements, for weight-maintenance of energy needs.
There are large differences in adipose tissue mass change after the obese and overweight participate in regular exercise. Why some obese individuals experience significant adipose tissue mass loss after exercise, whereas others lose little or gain adipose tissue is undetermined. This chapter will summarize a range of factors that have been shown to influence adipose tissue mass or have the potential to produce variability in the body adipose tissue response to exercise. Factors influencing fat intake and absorption such as eating traits and the digestion of nutrients that affect post-prandial blood lipid and glucose levels will be firstly discussed. Then factors influencing the fat oxidation contribution to adipose tissue mass loss such as amount of non-exercise physical activity and the exercise environment will be outlined. Finally, individual factors affecting adipose tissue balance such as genetic influence, body composition, and endocrine effects will be summarized.
The purpose of the study was to estimate the genetic effect for skeletal muscle characteristics using pairs of nontwin brothers (n = 32), dizygotic (DZ) twins (n = 26), and monozygotic (MZ) twins (n = 35). They were submitted to a needle biopsy of the vastus lateralis for the determination of fiber type distribution (I, IIa, IIb) and the following enzymes were assayed for maximal activity: creatine kinase, hexokinase, phosphofructokinase (PFK), lactate dehydrogenase, malate dehydrogenase, 3-hydroxyacyl CoA dehydrogenase, and oxoglutarate dehydrogenase (OGDH). For the percentage of type I fibers, intraclass correlations were 0.33 (p less than 0.05), 0.52 (p less than 0.01), and 0.55 (p less than 0.01) in brothers and DZ and MZ twins, respectively. MZ twins exhibited significant within-pair resemblance for all enzyme activities (0.30 less than or equal to r less than or equal to 0.68). In spite of these correlations, genetic analyses performed with the twin data alone indicated that there was no significant genetic effect for muscle fiber type I, IIa, and IIb distribution and fiber areas. Although there were significant correlations in MZ twins for all muscle enzyme activities, the often nonsignificant intraclass coefficients found in brothers and DZ twins suggest that variations in enzyme activities are highly related to common environmental conditions and nongenetic factors. However, genetic factors appear to be involved in the variation of regulatory enzymes of the glycolytic (PFK) and citric acid cycle (OGDH) pathways and in the variation of the oxidative to glycolytic activity ratio (PFK/OGDH ratio). Data show that these genetic effects reach only about 25-50% of the total phenotypic variation when data are adjusted for age and sex differences.
In order to study the influence of heredity on resting metabolic rate (RMR), 20 monozygotic and 19 dizygotic male twin pairs aged 20.6 (SD 2.9) and 21.4 (SD 3.1) years, gave their consent to participate in the experiment. Fat free weight (FFW) was estimated from underwater weighing. RMR was measured by indirect calorimetry using an open circuit system. RMR was expressed as kJ · min −1 , kJ/m 2 · h −1 , kJ/kg · h −1 and kJ/kgFFW · h −1 . Significant intraclass coefficients were observed in MZ twins for the different expressions of RMR. The values ranged from r = 0.45 (P < 0.05) to r = 0.81 (P < 0.01). However, DZ twins demonstrated lower intraclass coefficients for RMR, with a range from r = 0.21 to r = 0.44. Significant (P < 0.05) DZ resemblance was revealed only when RMR was expressed as kJ · min −1 and kJ/kg · h −1 . Results of the present study suggest that variations in RMR may have a genetic component. Implications for human energy balance and body fat are discussed.
Over the past 50 years a large number of methods have been proposed for estimating heritability from twin studies. The present paper describes the most commonly cited of these estimates as a first step in evaluating their usefulness. A critical review will then follow.
Twin methodology for the analysis of continuously distributed traits is presented as a guideline for initial steps in the analysis of twin data. Tests for heterogeneity of twin means and variances are reviewed along with estimates of genetic variance.
Analysis of twin data appears on the surface to be a rather simple task, but investigators may well be confused by the wealth of choices available for hypothesis testing. This paper is designed to help the less experienced investigator, with perhaps a modest amount of data, begin analysis with maximum attention to testing all testable assumptions of the twin model, and using recent examples of applications of the methods.
The use of correlation and regression as applied to the analysis of family resemblance is discussed. The application of these statistical techniques to family data is not routine because the number of siblings per family is in general variable. Topics dealt with include estimation of sib-sib (intraclass) correlation, parent-child (interclass) correlation and regression of child on parent. An example is given.
The role of the genotype in the response to short-term overfeeding was assessed by submitted six pairs of male monozygotic twins to a 4.2 MJ (1000 kcal) per day energy intake surplus for a period of 22 consecutive days. Individual differences in fat mass and fat-free mass gains were observed in response to overfeeding but they were not randomly distributed. Indeed, the within-pair resemblance in the response was striking when compared to the heterogeneity found among the pairs in adiposity and fat-free mass gains. The intrapair resemblance in the response to overfeeding as assessed by the intraclass coefficient computed with the individual changes, reached 0.88 for total fat mass and 0.76 for fat-free mass. A similar trend for a genetically determined pattern of adaptation to overfeeding was observed for resting metabolic rate (intraclass = 0.63), thermic effect of a meal (intraclass = 0.62), and energy cost of submaximal exercise (intraclass = 0.78) when the data were analysed in terms of changes in oxygen uptake. On the other hand, no major alterations in glucose and insulin response to a glucose load or a test meal, in cardio-pulmonary adaptation to submaximal exercise and in maximal exercise tolerance were found with overfeeding. In contrast, the response of suprailiac fat cell lipolysis (intraclass of about 0.7) and heparin releasable adipose tissue lipoprotein lipase (intraclass - 0.82) varied among individuals but was highly homogeneous within genotypes. Similarly, a genotype-overfeeding interaction effect was seen for serum triglycerides (intraclass = 0.69), HDL-cholesterol (intraclass = 0.85), and the HDL-cholesterol to total cholesterol ratio (intraclass = 0.82). Multiple correlation analyses suggest that much of the variance in the response of fat mass (R = 0.65) and fat-free mass (R = 0.81) is accounted for by alterations in the energy expenditure components assessed in the study. If one takes into account the measurement errors always present in such complex studies and the fact that only a limited fraction of the energy expenditure of activity was considered by design, one can conclude that the genotype determines to a large extent the response variation to short-term overfeeding. In particular, the genotype-overfeeding interaction effect for body composition changes seems to be mediated by the various energy expenditure components, themselves characterized by significant genotype-overfeeding interaction effects.(ABSTRACT TRUNCATED AT 400 WORDS)
Exercise-training has been shown to influence resting components of energy expenditure in lean and obese individuals. Moreover, experimental data suggest that the effect of training on these components could represent an acute effect of exercise. In this regard, the present study was undertaken to determine whether resting metabolic rate (RMR) and glucose-induced thermogenesis (GIT) could be modified depending on the delay elapsing between the last exercise session of a training program and calorimetric measurements. Eight trained individuals were tested 16 h after a 90-min exercise bout and following a 3-day interruption of training. A significant decrease in RMR (-6.6 percent, P less than 0.05) was observed in response to exercise cessation. On the other hand, an increased GIT was noted following the 3-day rest period and this effect was also statistically significant. These results show that short-term interruption of training can affect substantially RMR and GIT in trained individuals, indicating that the time elapsing since the last exercise session must be taken into account in the interpretation of the effects of physical training on both these parameters.
The contribution of reduced energy expenditure to the development of obesity has been a point of controversy. We measured 24-hour energy expenditure (adjusted for body composition, age, and sex), in a respiratory chamber, in 95 southwestern American Indians. Energy expenditure correlated with the rate of change in body weight over a two-year follow-up period (r = -0.39, P less than 0.001). The estimated risk of gaining more than 7.5 kg in body weight was increased fourfold in persons with a low adjusted 24-hour energy expenditure (200 kcal per day below predicted values) as compared with persons with a high 24-hour energy expenditure (200 kcal per day above predicted values; P less than 0.01). In another 126 subjects, the adjusted metabolic rate at rest at the initial visit was also found to predict the gain in body weight over a four-year follow-up period. When the 15 subjects who gained more than 10 kg were compared with the remaining 111 subjects, the initial mean (+/- SD) adjusted metabolic rate at rest was lower in those who gained weight (1694 +/- 103 vs. 1764 +/- 109 kcal per day; P less than 0.02) and increased to 1813 +/- 134 kcal per day (P less than 0.01) after a mean weight gain of 15.7 +/- 5.7 kg. In a group of 94 siblings from 36 families, values for adjusted 24-hour energy expenditure aggregated in families (intraclass correlation = 0.48). We conclude that a low rate of energy expenditure may contribute to the aggregation of obesity in families.
The purpose of this experiment was to assess the effects of short-term overfeeding (mixed diet) on the thermic effect of a meal (TEM) and associated hormonal changes and to investigate the role of the genotype in the observed changes. Six pairs of male sedentary monozygotic (MZ) twins consumed an extra 1,000 kcal per day over their individual level of energy expenditure while maintaining a sedentary existence. Resting metabolic rate (RMR) and TEM following a 4.2 MJ meal challenge was measured before and after 22 days of overfeeding. RMR did not change significantly (7% elevation) in response to the positive caloric stimulus, whereas significant increases (P less than 0.01) in TEM were observed. Moreover, postprandial insulin and glucose responses were not modified. Overfeeding did not significantly alter catecholamine levels but induced significant elevations in plasma levels of T3 and T4 (P less than 0.05). Changes in RMR exhibited moderate but nonsignificant within twin pair resemblance in response whereas significant within pair resemblance was noted in the magnitude of TEM changes induced by overfeeding (P less than 0.05). Hormonal responses exhibited a weaker genotype dependency. These results suggest that short-term overfeeding can induce an elevation in TEM with accompanying increases in T3 and T4. Large individual response variation in metabolic and hormonal measures were observed. The similarity of response within twin pairs suggests that sensitivity to change in TEM induced by short-term overfeeding is genetically influenced.
The purpose of this experiment was to assess the effects of a 22-day training program on resting metabolic rate (RMR), thermic effect of a meal (TEM), and associated hormonal changes. Six pairs of male monozygotic twins were submitted to a 22-day ergocycle exercise program designed to induce a deficit in energy balance of 4.2 MJ per day. RMR and TEM after a 4.2-MJ meal challenge were measured before and after training. Results indicated that RMR and TEM did not change significantly, although a large variation in response between twin pairs was observed. Moreover, training reduced (P less than 0.05) basal and postprandial insulin response, plasma thyroid hormones triiodothyronine (T3), thyroxine (T4), and FT4 (P less than 0.05). Absolute changes in RMR and TEM exhibited significant within-pair resemblance in response, with intraclass correlations reaching r = 0.81 (P less than 0.05) and r = 0.72 (P less than 0.05), respectively. Changes in T4 and FT4 also exhibited moderate within-pair resemblance (0.42 less than or equal to r less than or equal to 0.71). These results suggest that short-term exercise training does not modify RMR and TEM but can significantly decrease plasma levels of insulin and thyroid hormones. Moreover, the similarity of response within twin pairs suggests that heredity plays a role in determining RMR, TEM, and thyroid hormone adaptation to exercise training generating a negative energy balance.
We have described two counterbalancing mechanisms that affect energy balance in man. The one tends to limit storage of energy as fat by promoting the dissipation of nonessential dietary calories and tends to preserve mobility. It appears to be largely under control of the sympathetic nervous system. The other promotes storage of dietary fat in the form of fat, and tends to protect in time of famine. These two mechanisms operate in varying proportions in the heterogeneous animal that is man. The predominance of the second mechanism of fat storage and the insulin resistance that often accompanies it is associated with modern lifestyles and is closely related to the byproducts of obesity, hypertension, non-insulin-dependent diabetes, and hyperlipidemia. Continued research into the factors controlling these two main mechanisms is therefore of prime importance.
The present study investigated the role of heredity in determining changes in the energy cost of submaximal exercise in response to short-term overfeeding. Six pairs of monozygotic twins were subjected to a 1,000 kcal/day surplus for 22 days with careful experimental controls over food intake and physical activities. O2 consumption (VO2) was measured during a submaximal treadmill exercise test 165 min postprandially before and the morning after the overfeeding protocol. As expected, overfeeding induced significant increases in body weight and fat mass. No significant increase in mean exercise VO2 was observed after overfeeding. However, the interindividual variation in overfeeding-induced changes in exercise VO2 was large and not randomly distributed. When comparing intrapair variance for changes in exercise VO2 to interpair variance, a moderate to high within-pair resemblance in response, i.e., a genotype-overfeeding interaction, was observed. Changes in exercise VO2 were positively correlated with those in postexercise levels of blood catecholamines, particularly epinephrine. A negative correlation was found between changes in exercise VO2 and body fat gain. These results are consistent with the concept of a role for the sympathoadrenal system in the regulation of adaptive thermogenesis and the predisposition to store fat. Moreover, these data suggest that the sensitivity to adapt in exercise energy expenditure after overfeeding is inherited to a significant extent.
Human obesity is known to be a familial disorder. We studied 130 nondiabetic adult southwestern American Indians (74 men and 56 women) from 54 families to determine whether the resting metabolic rate, as measured by indirect calorimetry, is a familial trait that is independent of individual differences in fat-free mass (estimated mass of metabolically active tissue), age, and sex. We found that most of the variance in the resting metabolic rate (83 percent, P less than 0.0001) was accounted for by three covariates--fat-free mass, age, and sex--and that fat-free mass was the most important determinant. Family membership accounted for an additional 11 percent (P less than 0.0001) of the variance in the resting metabolic rate. Thus, resting metabolic rate is a familial trait in this population, and it is independent of differences in fat-free mass, age, and sex. We also found that persons from families with lower resting metabolic rates were no more obese than persons from families with higher metabolic rates. This finding may be partly explained by the close correlation between fat-free mass and percentage of body fat (r = 0.81, P less than 0.0001), which indicates that the resting metabolic rate, as adjusted for fat-free mass, is already partly adjusted for obesity. Only prospective studies will elucidate whether the familial dependence of the resting metabolic rate is a contributing mechanism to the familial predisposition to obesity.
Forty-two brothers, 66 dizygotic twins of both sexes and 106 monozygotic twins of both sexes, 16 to 34 yr of age, took part in this study that was designed to investigate the effect of heredity in aerobic performance. Maximal oxygen uptake (VO2 max), maximal heart rate (HR max), maximal ventilation, and maximal oxygen pulse were obtained from a progressive ergocycle test to exhaustion. Total work output in a 90-min maximal ergocycle test was also determined in the twins. Fat-free weight was estimated from body density measurements obtained through underwater weighing. Aerobic performance scores were adjusted for age (brothers), and age and sex (dizygotic and monozygotic twins) by regression procedures. Dizygotic twins and brothers of same sibship exhibited about the same level of resemblance for all variables or were only slightly different, with the exception of HR max. Monozygotic pairs were generally more alike than the other sibs, as suggested by the intra-class coefficients. Twin data were used to compute the genetic effects. The within-pair estimate of genetic variance revealed that it was significant (P less than or equal to 0.05) for all variables except VO2 max X kg-1 fat-free weight X min-1. In the case of HR max, the among-pairs component estimate had to be used, and it also proved significant (P less than or equal to 0.01). The size of the genetic effect was computed from three different methods, and it reached about 40% for VO2 max X kg-1 X min-1, 50% for HR max, 60% for maximal oxygen pulse and maximal ventilation, and 70% for 90-min work output X kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)
Fasting blood glucose and serum immunoreactive insulin (IRI) and the responses of blood glucose and serum IRI to peroral glucose challenge were investigated in middle-aged normoglycemic male twins of 17 monozygotic (MZ) and 18 dizygotic (DZ) pairs recruited from the Finnish Twin Cohort Study. Also, the role of obesity and diet in the regulation of glucose and insulin metabolism was estimated. The fasting and 2 hr postprandial (PP) glucose showed higher pairwise correlations in MZ (r = 0.78 and 0.56) than DZ (r = 0.08 and -0.05) pairs whereas fasting and PP insulin levels and the areas under the PP glucose and insulin curves were weakly and similarly correlated in MZ and DZ twins. The pairwise correlations of the 1/2 hr and 1 hr, but not the fasting and 2 hr insulin/glucose ratios, were somewhat higher in MZ (R = 0.51 and 0.53) than DZ (r = = 0.28 and 0.30) pairs. In MZ twins, the intrapair differences in the body mass index were significantly correlated with those in the fasting and 2 hr PP glucose and insulin levels and those in the fasting and 1/2 hr insulin/glucose ratios (r from 0.47 to 0.76). Also, the intrapair differences in the dietary fat calories were correlated positively, but those in the calories derived from carbohydrates negatively, with the intrapair differences in several parameters of the glucose and insulin metabolism. These data suggest that the environmental contribution to the regulation of glucose and insulin metabolism in subjects within the normoglycemic range may be quite strong.(ABSTRACT TRUNCATED AT 250 WORDS)
This paper describes a modification of the standard oxygen-dilution technique for determining residual lung volume, whereby rapid responding oxygen and carbon dioxide analyzers are used to determine the point of nitrogen equilibration, and a five-liter rebreathing bag is substituted for the standard spirometer. This simplified method reduced the total test time to five min or less for duplicate determinations, and eliminated the need for a nitrogen analyzer and a spirometer. This method was found to be both reliable (r = 0.99) and valid (r = 0.92), with a standard error of prediction of 125 ml, and a mean difference of only eight ml, when compared with the established oxygen-dilution technique on a sample of 76 healthy men and women, 19 to 55 years of age. In a subsample of 13 subjects, residual volume was also determined with the nitrogen washout technique, which correlated r = 0.89 and r = 0.91 with the established and modified oxygen-dilution techniques respectively. The use of assumed values for the initial and final alveolar concentrations of nitrogen did not appear to significantly influence the final results.
Genetics of body fat, energy expenditure and adipose tissue metabolism
- Bouchard
Une nouvelle méthode simple de transformation linéaire de la courbe standard dans le dosage radioimmunologique de l'insuline
- Nadeau
Reproducibility of body composition and adipose tissue measurements in humans
- Bouchard