Measurement of total energy expenditure in grossly obese women: comparison of the bicarbonate–urea method with whole-body calorimetry and free-living doubly labelled water

Gibney, Eileen R.; Murgatroyd, Peter R.; Wright, Antony; Jebb, Susan A.; Elia, Marinos

doi:10.1038/sj.ijo.0802302

Cited by 13 publications

(8 citation statements)

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“…To illustrate the magnitude of the elevated energy expenditure, TDEE was 840 kcal/d higher in the Class III obese compared to lean individuals. Our finding of high TDEE in the Class III obese (3244 kcal/d) confirms previous reports of high TDEE (3415 kcal/d 21 , 3310 kcal/d 33 , 3226 kcal/d 13 ,4036 kcal/d 34 ) in severely obese individuals. Based on the elevated TDEE, the Class III obese individuals would need to consume 35% more calories per day than lean individuals to maintain body weight.…”

Section: Discussionsupporting

confidence: 91%

High energy expenditure masks low physical activity in obesity

et al. 2012

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Objective To investigate energy expenditure in lean and obese individuals, focusing particularly on physical activity and severely obese individuals. Design Total daily energy expenditure (TDEE) was assessed using doubly labeled water, resting metabolic rate (RMR) by indirect calorimetry, activity EE (AEE) by difference and time spent in physical activity by multisensor activity monitors. Subjects 177 lean, Class I and severely obese individuals (age 31–56, BMI 20–64 kg/m2). Results All components of EE were elevated in obese individuals. For example, TDEE was 2404±95 kcal/d in lean and 3244 ± 48 kcal/d in Class III obese. After appropriate adjustment, RMR was similar in all groups. Analysis of AEE by body weight and obesity class indicated a lower AEE in the obese. Confirming lower physical activity, obese individuals spent less time engaged in moderate-to-vigorous physical activity (2.7±1.3, 1.8±0.6, 2.0±1.4 and 1.2±1.0 hr/d in lean, Class I, Class II and Class III), and more time in sedentary behaviors. Conclusions There was no indication of metabolic efficiency in even the severely obese, as adjusted RMR was similar across all groups. The higher AEE observed in the obese is consistent with a higher cost of activities due to higher body weight. However, the magnitude of the higher AEE (20 to 25% higher in obese) is lower than expected (weight approximately 100% higher in Class III). Confirming a lower volume of physical activity in the obese, the total time spent in moderate-to-vigorous physical activity and average daily MET level were lower with increasing obesity. These findings demonstrate that high body weight in obesity leads to a high TDEE and AEE which masks the fact that they are less physically active, which can be influenced by duration or intensity of activity, than lean individuals.

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Section: Discussionsupporting

confidence: 91%

High energy expenditure masks low physical activity in obesity

et al. 2012

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“…The same statistical test was used to define the best fit distributions of the resulting physiological daily inhalation rates per age group. The number of individual observations in fasting subjects reported in Gibney et al (2003) and Shepherd et al (2007) was insufficient (n = 8) for the use of the Anderson-Darling test. Therefore, individual H P (n = 102) values for subjects in the supine position were statically tested in order to characterize the distribution type for the H F value during nighttime sleep.…”

Section: Discussionmentioning

confidence: 90%

“…Variations observed were consistently <0.4% (Table 8) Results of H P and H F values calculated based on simultaneous VO 2 and VCO 2 measurements are not shown in tables. Values for an H F of 0.205 ± 0.003, 0.206 ± 0.003, and 0.207 ± 0.003 L of O 2 /kcal for subjects at rest in a semi-recumbent (Müeller et al 1989; n = 5), almost supine (Saltzman and Salzano 1971;n = 20) and supine position (Gibney et al 2003; n = 6) were calculated with VO 2 , E, and RER values varying from 0.225 ± 0.035 to 0.307 ± 0.044 L/min, 1.09 ± 0.05 to 1.47 ± 0.07 kcal/min, and 0.802 ± 0.057 to 0.858 ± 0.072, respectively. A mean H F value of 0.205 ± 0.001 L of O 2 /kcal was also calculated for adults aged 23-30 years (n = 27) performing exercise in the upright position below the anaerobic threshold (De Bock et al 2005; VO 2 of 2.83 ± 0.05 L/min, VCO 2 of 2.37 ± 0.05 L/ min, E of 13.41 ± 0.21 kcal/min, RER of 0.838 ± 0.023 with minimal and maximal values of 0.759 and 0.928, respectively).…”

Section: Resultsmentioning

confidence: 99%

Derivation of physiological inhalation rates in children, adults, and elderly based on nighttime and daytime respiratory parameters

Brochu

Brodeur

Krishnan

2011

Inhalation Toxicology

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The methodology developed in our previous studies ( Brochu et al. 2006a-c ) for the determination of physiological daily inhalation rates was improved by integrating into the calculation process, both nighttime and daytime respiratory parameters, namely oxygen uptake factors (H) and ventilatory equivalents (VQ). H values during fasting (0.2057±0.0018 L of O2/kcal; mean±SD) and postprandial phases (0.2059±0.0019 L of O2/kcal) as well as VQ values for subjects at rest (27.4±4.8 to 32.2±3.1, unitless) and during the aggregate daytime activities (29.9±4.2 to 33.7±7.2) were determined and combined with published doubly labeled water measurements for the calculation of daily inhalation rates in normal-weight males and females aged 0.22-96 years (n=1235). Depending upon the unit value chosen, the highest 99th percentiles for inhalation data were found in males aged 35 to <45 years (35.40 m3/day), 2.6 to <6 months (1.138 m3/kg-day), and 10 to <16.5 years (22.29 m3/m2-day). Means and percentiles expressed in m3/kg-day as well as in m3/m2-day suggest generally higher intakes of air pollutants in children than in adults and in males than in females (in g/kg-day or g/m2-day) for identical exposure concentrations and conditions. For instance, means in boys aged 2.6 to <6 months of 10.99±3.50 m3/m2-day and 0.572±0.191 m3/kg-day are 1.3- and 2.5-folds higher, respectively, than those in adult males 65?96 years old (8.42±2.13 m3/m2-day, 0.225±0.059 m3/kg-day).

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“…Parenteral feeding provided 7.5 MJ/day (1,800 kcal/day) for the first six postoperative days, but this would represent a sudden decrease in energy consumption. As body weight was 152 kg preoperatively, a daily intake of about 13.4 MJ/day (3,200 kcal/day) would be required for weight maintenance [7]. By 7 days postoperatively, fat mass had decreased by 4.4 kg and the fasting blood glucose level had fallen to 5.9 mmol/l (Fig.…”

Section: Time-course Of Reversal Of Pathogenic Factorsmentioning

confidence: 99%

Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause

2008

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The metabolic abnormalities of type 2 diabetes can be reversed reproducibly by bariatric surgery. By quantifying the major pathophysiological abnormalities in insulin secretion and insulin action after surgery, the sequence of events leading to restoration of normal metabolism can be defined. Liver fat levels fall within days and normal hepatic insulin sensitivity is restored. Simultaneously, plasma glucose levels return towards normal. Insulin sensitivity of muscle remains abnormal, at least over the weeks and months after bariatric surgery. The effect of the surgery is explicable solely in terms of energy restriction. By combining this information with prospective observation of the changes immediately preceding the onset of type 2 diabetes, a clear picture emerges. Insulin resistance in muscle, caused by inherited and environmental factors, facilitates the development of fatty liver during positive energy balance. Once established, the increased insulin secretion required to maintain plasma glucose levels will further increase liver fat deposition. Fatty liver causes resistance to insulin suppression of hepatic glucose output as well as raised plasma triacylglycerol. Exposure of beta cells to increased levels of fatty acids, derived from circulating and locally deposited triacylglycerol, suppresses glucose-mediated insulin secretion. This is reversible initially, but eventually becomes permanent. The essential time sequence of the pathogenesis of type 2 diabetes is now evident. Muscle insulin resistance determines the rate at which fatty liver progresses, and ectopic fat deposition in liver and islet underlies the related dynamic defects of hepatic insulin resistance and beta cell dysfunction. These defects are capable of dramatic reversal under hypoenergetic feeding conditions, completely in early diabetes and to a worthwhile extent in more established disease.

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Measurement of total energy expenditure in grossly obese women: comparison of the bicarbonate–urea method with whole-body calorimetry and free-living doubly labelled water

Cited by 13 publications

References 42 publications

High energy expenditure masks low physical activity in obesity

High energy expenditure masks low physical activity in obesity

Derivation of physiological inhalation rates in children, adults, and elderly based on nighttime and daytime respiratory parameters

Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause

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