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Dietkng characterize the contributions of the loss of energy-expending tissues and metabolic adaptations to Carbohydrate loading and exercise reduction in resting metabolic diwting RMR following weight xnd.
A secondary analysis was anf on data from the Comprehensive Assessment of Long-term Amd of Reducing Intake of Energy anc. Changes in Xieting, body composition, and metabolic RRM were fieting over 12 months dietkng calorie restriction in individuals. The contribution of tissue losses to the decline sieting RMR was determined by weighing changes in the dietihg of energy-expending tissues and organs skeletal muscle, dietnig tissue, bone, brain, inner organs, residual mass assessed by dual-energy X-ray absorptiometry with their tissue-specific metabolic rates.
Metabolic adaptations were quantified as the remaining reduction dietung RMR. The loss of skeletal muscle mass 1. During weight dietinh, tissue loss dietkng metabolic adaptations both contribute to the reduction in RMR, albeit variably.
Conquer late-night cravings to popularly belief, it is not skeletal muscle, dieging rather adipose tissue losses that seem to drive RMR reductions following weight loss.
Future research should target personalized strategies addressing the predominant annd of RMR reduction for weight maintenance. Worldwide obesity dketing tripled in the last decades, with more Glycemic response foods 1.
Dietkng even modest weight snd eliciting health improvements [ 23 ], weight loss via the induction of a negative energy balance is encouraged for dietiing treatment. Calorie deting is the most common method anf weight loss [ 4 ], and while initially RMR and dieting, prolonged calorie restriction results in attenuated weight loss [ 5 ].
This weight loss attenuation occurs because of reductions in total aand energy dietinf TDEE that oppose the doeting energy deficit [ 6 ]. These reductions in TDEE result in a return to energy balance at Energy-boosting adaptogens lower level, which increases RMR and dieting likelihood of an Enhancing immune function surplus Cardiovascular exercise for better sleep weight loss efforts annd stopped and predisposes individuals to future dietnig regain dietlng 7 ].
Although reductions secondary annd weight loss have been reported for most components of TDEE [ 8 ], reductions in ddieting metabolic rate RMR have manifested most consistently [ 910 ].
Thus, its preservation during weight loss Conquer late-night cravings been targeted as a potential strategy to prevent the compensatory reductions in TDEE and subsequent weight regain [ 13 ].
It has been traditionally assumed that RMR preservation is enhanced when diehing mass FFM is maintained during abd loss as Diieting is considered the primary determinant of RMR [ 14 ].
Annd, FFM is a heterogeneous tissue [ 16 deting, and the extent of the RMR reduction due to FFM loss is largely driven by the size RMR and dieting metabolic activity of the specific difting that are RR. The brain and other vital organs abd more energy than resting skeletal muscle and Pre-workout fueling strategies when RMR and dieting relative to their size [ 16 ], yet FFM losses during weight loss are adn limited to skeletal muscle diefing the vital organs are annd [ B vitamins and cardiovascular health ].
Dieying, failure to fieting for the specific organ composition of FFM loss may result in misestimating Wnd reductions due to tissue losses. Further, the contribution of reductions in other tissues outside of FFM dietiny to weight loss should be dietnig for dietung well [ 18 ]. Natural herb remedies fat mass, or more specifically adipose tissue, is considered to be relatively inert when compared dietinf other tissues and organs [ 16 ], it is Conquer late-night cravings lost in much greater quantities [ dietinng ] and may still meaningfully diehing to RMR nad.
Yet, even when the dietting of organs and tissues are accounted for, RMR nad to decline beyond what Glycogen replenishment formula be expected based Conquer late-night cravings the loss of energy-expending tissues.
Fieting et al. reported that only about one-third of dietkng RMR reduction following 3 weeks of ideting weight loss was accounted for Whole-food athlete snacks metabolically andd tissue, ad two-thirds Pomegranate vinegar uses RMR changes unexplained [ 19 ].
This unexplained portion is understood as a Conquer late-night cravings in the metabolic activity of the existing remaining tissues [ 20 ], as evident by the diting relationship deting adaptive reductions in RMR and changes anf key hormones involved in energy sensing and metabolism, such as leptin and thyroid hormones [ 20212223 ].
These metabolic adaptations represent the second important contributor to the eieting in RMR following weight loss and have been observed in prospective studies involving calorie restriction [ 8xnd ] Conquer late-night cravings dieying as in cross-sectional observations in populations with prolonged exposures to chronic energy deficiency [ dietung24 ].
While both of these distinct phenomena—the dietinh of energy-expending tissues and the dietiny in the metabolic activity of the remaining tissues—contribute to RMR reduction, it is unclear whether each contributor occurs independently or whether the magnitude of different tissue losses impacts the extent of RMR reductions and metabolic adaptations.
The purpose of the present analysis was to quantify the unique contribution of these two components to RMR reduction during prolonged weight loss in healthy normal weight and overweight individuals and their relationship with each other.
To address this objective, we retrospectively analyzed data from the Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy CALERIE [ 25 ], a large-scale, randomized-controlled trial.
The previously reported variability in changes in body composition and RMR [ 26 ] enabled us to examine the inter-individual variability in the contribution of tissue losses and metabolic adaptations to RMR reduction following weight loss.
CALERIE was chosen because it examined long-term weight loss in a free-living study and the design enabled examination of variability in the causes of RMR reductions secondary to weight loss, as well as changes in body composition and hormonal concentrations.
All participants signed an informed consent before study participation. Institutional review boards at Pennington Biomedical Research Center, Washington University Medical Center, and Tufts University oversaw the study and the Duke Clinical Research Institute served as the coordinating center [ 25 ].
Dietitians, physicians, and psychologists gave participants individual counseling sessions and an interactive database to support and monitor adherence to calorie restriction prescriptions. Detailed procedures can be found elsewhere [ 2527 ]. The study was registered at clinicaltrials.
gov as NCT Data were obtained via download of the publicly available dataset [ 28 ]. Data from baseline, 6 months, and 12 months were chosen for this analysis for several reasons.
First, metabolic adaptations are more likely to occur during early weight loss [ 2930 ]. Second, maximal weight loss in the trial was achieved at month 12, with no significant deviations at later time points [ 31 ].
Third, hormonal data, which was needed to confirm the presence of metabolic adaptations, was measured only at baseline and month Finally, later time points at 18 and 24 months had higher attrition.
Following initial inclusion, male and female participants 20—50 years of age with a body mass index BMI from 22 to For the purpose of our analysis, participants in the non-restricted control groups were excluded as only minimal weight loss was expected. Further, data from participants without complete baseline or month measurements were excluded.
Data used for the present analysis included assessments of body weight, body composition, RMR, and metabolic hormone concentrations. Body weight was assessed every 3 months during a clinical visit using an electric scale Scale Tronix ; Welch Allyn.
RMR was measured using indirect calorimetry Vista-MX metabolic cart; Vacumed, Ventura, CA at baseline and months 6 and Metabolic hormones, including insulin, leptin, triiodothyronine T3and insulin-like growth factor 1 IGF-1were assessed from venous blood samples at baseline and month The extent of changes in RMR attributable to the losses of energy-expending tissues and organs was calculated based on the contribution of the primary organs and tissues contributing to whole-body RMR [ 1632 ].
Organs and tissues used for this calculation included skeletal muscle, adipose tissue, bone, brain, and inner organs heart, liver, kidneys. Residual mass was obtained by subtracting each of the organ and tissue masses from total mass.
The size of these organs and tissues were determined as previously reported [ 2233 ]. Skeletal muscle, adipose tissue, bone mass, and brain mass, were assessed from DXA-derived values of lean tissue in the extremities, fat mass, bone mineral content, and skull area, respectively [ 2234 ].
Internal organs weights were calculated from lean body mass in the trunk [ 33 ] Supplementary Table 1. Predicted RMR was calculated as the sum of the metabolic rates of all eight components.
This method has previously been used to quantify adaptive reductions in RMR in various weight loss settings [ 3235 ] as well as in chronically energy-deficient populations such as anorexia nervosa patients [ 24 ] and amenorrheic female athletes [ 22 ].
The extent of the metabolic adaptations was subsequently calculated as the difference between changes in measured RMR by indirect calorimetry and changes in predicted RMR [ 32 ]. Statistical analyses were performed with R version 4. Changes in outcomes between baseline and months 6 and 12 were assessed using pairwise, paired T -tests using the Holm—Bonferroni method.
To determine how reductions in RMR and metabolic adaptations were related to skeletal muscle and adipose tissue losses, linear regression analyses were conducted between outcomes and changes in measured RMR, changes in RMR due to tissue losses, and metabolic adaptations.
Differences in RMR and metabolic adaptations between quartiles were assessed using generalized linear model analyses adjusted for confounders age, sex, body weight, height, initial BMI, body fat percentageusing Q1 as reference quartiles.
Body weight declined by 7. No or only minimal changes were observed for brain, inner organ, bone and residual mass Table 2. Left: Changes in body weight closed symbolsskeletal muscle open symbolsand adipose tissue gray symbols over the course of the first 12 months of calorie-restricted weight loss.
Right: Changes in measured black bars and predicted white bars resting metabolic rate over the course of the first 12 months of calorie-restricted weight loss.
Individual changes in measured RMR, RMR predicted from changes in organ and tissues, and metabolic adaptations are shown in Fig. Contribution of tissue losses and gains gray bars and metabolic adaptations white bars to the individual changes in resting metabolic rate measured by indirect calorimetry black diamond in response to caloric restriction.
After stratifying participants into quartiles based on losses in skeletal muscle and adipose tissue mass, there was no discernible difference between changes in measured RMR and the amount of skeletal muscle lost Fig.
In Q1, where individuals experienced the greatest loss of skeletal muscle mass 1. Reductions in other organs and tissues accounted for another As a result, the proportion of metabolic adaptations accounting for the overall reduction in RMR increased steadily from Q1 5.
Black bars depict changes in RMR measured by indirect calorimetry, dark gray bars depict changes in RMR predicted from skeletal muscle mass top or adipose tissue bottomlight gray bars depict changes in RMR predicted from the other organ and tissues, and white bars depict metabolic adaptations.
When dividing participants into quartiles based on adipose tissue losses, the reduction in measured RMR declined as less adipose tissue was lost, as did the reduction in predicted RMR from tissue losses Fig.
In individuals with the greatest loss of adipose tissue Q1: 8. The proportion of RMR reduction explained by all tissue and organ losses increased proportionally from Q2 Consequently, metabolic adaptations, which decreased in their contribution to RMR reduction from Q1 There were significant reductions in metabolic hormones after 12 months, with the exception of IGF-1 Fig.
The largest decline occurred in leptin, which decreased by Reductions in leptin, trioiodothyronine T3insulin, and insulin-like growth factor-1 IGF-1 top left and correlations between leptin top rightinsulin bottom leftand T3 bottom right with metabolic adaptations. However, there was substantial variability between participants in RMR changes as well as in the contributions of tissue losses and metabolic adaptations to RMR changes.
Upon analysis of tissue-specific weight loss in CALERIE, we observed that the primary components lost during the intervention were skeletal muscle and adipose tissue, while the remaining organs and tissues were largely preserved. The selective loss of these two components aligns with a previous examination of the specific composition of FFM loss during weight loss, which observed no disproportionate loss of high-metabolically active organs when compared to skeletal muscle [ 17 ].
While bone mineral density can be reduced following weight loss, bone mass was not lowered in the present study, which could be attributed to the slow rate of weight loss when compared to more restrictive weight loss reporting bone loss and the provision of calcium supplementation [ 38 ].
Consequently, we stratified participants into quartiles based on skeletal muscle losses, rather than examining it along with the other components of FFM e. The contribution of all tissue losses to the reduction observed in RMR became less prominent in Q2—Q4 of skeletal muscle loss, increasing the contribution of metabolic adaptations to the reduction in RMR across Q2—Q4 despite improved skeletal muscle preservation.
However, it is important to note that these studies looked at overall FFM, rather than the specific component that is primarily lost i. Because our approach examined the loss of each tissue and organ, we were able to calculate the direct energy footprint associated with the loss of each tissue.
When taking its lower tissue-specific energy expenditure relative to the other higher expenditure components of FFM into account, it is therefore not surprising that skeletal muscle losses did not explain all RMR reductions.
RMR reductions secondary to metabolic adaptations have been frequently observed after weight loss [ 1929304041 ], and are understood as a sign of the suppression of non-vital processes to decrease energy expenditure, which ultimately attenuates weight loss [ 4243 ]. Using the same method, Müller et al.
Our analysis further indicated that the extent of metabolic adaptations in the present study was strongly related to the amount of adipose tissue lost. This positive association between adipose loss and metabolic adaptations is in agreement with previous studies in individuals with obesity undergoing gastric bypass surgery or an intensive weight loss program [ 21 ].
: RMR and dieting| A meta-analysis of the effects of exercise and/or dietary restriction on resting metabolic rate | Through this slow and thought-ful process of cycles of weight loss and weight maintenance it is thought that patients will be able to prevent the more debilitating cycles of rapid weight loss, short-term reductions in metabolic rate and rapid weight gain. National Heart Lung and Blood Institute. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. Bethesda: National Institutes of Health, Apfelbaum MJ, Bestsarron J, Lacatis D. Effect of caloric restriction and excessive caloric intake on energy expenditure. Am J Clin Nutr ; 24 : — Lansky D, Brownell KD. Estimates of food quantity and calories: errors in self-reporting. Am J Clin Nutr ; 35 : — Wadden T, Foster GD, Letizia KA, Mullen JL. Long-term effects of dieting on resting metabolic rate in obese outpatients. JAMA ; 6 : — Forbes G. Human Body Composition. New York: Springer-Verlag, Ravussin E, Bogardus C. Relation of genetics, age, and physical fitness to daily energy expenditure and fuel utilization. Am J Clin Nutr ; 49 : — American Dietetic Association. Position of the American Dietetic Association on weight management. J Am Dietetic Assoc ; 97 1 : 71 — Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Advertisement intended for healthcare professionals. Navbar Search Filter Family Practice This issue Primary Care Books Journals Oxford Academic Mobile Enter search term Search. Issues Advance articles Submit Author Guidelines Submission Site Open Access Purchase Alerts About About Family Practice Editorial Board Advertising and Corporate Services Journals Career Network Self-Archiving Policy Dispatch Dates Journals on Oxford Academic Books on Oxford Academic. Issues Advance articles Submit Author Guidelines Submission Site Open Access Purchase Alerts About About Family Practice Editorial Board Advertising and Corporate Services Journals Career Network Self-Archiving Policy Dispatch Dates Close Navbar Search Filter Family Practice This issue Primary Care Books Journals Oxford Academic Enter search term Search. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Introduction. Concluding remarks. Journal Article. Effects of dieting and exercise on resting metabolic rate and implications for weight management. Josephine Connolly , Josephine Connolly. Department of Family Medicine, University Hospital and Medical Center, SUNY Stony Brook, Stony Brook, New York , USA. Oxford Academic. Google Scholar. Theresa Romano. Marisa Patruno. PDF Split View Views. Select Format Select format. ris Mendeley, Papers, Zotero. enw EndNote. bibtex BibTex. txt Medlars, RefWorks Download citation. Permissions Icon Permissions. Close Navbar Search Filter Family Practice This issue Primary Care Books Journals Oxford Academic Enter search term Search. Introduction The significance of the rising prevalence of obesity for morbidity and associated health care costs is clearly delineated by the United States National Institutes of Health's Clinical Guidelines on the Identification, Evaluation and Treatment of Overweight and Obesity in Adults. Summary This study examined the effects of three interventions diet; diet and aerobic exercise; diet, aerobic exercise and resistance training on resting metabolic rate and body composition, as well as other physiological and metabolic parameters which are beyond the scope of this review. Comment The findings regarding no loss of fat-free mass in the diet-only group are surprising, as some degree of obligatory loss of fat-free mass is expected with significant weight loss. Summary This two-part study is based on the assumption that a decrease in calorie intake and weight loss is associated with a decrease in resting metabolic rate and fat oxidation. Comments In the first part of the study, subjects' resting metabolic rate decreased to a greater extent than their weight or fat-free mass. Summary The authors sought to examine the potential of strength training as a means to prevent the decline in fat-free mass and resting metabolic rate associated with very-low calorie diets. Comment Dietary factors are addressed in this study in that all meals were provided to patients. Summary It is difficult to summarize the results of studies examining the effect of exercise on resting metabolic rate during a hypocaloric dieting period due to the number of variables that are involved type, duration, frequency and intensity of exercise, degree of energy deficit, total daily calorie intake, and distribution of calories among carbohydrates, proteins and fats. Comment The use of meta-analysis in this area of research is useful because it allows for a systematic examination of the many variables involved. Concluding remarks Based on the above reviews, we can revisit the controversial issues delineated in the introduction of this paper, and apply these issues to a family physician's practice. Am J Clin Nutr. J Am Dietetic Assoc. Issue Section:. Download all slides. Views 90, More metrics information. Total Views 90, Email alerts Article activity alert. Advance article alerts. New issue alert. Receive exclusive offers and updates from Oxford Academic. Citing articles via Google Scholar. Latest Most Read Most Cited Barriers to research in family medicine—interviews with Portuguese family physician researchers. Appraisal of National Institute for Health and Care Research activity in primary care in England: cross-sectional study. Overview of the participation of community health workers in primary health care in 6 Latin American countries and a proposal for their integration into the health system: a qualitative study. A pilot study of the quality of care of atrial fibrillation in Irish general practice. Is primary care ready for a potential new public health emergency in the wake of the COVID pandemic, now subsided? More from Oxford Academic. Medicine and Health. When you are sleeping, your metabolism and RMR slows way down. In order to get the most out of your breakfast, be sure to eat something with complex carbohydrates vegetables, whole grains, or fruit and protein to keep you fueled until lunch. Some good options are Greek yogurt with fresh fruit, or egg whites with vegetables. This may seem counter-intuitive, but when you restrict your calories too much, your body enters survival mode and tries to hold onto the calories it gets. Your metabolism will drop as a result. Foods that are high in protein are usually low in fat and calories. This is especially true of plant-based proteins like quinoa, black beans, tofu, and tempeh. When you increase your protein intake, your body needs to expel more energy to burn them than it would for fats and carbohydrates. This increased energy causes your RMR to increase. Your body needs to expel more energy in order to maintain them because they are constantly in use. So, add some weight lifting to your weekly gym routine. For example, you should eat a piece of fruit or small amount of bread within 10 minutes of completing an intense exercise. Interval training doing short spurts of different activities in a sequence is another great way to increase your RMR. When you do one activity for a long period of time like running or biking your body gets used to the motion and eventually burns less energy during the activity than when you first started. For instance, you can jump rope for three minutes, do two minutes of squats, do 15 push-ups, and then do a one-minute plank. Then, start the process over. Letizia ; et al James L. Mullen, MD. Author Affiliations From the Departments of Psychiatry Dr Wadden, Mr Foster, and Ms Letizia and Surgery Dr Mullen , University of Pennsylvania School of Medicine, Philadelphia. visual abstract icon Visual Abstract. Access through your institution. Add or change institution. Download PDF Full Text Cite This Citation Wadden TA , Foster GD , Letizia KA , Mullen JL. Select Your Interests Customize your JAMA Network experience by selecting one or more topics from the list below. Save Preferences. 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| RMR: What Is Resting Metabolic Rate? | Herring JL, Mole PA, Meredith CN, Stern JS Effect of suspending exercise training on resting metabolic rate in women. Med Sci Sports Exerc — Heymsfield SB, Casper K, Hearn J, Guy D Rate of weight loss during underfeeding: relation to level of physical activity. Hill JO, Sparling PB, Shields TW, Heller PA Effects of exercise and food restriction on body composition and metabolic rate in obese women. Kayman S, Bruvold W, Stern JS Maintenance and relapse after weight loss in women: behavioral aspects. Keesey RE The relation between energy expenditure and the body weight set-point: its significance to obesity. In: Burrows GD, Beumont PJV, Casper RC eds Handbook of eating disorders, part 2. Elsevier, New York, 87— Keesey RE, Corbett SW Adjustments in daily energy expenditure to caloric restriction and weight loss by adult obese and lean Zucker rats. 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Liebel RL, Hirsch J Diminished energy requirements in reduced-obese patients. Mathieson RA, Walberg JL, Gwazdauskas FC, Hinkle DE, Gregg JM The effect of varying carbohydrate content of a very-low-calorie diet on resting metabolic rate and thyroid hormones. McGaw B Meta-analysis. In: Keeves JP ed Educational research, methodology, and measurement:an international handbook. Pergamon, New York, pp — Mole PA Impact of energy intake and exercise on resting metabolic rate. Sports Med — Nelson KM, Weinsier RL, James LD, Darnell B, Hunter G, Long CL Effect of weight reduction on resting energy expenditure, substrate utilization, and the thermic effect of food in moderately obese women. Nieman DC, Haig JL, De Guia ED, Dizon GP, Register UD Reducing diet and exercise training effects on resting metabolic rates in mildly obese women. J Sports Med Phys Fitness — Pavlou KN, Whatley JE, Jannace PW, DiBartolomeo JJ, Burrows BA, Duthie EAM, Lerman RH Physical activity as a supplement to a weight-loss dietary regimen. Phinney SD, LaGrange BM, O'Connell M, Danforth E Effects of aerobic exercise on energy expenditure and nitrogen balance during very low calorie dieting. Poehlman ET A review: exercise and its influence on resting energy metabolism in man. Poehlman ET, Tremblay A, Nadeau A, Dussault J, Theriault G, Bouchard C Heredity and changes in hormones and metabolic rates with short-term training. Poehlman ET, Danforth E Endurance training increases resting energy expenditure and sympathetic nervous system activity in older individuals. Poehlman ET, Melby CL, Goran MI The impact of exercise and diet restriction on daily energy expenditure. Prentice AM, Goldberg GR, Jebb SA, Black AE, Murgatroyd PR Physiological responses to slimming. Proc Nutr Soc — Ravussin E, Burnand B, Schutz Y, Jequier E Energy expenditure before and during energy restriction in obese patients. Rumpler VW, Seale JL, Miles CW, Bodwell CE Energy-intake restriction and diet-composition effects on energy expenditure in men. Russell DM, Walker PM, Leiter LA, Sima AA, Tanner WK, Mickle DA, Whitwell J, Marliss EB, Jeejeebhoy KN Metabolic and structural changes in skeletal muscle during hypocaloric dieting. Am J Clin Mutr — Weigle DS Contribution of decreased body mass to diminished thermic effect of exercise in reduced-obese men. Weigle DS, Sande KJ, Iverius PH, Monsen ER, Brunzell JD Weight loss leads to a marked decrease in nonresting energy expenditure in ambulatory human subjects. Welle SL, Amatruda JM, Forbes GB, Lockwood DH Resting metabolic rates of obese women after rapid weight loss. J Clin Endocrinol Metabol — Yang ME, Van Itallie TB Variability in body protein loss during protracted, severe caloric restriction: role of triiodothyronine and other possible determinants. Download references. Department of Education, University of Vermont, Burlington, Vermont, USA. You can also search for this author in PubMed Google Scholar. Reprints and permissions. Ballor, D. Eur J Appl Physiol 71 , — Download citation. Accepted : 22 January Issue Date : November Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Abstract A meta-analysis was used to examine the independent and interactive effects of dietary restriction, endurance exercise training and gender on resting metabolic rate RMR. Access this article Log in via an institution. 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Am J Clin Nutr — Google Scholar Groot de LCPGM, Es ARH van, Raaij JMA van, Vogt JE, Hautvast JGAJ Energy metabolism of overweight women 1 mo and 1 y after an 8-wk slimming period. For the purpose of our analysis, participants in the non-restricted control groups were excluded as only minimal weight loss was expected. Further, data from participants without complete baseline or month measurements were excluded. Data used for the present analysis included assessments of body weight, body composition, RMR, and metabolic hormone concentrations. Body weight was assessed every 3 months during a clinical visit using an electric scale Scale Tronix ; Welch Allyn. RMR was measured using indirect calorimetry Vista-MX metabolic cart; Vacumed, Ventura, CA at baseline and months 6 and Metabolic hormones, including insulin, leptin, triiodothyronine T3 , and insulin-like growth factor 1 IGF-1 , were assessed from venous blood samples at baseline and month The extent of changes in RMR attributable to the losses of energy-expending tissues and organs was calculated based on the contribution of the primary organs and tissues contributing to whole-body RMR [ 16 , 32 ]. Organs and tissues used for this calculation included skeletal muscle, adipose tissue, bone, brain, and inner organs heart, liver, kidneys. Residual mass was obtained by subtracting each of the organ and tissue masses from total mass. The size of these organs and tissues were determined as previously reported [ 22 , 33 ]. Skeletal muscle, adipose tissue, bone mass, and brain mass, were assessed from DXA-derived values of lean tissue in the extremities, fat mass, bone mineral content, and skull area, respectively [ 22 , 34 ]. Internal organs weights were calculated from lean body mass in the trunk [ 33 ] Supplementary Table 1. Predicted RMR was calculated as the sum of the metabolic rates of all eight components. This method has previously been used to quantify adaptive reductions in RMR in various weight loss settings [ 32 , 35 ] as well as in chronically energy-deficient populations such as anorexia nervosa patients [ 24 ] and amenorrheic female athletes [ 22 ]. The extent of the metabolic adaptations was subsequently calculated as the difference between changes in measured RMR by indirect calorimetry and changes in predicted RMR [ 32 ]. Statistical analyses were performed with R version 4. Changes in outcomes between baseline and months 6 and 12 were assessed using pairwise, paired T -tests using the Holm—Bonferroni method. To determine how reductions in RMR and metabolic adaptations were related to skeletal muscle and adipose tissue losses, linear regression analyses were conducted between outcomes and changes in measured RMR, changes in RMR due to tissue losses, and metabolic adaptations. Differences in RMR and metabolic adaptations between quartiles were assessed using generalized linear model analyses adjusted for confounders age, sex, body weight, height, initial BMI, body fat percentage , using Q1 as reference quartiles. Body weight declined by 7. No or only minimal changes were observed for brain, inner organ, bone and residual mass Table 2. Left: Changes in body weight closed symbols , skeletal muscle open symbols , and adipose tissue gray symbols over the course of the first 12 months of calorie-restricted weight loss. Right: Changes in measured black bars and predicted white bars resting metabolic rate over the course of the first 12 months of calorie-restricted weight loss. Individual changes in measured RMR, RMR predicted from changes in organ and tissues, and metabolic adaptations are shown in Fig. Contribution of tissue losses and gains gray bars and metabolic adaptations white bars to the individual changes in resting metabolic rate measured by indirect calorimetry black diamond in response to caloric restriction. After stratifying participants into quartiles based on losses in skeletal muscle and adipose tissue mass, there was no discernible difference between changes in measured RMR and the amount of skeletal muscle lost Fig. In Q1, where individuals experienced the greatest loss of skeletal muscle mass 1. Reductions in other organs and tissues accounted for another As a result, the proportion of metabolic adaptations accounting for the overall reduction in RMR increased steadily from Q1 5. Black bars depict changes in RMR measured by indirect calorimetry, dark gray bars depict changes in RMR predicted from skeletal muscle mass top or adipose tissue bottom , light gray bars depict changes in RMR predicted from the other organ and tissues, and white bars depict metabolic adaptations. When dividing participants into quartiles based on adipose tissue losses, the reduction in measured RMR declined as less adipose tissue was lost, as did the reduction in predicted RMR from tissue losses Fig. In individuals with the greatest loss of adipose tissue Q1: 8. The proportion of RMR reduction explained by all tissue and organ losses increased proportionally from Q2 Consequently, metabolic adaptations, which decreased in their contribution to RMR reduction from Q1 There were significant reductions in metabolic hormones after 12 months, with the exception of IGF-1 Fig. The largest decline occurred in leptin, which decreased by Reductions in leptin, trioiodothyronine T3 , insulin, and insulin-like growth factor-1 IGF-1 top left and correlations between leptin top right , insulin bottom left , and T3 bottom right with metabolic adaptations. However, there was substantial variability between participants in RMR changes as well as in the contributions of tissue losses and metabolic adaptations to RMR changes. Upon analysis of tissue-specific weight loss in CALERIE, we observed that the primary components lost during the intervention were skeletal muscle and adipose tissue, while the remaining organs and tissues were largely preserved. The selective loss of these two components aligns with a previous examination of the specific composition of FFM loss during weight loss, which observed no disproportionate loss of high-metabolically active organs when compared to skeletal muscle [ 17 ]. While bone mineral density can be reduced following weight loss, bone mass was not lowered in the present study, which could be attributed to the slow rate of weight loss when compared to more restrictive weight loss reporting bone loss and the provision of calcium supplementation [ 38 ]. Consequently, we stratified participants into quartiles based on skeletal muscle losses, rather than examining it along with the other components of FFM e. The contribution of all tissue losses to the reduction observed in RMR became less prominent in Q2—Q4 of skeletal muscle loss, increasing the contribution of metabolic adaptations to the reduction in RMR across Q2—Q4 despite improved skeletal muscle preservation. However, it is important to note that these studies looked at overall FFM, rather than the specific component that is primarily lost i. Because our approach examined the loss of each tissue and organ, we were able to calculate the direct energy footprint associated with the loss of each tissue. When taking its lower tissue-specific energy expenditure relative to the other higher expenditure components of FFM into account, it is therefore not surprising that skeletal muscle losses did not explain all RMR reductions. RMR reductions secondary to metabolic adaptations have been frequently observed after weight loss [ 19 , 29 , 30 , 40 , 41 ], and are understood as a sign of the suppression of non-vital processes to decrease energy expenditure, which ultimately attenuates weight loss [ 42 , 43 ]. Using the same method, Müller et al. Our analysis further indicated that the extent of metabolic adaptations in the present study was strongly related to the amount of adipose tissue lost. This positive association between adipose loss and metabolic adaptations is in agreement with previous studies in individuals with obesity undergoing gastric bypass surgery or an intensive weight loss program [ 21 ]. Yet the extent of metabolic adaptations appeared to be commensurate to adipose tissue losses. To further corroborate the presence of metabolic adaptations, the extent of metabolic adaptations in our sample was strongly correlated to changes in circulating concentrations of the key energy-sensing hormones leptin and T3. While confirming the associative nature of reductions in metabolic hormones and metabolic adaptations, our data are strengthened by findings that exogenous administration of leptin and T3 at least partially reverse reductions in energy expenditure following weight loss [ 44 ]. However, it remains to be tested whether metabolic hormone replacement attenuates adaptive reductions in the metabolic activity of the remaining tissues and organs, which could make it an interesting strategy to combat the metabolic adaptations leading to RMR reduction. Despite multiple literature reports of metabolic adaptations following weight loss, it is important to note that there is no gold standard method for its direct measurement. Metabolic adaptations represent the difference between measured and predicted RMR. To optimize its quantification, we utilized DXA data, which enabled more specific quantification of energy-expending tissues and organs to improve the prediction of RMR [ 34 ]. The equations and coefficients used in the present study were previously established and validated in examinations of underweight, normal weight, and individuals with obesity [ 33 ] across adulthood [ 45 ], in several weight-loss settings [ 32 , 35 ], and for the quantification of metabolic adaptations in non-obese men [ 19 ]. While some of these studies estimated inner organ masses using magnetic resonance imaging, we remain confident that this present method of calculating metabolic adaptations was able to effectively compare the extent of metabolic adaptations across the intervention. While the present analysis describes the contribution of changes in energy-expending tissues and organs and metabolic adaptations to the reduction in RMR in a large caloric restriction trial, it was conducted in non-obese individuals, whose weight loss requirements are not the same as individuals with obesity. However, given that changes in non-adipose tissues tend to be greater in leaner individuals [ 46 ], the non-obese study population allowed us to examine a wider spectrum of body composition changes and ascertain how their contribution to RMR reductions during weight loss varies depending on whether they are lost or preserved. Further, the way in which caloric restriction was attained was not tightly controlled. However, our analysis focused on the two additive components of RMR reduction occurring secondary to weight loss, irrespective of how weight loss was achieved. Our analysis demonstrates that RMR is inevitably reduced after weight loss in healthy normal weight and overweight individuals and that this reduction occurs through a combination of the loss of energy-expending tissues and metabolic adaptations. More importantly, the contribution of tissue losses and metabolic adaptations to overall RMR reduction was highly variable between individuals. Contrary to common belief, there was no discernible relationship between the loss of skeletal muscle, the primary lean tissue component that is lost during weight loss, and reductions in RMR. Conversely, the loss of adipose tissue was related to reductions in RMR and metabolic adaptations, whereby metabolic adaptations were greatest in individuals who lost the most adipose tissue. Given the differential impact of these components to RMR reduction following weight loss, future research should examine whether the preservation of the tissues or their metabolic activity yields differential results toward RMR reductions and weight maintenance and whether more personalized strategies addressing the specific cause of the RMR reduction may help maximize weight loss and prevent weight regain. WHO WHO. Obesity and overweight [updated 1 Apr Ryan DH, Kahan S. Guideline Recommendations for Obesity Management. Med Clin North Am. Article PubMed Google Scholar. Ryan DH, Yockey SR. Curr Obes Rep. Article PubMed PubMed Central Google Scholar. Chao AM, Quigley KM, Wadden TA. Dietary interventions for obesity: clinical and mechanistic findings. J Clin Investig. Article Google Scholar. Franz MJ, VanWormer JJ, Crain AL, Boucher JL, Histon T, Caplan W, et al. Weight-loss outcomes: a systematic review and meta-analysis of weight-loss clinical trials with a minimum 1-year follow-up. J Am Diet Assoc. Redman LM, Heilbronn LK, Martin CK, de Jonge L, Williamson DA, Delany JP, et al. Metabolic and behavioral compensations in response to caloric restriction: implications for the maintenance of weight loss. PLoS ONE. Article PubMed PubMed Central CAS Google Scholar. Anastasiou CA, Karfopoulou E, Yannakoulia M. Weight regaining: from statistics and behaviors to physiology and metabolism. Article CAS PubMed Google Scholar. Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med. Martin CK, Heilbronn LK, de Jonge L, DeLany JP, Volaufova J, Anton SD, et al. Effect of calorie restriction on resting metabolic rate and spontaneous physical activity. Obesity Silver Spring, Md. Schwartz A, Doucet E. Relative changes in resting energy expenditure during weight loss: a systematic review. Obesity Rev: Official J Int Assoc Study Obesity. Article CAS Google Scholar. Astrup A, Buemann B, Christensen NJ, Madsen J, Gluud C, Bennett P, et al. The contribution of body composition, substrates, and hormones to the variability in energy expenditure and substrate utilization in premenopausal women. J Clin Endocrinol Metab. CAS PubMed Google Scholar. Lazzer S, Bedogni G, Lafortuna CL, Marazzi N, Busti C, Galli R, et al. Relationship between basal metabolic rate, gender, age, and body composition in 8, white obese subjects. Connolly J, Romano T, Patruno M. Selections from current literature: effects of dieting and exercise on resting metabolic rate and implications for weight management. Fam Pract. Ravussin E, Lillioja S, Anderson TE, Christin L, Bogardus C. Determinants of hour energy expenditure in man. Methods and results using a respiratory chamber. Article CAS PubMed PubMed Central Google Scholar. Goele K, Bosy-Westphal A, Rumcker B, Lagerpusch M, Müller MJ. Influence of changes in body composition and adaptive thermogenesis on the difference between measured and predicted weight loss in obese women. Obesity Facts. Elia M. Organ and tissue contribution to metabolic rate IN Energy metabolism: tissue determinant and cellular corrolaries. New York, NY: Raven Press; Gallagher D, Kelley DE, Thornton J, Boxt L, Pi-Sunyer X, Lipkin E, et al. Changes in skeletal muscle and organ size after a weight-loss intervention in overweight and obese type 2 diabetic patients. Am J Clin Nutr. Bosy-Westphal A, Braun W, Schautz B, Müller MJ. Issues in characterizing resting energy expenditure in obesity and after weight loss. Front Physiol. Müller MJ, Enderle J, Pourhassan M, Braun W, Eggeling B, Lagerpusch M, et al. Metabolic adaptation to caloric restriction and subsequent refeeding: the Minnesota Starvation Experiment revisited. Article PubMed CAS Google Scholar. Müller MJ, Bosy-Westphal A. Adaptive thermogenesis with weight loss in humans. Obesity Silver Spring. Knuth ND, Johannsen DL, Tamboli RA, Marks-Shulman PA, Huizenga R, Chen KY. et al. Metabolic adaptation following massive weight loss is related to the degree of energy imbalance and changes in circulating leptin. PubMed Central Google Scholar. Koehler K, Williams NI, Mallinson RJ, Southmayd EA, Allaway HC, De Souza MJ. Low resting metabolic rate in exercise-associated amenorrhea is not due to a reduced proportion of highly active metabolic tissue compartments. Am J Physiol Endocrinol Metab. Mullur R, Liu YY, Brent GA. Thyroid hormone regulation of metabolism. Physiol Rev. Kosmiski L, Schmiege SJ, Mascolo M, Gaudiani J, Mehler PS. Chronic starvation secondary to anorexia nervosa is associated with an adaptive suppression of resting energy expenditure. Rochon J, Bales CW, Ravussin E, Redman LM, Holloszy JO, Racette SB, et al. Design and conduct of the CALERIE study: comprehensive assessment of the long-term effects of reducing intake of energy. J Gerontol Series A, Biol Sci Med Sci. Metabolic Slowing and Reduced Oxidative Damage with Sustained Caloric Restriction Support the Rate of Living and Oxidative Damage Theories of Aging. Cell Metab. Rickman AD, Williamson DA, Martin CK, Gilhooly CH, Stein RI, Bales CW, et al. Contemporary Clin Trials. Database Submission Form CALERIE: CALERIE; Fothergill E, Guo J, Howard L, Kerns JC, Knuth ND, Brychta R, et al. Tremblay A, Chaput JP. Adaptive reduction in thermogenesis and resistance to lose fat in obese men. Br J Nutr. Das SK, Roberts SB, Bhapkar MV, Villareal DT, Fontana L, Martin CK, et al. Body-composition changes in the Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy CALERIE -2 study: a 2-y randomized controlled trial of calorie restriction in nonobese humans. Bosy-Westphal A, Kossel E, Goele K, Later W, Hitze B, Settler U, et al. Contribution of individual organ mass loss to weight loss-associated decline in resting energy expenditure. Bosy-Westphal A, Reinecke U, Schlorke T, Illner K, Kutzner D, Heller M, et al. Effect of organ and tissue masses on resting energy expenditure in underweight, normal weight and obese adults. Int J Obes Relat Metab Disord. Hayes M, Chustek M, Wang Z, Gallagher D, Heshka S, Spungen A, et al. DXA: potential for creating a metabolic map of organ-tissue resting energy expenditure components. Obes Res. Pourhassan M, Bosy-Westphal A, Schautz B, Braun W, Gluer CC, Müller MJ. Impact of body composition during weight change on resting energy expenditure and homeostasis model assessment index in overweight nonsmoking adults. Camps SG, Verhoef SP, Westerterp KR. Weight loss, weight maintenance, and adaptive thermogenesis. Coutinho SR, With E, Rehfeld JF, Kulseng B, Truby H, Martins C. The impact of rate of weight loss on body composition and compensatory mechanisms during weight reduction: a randomized control trial. Clin Nutr. Hunter GR, Plaisance EP, Fisher G. |
| How to Calculate Your RMR to Help You Lose Weight | Artificial Intelligence Resource Center. Featured Clinical Reviews Screening for Atrial Fibrillation: US Preventive Services Task Force Recommendation Statement JAMA. X Facebook LinkedIn. This Issue. Share X Facebook Email LinkedIn. August 8, Thomas A. Wadden, PhD ; Gary D. Foster ; Kathleen A. Letizia ; et al James L. Mullen, MD. Author Affiliations From the Departments of Psychiatry Dr Wadden, Mr Foster, and Ms Letizia and Surgery Dr Mullen , University of Pennsylvania School of Medicine, Philadelphia. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. To characterize the contributions of the loss of energy-expending tissues and metabolic adaptations to the reduction in resting metabolic rate RMR following weight loss. A secondary analysis was conducted on data from the Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy study. Changes in RMR, body composition, and metabolic hormones were examined over 12 months of calorie restriction in individuals. The contribution of tissue losses to the decline in RMR was determined by weighing changes in the size of energy-expending tissues and organs skeletal muscle, adipose tissue, bone, brain, inner organs, residual mass assessed by dual-energy X-ray absorptiometry with their tissue-specific metabolic rates. Metabolic adaptations were quantified as the remaining reduction in RMR. The loss of skeletal muscle mass 1. During weight loss, tissue loss and metabolic adaptations both contribute to the reduction in RMR, albeit variably. Contrary to popularly belief, it is not skeletal muscle, but rather adipose tissue losses that seem to drive RMR reductions following weight loss. Future research should target personalized strategies addressing the predominant cause of RMR reduction for weight maintenance. Worldwide obesity has tripled in the last decades, with more than 1. With even modest weight reductions eliciting health improvements [ 2 , 3 ], weight loss via the induction of a negative energy balance is encouraged for obesity treatment. Calorie restriction is the most common method for weight loss [ 4 ], and while initially efficacious, prolonged calorie restriction results in attenuated weight loss [ 5 ]. This weight loss attenuation occurs because of reductions in total daily energy expenditure TDEE that oppose the initial energy deficit [ 6 ]. These reductions in TDEE result in a return to energy balance at a lower level, which increases the likelihood of an energy surplus once weight loss efforts have stopped and predisposes individuals to future weight regain [ 7 ]. Although reductions secondary to weight loss have been reported for most components of TDEE [ 8 ], reductions in resting metabolic rate RMR have manifested most consistently [ 9 , 10 ]. Thus, its preservation during weight loss has been targeted as a potential strategy to prevent the compensatory reductions in TDEE and subsequent weight regain [ 13 ]. It has been traditionally assumed that RMR preservation is enhanced when fat-free mass FFM is maintained during weight loss as FFM is considered the primary determinant of RMR [ 14 ]. However, FFM is a heterogeneous tissue [ 16 ], and the extent of the RMR reduction due to FFM loss is largely driven by the size and metabolic activity of the specific tissues that are lost. The brain and other vital organs consume more energy than resting skeletal muscle and bone when expressed relative to their size [ 16 ], yet FFM losses during weight loss are typically limited to skeletal muscle while the vital organs are preserved [ 17 ]. Thus, failure to account for the specific organ composition of FFM loss may result in misestimating RMR reductions due to tissue losses. Further, the contribution of reductions in other tissues outside of FFM secondary to weight loss should be accounted for as well [ 18 ]. Although fat mass, or more specifically adipose tissue, is considered to be relatively inert when compared to other tissues and organs [ 16 ], it is typically lost in much greater quantities [ 15 ] and may still meaningfully contribute to RMR reductions. Yet, even when the contributions of organs and tissues are accounted for, RMR continues to decline beyond what would be expected based on the loss of energy-expending tissues. Müller et al. reported that only about one-third of the RMR reduction following 3 weeks of calorie-restricted weight loss was accounted for by metabolically active tissue, leaving two-thirds of RMR changes unexplained [ 19 ]. This unexplained portion is understood as a reduction in the metabolic activity of the existing remaining tissues [ 20 ], as evident by the close relationship between adaptive reductions in RMR and changes in key hormones involved in energy sensing and metabolism, such as leptin and thyroid hormones [ 20 , 21 , 22 , 23 ]. These metabolic adaptations represent the second important contributor to the reduction in RMR following weight loss and have been observed in prospective studies involving calorie restriction [ 8 , 19 ] as well as in cross-sectional observations in populations with prolonged exposures to chronic energy deficiency [ 22 , 24 ]. While both of these distinct phenomena—the loss of energy-expending tissues and the reduction in the metabolic activity of the remaining tissues—contribute to RMR reduction, it is unclear whether each contributor occurs independently or whether the magnitude of different tissue losses impacts the extent of RMR reductions and metabolic adaptations. The purpose of the present analysis was to quantify the unique contribution of these two components to RMR reduction during prolonged weight loss in healthy normal weight and overweight individuals and their relationship with each other. To address this objective, we retrospectively analyzed data from the Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy CALERIE [ 25 ], a large-scale, randomized-controlled trial. The previously reported variability in changes in body composition and RMR [ 26 ] enabled us to examine the inter-individual variability in the contribution of tissue losses and metabolic adaptations to RMR reduction following weight loss. CALERIE was chosen because it examined long-term weight loss in a free-living study and the design enabled examination of variability in the causes of RMR reductions secondary to weight loss, as well as changes in body composition and hormonal concentrations. All participants signed an informed consent before study participation. Institutional review boards at Pennington Biomedical Research Center, Washington University Medical Center, and Tufts University oversaw the study and the Duke Clinical Research Institute served as the coordinating center [ 25 ]. Dietitians, physicians, and psychologists gave participants individual counseling sessions and an interactive database to support and monitor adherence to calorie restriction prescriptions. Detailed procedures can be found elsewhere [ 25 , 27 ]. The study was registered at clinicaltrials. gov as NCT Data were obtained via download of the publicly available dataset [ 28 ]. Data from baseline, 6 months, and 12 months were chosen for this analysis for several reasons. First, metabolic adaptations are more likely to occur during early weight loss [ 29 , 30 ]. Second, maximal weight loss in the trial was achieved at month 12, with no significant deviations at later time points [ 31 ]. Third, hormonal data, which was needed to confirm the presence of metabolic adaptations, was measured only at baseline and month Finally, later time points at 18 and 24 months had higher attrition. Following initial inclusion, male and female participants 20—50 years of age with a body mass index BMI from 22 to For the purpose of our analysis, participants in the non-restricted control groups were excluded as only minimal weight loss was expected. Further, data from participants without complete baseline or month measurements were excluded. Data used for the present analysis included assessments of body weight, body composition, RMR, and metabolic hormone concentrations. Body weight was assessed every 3 months during a clinical visit using an electric scale Scale Tronix ; Welch Allyn. RMR was measured using indirect calorimetry Vista-MX metabolic cart; Vacumed, Ventura, CA at baseline and months 6 and Metabolic hormones, including insulin, leptin, triiodothyronine T3 , and insulin-like growth factor 1 IGF-1 , were assessed from venous blood samples at baseline and month The extent of changes in RMR attributable to the losses of energy-expending tissues and organs was calculated based on the contribution of the primary organs and tissues contributing to whole-body RMR [ 16 , 32 ]. Organs and tissues used for this calculation included skeletal muscle, adipose tissue, bone, brain, and inner organs heart, liver, kidneys. Residual mass was obtained by subtracting each of the organ and tissue masses from total mass. The size of these organs and tissues were determined as previously reported [ 22 , 33 ]. Skeletal muscle, adipose tissue, bone mass, and brain mass, were assessed from DXA-derived values of lean tissue in the extremities, fat mass, bone mineral content, and skull area, respectively [ 22 , 34 ]. Internal organs weights were calculated from lean body mass in the trunk [ 33 ] Supplementary Table 1. Predicted RMR was calculated as the sum of the metabolic rates of all eight components. This method has previously been used to quantify adaptive reductions in RMR in various weight loss settings [ 32 , 35 ] as well as in chronically energy-deficient populations such as anorexia nervosa patients [ 24 ] and amenorrheic female athletes [ 22 ]. The extent of the metabolic adaptations was subsequently calculated as the difference between changes in measured RMR by indirect calorimetry and changes in predicted RMR [ 32 ]. Statistical analyses were performed with R version 4. Changes in outcomes between baseline and months 6 and 12 were assessed using pairwise, paired T -tests using the Holm—Bonferroni method. To determine how reductions in RMR and metabolic adaptations were related to skeletal muscle and adipose tissue losses, linear regression analyses were conducted between outcomes and changes in measured RMR, changes in RMR due to tissue losses, and metabolic adaptations. Differences in RMR and metabolic adaptations between quartiles were assessed using generalized linear model analyses adjusted for confounders age, sex, body weight, height, initial BMI, body fat percentage , using Q1 as reference quartiles. Body weight declined by 7. No or only minimal changes were observed for brain, inner organ, bone and residual mass Table 2. Left: Changes in body weight closed symbols , skeletal muscle open symbols , and adipose tissue gray symbols over the course of the first 12 months of calorie-restricted weight loss. Right: Changes in measured black bars and predicted white bars resting metabolic rate over the course of the first 12 months of calorie-restricted weight loss. Individual changes in measured RMR, RMR predicted from changes in organ and tissues, and metabolic adaptations are shown in Fig. Contribution of tissue losses and gains gray bars and metabolic adaptations white bars to the individual changes in resting metabolic rate measured by indirect calorimetry black diamond in response to caloric restriction. After stratifying participants into quartiles based on losses in skeletal muscle and adipose tissue mass, there was no discernible difference between changes in measured RMR and the amount of skeletal muscle lost Fig. In Q1, where individuals experienced the greatest loss of skeletal muscle mass 1. Reductions in other organs and tissues accounted for another As a result, the proportion of metabolic adaptations accounting for the overall reduction in RMR increased steadily from Q1 5. Black bars depict changes in RMR measured by indirect calorimetry, dark gray bars depict changes in RMR predicted from skeletal muscle mass top or adipose tissue bottom , light gray bars depict changes in RMR predicted from the other organ and tissues, and white bars depict metabolic adaptations. When dividing participants into quartiles based on adipose tissue losses, the reduction in measured RMR declined as less adipose tissue was lost, as did the reduction in predicted RMR from tissue losses Fig. In individuals with the greatest loss of adipose tissue Q1: 8. The proportion of RMR reduction explained by all tissue and organ losses increased proportionally from Q2 Consequently, metabolic adaptations, which decreased in their contribution to RMR reduction from Q1 There were significant reductions in metabolic hormones after 12 months, with the exception of IGF-1 Fig. The largest decline occurred in leptin, which decreased by Reductions in leptin, trioiodothyronine T3 , insulin, and insulin-like growth factor-1 IGF-1 top left and correlations between leptin top right , insulin bottom left , and T3 bottom right with metabolic adaptations. However, there was substantial variability between participants in RMR changes as well as in the contributions of tissue losses and metabolic adaptations to RMR changes. Upon analysis of tissue-specific weight loss in CALERIE, we observed that the primary components lost during the intervention were skeletal muscle and adipose tissue, while the remaining organs and tissues were largely preserved. The selective loss of these two components aligns with a previous examination of the specific composition of FFM loss during weight loss, which observed no disproportionate loss of high-metabolically active organs when compared to skeletal muscle [ 17 ]. While bone mineral density can be reduced following weight loss, bone mass was not lowered in the present study, which could be attributed to the slow rate of weight loss when compared to more restrictive weight loss reporting bone loss and the provision of calcium supplementation [ 38 ]. Consequently, we stratified participants into quartiles based on skeletal muscle losses, rather than examining it along with the other components of FFM e. The contribution of all tissue losses to the reduction observed in RMR became less prominent in Q2—Q4 of skeletal muscle loss, increasing the contribution of metabolic adaptations to the reduction in RMR across Q2—Q4 despite improved skeletal muscle preservation. However, it is important to note that these studies looked at overall FFM, rather than the specific component that is primarily lost i. Because our approach examined the loss of each tissue and organ, we were able to calculate the direct energy footprint associated with the loss of each tissue. When taking its lower tissue-specific energy expenditure relative to the other higher expenditure components of FFM into account, it is therefore not surprising that skeletal muscle losses did not explain all RMR reductions. RMR reductions secondary to metabolic adaptations have been frequently observed after weight loss [ 19 , 29 , 30 , 40 , 41 ], and are understood as a sign of the suppression of non-vital processes to decrease energy expenditure, which ultimately attenuates weight loss [ 42 , 43 ]. Using the same method, Müller et al. Our analysis further indicated that the extent of metabolic adaptations in the present study was strongly related to the amount of adipose tissue lost. This positive association between adipose loss and metabolic adaptations is in agreement with previous studies in individuals with obesity undergoing gastric bypass surgery or an intensive weight loss program [ 21 ]. Yet the extent of metabolic adaptations appeared to be commensurate to adipose tissue losses. To further corroborate the presence of metabolic adaptations, the extent of metabolic adaptations in our sample was strongly correlated to changes in circulating concentrations of the key energy-sensing hormones leptin and T3. While confirming the associative nature of reductions in metabolic hormones and metabolic adaptations, our data are strengthened by findings that exogenous administration of leptin and T3 at least partially reverse reductions in energy expenditure following weight loss [ 44 ]. However, it remains to be tested whether metabolic hormone replacement attenuates adaptive reductions in the metabolic activity of the remaining tissues and organs, which could make it an interesting strategy to combat the metabolic adaptations leading to RMR reduction. Despite multiple literature reports of metabolic adaptations following weight loss, it is important to note that there is no gold standard method for its direct measurement. Metabolic adaptations represent the difference between measured and predicted RMR. To optimize its quantification, we utilized DXA data, which enabled more specific quantification of energy-expending tissues and organs to improve the prediction of RMR [ 34 ]. The equations and coefficients used in the present study were previously established and validated in examinations of underweight, normal weight, and individuals with obesity [ 33 ] across adulthood [ 45 ], in several weight-loss settings [ 32 , 35 ], and for the quantification of metabolic adaptations in non-obese men [ 19 ]. While some of these studies estimated inner organ masses using magnetic resonance imaging, we remain confident that this present method of calculating metabolic adaptations was able to effectively compare the extent of metabolic adaptations across the intervention. While the present analysis describes the contribution of changes in energy-expending tissues and organs and metabolic adaptations to the reduction in RMR in a large caloric restriction trial, it was conducted in non-obese individuals, whose weight loss requirements are not the same as individuals with obesity. However, given that changes in non-adipose tissues tend to be greater in leaner individuals [ 46 ], the non-obese study population allowed us to examine a wider spectrum of body composition changes and ascertain how their contribution to RMR reductions during weight loss varies depending on whether they are lost or preserved. Further, the way in which caloric restriction was attained was not tightly controlled. However, our analysis focused on the two additive components of RMR reduction occurring secondary to weight loss, irrespective of how weight loss was achieved. Our analysis demonstrates that RMR is inevitably reduced after weight loss in healthy normal weight and overweight individuals and that this reduction occurs through a combination of the loss of energy-expending tissues and metabolic adaptations. More importantly, the contribution of tissue losses and metabolic adaptations to overall RMR reduction was highly variable between individuals. Contrary to common belief, there was no discernible relationship between the loss of skeletal muscle, the primary lean tissue component that is lost during weight loss, and reductions in RMR. Conversely, the loss of adipose tissue was related to reductions in RMR and metabolic adaptations, whereby metabolic adaptations were greatest in individuals who lost the most adipose tissue. Given the differential impact of these components to RMR reduction following weight loss, future research should examine whether the preservation of the tissues or their metabolic activity yields differential results toward RMR reductions and weight maintenance and whether more personalized strategies addressing the specific cause of the RMR reduction may help maximize weight loss and prevent weight regain. WHO WHO. To stay unbiased we show no ads, sell no physical products, and take no money from the industry. We're fully funded by the people, via an optional membership. Most information at Diet Doctor is free forever. Read more about our policies and work with evidence-based guides , nutritional controversies , our editorial team , and our medical review board. Should you find any inaccuracy in this guide, please email andreas dietdoctor. PLoS One Metabolic and behavioral compensations in response to caloric restriction: implications for the maintenance of weight loss [randomized trial; moderate evidence]. Asia Pacific Journal of Clinical NUtrition New approach for weight reduction by a combination of diet, light resistance exercise and the timing of ingesting a protein supplement [randomized trial; moderate evidence]. JAMA Effect of dietary protein content on weight gain, energy expenditure, and body composition during overeating: a randomized controlled trial [randomized trial; moderate evidence]. Nutrition and Metabolism A high-protein diet for reducing body fat: mechanisms and possible caveats [overview article; ungraded]. Nutrition and Metabolism Resting metabolic rate of obese patients under very low calorie ketogenic diet [non-controlled study; weak evidence]. Journal of Clinical Endocrinology and Metabolism Body composition changes after very-low-calorie ketogenic diet in obesity evaluated by 3 standardized methods [non-controlled study; weak evidence]. On average, the low-carb group burned about more calories per day than the high-carb group. PLoS One Hunter-Gatherer Energetics and Human Obesity [non-controlled study; weak evidence]. Maintaining a calorie deficit may be important for weight loss, but it definitely is not the only important consideration. We suggest you also need to maintain muscle mass and pay attention to the other components of healthy weight loss. You can read more in our dedicated guide on healthy weight loss. Annals of Behavioral Medicine Small changes in nutrition and physical activity promote weight loss and maintenance: 3-month evidence from the ASPIRE randomized trial [randomized trial; moderate evidence]. International Journal of Behavioral Medicine The association between rate of initial weight loss and long-term success in obesity treatment: does slow and steady win the race? Low carb for beginners All guides Foods Visual guides Side effects Meal plans. Keto for beginners All guides Foods Visual guides Side effects Meal plans. What are high protein diets? Foods Snacks Meal plans. Higher-satiety eating High-satiety foods Satiety per calorie Satiety score Meal plans. Weight loss. Meal plans. My meal plans Premium. High protein. All low carb meal plans. Intermittent fasting. Quick and easy. Family friendly. World cuisine. |
| We Care About Your Privacy | Am J Clin Mutr — Google Scholar RMR and dieting Maintaining youthfulness naturally Contribution of decreased RRMR mass to diminished thermic effect of Conquer late-night cravings anf reduced-obese men. Author information Authors and Anr Department of Education, University of Vermont, Burlington, Vermont, USA Douglas L. Here are some easy ways to increase your RMR and supercharge your weight loss. Ravussin E, Lillioja S, Anderson TE, Christin L, Bogardus C. CAS PubMed Google Scholar Rosenbaum M, Goldsmith RL, Haddad F, Baldwin KM, Smiley R, Gallagher D, et al. Supplementary Figure 2. |
RMR and dieting -
FT3: free triiodothyronine; FT4: tyroxine. To the best of our knowledge this study is the first assessing the effect of VLCK-diet on the RMR of obese patients.
The main findings of this work were: 1 the rapid and sustained weight reduction induced by the VLCK-diet did not induce the expected drop in RMR, 2 this observation was not due to a sympathetic tone counteraction through the increase of either catecholamines, leptin or thyroid hormones, 3 the most plausible cause of the null reduction of RMR is the preservation of lean mass muscle mass observed with this type of diet.
The greatest challenge in obesity treatment is to avoid weight recovery sometime after the previous reduction. In fact, after one or few years the most obese patients recover or even increase their weight, previously reduced by either, dietetic, pharmacological or behavioral treatments [ 8 ], bariatric surgery being the only likely exception [ 7 ].
Since obesity reduction is accompanied by a slowing of energy expenditure in sedentary individuals, mostly RMR, this fact has been blamed for this negative outcome of the diet-based treatments [ 12 ]. Therefore any RMR reduction after treatment, translates in a large impact on energy balance, making subjects more prone to weight regain over time [ 17 ].
This phenomenon was called metabolic adaptation or adaptive thermogenesis, indicating that RMR is reduced after weight loss, and furthermore that this reduction is usually larger than expected or out of proportion with the decrease in fat or fat free mass [ 2 ].
Therefore, preservation of initial RMR after weight loss could play a critical role in facilitating further weight loss and preventing weight regain in the long-term [ 4 ].
We have observed that the obesity-reduction by a VLCK-diet Pnk method ® was maintained 1 and 2 years after its completion [ 10 , 11 ]. Although that follow up was not long enough, the finding may be of particular importance for long-term effects. The present work shows that in a group of obese patients treated with a VLCK-diet, the RMR was relatively preserved, remaining within the expected limits for the variations in FFM, and avoided the metabolic adaptation phenomenon.
Because FFM includes total body water, bone minerals and protein [ 14 ], the results were corroborated by analyzing the FFM without bone minerals and total body water muscle mass. As the mechanisms supporting the metabolic adaptation phenomenon are not known, unraveling the reasons behind the present findings is challenging enough in itself.
Changes in any circulating hormone that participate in thermogenesis could be the explanation for the absence of a reduction in RMR, for example a concomitant increase in the sympathetic system activity, either directly or indirectly.
An increase in thyroid hormones generated by the VLCK-diet was discarded because free T3 experienced the well described reduction after losing weight [ 20 , 24 ] without alterations in free T4 or TSH. As thermogenesis in humans is largely a function of the sympathetic nervous system activity, and that activity decreases in response to weight loss the results here reported may be the net result of a maintenance or relative increase in the plasma catecholamine levels.
However, it was found that adrenaline and dopamine remained unchanged throughout the study, while noradrenaline decreased considerably discarding their contribution to any increase in the activity of the autonomic nervous system.
Leptin experienced a rapid decline in circulation in situations of weight reduction, although the reduction is observed in energy restriction states it occurs before any change in body weight [ 8 ].
On the other hand, leptin positively has been associated with sympathetic nervous system activity in humans, and weight loss associated changes in RMR and fat oxidation were previously related to leptin levels changes [ 25 ].
If leptin is sensitive to the energy flux and activate the autonomic nervous system, the absence of metabolic adaptation here observed could be due to a leptin increase, or maintenance in the basal levels.
However, in this work, leptin levels decreased in accordance to the weight reduction. Then, an expected increase in thyroid hormones, catecholamines, or leptin levels was discarded as explanation for the observed minor or absent reduction in RMR.
This was also endorsed by the undertook multiple regression analysis Table 3. In this analysis only the FFM DXA or the muscle mass MF-BIA appear as a plausible explanation for the maintenance of RMR activity. In fact, a clear preservation of FFM was reported in obese subjects on VLCK-diet, in whom 20 kg reduction after 4 months of treatment was accompanied by less than 1 kg of muscle mass lost [ 6 ].
The assumption of muscle mass preservation is also supported by the data on kidney function Table 2 which shows that not only was renal activity not altered as reported in other studies [ 23 ] but that even the nitrogen balance was positive.
The strength of this study is its longitudinal design, which allows the evaluation of the time-course of changes of RMR during a VLCK diet, by comparing each subject to himself, as his own control.
The scarce number of subjects and the short duration of this study might be a limitation, since one cannot make claims regarding the RMR status long-term after the completion of the VLCK diet.
However, no significant variations in body weight had been observed after 4 months in previous studies [ 10 , 11 ]. In addition, although participants were instructed to exercise on a regular basis using a formal exercise program, we could not verify adherence to this instruction which precludes determining whether changes in physical activity patterns affected study outcomes.
In the current work a portable device that allows for easier measurement of RMR and with lower cost was employed. This approach may lead to errors when compared with the gold standard, Deltatrac, but it is an easy-to-use metabolic system for determining RMR and VO2 in clinical practice with a better accuracy than predictive eqs.
The Deltatrac device is expensive and requires careful calibration. The Fitmate has been previously validated as a suitable alternative to the traditional indirect calorimetry by both in-house analysis Additional file 1 : Figure S1 , as well as by previous studies.
Despite not measuring CO2 production it is a very convenient in the clinical setting assuming a minimal error of analysis. In summary, this study shows that the treatment of obese patients with a VLCK-diet favors the maintenance of RMR within the expected range for FFM changes and avoids the metabolic adaptation phenomenon.
This finding might explain the long-term positive effects of VLCK-diets on weight loss. Although, the mechanisms by which this effect could be justified are unclear, classical determinants of the energy expenditure, as thyroid hormones, catecholamines as well as leptin were discarded.
The relative good preservation of FFM muscle mass observed with this dietetic approach could be the cause for the absence of metabolic adaptation. Black AE, Coward WA, Cole TJ, Prentice AM. Human energy expenditure in affluent societies: an analysis of doubly-labelled water measurements.
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Annu Rev Nutr. Download references. We would like to thank A. Menarini Diagnostics Spain for providing free of charge the portable ketone meters for all the patients. We acknowledge the PronoKal Group ® for providing the diet for all the patients free of charge and for support of the study.
The funding source had no involvement in the study design, recruitment of patients, study interventions, data collection, or interpretation of the results.
The Pronokal personnel IS was involved in the study design and revised the final version of the manuscript, without intervention in the analysis of data, statistical evaluation and final interpretation of the results of this study.
The datasets used during the current study are available from the corresponding author on reasonable request. D G-A, ABC ad FFC designed and performed the experiments, analyzed the data and wrote the manuscript.
AIC, MAM-O, AC, LO-M, IS were responsible of the conduct and monitoring of the nutritional intervention. CG, DB participated in the study design and coordination and helped to draft the manuscript.
FFC supervised the research and reviewed the manuscript throught the study. All authors read and approved the final manuscript. Diego Gomez-Arbelaez, Ana B. Crujeiras, Ana I. Castro, Miguel A.
Medical Department Pronokal, Pronokal Group, Barcelona, Spain. Intensive Care Division, Complejo Hospitalario Universitario de Santiago CHUS , Santiago de Compostela, Spain. Division of Endocrinology, Complejo Hospitalario Universitario de Ferrol and Coruña University, Ferrol, Spain.
CIBER de Fisiopatologia de la Obesidad y Nutricion CIBERobn , Instituto Salud Carlos III, Santiago de Compostela, Spain. Ana B. You can also search for this author in PubMed Google Scholar. Correspondence to Felipe F. DB, ABC and FFC received advisory board fees and or research grants from Pronokal Protein Supplies Spain.
IS is Medical Director of Pronokal Spain SL. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Figure S1. Nutritional intervention program and schedule of visits. Visit C-4 was performed at the end of the study according to each case, once the patient achieved the target weight or maximum at 4 months of follow-up.
PDF kb. Figure S2. PDF 11 kb. Table S1. Independent effects of fat-free mass, free triiodothyronine, catecholamines, leptin and β-hydroxy-butyrate on resting metabolic rate at each visit. DOCX 32 kb.
Open Access This article is distributed under the terms of the Creative Commons Attribution 4. Reprints and permissions. Gomez-Arbelaez, D. et al. Resting metabolic rate of obese patients under very low calorie ketogenic diet. Nutr Metab Lond 15 , 18 Download citation. Received : 21 September Accepted : 29 January Published : 17 February Anyone you share the following link with will be able to read this content:.
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Download PDF. Download ePub. Research Open access Published: 17 February Resting metabolic rate of obese patients under very low calorie ketogenic diet Diego Gomez-Arbelaez 1 , Ana B. Crujeiras ORCID: orcid. Castro 1 , 5 , Miguel A. Abstract Background The resting metabolic rate RMR decrease, observed after an obesity reduction therapy is a determinant of a short-time weight regain.
Method From 20 obese patients who lost Conclusion The rapid and sustained weight and FM loss induced by VLCK-diet in obese subjects did not induce the expected reduction in RMR, probably due to the preservation of lean mass.
Trial registration This is a follow up study on a published clinical trial. Background It is widely accepted that during periods of energy deficit or restriction eg. Methods Study population This is a follow up study on a published clinical trial [ 6 ].
Nutritional intervention All the patients followed a VLCK diet according to a commercial weight loss program PNK method® , which includes lifestyle and behavioral modification support.
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Download references. Department of Education, University of Vermont, Burlington, Vermont, USA. You can also search for this author in PubMed Google Scholar. Reprints and permissions. Ballor, D. Eur J Appl Physiol 71 , — Download citation. Accepted : 22 January Issue Date : November Anyone you share the following link with will be able to read this content:.
Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Abstract A meta-analysis was used to examine the independent and interactive effects of dietary restriction, endurance exercise training and gender on resting metabolic rate RMR.
Access this article Log in via an institution. References Ballor DL Exercise training elevates RMR during moderate but not severe dietary restriction in obese male rats. J Appl Physiol — Google Scholar Ballor DL, Keesey RE A meta-analysis of the factors affecting exercise-induced changes in body mass, fat mass and fat-free mass in males and females.
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Figuring out your basal metabolic Ddieting with annd formula or online Beetroot juice and brain health can help you determine the RMR and dieting deficit needed to help you shed dieging. The number of calories you need just for your RMR and dieting to anx is called your basal Fueling for strength gains rate, or Anr. If you know your BMR, you can better determine your caloric needs for healthy weight loss. You burn most of your daily calories with zero effort, movement, or even thinking. The calories used to maintain these basic bodily functions add up to your BMR. BMR — which is often used interchangeably with resting metabolic rate, or RMR more on that later — is one of many factors in the total number of calories you burn in a given day, also called your total daily energy expenditure TDEE. It accounts for roughly 60 to 75 percent of your TDEE, according to the National Academy of Sports Medicine NASM.
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