high amounts of fatty acids are broken down and subsequently flood the mitochondria. These ketone bodies are rich in energy and the preferred source of energy for people following low-carb, ketogenic, and zero carb diets. Since most people entering the fitness space are wanting to lose fat, it would make sense to discuss what things we can do to enhance fat oxidation and accelerate fat loss.

One of these ways is by reducing caloric expenditure, i. creating a calorie deficit. This is why in order to lose fat, cutting calories is one of the main things you have to do.

Weight loss ultimately boils down to energy balance in the body, i. calories in vs calories out. Earlier in this article, we discussed the importance of hormone-sensitive lipase in the liberating of stored fatty acids from adipose tissue.

Insulin is the hormone in your body that is responsible for driving nutrients into your cells, including muscle and fat cells, which can then be used for energy production. The main macronutrient that causes insulin levels to rise is carbohydrates and seeing that insulin effectively shuts off the fat burning process, maintaining low levels of insulin is essential to maximizing fat burning.

This is why so many ketogenic, low carb, no carb diets restrict carbohydrate intake. You can still have your carbs and burn body fat, but it requires some proper nutritional selections on your part.

Simple sugars create larger insulin spikes in the body than complex carbohydrates or protein. As we stated above, increasing your calories out is one of the ways you can tip energy balance in favor of fat loss. This, of course, is accomplished through exercise, and we can maximize fat burning by performing the right types of exercise.

Science has pretty clearly shown that during exercise, your muscles can use both dietary carbohydrate and fat operate as substrates used for energy. Your body has a finite amount of glycogen stored in the muscle. Once these stores are exhausted, the body will start pulling from your fat stores for energy.

Low to moderate intensity forms of exercise primarily use fat as their source of energy. The higher you go with exercise intensity, the more you shift to burning glycogen and glucose.

The longer you train, the more you deplete glycogen and once those stores are depleted, you will switch to burning fat for fuel. Additionally, the more fit you are, the lower your resting insulin levels will be, thus allowing you to burn more fat outside of your eating windows.

Due to these factors, you can begin to understand why most fasted cardio sessions are performed at a relatively low intensity -- it maximizes fat burning in the body. The oxygen deficit created by high-intensity forms of training such as weight lifting or interval training leads to greater overall calorie burning as your body works to restore homeostasis.

The point of this is to say that both steady-state and high-intensity interval training can be used to lose body fat. The mechanisms by which they work are different, but the end result is the same.

Fat burning is a billion-dollar industry, yet very few people actually understand the theory and science of what it takes to burn fat, and even fewer know how to apply it to daily life. And, if you need some help burning extra calories and shifting your body towards a greater fat burning environment, check out Steel Sweat.

Steel Sweat is the ideal pre-workout for fasted training. Not only does it include ingredients such as caffeine which help release fatty acids to be burned for energy it also includes several pro-fat burning compounds, such as L-Carnitine L-Tartrate and Paradoxine, which take those liberated fatty acids and burn them for energy.

The Complete Guide to Thermogenesis. How Nutrients Get Absorbed into Muscles. Close 🍪 Cookie Policy We use cookies and similar technologies to provide the best experience on our website. ANP, atrial natriuretic peptide; FFAs, free fatty acids; SAT, subcutaneous adipose tissue; VAT, visceral adipose tissue.

Abildgaard, J. Menopause is associated with decreased whole body fat oxidation during exercise. doi: PubMed Abstract CrossRef Full Text Google Scholar. Brooks, G.

Chronicle of the Institute of Medicine physical activity recommendation: how a physical activity recommendation came to be among dietary recommendations. Buemann, B. Metabolism 43, — Google Scholar. Coelho, M. Biochemistry of adipose tissue: an endocrine organ. Davitt, P. Postprandial triglyceride and free fatty acid metabolism in obese women after either endurance or resistance exercise.

Donnelly, J. Appropriate physical activity intervention strategies for weight loss and prevention of weight regain for adults. Sports Exerc. Ebbert, J. Fat depots, free fatty acids, and dyslipidemia. Nutrients 5, — CrossRef Full Text Google Scholar.

Fox, C. Abdominal visceral and subcutaneous adipose tissue compartments: association with metabolic risk factors in the Framingham Heart Study. Circulation , 39— Gonzalez-Gil, A. The role of exercise in the interplay between myokines, hepatokines, osteokines, adipokines, and modulation of inflammation for energy substrate redistribution and fat mass loss: a review.

Nutrients Hargreaves, M. Skeletal muscle energy metabolism during exercise. Haufe, S. Determinants of exercise-induced fat oxidation in obese women and men. Holloszy, J. Regulation of carbohydrate and fat metabolism during and after exercise.

Horowitz, J. Whole body and abdominal lipolytic sensitivity to epinephrine is suppressed in upper body obese women.

Isacco, L. Hackney Chapel Hill, NC: Springer Nature , 35— Fat mass localization alters fuel oxidation during exercise in normal weight women. Gender-specific considerations in physical activity, thermogenesis and fat oxidation: implications for obesity management.

Effects of adipose tissue distribution on maximum lipid oxidation rate during exercise in normal-weight women. Diabetes Metab. Jensen, M. Lipolysis: contribution from regional fat. Influence of body fat distribution on free fatty acid metabolism in obesity.

Jeukendrup, A. Regulation of fat metabolism in skeletal muscle. Jocken, J. Catecholamine-induced lipolysis in adipose tissue and skeletal muscle in obesity. Johnson, L. Substrate utilization during exercise in postmenopausal women on hormone replacement therapy.

Kanaley, J. Abdominal fat distribution in pre- and postmenopausal women: the impact of physical activity, age, and menopausal status. Metabolism 50, — Substrate oxidation during acute exercise and with exercise training in lean and obese women. Kelley, D. Skeletal muscle fat oxidation: timing and flexibility are everything.

Lange, K. Subcutaneous abdominal adipose tissue lipolysis during exercise determined by arteriovenous measurements in older women. Lovejoy, J. Increased visceral fat and decreased energy expenditure during the menopausal transition.

Maillard, F. Effect of high-intensity interval training on total, abdominal and visceral fat mass: a meta-analysis.

Sport Med. Manolopoulos, K. Gluteofemoral body fat as a determinant of metabolic health. Martin, M. Effects of body fat distribution on regional lipolysis in obesity.

Mauriège, P. Regional differences in adipose tissue metabolism between sedentary and endurance-trained women. Melanson, E. When energy balance is maintained, exercise does not induce negative fat balance in lean sedentary, obese sedentary, or lean endurance-trained individuals.

Exercise improves fat metabolism in muscle but does not increase h fat oxidation. Sport Sci. Nicklas, B. Visceral adiposity is associated with increased lipid oxidation in obese, postmenopausal women. Visceral adiposity, increased adipocyte lipolysis, and metabolic dysfunction in obese postmenopausal women.

Exercise blunts declines in lipolysis and fat oxidation after dietary-induced weight loss in obese older women. Numao, S. Sex differences in substrate oxidation during aerobic exercise in obese men and postmenopausal obese women.

Metabolism 58, — Effects of obesity phenotype on fat metabolism in obese men during endurance exercise. Ormsbee, M. Regulation of fat metabolism during resistance exercise in sedentary lean and obese men. Petridou, A.

Exercise in the management of obesity. Metabolism 92, — Power, M. Sex differences in fat storage, fat metabolism, and the health risks from obesity: possible evolutionary origins.

Ravussin, E. Metabolic predictors of obesity: cross-sectional versus longitudinal data. Reynisdottir, S. Effects of weight reduction on the regulation of lipolysis in adipocytes of women with upper-body obesity. Romijn, J.

Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. After exercise and upon recovery in the fasted state, however, we observed an increase in IHL [ 41 ].

Additionally, IHL increases upon an exercise bout in active lean participants who consumed a light meal before the start of the exercise [ 52 ]. Interestingly, in both studies [ 41 , 52 ], increased IHL content after exercise occurred in the presence of elevated plasma NEFA levels.

If this rise in plasma NEFAs is prevented by providing a glucose drink every half hour during and after exercise, IHL does not increase. This indicates that the rise in plasma NEFA levels upon exercise drives the increased IHL content after an exercise bout.

IHL can be used during exercise, upon secretion of VLDL-triacylglycerols into the bloodstream. VLDL-triacylglycerol kinetic analyses during an acute exercise bout in the fasted state show that VLDL-triacylglycerol secretion rates drop during exercise and that the contribution of these particles to total energy expenditure is decreased [ 53 ].

Thus, besides the increase in NEFA influx, the lower VLDL-triacylglycerol secretion rates during exercise may also contribute to the increase in IHL content after acute exercise in the fasted state Fig.

In lean, normoglycaemic but insulin-resistant individuals, postprandial IHL synthesis and de novo lipogenesis is lower after a single bout of exercise compared with rest [ 54 ].

Overall, IHL may increase upon acute exercise, but is lower after training, possibly due to lower postprandial de novo lipogenesis during recovery. It is also lower in endurance-trained individuals.

It is currently unknown how the apparent increase in IHL after acute exercise turns into reduced IHL content after endurance training. We cannot exclude that training, per se, is not the major determinant of IHL but that the dietary habits of trained individuals may also make an important contribution.

IMCL and IHL content are increased, and fat oxidative capacity decreased in metabolically compromised individuals, such as obese individuals and those with type 2 diabetes. While endurance exercise training reduces total intracellular fat content in the liver, the effects in muscle indicate remodelling rather than lowering of the myocellular lipid droplet pool.

In fact, in most populations and under most conditions, endurance exercise training augments IMCL content. Thus, the ability of exercise to modulate lipid droplet dynamics in the liver and muscle contributes to differences in fat oxidative metabolism. Endurance training in individuals with type 2 diabetes remodels IMCL content towards an athlete-like phenotype, while IHL content is reduced.

While many training intervention studies have been performed in metabolically compromised individuals, the effects of acute exercise have not been extensively studied, particularly not in participants with type 2 diabetes.

Thus, it is unclear why IMCL utilisation during exercise is lower in individuals with type 2 diabetes and whether the observed IMCL remodelling towards the athlete-like phenotype in these individuals also translates into the anticipated increase in IMCL utilisation during exercise.

Study findings on the effects of sex differences and exercise intensity on IMCL use during exercise or lipid droplet remodelling upon training are either contradictory or lacking. Compared with skeletal muscle, the underlying mechanisms of the effects of exercise and training on IHL are even more poorly understood.

The reduction in IHL content upon training that is observed in metabolically compromised individuals may partly originate from reduced postprandial de novo lipogenesis.

Since diurnal rhythms are present in lipid metabolism, future studies should also focus on the effect of timing of exercise on the parameters discussed in this review in order to elucidate the optimal conditions for exercise-induced improvements in insulin sensitivity in individuals with type 2 diabetes.

Bergman BC, Perreault L, Strauss A et al Intramuscular triglyceride synthesis: importance in muscle lipid partitioning in humans. Am J Physiol Endocrinol Metab 2 :E—E Article CAS PubMed Google Scholar.

Kiens B Skeletal muscle lipid metabolism in exercise and insulin resistance. Physiol Rev 86 1 — van Loon LJ, Greenhaff PL, Constantin-Teodosiu D, Saris WH, Wagenmakers AJ The effects of increasing exercise intensity on muscle fuel utilisation in humans.

J Physiol 1 — Article PubMed PubMed Central Google Scholar. Goodpaster BH, He J, Watkins S, Kelley DE Skeletal muscle lipid content and insulin resistance: evidence for a paradox in endurance-trained athletes. J Clin Endocrinol Metab 86 12 — Mol Metab — Article CAS PubMed PubMed Central Google Scholar.

Gemmink A, Daemen S, Brouwers B et al Dissociation of intramyocellular lipid storage and insulin resistance in trained athletes and type 2 diabetes patients; involvement of perilipin 5? J Physiol 5 — Boon H, Blaak EE, Saris WH, Keizer HA, Wagenmakers AJ, van Loon LJ Substrate source utilisation in long-term diagnosed type 2 diabetes patients at rest, and during exercise and subsequent recovery.

Diabetologia 50 1 — Chee C, Shannon CE, Burns A et al Relative contribution of intramyocellular lipid to whole-body fat oxidation is reduced with age but subsarcolemmal lipid accumulation and insulin resistance are only associated with overweight individuals. Diabetes 65 4 — van Loon LJ, Manders RJ, Koopman R et al Inhibition of adipose tissue lipolysis increases intramuscular lipid use in type 2 diabetic patients.

Diabetologia 48 10 — Gemmink A, Goodpaster BH, Schrauwen P, Hesselink MKC Intramyocellular lipid droplets and insulin sensitivity, the human perspective. Biochim Biophys Acta Mol Cell Biol Lipids 10 Pt B — Nielsen J, Mogensen M, Vind BF et al Increased subsarcolemmal lipids in type 2 diabetes: effect of training on localization of lipids, mitochondria, and glycogen in sedentary human skeletal muscle.

Am J Physiol Endocrinol Metab 3 :E—E Feng YZ, Lund J, Li Y et al Loss of perilipin 2 in cultured myotubes enhances lipolysis and redirects the metabolic energy balance from glucose oxidation towards fatty acid oxidation.

J Lipid Res 58 11 — Covington JD, Noland RC, Hebert RC et al Perilipin 3 differentially regulates skeletal muscle lipid oxidation in active, sedentary and type 2 diabetic males.

J Clin Endocrinol Metab 10 — Shepherd SO, Cocks M, Tipton KD et al Sprint interval and traditional endurance training increase net intramuscular triglyceride breakdown and expression of perilipin 2 and 5.

J Physiol 3 — Shepherd SO, Cocks M, Tipton KD et al Preferential utilization of perilipin 2-associated intramuscular triglycerides during 1 h of moderate-intensity endurance-type exercise. Exp Physiol 97 8 — Koh HE, Nielsen J, Saltin B, Holmberg HC, Ortenblad N Pronounced limb and fibre type differences in subcellular lipid droplet content and distribution in elite skiers before and after exhaustive exercise.

J Physiol 17 — Shaw CS, Jones DA, Wagenmakers AJ Network distribution of mitochondria and lipid droplets in human muscle fibres. Histochem Cell Biol 1 — Gemmink A, Daemen S, Kuijpers HJH et al Super-resolution microscopy localizes perilipin 5 at lipid droplet-mitochondria interaction sites and at lipid droplets juxtaposing to perilipin 2.

Biochim Biophys Acta Mol Cell Biol Lipids 11 — Bleck CKE, Kim Y, Willingham TB, Glancy B Subcellular connectomic analyses of energy networks in striated muscle.

Nat Commun 9 1 Benador IY, Veliova M, Mahdaviani K et al Mitochondria bound to lipid droplets have unique bioenergetics, composition, and dynamics that support lipid droplet expansion. Cell Metab 27 4 — Devries MC, Samjoo IA, Hamadeh MJ et al Endurance training modulates intramyocellular lipid compartmentalization and morphology in skeletal muscle of lean and obese women.

J Clin Endocrinol Metab 98 12 — Samjoo IA, Safdar A, Hamadeh MJ et al Markers of skeletal muscle mitochondrial function and lipid accumulation are moderately associated with the homeostasis model assessment index of insulin resistance in obese men.

PLoS One 8 6 :e Devries MC, Lowther SA, Glover AW, Hamadeh MJ, Tarnopolsky MA IMCL area density, but not IMCL utilization, is higher in women during moderate-intensity endurance exercise, compared with men. Am J Physiol Regul Integr Comp Physiol 6 :R—R Devries MC Sex-based differences in endurance exercise muscle metabolism: impact on exercise and nutritional strategies to optimize health and performance in women.

Exp Physiol 2 — Article PubMed Google Scholar. Meex RC, Schrauwen-Hinderling VB, Moonen-Kornips E et al Restoration of muscle mitochondrial function and metabolic flexibility in type 2 diabetes by exercise training is paralleled by increased myocellular fat storage and improved insulin sensitivity.

Diabetes 59 3 — Kelley DE, He J, Menshikova EV, Ritov VB Dysfunction of mitochondria in human skeletal muscle in type 2 diabetes. Diabetes 51 10 — Phielix E, Schrauwen-Hinderling VB, Mensink M et al Lower intrinsic ADP-stimulated mitochondrial respiration underlies in vivo mitochondrial dysfunction in muscle of male type 2 diabetic patients.

Diabetes 57 11 — De Feyter HM, van den Broek NM, Praet SF, Nicolay K, van Loon LJ, Prompers JJ Early or advanced stage type 2 diabetes is not accompanied by in vivo skeletal muscle mitochondrial dysfunction.

Eur J Endocrinol 5 — Pino MF, Stephens NA, Eroshkin AM et al Endurance training remodels skeletal muscle phospholipid composition and increases intrinsic mitochondrial respiration in men with type 2 diabetes. Physiol Genomics 51 11 — Bruce CR, Thrush AB, Mertz VA et al Endurance training in obese humans improves glucose tolerance and mitochondrial fatty acid oxidation and alters muscle lipid content.

Am J Physiol Endocrinol Metab 1 :E99—E Schrauwen P, van Aggel-Leijssen DP, Hul G et al The effect of a 3-month low-intensity endurance training program on fat oxidation and acetyl-CoA carboxylase-2 expression.

Diabetes 51 7 — He J, Goodpaster BH, Kelley DE Effects of weight loss and physical activity on muscle lipid content and droplet size. Obes Res 12 5 — Shepherd SO, Cocks M, Meikle PJ et al Lipid droplet remodelling and reduced muscle ceramides following sprint interval and moderate-intensity continuous exercise training in obese males.

Int J Obes 41 12 — Article CAS Google Scholar. Tarnopolsky MA, Rennie CD, Robertshaw HA, Fedak-Tarnopolsky SN, Devries MC, Hamadeh MJ Influence of endurance exercise training and sex on intramyocellular lipid and mitochondrial ultrastructure, substrate use, and mitochondrial enzyme activity.

Am J Physiol Regul Integr Comp Physiol 3 :R—R Van Proeyen K, Szlufcik K, Nielens H et al High-fat diet overrules the effects of training on fiber-specific intramyocellular lipid utilization during exercise. J Appl Physiol 1 — Koh HE, Ortenblad N, Winding KM, Hellsten Y, Mortensen SP, Nielsen J High-intensity interval, but not endurance, training induces muscle fiber type-specific subsarcolemmal lipid droplet size reduction in type 2 diabetic patients.

Am J Physiol Endocrinol Metab 5 :E—E Van Proeyen K, Szlufcik K, Nielens H, Ramaekers M, Hespel P Beneficial metabolic adaptations due to endurance exercise training in the fasted state.

Louche K, Badin PM, Montastier E et al Endurance exercise training up-regulates lipolytic proteins and reduces triglyceride content in skeletal muscle of obese subjects. Peters SJ, Samjoo IA, Devries MC, Stevic I, Robertshaw HA, Tarnopolsky MA Perilipin family PLIN proteins in human skeletal muscle: the effect of sex, obesity, and endurance training.

Appl Physiol Nutr Metab 37 4 — Shaw CS, Shepherd SO, Wagenmakers AJ, Hansen D, Dendale P, van Loon LJ Prolonged exercise training increases intramuscular lipid content and perilipin 2 expression in type I muscle fibers of patients with type 2 diabetes.

Am J Physiol Endocrinol Metab 9 :E—E Bilet L, Brouwers B, van Ewijk PA et al Acute exercise does not decrease liver fat in men with overweight or NAFLD. Sci Rep 5 1

Fat max values were also significantly higher on the treadmill Exercising on a treadmill maximizes fat oxidation to a greater extent than elliptical and rowing exercises, and remains an important exercise modality to improve fat oxidation, and consequently, cardio-metabolic health.

Key Points The ability to oxidize fat has been associated with improved oxidative enzymes activity and mitochondrial biogenesis. The present study examined the effects of treadmill, elliptical, and rower exercises on maximal fat oxidation rates MFO , the intensity were MFO was observed Fat max and on fat oxidation curves in healthy and young participants.

Both MFO and Fat max were higher during treadmill exercise. Multiple linear mixed-effects regression analyses further revealed an effect of exercise modality on fat oxidation curves. Adequate selection of exercise modality during training may have a meaningful impact on substrate oxidation.

Treadmill exercise should be considered in training design for those looking to maintain or improve metabolic profiling. pH, temperature, substrate availability, etc.

Gevers, ; Robergs et al. The oxidation of substrates is also known to be further altered extrinsically, via exercise duration Phillips et al. Substrate metabolism shifts towards greater fat oxidation and reaches higher rates of maximal fat oxidation MFO during walking and running compared to cycling Achten et al.

These results are believed to stem from differences in muscle recruitment patterns and Type II muscle fiber recruitment in cycling from lower muscle mass contribution to total energy production Achten et al. Additionally, Chenevière et al. Intrinsically, as exercise intensity increases, greater glycolytic activity results in an increased accumulation of lactate and hydrogen ions, decreasing muscle pH.

Reductions in fatty acid oxidation are strongly correlated with the accumulation of plasma lactate Achten and Jeukendrup, Achten and Jeukendrup also found that the initial rise in plasma lactate occurred at the same intensity that elicited MFO.

It is suggested that decreased muscle pH, due to the accumulation of glycolytic by-products, inhibits the transport of long-chain fatty acid into the mitochondria, reducing fatty acid oxidation Achten and Jeukendrup, ; Sidossis et al.

The elliptical and rower are two modalities increasing in popularity for their ability to offer meaningful aerobic benefits Brown et al. They further provide alternatives to those with limited range of motions and physical disabilities, such as cerebral palsy, multiple sclerosis, and others.

Importantly, it has been reported that heart rate and oxygen uptake during elliptical exercise is similar to treadmill when both exercises are performed at self-selected intensities Porcari et al. Carey et al. Despite some aerobic similarities, MFO and Fat max was reported higher during rowing compared to cycling Egan et al.

The crossover point, where energy contribution from CHO and fat to total energy expenditure is equal Brooks and Mercier, , was also reported to occur at a higher relative exercise intensity during rowing than cycling Egan et al. Although the elliptical and rower involve a large level of muscle mass Egan et al.

The muscles of the upper limbs have a relatively smaller surface area than those of the lower body Young et al. This could possibly result in not only a greater production of lactate, but also an earlier reliance on carbohydrate oxidation.

Fat oxidation during exercise has been associated to increases in oxidative enzymatic activity and mitochondrial biogenesis in skeletal muscle Little et al. Training designed to improve fat oxidation could help to gain or maintain a healthy metabolic profile via an appropriate selection of exercise modality.

We consequently investigated the effects of treadmill, elliptical and rowing exercise on MFO, Fat max , the crossover point, and rates of fat oxidation.

It was hypothesized that MFO, Fat max , the crossover point, and absolute fat oxidation would be greater during the treadmill exercise compared to the elliptical or rowing exercises. Nine healthy males age: 22 ± 1. Informed written consent was provided prior to testing.

Participants were screened with a Get Active Questionnaire and a health screening form for health conditions or diseases that could be aggravated by exercise. None of the participants were on prescribed medications. Participants reported to the laboratory, following a hour fasted state, for one familiarization session, followed by three experimental exercise sessions, in a balanced design, consisting of an adapted incremental V̇O 2peak protocol to exhaustion during either: 1 treadmill exercise TM , 2 elliptical exercise EL , or 3 rowing exercise ROW.

Participants performed each exercise session at the same time of day, between h and h, five to seven days apart, to minimize the influence of circadian variance.

Participants were also requested to avoid alcohol consumption, strenuous exercise, caffeine and tobacco 24 hours prior to each experimental exercise session. To control for dietary influences on metabolism during exercise, participants maintained the same diet each day prior to their exercise sessions, with the built-in assumption that this energy standardization method yields significant variability in food intake between participants Jeacocke and Burke, Familiarization session.

Participants completed one familiarization session to become accustomed to the exercise protocols, instrumentation, and each of the exercise modalities.

Additionally, anthropometric measures were collected, and percent body fat was estimated Jackson and Pollock, Treadmill Exercise TM. An adapted incremental V̇O 2peak exercise protocol was used to ensure that there was a sufficient number of stages to build substrate oxidation curves Achten et al.

Participants began walking at 3. Following the first stage, the speed was increased every three minutes to 4. Elliptical Exercise EL. An adapted incremental V̇O 2peak exercise protocol was used to ensure that there was a sufficient number of stages to build substrate oxidation curves Dalleck et al.

Participants began exercising at 30 W for the first three-minute stage on the elliptical S70 Ascent Trainer, Vision Fitness, Cottage Grove, Wisconsin, USA.

The placement of hands and feet on the elliptical were standardized for all participants. The gradient was maintained at a midpoint between the low to high ranges, pre-determined on the elliptical, and was maintained throughout the entire test Dalleck et al.

Every three minutes, the power output was increased by 20 W until participants reached an RER of 1. Power output was then increased by 20 W every minute until V̇O 2peak was reached.

Participants were required to maintain the appropriate exercise intensity by keeping the average power output at the target value. Rowing Exercise ROW. An adapted incremental V̇O 2peak exercise protocol was used to ensure that there was a sufficient number of stages to build substrate oxidation curves Egan et al.

Participants began rowing at 30 W for the first three-minute stage on the rower Model D Rowing Ergometer, Concept2 Inc. To standardize the level of drag for all participants, the coefficient of drag was maintained at during all subsequent stages Egan et al. The power output was increased by 30 W every three minutes until participants reached an RER of 1.

Power output was then increased by 30 W every minute until V̇O 2peak was reached. For exercise on all three modalities, V̇O 2 was considered to be peak when at least two of the three following conditions occurred, 1 if heart rate did not significantly increase with increasing workload defined as an increase of no more than 5 bpm , 2 if RER was greater than 1.

Heart rate HR was recorded continuously using a Polar Heart Rate Monitor H Fingertip blood samples were collected using a contact-activated lancet BD Microtainer, BD, USA prior to, and immediately following, each exercise session to assess blood lactate Lactate Pro Test Strip, Arkray, Kyoto, Japan and glucose FreeStyle Precision Neo, Abbott Point of Care, Illinois, USA concentrations.

Venous blood samples, from an antecubital vein, were also collected prior to, and immediately following each exercise session to assess concentrations of pH levels, base excess of extracellular fluid BEecf , bicarbonate levels HCO 3 - , partial pressure of oxygen pO 2 , partial pressure of carbon dioxide pCO 2 , total carbon dioxide levels TCO 2 , and oxygen saturation SO 2 i-STAT Handheld, Abbott Point of Care, Illinois, USA.

Breath-by-breath cardiorespiratory data were collected continuously during exercise using an open circuit ergospirometer in breath-by-breath mode CPX, MGC Diagnostics, Saint Paul, MN to obtain measures of oxygen consumption V̇O 2 , carbon dioxide production V̇CO 2 , respiratory exchange ratio RER , and ventilation rate V̇E.

Gas flow was measured through a bidirectional pitot tube flow sensor attached to the face-fitting mask worn by all participants during the exercise sessions. For each three-minute stage of the V̇O 2peak protocols, the last thirty seconds was averaged for the following measures: HR, V̇O 2 , V̇CO 2 , and V̇E.

The highest mean value over the entire exercise protocol for both HR and V̇E was used to determine peak heart rate HR peak , and peak ventilation rate V̇E peak values for each participant.

Protein oxidation was not directly calculated as short-term exercise does not alter its contribution Vallerand and Jacobs, Normal distribution of the data was verified via skewness and kurtosis tests, Kolmogorov-Smirnov and Shapiro-Wilk tests, and visual inspection of histograms.

When a significant F ratio was observed, pairwise comparisons with Bonferroni correction was conducted. Statistical analyses were completed using SPSS statistical package Version 24, IBM, Armonk, NY, Mean MFO was higher in TM vs.

Similarly, Fat max was higher in TM vs. Figure 2 presents absolute rates of fat and CHO oxidation across the exercise intensity spectrum during treadmill, elliptical and rower exercise. Examination of the fat oxidation curves revealed that curves became linear, and the distribution of the data was greater in the elliptical and rower exercises.

The CHO oxidation curves were similar in shape between exercise modalities, but a greater distribution of the data was found in the elliptical condition. Results of the regression model for the relative fat and CHO oxidation are presented in Table 1.

Additionally, pO 2 was higher post-exercise in TM vs. BEecf was also significantly lower post-exercise during ROW exercise compared vs. Mean TCO 2 was significantly lower post-exercise The present study investigated the influence of whole-body exercises, including treadmill, elliptical, and rower exercise, on fat oxidation parameters in healthy individuals.

The main findings of this study were: i MFO and Fat max were higher during the treadmill condition compared to both the elliptical and rower conditions, ii there was no difference in crossover points between the three conditions, and iii exercise modality influenced absolute rates of CHO and fat oxidation, and thereby modulated their respective curves across the exercise intensity spectrum.

The present study supports previous work demonstrating that treadmill exercise results in higher MFO rates than other exercise modalities, and greater metabolic benefits may stem from walking and running exercise Achten et al.

This work provides critical metabolic insights that may promote further research focused on those suffering from metabolic conditions and physical disabilities.

V̇O 2peak values were similar between all three exercise modalities. Maximal V̇O 2 values reflect the quantity of active muscle mass during exercise, indicating that all three modalities elicited similar levels of muscle activation.

Previous research has identified level of active muscle mass as a mechanism for differences in fat oxidation, particularly between cycling and other whole-body modalities. Achten et al. Walking and running on a treadmill utilizes different muscle contraction regimes and elicits greater mechanical efficiency compared to cycling, which may be extended to include elliptical and rowing exercise.

Additionally, the return of elastic energy may reduce recruitment of larger motor units consisting of greater Type II muscle fibres, influencing CHO metabolism, lactate production, and onset of peripheral fatigue Carter et al.

Egan et al. However, the mean MFO rates and Fat max values in the present study were lower on the rowing ergometer than Egan et al. Modality-specific training status is highly correlated with MFO and metabolic efficiency, promoting greater fat oxidation Hagerman, The present study used healthy males with no explicit training in rowing, while Egan et al.

However, this study was designed to provide information for, and reflect how recreational individuals respond to different exercise modalities. Despite this, the lack of familiarization and training with alternative whole-body exercises, particularly during rowing, may have led to decreased efficiency and greater reliance on the muscles of the upper body compared to those who utilize these modalities more often.

While untrained rowers display similar muscle synergies spatiotemporal pattern of muscle activation as trained rowers Shaharudin and Agrawal, , body posture and stroke technique can vary greatly between trained and untrained rowers Cerne et al.

Secher also detailed that untrained individuals will utilize less upper body movement and focus on the drive of the legs during rowing strokes with increased training.

Therefore, even though similar levels in activation of muscle mass occurred between exercise modalities, as indicated by similar V̇O 2peak values, the specific muscles utilized for each modality may explain differences in fat oxidation.

Moreover, the lower MFO and Fat max in elliptical and rower vs. treadmill could be associated with an increased recruitment of Type II muscle fibers Achten et al.

The present study demonstrated higher blood lactate concentrations post-exercise in both the elliptical and rowing conditions. Type II muscle fibres are less efficient than Type I muscle fibers since they rely primarily on carbohydrates as their energy source and produce lactate as a by-product Knechtle et al.

Treadmill exercise primarily uses muscles of the lower extremities, such as the gastrocnemius Sozen, , composed of a high percentage of Type I fibres Costill et al. The elliptical and rower involve greater activation of many muscles of the upper body compared to the treadmill Bazzucchi et al.

Although not all of the muscles of the upper body are mainly composed of Type II muscle fibres, the muscles of the upper limbs i. Biceps Brachii, Triceps Brachii have been known to have a greater percentage of these fibres Klein et al.

Finally, these muscles also generally have a smaller surface area than those of the lower body Young et al. The increased reliance on muscles of the upper body, and subsequently Tyle II muscle fibres, may have influenced the overall fat oxidation curves for elliptical and rowing exercises Figure 2.

Visually, curve fitting demonstrated a loss of curvilinearity of the fat oxidation curves in the elliptical and rowing exercise, as the apex of the curve i. the point of maximal fat oxidation occurred at low exercise intensities.

Fat max values for elliptical and rowing exercises were similar to those observed in overweight Bogdanis et al. The reduced ability of muscles to oxidize fat observed in obesity is suggested to result from increased intracellular lipid accumulation, leading to production of reactive oxygen species and disruption of mitochondiral oxidative enzymes Wells et al.

Therefore, factors such as exercise modalitiy and body weight, can heavily influence intrinsic cellular processes in skeletal muscle, altering substrate metabolism in these tissues. The accumulation of lactate, and subsequent decrease in pH, lowers fatty acid oxidation with increasing exercise intensities Achten and Jeukendrup, as they are known to inhibit long-chain fatty acid entry into the mitochondria Sidossis et al.

Lower muscle pH decreases the activity of carnitine palmitoyl transferase 1 CPT-1 , responsible for transporting long-chain fatty acids into the mitochondria Starritt et al.

Even though we did not observe a difference in plasma pH at the end of exercise between modalities, lactate concentrations were different between treadmill and rower, and it has been suggested that plasma lactate concentrations reflect changes in muscle pH MacLean et al.

Our results further substantiate this response with higher base excess of extracellular fluid in the treadmill and elliptical compared to the rower condition. Previous research has shown that the lactate threshold occurs at a lower V̇O 2 during incremental rowing exercise compared to treadmill, even when the same V̇O 2max is attained Weltman et al.

Blood lactate increases in a curvilinear fashion with increasing exercise intensity, resulting in an exponential increase during work above the lactate threshold Goodwin et al. The onset of blood lactate accumulation is also highly correlation with the onset of muscle deoxygenation Grassi et al.

The potential for increased lactate accumulation at an earlier stage lower V̇O 2 during rowing exercise may have resulted in a prompter shift in metabolism, and therefore a higher concentrations of lactate at the end of exercise compared to the treadmill.

Interestingly, a higher venous partial pressure of O 2 was observed in the treadmill condition compared to the rower at the end of exercise. Increases in pO 2 are generally indicative of impaired diffusive O 2 capacity from the circulatory system to active muscles, as observed in mitochondrial myopathic patients Taivassalo et al.

Additionally, minute ventilation and oxygen pulse remained unchanged across conditions, thereby eliminating the possibility of a higher O 2 uptake at the pulmonary level. While a direct relationship would conclude that higher O 2 availability in venous blood would be the by-product of lower O 2 extraction in the rower condition, V̇O 2peak was similar across conditions.

However, without blood flow or arterial blood gases we cannot conclusively state that lower O 2 extraction was at play in the present results.

treadmill in normal exercise routines may have impacted our results, as familiarity and technique with the elliptical and rowing ergometer varied between participants.

Even though proper technical instructions and a familiarization session were provided, we cannot ignore possible influence of technique and lower mechanical efficiency, especially during rowing, on substrate oxidation.

Therefore, these results may not be generalizable to individuals who use an elliptical or rowing ergometer frequently.

Additionally, blood samples were only obtained from the antecubital vein for all three exercise modalities. Blood samples for the rowing and elliptical exercises may have been influenced by the metabolic activity of the arm due to greater upper extremity muscle activation during these exercises.

Moreover, the sample used in the present study was composed of young and healthy individuals. Whether clinical or pathological populations would present similar metabolic responses to a variety of exercise modalities remains unknown.

While treadmill, elliptical and rower exercise modalities yield similar V̇O 2peak values, the research findings of the present study demonstrated that treadmill exercise elicited higher MFO, Fat max , and absolute rates of fat oxidation compared to elliptical and rower exercise, and that substrate oxidation curves were clearly influenced by exercise modality.

greater than predicted for the change in body composition. To determine whether such metabolic adaptation occurs in response to spontaneous long term weight change, we conducted a longitudinal study in which h energy expenditure EE and h respiratory quotient RQ; i.

fat to carbohydrate oxidation were repeatedly measured in Pima Indians at baseline and after a mean follow-up of 3. Changes in EE and RQ varied substantially among individuals. Thus, on the average, spontaneous long term weight changes are accompanied by small metabolic adaptations in both energy expenditure and fat oxidation.

The metabolic responses to weight changes are highly variable among individuals, however. To develop successful prevention and treatment strategies, it is important to understand the physiological mechanisms underlying the long term regulation of body weight. Differences in energy metabolism may play a role in long term body weight regulation and the pathogenesis of human obesity 2 — Several 2 — 7 , but not all 8 — 10 , prospective studies have shown that a relatively low energy expenditure 2 — 5 and a relatively high respiratory quotient, i.

a low fat to carbohydrate oxidation rate 6 , 7 predict body weight gain. Longitudinal studies, however, in which energy metabolism was assessed not only at baseline but also at follow-up, indicate that upon gaining weight, energy expenditure and fat oxidation increase 2 , 6 , Metabolic propensity to obesity might thus depend not only on initial rates of energy expenditure and fat oxidation, but also on how these measures change in response to weight change Results from most overfeeding studies indicate that short term experimental weight gain is accompanied by an overcompensatory increase in energy expenditure, i.

an increase in energy expenditure that is greater than predicted for the changes in body size and composition 14 — Similarly, most underfeeding studies reveal that in the short term, intentional weight loss leads to a decrease in energy expenditure beyond predicted values 23 — Such overcompensatory metabolic changes act to oppose further weight change and have thus been referred to as metabolic adaptation 13 , 24 , Although metabolic adaptation thus seems to occur in response to large perturbations in body weight over relatively short periods of time, it is unknown whether similar adaptive mechanisms also occur in response to spontaneous long term weight changes in free living conditions.

To examine this question, we analyzed data from an ongoing longitudinal study of the pathogenesis of obesity initiated in among the Pima Indians of Arizona, a population with a very high prevalence of obesity, in whom low rates of energy expenditure and fat oxidation predict body weight gain 2 , 6.

We present results from over subjects in whom h energy expenditure and h substrate oxidation were repeatedly measured in a whole body respiratory chamber before and after an average follow-up of 3.

The aims of this study were 1 to test whether metabolic adaptation in h energy expenditure and h substrate oxidation occur in response to spontaneous long term weight change, 2 to quantify and explain the variability in these changes among individuals, and 3 to determine the relationship between changes in energy expenditure and substrate oxidation in response to weight gain and weight loss.

Since , Pima Indians have been admitted to the metabolic ward of the Clinical Diabetes and Nutrition Section of the NIH in Phoenix, Arizona, for an ongoing longitudinal study of the pathogenesis of obesity that includes the repeated assessment of h energy expenditure and h substrate oxidation in a whole body respiratory chamber.

Among the subjects meeting these criteria, subjects had been studied on at least 2 occasions. In subjects studied more than twice, the visit with the greatest weight change was selected for follow-up. Among the subjects, 31 subjects had lost weight and 71 had gained weight at follow-up. All subjects were between 18—50 yr of age at baseline and follow-up, healthy according to a physical examination and routine laboratory tests, and did not smoke or take medications at baseline or follow-up Table 1.

Physical and metabolic characteristics of the entire study population and of the subset of subjects with follow-up. At baseline, all measurements in the follow-up group were comparable to those in the entire population. The P values refer to the changes over time determined by paired t -test.

Glucose tolerance was assessed by a g oral glucose tolerance test The study protocol was approved by the Institutional Review Board of the NIDDK and by the Tribal Council of the Gila River Indian Community, and all subjects provided written informed consent before participation.

Body composition was estimated by underwater weighing, with determination of residual lung volume by helium dilution 39 , or by total body dual energy x-ray absorptiometry DPX-L, Lunar Corp. Percent body fat, fat mass FM , and fat-free mass FFM were calculated as previously described 41 , and a conversion equation 42 was used to make measurements comparable between the two methods.

Waist and thigh circumferences were measured at the umbilicus and the gluteal fold in the supine and standing positions, respectively, and the waist to thigh ratio WTR was calculated as an index of body fat distribution The measurement of energy expenditure and substrate oxidation in the respiratory chamber has previously been described 44 and did not differ at baseline and follow-up.

In brief, volunteers entered the chamber at h after an overnight fast and remained there until h the following morning. Subjects were fed a standardized diet with the amount of calories calculated according to previously determined equations to achieve energy balance Meals were provided at , , and h, and an evening snack was given at h.

The rate of energy expenditure was measured continuously, calculated for each min interval of the 23 h in the chamber, and then extrapolated to 24 h h energy expenditure, EE.

Spontaneous physical activity SPA was detected by radar sensors and expressed as the percentage of time over the h period in which activity was detected Carbon dioxide production VCO 2 and oxygen consumption VO 2 were calculated at min intervals, summed for the 23 h in the chamber, and then extrapolated to 24 h.

Based upon RQ, EE, and h urinary nitrogen excretion, the rates of h fat, carbohydrate, and protein oxidation were determined as previously described Statistical analyses were performed using the procedures of the SAS Institute, Inc.

Cary, NC Results are given as the mean ± sd. Data from the entire group of subjects were used to assess the cross-sectional relationships between EE and RQ vs. Changes in anthropometric and metabolic parameters were assessed in the subset of subjects with follow-up measurements.

Changes Δ in EE and RQ were calculated as the difference between follow-up and baseline measurements for both the unadjusted and the adjusted values.

Paired t tests were used to test whether measurements at follow-up were significantly different from those at baseline. Pearson correlation coefficients were calculated to assess the relation of the changes in unadjusted and adjusted EE and RQ to the change in body weight.

The changes in EE and RQ predicted for a kg weight loss or kg weight gain were determined from the regression equation of the relationships between Δ EE andΔ RQ vs.

Δ weight. body weight, as assessed in the entire study population of subjects. The residuals of the relationships between Δ EE and Δ RQ vs. Δ weight were calculated using general linear regression models. The anthropometric and metabolic characteristics of the entire study population and of the subset of individuals with follow-up studies are summarized in Table 1.

The baseline anthropometric and metabolic characteristics of the subjects with repeated measurements of energy metabolism were similar to those of the entire study population. The follow-up duration ranged from 0.

A, Relationship between Δ EE and Δ weight over 3. B, Relationship between Δ EE and Δ weight after adjustment of EE for FFM, FM, WTR, and age.

A, Relationship between changes in RQ, adjusted for energy balance, and Δ weight over 3. B, Relationship between Δ RQ and Δ weight after adjustment of RQ for percent body fat, age, and sex in addition to energy balance.

Changes in h energy expenditure. The correlation between Δ EE and Δ weight remained significant when baseline and follow-up EE were adjusted for FFM, FM, WTR, age, and sex Fig. Sex, age, glucose tolerance status normal or impaired , initial body weight, and follow-up duration were not significant determinants of Δ EE.

Changes in h respiratory quotient and substrate oxidation. There was a negative linear correlation between Δ RQ and Δ weight, but for any given Δ weight there was considerable interindividual variability in Δ RQ sd , 0. The correlation between Δ RQ andΔ weight remained significant when baseline and follow-up RQ were adjusted for percent body fat, age, and sex in addition to energy balance in the chamber Fig.

Responses in energy expenditure vs. responses in substrate oxidation. Based on the relationship between Δ EE and Δ weight Fig. The changes in RQ Fig. In response to weight gain there was a negative correlation between the residuals of Δ EE and the residuals of Δ RQ Fig.

subjects with metabolic adaptation in EE positive residuals also tended to have metabolic adaptation in substrate oxidation negative residuals in RQ and vice versa. In response to weight loss, the residuals in Δ EE and Δ RQ were unrelated, i. metabolic adaptation in EE did not tend to be accompanied by metabolic adaptation in substrate oxidation Fig.

In the present longitudinal study we examined the changes in h energy expenditure and h substrate oxidation associated with spontaneous long term weight changes in more than Pima Indians who spent h in a respiratory chamber at baseline and after a mean follow-up of 3.

The results indicate that metabolic adaptation, i. changes in energy expenditure and substrate oxidation greater than predicted for the change in body size and composition, can occur in response to spontaneous long term weight changes.

On the average, the metabolic changes were only slightly greater than predicted, but varied substantially among individuals. Finally, we found that in response to weight gain, adaptations in energy expenditure and substrate oxidation were related to one another, such that subjects with the most pronounced metabolic adaptation in energy expenditure also had the most pronounced metabolic adaptation in fat oxidation and vice versa.

This was not the case for weight loss. Most previous intervention studies have demonstrated metabolic adaptation in response to experimental short term weight change induced by controlled over- and underfeeding regimens 14 — Whether similar overcompensatory changes in energy expenditure and fat oxidation occur in the natural history of weight changes has been a matter of contention 9 — 13 , 16 , The present study demonstrates, for the first time, that metabolic adaptation can occur in response to spontaneous long term weight changes, but also reveals that, on the average, these overcompensatory changes are small.

In practical terms, these adaptations translate into the caloric content of approximately one half of an apple, one fifth of a bagel, or one tenth of a cheeseburger for the adaptation in h energy expenditure or the fat content of two teaspoons of peanut butter or seven potato chips for the metabolic adaptation in h fat oxidation , respectively.

The results also indicate that even a large decrease in body weight over several years is, on the average, not accompanied by a profound slowing of energy metabolism, as occasionally implied to explain the high rate of weight recidivism in the medical treatment of obesity.

However, several aspects need to be considered in this respect. Second, the present study was observational in design, which has both advantages and disadvantages. On the one hand, we have no information on the exact causes of the weight changes.

In some individuals, weight loss might have been secondary to illness, although this is unlikely because subjects in our studies typically remain in close contact with the research unit and receive a comprehensive medical examination before each admission.

An advantage of the observational design, on the other hand, is that it allows us to examine the metabolic responses to spontaneous long term weight changes that probably more closely resemble the typical pattern of weight change under free living conditions than imposed by over- and underfeeding regimens.

The fact that the magnitude of metabolic adaptation in response to such gradual weight change was small, on the average, agrees with cross-sectional findings indicating that energy expenditure is only marginally reduced in formerly obese individuals who had returned to a normal body weight and had successfully maintained the weight loss over months or years postobese individuals Some previous intervention studies suggest that the suppression in energy expenditure in response to weight loss might be larger shortly after a more rapid decrease in body weight 26 , 27 , 29 , 31 , It is also important to point out that energy expenditure in the present study was measured in the restricted environment of a respiratory chamber, which significantly reduces physical activity.

Although nonexercise activity thermogenesis, of which spontaneous physical activity is a component, has recently been suggested to play an important role in the adaptation to overfeeding 21 , our findings do not suggest a major role of spontaneous physical activity i.

fidgeting in the metabolic response to long term weight change. To what extent changes in volitional physical activities such as exercise habits contribute to the overall metabolic responses to long term weight change remains unknown.

Our study also provides no information on the role of spontaneous adaptations in energy intake. Thus, as with the metabolic adaptation in energy expenditure, small differences in the adaptation in energy intake may play an important role in determining whether body weight remains stable or continues to increase.

Rather, some individuals will experience relatively large overcompensatory responses, whereas others will have subnormal responses. Such interindividual variability in metabolic responses has also been found in response to experimental over- and underfeeding and has been used to explain why the amount of weight gained or lost under standardized dietary regimens can differ substantially among individuals 14 , 19 , 22 , The large number of subjects in the present study allowed us to quantify the interindividual variability in metabolic responses to weight changes and to search for possible underlying determinants.

We found that the change in h energy expenditure was explained not only by the changes in FFM and FM, but also independently by the changes in body fat distribution and spontaneous physical activity. The only additional determinant of the change in h respiratory quotient was age at baseline.

As only a small part of this variability can be attributed to the variability of the method 2 , 6 , 44 , other factors must be involved. Moreover, there is strong evidence from overfeeding studies in identical twins that the metabolic responses to weight changes are in part genetically determined 55 , Another interesting observation in the present study was that in response to weight gain, the changes in h energy expenditure and h substrate oxidation were related to one another, in that individuals with the most pronounced adaptation in energy expenditure also tended to have the most pronounced adaptation in fat oxidation and vice versa.

Interestingly, this was not the case in response to weight loss, where adaptations in energy expenditure and substrate oxidation were unrelated. The above findings may have important implications for our understanding of the role of energy metabolism in the long term regulation of body weight and the pathogenesis of human obesity.

To illustrate this, we have developed a schematic model that integrates previous cross-sectional and prospective findings with those from the present longitudinal study Fig.

Schematic model integrating cross-sectional, prospective, and longitudinal findings to illustrate the potential role of energy expenditure and substrate oxidation in the long term regulation of body weight.

Cross-sectionally, energy expenditure and the rate of fat to carbohydrate oxidation increase with increasing body size prediction line , but at any given body size, both measures vary considerably among individuals 44 , 51 , Our present longitudinal data indicate that upon gaining weight, the initially low rates of energy expenditure and fat oxidation tend to normalize, on the average, but as with the cross-sectional relationship, there is substantial interindividual variability in these responses.

Accordingly, the metabolic drive to weight gain may soon diminish in some individuals, thereby limiting the amount of weight gain metabolic adaptation; arrow 1A , whereas it may be sustained in others, who will thus be predisposed to gain further weight arrow 1B.

Of note, these considerations apply to spontaneous long term weight changes. Further studies are needed to confirm the role of low energy expenditure and fat oxidation as predictors of weight gain and to formally test the effect of metabolic adaptation on further weight change. It will also be important to examine the role of adaptation in energy and substrate intake to weight change.

These are probably complex and could include changes in the perception of hunger and satiation as well as in caloric intake and food preferences.

In summary, the results of this longitudinal study indicate that the changes in h energy expenditure and h respiratory quotient i. in substrate oxidation associated with long term weight changes 1 are greater than those predicted for the change in body size and composition, 2 vary substantially among individuals, and 3 are related to one another in response to weight gain.

We conclude that metabolic adaptation can occur not only in response to experimental short term perturbations in body weight, but also in response to spontaneous long term weight changes.

These responses, albeit small on the average, vary substantially among individuals and may thus play a role in the long term regulation of body weight and the pathogenesis of human obesity. We gratefully acknowledge Mr. Tom Anderson, Mrs. Carol Massengill, and the nurses of the Clinical Research Unit as well as the staff of the metabolic kitchen for their care of the patients in the studies, and the Clinical Diabetes and Nutrition Section technical staff for assisting with the chamber measurements and laboratory analyses.

We thank the members and leaders of the Gila River Indian Community, without whose continuing cooperation this study would not have been possible. Flegal KM , Carroll MD , Kuczmarski RJ , Johnson CL. Int J Obes. Google Scholar. Ravussin E , Lillioja S , Knowler WC , et al.

N Engl J Med. Buscemi S, Di Maggio O, Blunda G, Maneri R, Verga S, Bompiani GD. Griffiths M , Payne PR , Stunkard AJ , Rivers JPW , Cox M. Roberts SB , Savage J , Coward WA , Chew B , Lucas A.

Zurlo F , Lillioja S , Puente A , et al. Am J Physiol. Seidell JA , Muller DC , Sorkin JD , Andres R. Davies PSW , Day JME , Lucas A. Weinsier RL , Nelson KM , Hensrud DD , Darnell BE , Hunter GR , Schutz Y. Contributions of resting energy expenditure, thermic effect of food, and fuel utilization to four-year weight gain in post-obese and never-obese women.

J Clin Invest. Amatruda JM , Statt MC , Welle SL. Flatt JP. Diabetes Metab Rev. Ravussin E , Swinburn BA. Diabetes Rev. In: Stunkard AJ, Wadden TA, eds. Obesity: theory and therapy, 2nd Ed. New York : Raven Press; 97— Miller DS , Mumford P , Stock MJ.

Thermogenesis in overeating man. Am J Clin Nutr. Sims EAH , Danforth Jr E , Horton ES , Bray GA , Glennon JA , Salans LB. Recent Prog Horm Res. Garrow JS. In: Bray GA, ed.