Browsing by Author "Melby, Christopher, committee member"
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- ItemOpen Access1 month effect of breaking up sedentary activity on insulin sensitivity and glucose homeostasis in free-living overweight/obese adults(Colorado State University. Libraries, 2019) Schreck, Laura M., author; Hickey, Matthew, advisor; Bergouignan, Audrey, advisor; Broussard, Josiane, committee member; Melby, Christopher, committee memberSedentary behavior (SB) triggers an inability to adjust substrate use to substrate availability (low metabolic flexibility, MF), which may precede glucose intolerance in the pathogenesis of insulin resistance. We and others have shown that frequent interruptions in SB leads to improved glycemic control, however the underlying role of MF in this process is unknown. This study examined the effects of breaking up SB on MF and glucose metabolism in free-living overweight and obese adults. To distinguish effects of breaking up SB from being physically active, we also studied a group where participants performed a single energy matched continuous bout of exercise. Physically inactive, adults (12F/9M, mean±SD, age: 33±8 yr, BMI: 29.5±3.3 kg/m2) were randomly assigned to a 4 week intervention consisting of brisk walking for 5 min each hour for 10h, 5 d/wk (MICRO, n=10), or 4 weeks of an intervention consisting of one continuous 45 min bout of exercise per day, 5d/wk (ONE, n=9). Outcomes assessed at baseline and after each intervention included: MF (waking respiratory quotient, RQ, minus sleeping RQ as measured in a whole room calorimeter), insulin sensitivity (SI, IVGTT), 24h glycemia (continuous glucose monitor), 24h glucose oxidation (U13C glucose tracer), SB, time spent standing, time spent stepping (ActivPAL) and TEE (double labeled water). Groups were similar on all outcome variables at baseline. Linear mixed models evaluated intervention and intervention-by-group effects. MICRO and ONE decreased time sitting and increased time stepping with no significant changes in TEE. Compared to ONE, MICRO decreased 24h glycemic variability (p=0.06), improved the acute whole body insulin sensitivity (p=0.08) and acute insulin response to glucose (AIRg) (p=0.02) , maintained exogenous glucose oxidation (p<0.03) and improved MF (p=0.02). Independent of time sitting and stepping, breaking up SB improves glucose homeostasis and MF. The effects of such an intervention in persons with type 2 diabetes warrants further study.
- ItemOpen AccessAccuracy of walking metabolic prediction equations using a large diverse data set(Colorado State University. Libraries, 2014) Woods, Rachel M., author; Browning, Raymond C., advisor; Hickey, Mathew, committee member; Melby, Christopher, committee memberWalking metabolic rate prediction equations are commonly used to estimate oxygen consumption, exercise intensity and energy expenditure across a wide range of ages and anthropometrics. Despite their widespread use, independent validations of these equations using metabolic data from a large number of individuals are uncommon. PURPOSE: To assess the accuracy of the commonly used ACSM and Pandolf walking metabolic rate prediction equations, along with two new walking metabolic rate predictions equations developed by Weyand et al. and Browning et al., using data from a large number of adults. METHODS: We used demographic, anthropometric, walking speed, and oxygen consumption data from several laboratories (N = 450 (164 Males, 286 females), 18-85 years old, 16.5-44 kg/m2). We estimated oxygen consumption using each prediction equation in 1,078 walking trials ranging from 0.55-2.18 m/s, and 0.5-12% grade. Comparisons between predictive methods were made for all walking trials, as well as among normal weight participants during level and gradient walking, and overweight and obese participants during level and gradient walking. We computed the mean prediction difference (MPD) as the difference between predicted vs. measured rates of oxygen consumption (ml/kg/min) for each trial, and examined the relationship between the MPD and measured oxygen consumption (ml/kg/min) using modified Bland-Altman plots. Linear regression was used to determine the intercept (fixed bias) and slope (proportional bias) for each equation. The absolute value of the mean prediction difference, and Root Mean Square Error (RMSE) values were also calculated for each equation and population. RESULTS: For level walking, all prediction equations had mean prediction differences that were statistically different from zero (P ≤ 0.05) except for the Browning et al., equation when applied to normal weight individuals and the Pandolf equation when applied to overweight and obese individuals. Most importantly, all prediction equations had significant (P ≤ 0.05) fixed and proportional bias, and demonstrated large RMSE (7.8-23.5% of mean measured metabolic rate) that were similar across equations and population. In addition, prediction error increased as measured metabolic rate increased for all equations. CONCLUSION: The metabolic prediction equations evaluated here each had considerable error when compared to measured values, regardless of the population in which the equation was created and/or validated. Improvements in prediction equations may require using approaches that aim to minimize RMSE and/or developing population/intensity specific equations.
- ItemEmbargoCaffeine augments the lactate and interleukin-6 response to moderate-intensity exercise in males but not females(Colorado State University. Libraries, 2022) Abbotts, Kieran Shay Struebin, author; Bell, Christopher, advisor; Hamilton, Karyn, committee member; Melby, Christopher, committee memberThe release of interleukin (IL)-6 from contracting skeletal muscle is thought to contribute to some of the health benefits bestowed by exercise. This IL-6 response appears proportional to exercise volume. Unfortunately, high volumes of exercise are not feasible for all people. Caffeine augments the magnitude of increase in circulating concentration of IL-6 in response to high-intensity and long-duration exercise, in males. Caffeine is also known to increase circulating concentrations of lactate during exercise. One of the mechanisms thought to contribute to IL-6 release from exercising skeletal muscle is lactate production. We hypothesized that caffeine, ingested prior to moderate-intensity exercise, would lead to greater circulating concentrations of lactate and IL-6 in a study population comprising both males and females. 15 healthy adults (9 males and 6 females, aged 26±7 years, (mean ± SD)) completed 30-minutes of moderate-intensity cycle ergometer exercise, equivalent to the ventilatory threshold, after ingesting either caffeine (6 mg/kg) or placebo. Arterialized-venous blood was collected throughout each of the exercise sessions. Compared with placebo, caffeine increased end-exercise circulating concentrations of lactate (5.72±3.95 vs. 7.14±4.66 mmol/L, P<0.001) but not end-exercise IL-6 (1.84±0.97 vs. 2.37±1.04 pg/mL, P=0.139). However, when females were excluded from the analysis, caffeine augmented (P=0.04) the magnitude of increase of end-exercise IL-6 concentration (1.80±0.86 vs. 2.57±1.21 pg/mL); this effect was further exaggerated after 30-minutes of inactive recovery (3.81±2.32 vs. 5.06±3.22 pg/mL). Noteworthy, caffeine evoked greater end-exercise lactate concentrations in data sets containing only males (P=0.02) and only females (P=0.002) but did not influence the IL-6 response in females (P=0.94). Our preliminary data imply that in males unable/unwilling to perform high-intensity and/or long-duration exercise, caffeine may potentially enhance the IL-6 mediated health benefits of relatively short, moderate-intensity exercise.
- ItemOpen AccessDevelopment and evaluation of the America On the Move program for university students(Colorado State University. Libraries, 2013) Dadkhah, Maryam, author; Anderson, Jennifer, advisor; Hill, James, advisor; Melby, Christopher, committee member; Long, Marilee, committee memberTo view the abstract, please see the full text of the document.
- ItemOpen AccessFADS2 expression modulates effect of dietary polyunsaturated fatty acids on western diet-induced glucose intolerance(Colorado State University. Libraries, 2017) Linde, Peter, author; Chicco, Adam, advisor; Melby, Christopher, committee member; Bouma, Gerrit, committee memberFatty Acid Desaturase 2 (FADS2) haplotypes associated with hyperactivity of its gene product, delta-6-desaturase (D6D), are associated with obesity and type-2 diabetes in humans. D6D regulates long-chain polyunsaturated fatty acid (PUFA) biosynthesis and is upregulated in several rodent models of obesity/insulin resistance, but its direct influence on diabetes is unclear. D6D activity might favor pathogenic effects of omega-6 FA linoleic acid (LA) by enhancing production of its product arachidonic acid (AA). Conversely, D6D may promote protective effects of omega-3 FA α-linolenic acid (ALA) by enhancing production of ALA to long-chain PUFAs that displace AA in cell membranes. It is hypothesized that abundant LA found in the modern western diet will be converted to AA promoting an inflammatory phenotype. The present study is to determine the interaction of heterozygous knockout (HET) or transgenic overexpression (TG) of FADS2 in mice fed high fat diets (HFD), as well as the interaction of LA:ALA content in the HFD. Adult male mice with HET (low), wild type (WT; medium), and TG (high) expression of FADS2 were fed HFD (45% w/w) containing 8% PUFA supplied by a balanced mix of LA and ALA (1:1), LA-rich (41:1), or ALA-rich (1:4) for 16 weeks. Glucose intolerance developed in WT mice, with no difference between diets. In HET mice, glucose intolerance was attenuated but this protection was removed by ALA rich diet. TG mice developed more glucose intolerance than WT. TG mice fed high LA diets were more glucose tolerant than high ALA and mixed diets. In conclusion, FADS2 expression modulates metabolic responses to high fat feeding. HET provides some protection against glucose intolerance, except when given an ALA rich diet. Transgenic overexpression increases glucose intolerance while a high LA diet attenuates this effect. This is inconsistent with current hypotheses that AA production from LA increases metabolic risk.
- ItemEmbargoGlucocorticoid receptor signaling is required for acclimation of skeletal muscle to hypobaric hypoxia(Colorado State University. Libraries, 2022) Whitcomb, Luke, author; Chicco, Adam, advisor; Maresh, Ryan, advisor; Melby, Christopher, committee memberHypobaric hypoxia (HH) encountered at high altitudes acutely impairs aerobic exercise capacity, which partially recovers following 1-2 weeks of acclimation to chronic HH. Persistent elevations in serum glucocorticoids occur during HH exposure, but their role in these acute and chronic physiological responses is unclear. We tested the hypothesis that glucocorticoid signaling is essential for the acclimation of aerobic exercise capacity to chronic HH, in part by mediating adaptive changes in skeletal muscle metabolism. Male F344 rats were administered the glucocorticoid receptor antagonist RU486 (RU; 60 mg/kg/d in chow) or no drug for 5 days prior to 15 days of continued normoxia (Fort Collins, CO; elevation 5,003 feet) or HH (simulated 17,200 feet in a hypobaric chamber) with or without continuous RU treatment (N=4-8/group). Graded treadmill exercise tests (GXT) were conducted on a motorized treadmill in normoxia, during acute HH exposure, and in HH after 15 days of HH acclimation. As expected, acute HH reduced GXT performance compared to normoxia in all rats, which improved following 15 days of acclimation to HH. RU pretreatment did not impact hypoxic GXT performance, but continuous treatment abolished improvements in GXT performance following chronic HH. RU attenuated HH-induced increases in hematocrit and muscle fatty acid oxidation efficiency assessed by high-resolution respirometry ex vivo, suggesting that glucocorticoid signaling may improve muscle oxygen utilization in response to chronic HH. RU also prevented HH-induced decreases in pyruvate dehydrogenase expression and increases in Krüppel-like factor 15, proteolysis and branched-chain amino acid aminotransferase in glycolytic muscle, implicating glucocorticoid signaling in a rewiring of glucose and protein catabolism to rid the cell of excess nitrogen in HH. In conclusion, these results demonstrate that glucocorticoid receptor signaling is essential for the acclimation of aerobic exercise capacity to HH, perhaps by mediating improvements in the bioenergetic efficiency of skeletal muscle metabolism.
- ItemOpen AccessImpact of timing of protein intake on nitrogen balance in exercising older individuals on a hypercaloric diet(Colorado State University. Libraries, 2011) Minor, Brian, author; Miller, Benjamin, advisor; Hamilton, Karyn, committee member; Melanson, Ed, committee member; Hickey, Matthew, committee member; Melby, Christopher, committee memberWe have previously shown that in older adults, consumption of protein in the form of chocolate milk immediately after exercise enhances nitrogen balance (NBAL) when energy balance is maintained. Since it is known that hypercaloric diets increase nitrogen (N) retention, it is important to know if the timing of protein intake after aerobic exercise provides further increases in N retention compared to the consumption of carbohydrate only post exercise. PURPOSE: To investigate if consumption of protein and carbohydrate (PRO + CHO) immediately after exercise as opposed to earlier in the day can improve NBAL in older individuals consuming a hypercaloric diet. METHODS: In a randomized cross-over design, subjects completed two separate 3-day exercise and nutrition interventions. Exercise (60 minutes of stationary cycling at 55% of VO2max) was performed daily at 4:30 PM. Diets were hypercaloric (calculated at +15% daily intake), with a PRO+CHO or carbohydrate only (CHO) drink consumed at 10 am and the opposite drink consumed after exercise (5:30 PM). Both diets (1.2 g protein/kg bodyweight, 30% fat, and balance as carbohydrate) were isonitrogenous and isocaloric with only the timing of the drinks differing. A 24 hour stay in a metabolic chamber confirmed positive energy balance while 24-hour urine collections determined NBAL. RESULTS: The 3-day mean NBAL was not significantly different (p=.0881) (n=6) between the CHO trial (.970 ± .517 g N) and the PRO + CHO trial (1.659 ± .430 g N) although a trend toward increased NBAL with PRO+CHO was apparent. The mean energy balance was not significantly different (p=.2906) between the CHO trial (+13.09 ± 1.94%) and the PRO + CHO trial (+ 14.28 ± 1.75%). Further analyses comparing the positive energy balance cohort to previously completed negative, and even energy balance cohorts distinguished the role of energy balance and timing of nutrition effects. CONCLUSION: Older individuals in positive energy balance do not maintain a significantly more positive NBAL balance by consuming protein after aerobic exercise as opposed to earlier in the day although energy balance does change the effect of protein timing on NBAL.
- ItemOpen AccessNrf2 activation but not vitamin C treatment promotes proteostatic maintenance during an oxidative challenge(Colorado State University. Libraries, 2016) Ehrlicher, Sarah E., author; Miller, Benjamin F., advisor; Hamilton, Karyn L., advisor; Melby, Christopher, committee memberImproved proteostasis may be a mechanism of stress resistance, and it is likely that the increased protein turnover with exercise training contributes to adaptation to stress. Exogenous antioxidant treatments such as vitamin C (VitC) target the detrimental effects of reactive oxygen species (ROS), but may simultaneously prevent the beneficial redox signaling associated with exercise. A possible alternative strategy to prevent oxidative damage while permitting redox-sensitive signaling is to increase endogenous antioxidants. The transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2) increases the transcription of endogenous antioxidants by binding to the antioxidant response element in the promoter region of target genes. Protandim (Pro, LifeVantage), a combination of five phytochemicals, activates Nrf2 by increasing its translocation to the nucleus. We hypothesized that, compared to VitC, treatment with the Nrf2 activator Pro would not blunt ROS induced proteostatic maintenance. To mimic ROS signaling, C2C12 myoblasts were treated with H2O2. Treatment occurred alone or in combination with either VitC or Pro. Deuterium oxide labeling was used to measure protein synthesis in the mitochondrial and cytosolic cell fractions after 2, 4, 8, and 12 hours of treatment. Simultaneously cell proliferation was measured by deuterium incorporation into DNA. Compared to the untreated control, H2O2 alone increased DNA synthesis but did not increase mitochondrial protein synthesis, resulting in decreased proteostasis. Compared to H2O2 alone, Pro decreased protein synthesis in both cytosolic and mitochondrial fractions. However, Pro also decreased DNA synthesis. This resulted in a greater protein to DNA ratio suggesting maintenance of proteostasis. VitC with H2O2 increased DNA synthesis and decreased proteostasis, similar to H2O2 treatment alone. From these data, it appears that although treatment with exogenous antioxidants increases proliferation, activation of Nrf2 maintains mitochondrial protein synthesis despite a reduction in proliferation. Further study into the role of Nrf2 in improving mitochondrial proteostasis to promote stress resistance is warranted.
- ItemOpen AccessObesity accelerates mammary carcinogenesis in a rat model of polygenic obesity susceptibility(Colorado State University. Libraries, 2015) Matthews, Shawna Beth, author; Thompson, Henry J., advisor; Henry, Charles, committee member; Hickey, Matthew, committee member; Melby, Christopher, committee memberGiven the ongoing obesity epidemic, in which more women in the US are overweight or obese than are lean, the impact of obesity on the development of breast cancer is an important public health concern. Obese women with breast cancer generally have larger tumors and poorer prognosis than lean women with breast cancer. In an effort to deconstruct the biological mechanisms that link obesity and breast cancer, we have developed a novel rat model with high relevance to the polygenic development of obesity and breast cancer in humans. These rats have differing susceptibility to obesity when fed a diet of similar macronutrient composition as that consumed by the average American woman. Diet susceptible (DS) rats rapidly accumulate excess body fat and display metabolic perturbations, including resistance to insulin and leptin, which normally provide "stop eating" anorexigenic cues. In contrast, diet resistant (DR) rats remain lean despite being fed the same diet. Findings from experiments conducted in our novel rat model have provided several critical pieces of information. When DR and DS rats were treated with a chemical carcinogen, DS rats displayed markedly accelerated mammary cancer formation compared to DR rats, including higher cancer incidence, multiplicity, and tumor burden, in conjunction with reduced cancer latency. The larger tumor mass in DS rats was found to be attributable to higher growth rates in DS vs. DR tumors, due to a combination of accelerated cell cycle progression and reduced apoptotic efficiency. Importantly, DS rats tended to develop more tumors that were negative for sex hormone receptor expression, a subtype of breast cancer with high rates of breast cancer mortality. This observation was corroborated by an endocrine ablation experiment, i.e., bilateral ovariectomy. Removal of the ovaries puts a strong selection pressure on expansion of cell populations that can grow in the absence of high circulating levels of sex hormones. In addition to removal of the primary source of circulating sex hormones, several experiments failed to provide evidence in support of peripheral production of estrogen by adipose tissue. In spite of the lack of estrogen at the host systemic and local (mammary gland) level, ovariectomized DS rats displayed elevated cancer multiplicity and sum tumor weight compared to ovariectomized DR rats, indicating that obesity in DS rats promotes the growth of cancer cells in an estrogen-independent manner. Clinically, chronic inflammation in adipose tissue as a consequence of obesity has been shown to create a permissive environment for the development of breast cancer. While DS rats display evidence of heightened fat storage in the form of adipocyte hypertrophy, there was no evidence of inflammation accompanying this hypertrophy in the rat mammary gland in the current studies. Thus, peripheral production of estrogen by fat tissue and chronic inflammation in fat tissue—two of the mainstream mechanisms proposed to link excess fat and breast cancer—do not appear to be obligatory biological processes for the effect of obesity on the increased cancer response in DS rats in our model. These findings suggest that our novel rat model represents a preclinical tool that facilitates investigation of mechanisms beyond those currently considered to link obesity to carcinogenesis of the breast. Breast cancer is a highly heterogeneous disease, and the integrated rat model reported herein is a tool that complements monogenic models of obesity and breast cancer in an effort to deconstruct the complex problem of breast cancer in clinical subpopulations whose disease is not explained via traditional mechanisms.
- ItemOpen AccessPotato and grape polyphenols, respectively, suppress high-fat diet-elevated oxidative stress/innate inflammation markers in porcine model and induce apoptosis in HCT-116 p53 +/+ and p53 -/- human colon cancer cell lines in vitro(Colorado State University. Libraries, 2014) Radhakrishnan, Sridhar, author; Vanamala, Jairam, advisor; Kim, Sung Woo, committee member; Melby, Christopher, committee member; Pagliassotti, Michael, committee member; Veeramachaneni, DN Rao, committee memberTo view the abstract, please see the full text of the document.
- ItemOpen AccessSprint interval training: the influence of exercise modality(Colorado State University. Libraries, 2013) Giordano, Gregory Robert, author; Bell, Christopher, advisor; Hickey, Matthew, committee member; Melby, Christopher, committee memberSprint interval training (SIT), whether performed on a cycle ergometer or non-motorized treadmill, enhances exercise capacity and evokes favorable metabolic and cardiopulmonary adaptations. However, despite known differences between cycling and running, the influence of exercise modality on the adaptive response to SIT has not been directly addressed. Additionally, the effect of SIT on the angiogenic factors, pigment epithelial-derived factor (PEDF) and vascular endothelial growth factor (VEGF), has not been well characterized. PURPOSE: To examine the influence of exercise modality on the adaptive response to SIT, we compared the effects of SIT performed on one of three different exercise machines: non-motorized treadmill, cycle ergometer, or plyometrics platform. Additionally, we sought to characterize the changes in circulating and skeletal muscle PEDF and VEGF following three weeks of SIT. METHODS: Twenty-seven healthy, sedentary or recreationally active adults (age: 23 ± 5 years; body mass index: 25.7 ± 4.7 kg m-2; VO2peak: 36.7 ± 6.1 ml kg-1 min-1 (mean ± SE)) completed nine sessions of repeated (four to eight) 30-s bouts of maximal exercise on a non-motorized treadmill (RUN), cycle ergometer (CYC), or plyometrics platform (JMP) over 21 days. Prior to and following completion of SIT, peak oxygen uptake (VO2peak) and time to exhaustion at 80% VO2peak were measured. Additionally, blood and skeletal muscle was sampled prior to and following completion of SIT to measure PEDF and VEGF. RESULTS: Three weeks of SIT increased time to exhaustion (40.0 min ± 3.2 vs.51.3 ± 5.5 min, P = 0.006). The interaction with exercise modality did not achieve statistical significance (P = 0.08), however, it appears that time to exhaustion increased in the RUN (43.2 ± 5.2 vs. 57.4 ± 9.2 min) and CYC (41.7 ± 6.1 vs. 62.3 ± 11.6 min) groups, but not the JMP group (35.5 ± 5.6 vs. 35.0 ± 4.9 min). Circulating and skeletal muscle VEGF and PEDF were not altered by three weeks of SIT (P > 0.05). DISCUSSION: Independent of exercise modality, three weeks of SIT improves endurance exercise capacity and does not alter circulating or skeletal muscle PEDF or VEGF.
- ItemOpen AccessThe influence of Dapagliflozin on dietary mediated physiological and behavioral changes(Colorado State University. Libraries, 2019) Ryan, Shane P. P., author; Bell, Christopher, advisor; Melby, Christopher, committee member; Braun, Barry, committee memberThe diabetes medication, Dapagliflozin, is a sodium-glucose co-transporter 2 (SGLT2) inhibitor. The mechanism of action is decreasing renal absorption of glucose, leading to glucosuria, and modest weight loss. We hypothesized that SGLT2 inhibition would potentiate the favorable influence of dietary counseling on body composition and physiological adaptations in overweight or obese adults. Fifty sedentary overweight/obese men (n = 12) and women (n = 38) were randomly assigned to 12 weeks of dietary counseling for weight loss, supplemented with daily ingestion of either placebo or Dapagliflozin (up to 10 mg/day); coded as Pill A and Pill B. Dietary counseling consisted of weekly, one-on-one, 30-minute meetings targeting modest calorie restriction. Before and after treatment, body composition, resting metabolic rate (RMR), insulin sensitivity, appetite and satiety were measured. Twelve weeks of dietary counseling decreased (P < 0.049) body mass, fat mass, and RMR; neither variable was influenced by pill assignment (interaction: P > 0.264). Dietary counseling also decreased lean mass (treatment main effect: P < 0.001), however the decrease in lean mass was greater in Pill B than in Pill A (interaction: P = 0.037). Neither dietary counseling nor SGLT2 inhibition influenced insulin sensitivity (P > 0.055). Overall, 12-weeks of dietary counseling leads to favorable modification of body mass and fat mass regardless of pill assignment. However, Pill A appears to reduce the dietary counseling mediated loss in lean mass. Except for lean mass, the effects of dietary counseling for weight loss were not influenced by SGLT2 inhibition.
- ItemOpen AccessWhat goes down need not go back up: decreasing the biological drive toward weight regain by increasing energy flux(Colorado State University. Libraries, 2014) Paris, Hunter Louis Ross, author; Bell, Christopher, advisor; Melby, Christopher, committee member; Hickey, Matthew, committee memberINTRODUCTION: Weight regain after weight loss is the experience of most obese dieters. Metabolic adjustments characterized by decreased resting metabolic rate (RMR) and increased hunger can prevent long-term success. Possibly this energy gap could be attenuated by a high flux (HF) state (higher expenditure coupled with higher intake). METHODS: 6 obese adults [age (mean±SE) = 42±12 y; body mass index (BMI)=35.7±3.7 kg/m2] underwent 7% diet-induced weight loss and were stabilized at this weight for 3 weeks. RMR via indirect calorimetry, and hunger via visual analog scale were then examined during two 4-day conditions of energy balance in random order--Low Flux (LF): sedentary with energy intake (EI)=RMR x1.35; and HF: daily exercise net energy cost of ~500 kcal/d and EI= RMR x1.7. RESULTS: Average 5-day weight did not differ between HF (103.4±4.7 kg) and LF (103±4.8 kg) (P>0.10). Average daily RMR was higher during HF (1926±138 kcal/day) compared to LF (1847±126 kcal/day; P = 0.05). Resting fat oxidation was also higher during HF (0.073+0.010 g/min) compared to LF (0.059+0.012 g/min; P<0.05). Average daily, perceived end-of-day hunger was lower during HF compared to LF (P<0.05). CONCLUSION: These preliminary data suggest that compared to a sedentary LF state of energy balance, a HF energy balance state is associated with a greater RMR, resting fat oxidation, and less hunger - all of which may attenuate the energy gap and protect against weight regain.