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Aerobic capacity is negatively related to locomotion economy. The purpose of this paper is to determine what effect aerobic exercise training has on the relationship between net cycling oxygen uptake (inverse of economy) and aerobic capacity [peak oxygen uptake (V̇o2peak)], as well as what role mitochondrial coupled and uncoupled respiration may play in whole body aerobic capacity and cycling economy. Cycling net oxygen uptake and V̇o2peak were evaluated on 31 premenopausal women before exercise training (baseline) and after 8–16 wk of aerobic training. Muscle tissue was collected from 15 subjects at baseline and post-training. Mitochondrial respiration assays were performed using high-resolution respirometry. Pre- ( r = 0.46, P < 0.01) and postexercise training ( r = 0.62, P < 0.01) V̇o2peak and cycling net oxygen uptake were related. In addition, uncoupled and coupled fat respiration were related both at baseline ( r = 0.62, P < 0.01) and post-training ( r = 0.89, P < 01). Post-training coupled ( r = 0.74, P < 0.01) and uncoupled carbohydrate respiration ( r = 0.52, P < 05) were related to cycle net oxygen uptake. In addition, correlations between V̇o2peak and cycle net oxygen uptake persist both at baseline and after training, even after adjusting for submaximal cycle respiratory quotient (an index of fat oxidation). These results suggest that the negative relationship between locomotion economy and aerobic capacity is increased following exercise training. In addition, it is proposed that at least one of the primary factors influencing this relationship has its foundation within the mitochondria. Strong relationships between coupled and uncoupled respiration appear to be contributing factors for this relationship. NEW & NOTEWORTHY The negative relationship between cycle economy and aerobic capacity is increased following exercise training. The strong relationship between coupled and uncoupled respiration, especially after training, appears to be contributing to this negative relationship between aerobic capacity and cycling economy, suggesting that mitochondrial economy is not increased following aerobic exercise training. These results are suggestive that training programs designed to improve locomotion economy should focus on changing biomechanics.

Objective Insulin sensitivity is lower in African American (AA) versus Caucasian American (CA). We tested the hypothesis that lower insulin sensitivity in AA could be explained by mitochondrial respiratory rates, coupling efficiency, myofiber composition, or H2O2 emission. A secondary aim was to determine whether sex affected the results. Methods AA and CA men and women, 19–45 years, BMI 17–43 kg m2, were assessed for insulin sensitivity (SIClamp) using a euglycemic clamp at 120 mU/m2/min, muscle mitochondrial function using high‐resolution respirometry, H2O2 emission using amplex red, and % myofiber composition. Results SIClamp was greater in CA (p, Present results do not support a role for mitochondrial function or fiber type in determining lower insulin sensitivity in African Americans. The source of lower skeletal‐muscle insulin sensitivity in African Americans remains unclear. Future research could focus on aspects of skeletal muscle composition, such as lipid species, and their association with insulin sensitivity in African Americans.

Exercise is known to improve insulin sensitivity (SI); however, studies to date have been confounded by negative energy deficits after exercise. PURPOSE The primary objective of this study was to assess the effect of 8 to 16 wk of aerobic exercise training on the SI of untrained women under rigorously controlled energy-balanced conditions. The secondary objective was to determine if one acute bout of moderate-intensity continuous (MIC) or high-intensity interval (HII) exercise further affected SI. METHODS Insulin sensitivity was assessed in 28 untrained women at baseline, after 8 to 16 wk of training with no-exercise (NE) before assessment, 22 h after MIC (50% V˙O2peak), and 22 h after HII (84% V˙O2peak) using a hyperinsulinemic-euglycemic clamp. Participants were in a whole-room indirect calorimeter during each condition, and food intake was adjusted to ensure energy balance across 23 h before each clamp. RESULTS There were no significant differences in acute energy balance between each condition. Results indicated a significant main effect of time, such that SI was higher during the HII condition compared with both baseline and NE (P < 0.05). No significant differences in SI were observed after NE or MIC. CONCLUSIONS Widely reported improvements in SI in response to chronic exercise training may be mediated in part by shifts in energy balance. However, an acute bout of HII exercise may increase SI even in the context of energy balance.

Reduction of salivary nitrate to nitrite by oral nitrate reductase (NR) expressing bacteria has emerged as an integral pathway in regulating nitric oxide (NO) homeostasis and signaling. The oral microbiome is critical for this pathway. Variations in this pathway may underlie variable responses in the magnitude by which dietary or therapeutic nitrate modulates NO-signaling. The relationships between oral microbes and NR activity, and the factors that affect this relationship remain unclear however. Using a cross-sectional study design, the objective of this study was to determine the relationships between oral microbes and oral NR activity using a protocol that directly measures initial NR activity. Tongue swabs were collected from 28 subjects ranging in age from 21 to 73y. Initial NR activity showed a bell-shaped dependence with age, with activity peaking at ~40-50y and being lower but similar between younger (20-30y) and older (51-73) individuals. Microbiome relative abundance and diversity analyses, using 16s sequencing, demonstrated differences across age and identified both NR expressing and non-expressing bacteria in modulating initial NR activity. Finally, initial NR activity was measured in 3mo and 13mo old C57BL/6J mice. No differences in bacterial number were observed. However initial NR activity was significantly (80%) lower in 13mo old mice. Collectively, these data suggest that age is a variable in NR activity and may modulate responsiveness to dietary nitrate.

Background Exercise training improves health outcomes in individuals with obesity (IO); however, it remains challenging for IO to adhere to exercise. Thus, it is critical to identify novel strategies that improve exercise tolerance (ET) and adherence in IO. Beetroot juice (BRJ), high in inorganic dietary nitrate, consistently improves exercise performance in athletes, individuals with cardiopulmonary diseases, and nonobese lean individuals. These improvements may be explained by reduced oxygen uptake (VO2) during exercise, enhanced blood flow, and greater mitochondrial efficiency. To date, we are aware of no studies that have compared the effects of BRJ, sodium nitrate (NaNO3), and nitrate‐depleted BRJ (PLA) for improving ET and cardiometabolic health in IO. Purpose Determine if BRJ improves ET, exercise efficiency (EE), and cardiometabolic health in IO and identify possible mechanisms of action. Methods Vascular hemodynamic, submaximal‐ and maximal‐exercise VO2, and time to exhaustion (TTE) were assessed in 16 participants 2.5 hr following consumption of: 1) BRJ, 2) NaNO3, 3) PLA, or 4) CON. Results A significant treatment effect was observed for submaximal exercise VO2 (p = .003), and TTE (p, Exercise training improves health outcomes in individuals with obesity, however it remains challenging for individuals with obesity to adhere to exercise. Evidence suggests beetroot supplementation improves exercise‐related outcomes in athletes and the non‐obese lean, however the crossover of these effects onto adults with obesity is not clear. This study primarily aimed to determine if beetroot juice improves exercise tolerance and efficiency in individuals with obesity. Supplementation with beetroot juice significantly reduced oxygen uptake during submaximal exercise (~7%), and increased by ~9% during severe‐intensity exercise. Perhaps most notable was a ~22% improvement in time to exhaustion observed following beetroot juice intake compared to control. Taken together acute supplementation with BRJ may be effective for improving exercise tolerance and efficiency in individuals with obesity.

BACKGROUND: Race differences in body composition and fat distribution may in part explain the differences in insulin sensitivity and the disproportionate burden of type 2 diabetes in African Americans. OBJECTIVE: To determine if differences in body composition and fat distribution explain race differences in insulin sensitivity and identify obesity measures that were independently associated with insulin sensitivity. METHODS: Participants were 113 lean, overweight, and obese African-American and Caucasian-American adults without diabetes. Skeletal muscle insulin sensitivity was determined using a hyperinsulinemic-euglycemic clamp (SI(Clamp), insulin rate:120 mU/m(2)/min). Subcutaneous abdominal adipose tissue (SAAT), intra-abdominal adipose tissue (IAAT), and liver fat were measured by MRI; leg fat, total fat, and lean mass were measured by DXA. RESULTS: Race-by-adiposity interactions were significant in cross-sectional analyses utilizing multiple linear regression models for SI(Clamp) (P

Age-related declines in health and function make locomotion increasingly difficult leading to reductions in non-exercise activity thermogenesis (NEAT), skeletal muscle size and strength, and increased adiposity. Exercise is an important strategy to attenuate loss of function through the life cycle. Despite claims to the contrary, high-intensity exercise is important for the prevention of obesity and sarcopenia with advancing age. Therefore, the purpose of this mini-review is to present literature supporting the contention that low volume, high-intensity aerobic and/or resistance training can slow sarcopenia, sustain ease of movement, stimulate NEAT, and attenuate the accretion of fat mass.

IntroductionResting energy expenditure (REE) increases after an intense exercise; however, little is known concerning mechanisms.PurposeThe purpose of this study was to determine effects of a single bout of moderate-intensity continuous (MIC) aerobic exercise, or high-intensity interval (HII

Calorie restriction (CR) decreases adiposity, but the magnitude and defense of weight loss is less than predicted due to reductions in total daily energy expenditure (TEE). The purpose of the current investigation was to determine whether high-intensity interval training (HIIT) would increase markers of sympathetic activation in white adipose tissue (WAT) and rescue CR-mediated reductions in EE to a greater extent than moderate-intensity aerobic exercise training (MIT). Thirty-two 5-wk-old male C57BL/6J mice were placed on ad libitum HFD for 11 wk, followed by randomization to one of four groups ( n = 8/group) for an additional 15 wk: 1) CON (remain on HFD), 2) CR (25% lower energy intake), 3) CR + HIIT (25% energy deficit created by 12.5% CR and 12.5% EE through HIIT), and 4) CR + MIT (25% energy deficit created by 12.5% CR and 12.5% EE through MIT). Markers of adipose thermogenesis ( Ucp1, Prdm16, Dio2, and Fgf21) were unchanged in either exercise group in inguinal or epididymal WAT, whereas CR + HIIT decreased Ucp1 expression in retroperitoneal WAT and brown adipose tissue. HIIT rescued CR-mediated reductions in lean body mass (LBM) and resting energy expenditure (REE), and both were associated with improvements in glucose/insulin tolerance. Improvements in glucose metabolism in the CR + HIIT group appear to be linked to a molecular signature that enhances glucose and lipid storage in skeletal muscle. Exercise performed at either moderate or high intensity does not increase markers of adipose thermogenesis when performed in the presence of CR but remodels skeletal muscle metabolic and thermogenic capacity.

African American (AA) and European American (EA) women often exhibit differences in hemoglobin (Hb) and 25-hydroxyvitamin D [25(OH)D], both of which can be altered by calorie restriction leading to weight loss. Given these known differences, it is of clinical interest to examine the potential for race-specific, adverse responses to weight loss. Sixty-four overweight (BMI 27–29.9 kg/m2), premenopausal women consumed a standardized, very-low calorie diet to reduce BMI < 25 kg/m2. Ancestry informative markers provided estimates of African admixture, an objective mean of expressing race. Blood sampling and anthropometric measures were performed at baseline and upon meeting target BMI. At baseline, in the overweight state, Hb (g/dL) (AA, 11.7 ± 0.9 vs. EA, 12.5 ± 0.8; p < .01) and 25(OH)D (nmol/L) (AA, 35.7 ± 12.9 vs. EA, 57.0 ± 20.0; p < .01) were lower in AAs. After weight loss, Hb decreased (AA, -0.5 ± 0.7 vs. EA, -0.4 ± 0.6; p = .48) to a similar extent among races. Conversely, 25(OH)D increased (AA, 43.4 ± 14.0 vs. EA 68.2 ± 24.3; p < .01) though the magnitude of change (Δ) was not different (AA, +7.8 ± 13.5 vs. EA, +11.2 ± 16.7; p = .37) between races. Multiple linear regression revealed a positive association between ΔHb and Δ25(OH)D (r = .386; p < .01) adjusted for African admixture, Δtestosterone, and Δbody fat%. Path analyses revealed a significant indirect effect of Δbody fat% on ΔHb through Δ25(OH)D, β =-0.023, CI [-0.06, -0.004]. Following 15% weight loss, participants with the largest increase in serum 25(OH)D exhibited the smallest decrease in Hb. Future research should clarify the optimal degree of calorie restriction to stimulate weight loss while mitigating the potential risk of anemia associated with dieting efforts.

Higherin vivofatty acid (FA) oxidation rates have been reported in obese individuals compared to lean counterparts; however whether this reflects a shift in substrate-specific oxidative capacity at the level of the skeletal muscle mitochondria has not been examined. The purpose of this study was to test the hypothesis that in situ measures of skeletal muscle mitochondria FA oxidation would be positively associated with total body fat. Participants were 38 premenopausal women (BMI=26.5±4.3 kg/m2). Total and regional fat were assessed by dual-energy X-ray absorptiometry (DXA). Mitochondrial FA oxidation was assessed in permeabilized myofibers using high-resolution respirometry and a palmitoyl carnitine substrate. We found positive associations of total fat mass with State 3 (ADP-stimulated respiration) (r=0.379,p<0.05) and the respiratory control ratio (RCR, measure of mitochondrial coupling) (r=0.348,p<0.05). When participants were dichotomized by high or low body fat percent, participants with high total body fat displayed a higher RCR compared to those with low body fat (p<0.05). There were no associations between any measure of regional fat and mitochondrial FA oxidation independent of total fat mass. In conclusion, greater FA oxidation in obesity may reflect molecular processes that enhance FA oxidation capacity at the mitochondrial level.

INTRODUCTION/PURPOSE: Aerobic exercise training (AET) has been shown to improve mitochondrial bioenergetics and upregulate proteins related to lipid metabolism. However, it remains to be determined if these alterations associated with AET persist when measured in energy balance (EB) in the days following the last bout of training.. The purpose of the study was to test the hypothesis that improvements in skeletal muscle mitochondrial function induced by AET observed in previous literature would persist when measured after restoring EB conditions 72 hours removed from the last exercise bout. METHODS: Participants were 14 premenopausal women (age = 31.2 ± 6.7 years, BMI = 26.6 ± 5.1 kg/m(2)). The AET program required 3 monitored training sessions per week for 8–16 weeks. Skeletal muscle biopsies were obtained at baseline and following 8–16 weeks of AET (≥72 hrs after the last exercise bout). All food was provided for 72 hours prior to biopsies and EB was managed 24 hours prior to testing within ±100 kcal of measured energy requirements using a whole-room calorimeter. Mitochondrial oxidative capacity was quantified in permeabilized muscle fibers from the vastus lateralis. RESULTS: We found that AET increased coupled respiration (154%) and uncoupled respiration (90%) rates using a fatty acid substrate (palmitoyl carnitine) (P

Aerobic capacity is negatively related to locomotion economy. The purpose of this paper is to determine what effect aerobic exercise training has on the relationship between net cycling oxygen uptake (inverse of economy) and aerobic capacity [peak oxygen uptake (V̇o(2peak))], as well as what role mitochondrial coupled and uncoupled respiration may play in whole body aerobic capacity and cycling economy. Cycling net oxygen uptake and V̇o(2peak) were evaluated on 31 premenopausal women before exercise training (baseline) and after 8–16 wk of aerobic training. Muscle tissue was collected from 15 subjects at baseline and post-training. Mitochondrial respiration assays were performed using high-resolution respirometry. Pre- (r = 0.46, P < 0.01) and postexercise training (r = 0.62, P < 0.01) V̇o(2peak) and cycling net oxygen uptake were related. In addition, uncoupled and coupled fat respiration were related both at baseline (r = 0.62, P < 0.01) and post-training (r = 0.89, P < 01). Post-training coupled (r = 0.74, P < 0.01) and uncoupled carbohydrate respiration (r = 0.52, P < 05) were related to cycle net oxygen uptake. In addition, correlations between V̇o(2peak) and cycle net oxygen uptake persist both at baseline and after training, even after adjusting for submaximal cycle respiratory quotient (an index of fat oxidation). These results suggest that the negative relationship between locomotion economy and aerobic capacity is increased following exercise training. In addition, it is proposed that at least one of the primary factors influencing this relationship has its foundation within the mitochondria. Strong relationships between coupled and uncoupled respiration appear to be contributing factors for this relationship. NEW & NOTEWORTHY The negative relationship between cycle economy and aerobic capacity is increased following exercise training. The strong relationship between coupled and uncoupled respiration, especially after training, appears to be contributing to this negative relationship between aerobic capacity and cycling economy, suggesting that mitochondrial economy is not increased following aerobic exercise training. These results are suggestive that training programs designed to improve locomotion economy should focus on changing biomechanics.

Background: Recent studies in nondisabled individuals have demonstrated that low-volume high-intensity interval training (HIIT) can improve cardiometabolic health similar to moderate-intensity training (MIT) despite requiring 20% of the overall time commitment. To date, there have been no studies assessing the effects of HIIT for improving cardiometabolic health in individuals with SCI. Objectives: The primary purpose of this pilot study was to compare the effects of 6 weeks of low-volume HIIT vs MIT using arm crank ergometer exercise to improve body composition, cardiovascular fitness, glucose tolerance, blood lipids, and blood pressure in a cohort of individuals with longstanding SCI. Methods: Participants were randomized to 6 weeks of HIIT or MIT arm crank exercise training. Aerobic capacity, muscular strength, blood lipids, glucose tolerance, blood pressure, and body composition were assessed at baseline and 6 weeks post training. Results: Seven individuals (6 male, 1 female; n = 3 in MIT and n = 4 in HIIT; mean age 51.3 ± 10.5 years) with longstanding SCI completed the study. The preliminary findings from this pilot study demonstrated that individuals with SCI randomized to either 6 weeks of HIIT or MIT displayed improvements in (a) insulin sensitivity, (b) cardiovascular fitness, and (c) muscular strength ( p < .05). However, MIT led to greater improvements in arm fat percent and chest press strength compared to HIIT ( p < .05). Conclusion: No differences between MIT and HIIT were observed. Both conditions led to improvements in insulin sensitivity, aerobic capacity, muscle strength, and blood lipids in individuals with SCI. Future larger cohort studies are needed to determine if the shorter amount of time required from HIIT is preferable to current MIT exercise recommendations.

Hunter, GR, Neumeier, WH, Chandler-Laney, PC, Carter, SJ, Borges, JH, Hornbuckle, LM, Plaisance, EP, and Fisher, G. Ratings of perceived exertion during walking predicts endurance independent of physiological effort in older women. J Strength Cond Res 34(5): 1340-1344, 2020-This study aimed to determine whether ratings of perceived exertion (RPE) and physiological effort at different exercise intensities relate to exercise endurance. Ninety-eight sedentary women (older than 60 years) completed 3 submaximal locomotion tasks: (a) stair climbing, (b) flat walking at 2 mph, and (c) grade walking at 2 mph. Maximal treadmill endurance was measured at least 3 days before the submaximal tests. Oxygen uptake was measured during all tests, and RPE were collected for the submaximal tasks. Ratings of perceived exertion during moderate-intensity exercise (walking on the flat at 43% V[Combining Dot Above]O2max, partial R = -0.35, p0.01), but not higher intensity exercise (grade walk at 59% V[Combining Dot Above]O2max, p = 0.49, and stair climbing at 67% V[Combining Dot Above]O2max, p = 0.17), were related to endurance even after adjusting for aerobic capacity and physiological effort (composite of maximal heart rate, ventilation, and respiratory exchange ratio). However, physiological effort was significantly related to endurance for the higher intensity exercise (both grade walk and stair climbing partial R-0.24, p0.02). Similar to previous findings that subjective ratings of fatigue at rest were related to RPE during low/moderate-intensity exercise, but not higher intensity exercise, these data further support Ekkekakis's dual-mode hypothesis that cognitive factors influence RPE during low/moderate-intensity exercise. A practical application is that the coach and personal trainer should know that physiological effort seems to play a greater role in influencing endurance than RPE as intensity of exercise increases.

Youth with inflammatory bowel disease (IBD) demonstrate deficits in lean mass (LM) placing them at increased risk for future health problems, including reduction of bone mass and impaired bone architecture. Research suggests that deficits in LM are multifactorial, including influences from the disease and its treatment, and health behaviors such as diet and physical activity. Based on a systematic literature review examining factors related to LM deficits in IBD, this article presents a conceptual model to explain the development of LM in youth with IBD. The model considers predictors of LM across 4 domains: demographic; medical; diet; and physical activity. Much existing research is cross-sectional, but suggests multiple factors work together to promote or inhibit LM accrual in youth with IBD. The conceptual model, developed based on empirical findings to date, can be used to understand and further elucidate the process through which LM is developed and maintained, to inform the development of empirically supported clinical interventions, and to guide future research objectives and priorities.

Sarcopenia not only affects the ability to lead an active lifestyle but also contributes to increased obesity, reduced quality of life, osteoporosis, and metabolic health, in part due to reduced locomotion economy and ease. On the other hand, increased obesity, decreased quality of life, and reduced metabolic health also contribute to sarcopenia. The purpose of this mini-review is to discuss the implications sarcopenia has for the development of obesity and comorbidities that occur with aging.

The dietary R-3-hydroxybutyrate-R-1,3-butanediol monoester increases resting energy expenditure (REE) and markers of brown and white adipose thermogenesis in lean mice. The purpose of this investigation was to determine whether the ketone ester, R,S-1,3-butanediol diacetoacetate (BD-AcAc(2)), increases energy expenditure and markers of adipose tissue thermogenesis in the context of high-fat diet (HFD)–induced obesity. Thirty-five-week–old male C57BL/6J mice were placed on an ad libitum HFD (45% kcal) for 10 wk. The mice were then randomized to 1 of 3 groups (n = 10 per group) for an additional 12 wk: 1) control (Con), continuous HFD, 2) pair-fed (PF) to ketone ester (KE); and 3) KE: HFD+30% energy from BD-AcAc(2). Mean energy intake throughout the study was ∼26% lower in the KE compared to the Con group (8.2 ± 0.5 vs. 11.2 ± 0.7 kcal/d; P < 0.05). Final body weight (26.8 ± 3.6 vs. 34.9 ± 4.8 g; P < 0.001) and fat mass (5.2 ± 1.2 vs. 11.3 ± 4.5 g; P < 0.001) of the KE group was significantly lower than PF, despite being matched for energy provisions. Differences in body weight and adiposity were accompanied by higher REE and total energy expenditure in the KE group compared to PF after adjustment for lean body mass and fat-mass (P = 0.001 and 0.007, respectively). Coupled or uncoupled mitochondrial respiratory rates in skeletal muscle were not different among groups, but markers of mitochondrial uncoupling and thermogenesis (uncoupling protein-1, deiodinase-2, and peroxisome proliferator-activated receptor γ coactivator-1α) were higher in interscapular brown adipose tissue (BAT) of mice receiving the KE diet. The absence of mitochondrial uncoupling in skeletal muscle and increased markers of mitochondrial uncoupling in BAT suggest that BD-AcAc(2) initiates a transcriptional signature consistent with BAT thermogenesis in the context of HFD-induced obesity.—Davis, R. A. H., Deemer, S. E., Bergeron, J. M., Little, J. T., Warren, J. L., Fisher, G., Smith, D. L., Jr., Fontaine, K. R., Dickinson, S. L., Allison, D. B., Plaisance, E. P. Dietary R,S-1,3-butanediol diacetoacetate reduces body weight and adiposity in obese mice fed a high-fat diet.

Hunter, GR, Fisher, G, Bryan, DR, Borges, JH, and Carter, SJ. Divergent blood pressure response after high-intensity interval exercise: a signal of delayed recovery? J Strength Cond Res 32(11): 3004-3010, 2018-The objective of this commentary is to highlight potential factors influential to the adaptation of high-intensity exercise. Herein, we present a rationale supporting the contention that elevated systolic blood pressure, after a bout of high-intensity exercise, may be indicative of delayed/incomplete recovery. Relative to type I skeletal muscle fibers, the unique cellular/vascular characteristics of type II muscle fibers may necessitate longer recovery periods, especially when exposed to repeated high-intensity efforts (i.e., intervals). In addition to the noted race disparities in cardiometabolic disease risk, including higher mean blood pressures, African Americans may have a larger percentage of type II muscle fibers, thus possibly contributing to noted differences in recovery after high-intensity exercise. Given that optimal recovery is needed to maximize physiological adaptation, high-intensity training programs should be individually-tailored and consistent with recovery profile(s). In most instances, even among those susceptible, the risk to nonfunctional overreaching can be largely mitigated if sufficient recovery is integrated into training paradigms.

Objectives This study investigated the effect of weight loss and weight regain on accuracy of perceived exertion (APE) in previously overweight African American (AA) and European American (EA) women. Methods Formerly overweight women (n = 102, age 20–44 years) completed a weight loss program to achieve BMI

AB Purpose: This study aims to determine the effects of aerobic or resistance training on activity-related energy expenditure (AEE; kcal[middle dot]d-1) and physical activity index (activity-related time equivalent (ARTE)) following weight loss. It was hypothesized that weight loss without exercise training would be accompanied by decreases in AEE, ARTE, and nontraining physical activity energy expenditure (nonexercise activity thermogenesis (NEAT)) and that exercise training would prevent decreases in free-living energy expenditure. Methods: One hundred forty premenopausal women had an average weight loss of 25 lb during a diet (800 kcal[middle dot]d-1) of furnished food. One group aerobically trained 3 times per week (40 min[middle dot]d-1), another group resistance-trained 3 times per week (10 exercises/2 sets x 10 repetitions), and the third group did not exercise. Dual-energy x-ray absorptiometry was used to measure body composition, indirect calorimetry was used to measure resting energy expenditure (REE) and walking energy expenditure, and doubly labeled water was used to measure total energy expenditure (TEE). AEE, ARTE, and nontraining physical activity energy expenditure (NEAT) were calculated. Results: TEE, REE, and NEAT all decreased following weight loss for the no-exercise group, but not for aerobic and resistance trainers. Only REE decreased in the two exercise groups. Resistance trainers increased ARTE. HR and oxygen uptake while walking on the flat and up a grade were consistently related to TEE, AEE, NEAT, and ARTE. Conclusions: Exercise training prevents a decrease in energy expenditure, including free-living energy expenditure separate from exercise training, following weight loss. Resistance training increases physical activity, whereas economy/ease of walking is associated with increased TEE, AEE, NEAT, and ARTE.

Cardiometabolic disease remains a leading cause of morbidity and mortality in developed nations. Consequently, identifying and understanding factors associated with underlying pathophysiological processes leading to chronic cardio metabolic conditions is critical. Metabolic health, arterial elasticity, and insulin sensitivity (SI) may impact disease risk, and may be determined in part by myofiber type. Therefore, the purpose of this study was to test the hypothesis that type I myofiber composition would be associated with high SI, greater arterial elasticity, lower blood pressure, and blood lipids; whereas, type IIx myofibers would be associated with lower SI, lower arterial elasticity, higher blood pressure, blood lipids. Muscle biopsies were performed on the vastus lateralis in 16 subjects (BMI = 27.62 ± 4.71 kg/m2, age = 32.24 ± 6.37 years, 43% African American). The distribution of type I, IIa, and IIx myofibers was determined via immunohistochemistry performed on frozen cross-sections. Pearson correlation analyses were performed to assess associations between myofiber composition, SI, arterial elasticity, blood pressure, and blood lipid concentrations. The percentage of type I myofibers positively correlated with SI and negatively correlated with systolic blood pressure SBP, diastolic blood pressure, and mean arterial pressure (MAP); whereas, the percentage of type IIx myofibers were negatively correlated with SI and large artery elasticity, and positively correlated with LDL cholesterol, SBP, and MAP. These data demonstrate a potential link between myofiber composition and cardiometabolic health outcomes in a cohort of premenopausal women. Future research is needed to determine the precise mechanisms in which myofiber composition impacts the pathophysiology of impaired glucose and lipid metabolism, as well as vascular dysfunction.