Resting energy expenditure and delayed-onset muscle soreness after full-body resistance training with an eccentric concentration

The purpose of this investigation was to determine the effect of an acute bout of high-volume, full-body resistance training with an eccentric concentration on resting energy expenditure (REE) and indicators of delayed-onset muscle soreness (DOMS). Eight resistance trained (RT) and eight untrained (UT) participants (mean: age = 23.5 years; height = 180.76 cm; weight = 87.58 kg; body fat = 19.34%; lean mass = 68.71 kg) were measured on four consecutive mornings for REE and indicators of DOMS: creatine kinase (CK) and rating of perceived muscle soreness (RPMS). Delayed-onset muscle soreness was induced by performing eight exercises, eight sets, and six repetitions using a 1-second concentric and 3-second eccentric muscle action duration. A two-factor repeated-measures analysis of variance revealed that REE was significantly (p < 0.05) elevated at 24, 48, and 72 hours post compared with baseline measures for both UT and RT groups. Ratings of perceived muscle soreness were significantly elevated within groups for UT and RT at 24 and 48 hours post and for UT only at 72 hours post compared with baseline (p < 0.05). Nonparametric analyses revealed that CK was significantly increased at 24 hours post for both UT and RT and at 48 and 72 hours post for UT only compared with baseline (p < 0.05). Resting energy expenditure and indicators of DOMS were higher in UT compared with RT on all measures, but no significant differences were determined. The main finding of this investigation is that full-body resistance training with an eccentric concentration significantly increased REE up to 72 hours postexercise in UT and RT participants.     

Restriction of energy intake, energy expenditure, and aging

Energy restriction (ER), without malnutrition, increases maximum life span and retards the development of a broad array of pathophysiological changes in laboratory rodents. The mechanism responsible for the retardation of aging by ER is, however, unknown. One proposed explanation is a reduction in energy expenditure (EE). Reduced EE may increase life span by decreasing the number of oxygen molecules interacting with mitochondria, thereby lowering reactive oxygen species (ROS) production. As a step toward testing this hypothesis, it is important to determine the effect of ER on EE. Several whole-body, organ, and cellular studies have measured the influence of ER on EE. In general, whole-body studies have reported an acute decrease in mass-adjusted EE that disappears with long-term ER. Organ-specific studies have shown that decreases in EE of liver and gastrointestinal tract are primarily responsible for initial reductions in EE with ER. These data, however, do not determine whether cellular EE is altered with ER. Three major processes contributing to resting EE at the cellular level are mitochondrial proton leak, Na(+)-K(+)-ATPase activity, and protein turnover. Studies suggest that proton leak and Na(+)-K(+)-ATPase activity are decreased with ER, whereas protein turnover is either unchanged or slightly increased with ER. Thus, two of the three major processes contributing to resting EE at the cellular level may be decreased with ER. Although additional cellular measurements are needed, the current results suggest that a lowering of EE could be a mechanism for the action of ER.     

Resting energy expenditure in young adults born preterm--the Helsinki study of very low birth weight adults

Background

Adults born preterm with very low birth weight (VLBW; <1500g) have higher levels of cardiovascular and metabolic risk factors than their counterparts born at term. Resting energy expenditure (REE) could be one factor contributing to, or protecting from, these risks. We studied the effects of premature birth with VLBW on REE.

Methodology/Principal Findings

We used indirect calorimetry to measure REE and dual x-ray absorptiometry (DXA) to measure lean body mass (LBM) in 116 VLBW and in 118 term-born control individuals (mean age: 22.5 years, SD 2.2) participating in a cohort study. Compared with controls VLBW adults had 6.3% lower REE (95% CI 3.2, 9.3) adjusted for age and sex, but 6.1% higher REE/LBM ratio (95% CI 3.4, 8.6). These differences remained similar when further adjusted for parental education, daily smoking, body fat percentage and self-reported leisure time exercise intensity, duration and frequency.

Conclusions/Significance

Adults born prematurely with very low birth weight have higher resting energy expenditure per unit lean body mass than their peers born at term. This is not explained by differences in childhood socio-economic status, current fat percentage, smoking or leisure time physical activity. Presence of metabolically more active tissue could protect people with very low birth weight from obesity and subsequent risk of chronic disease.     

Activity and energy expenditure

The influence of small changes in activity on energy expenditure and hence on energy requirements and energy balance is assessed. Evidence from direct and indirect calorimetry suggests that differences in spontaneous minor activity could readily alter 24-h energy expenditure by as much as 20%. This compares with values in the order of 10% for moderate overfeeding and somewhat less than this during mild cold exposure. Individual variability in 24-h energy expenditure can therefore be accounted for not only by differences in resting metabolism and the thermic responses to energy intake and temperature but also by differences in minor activity. Interactions between activity and environmental factors such as nutrition and temperature can modify the effect of activity on energy balance. Very little is known about mechanisms that could account for differences in spontaneous activity and these need to be the subject of future investigations.     

Comparison of energy expenditure and substrate oxidation between walking and running in men and women

[Purpose]The present study compared energy metabolism between walking and running at equivalent speeds during two incremental exercise tests.[Methods]Thirty four university students (18 males, 16 females) were recruited. Each participant completed two trials, consisting of walking (Walk) and running (Run) trials on different days, with 2-3 days apart. Exercise on a treadmill was started from initial stage of 3 min (3.0 k/m in Walk trial, 5.0 km/h in Run trial), and the speed for walking and running was progressively every minute by 0.5 km/h. The changes in metabolic variables, heart rate (HR), and rating of perceived exertion (RPE) during exercise were compared between the trials.[Results]Energy expenditure (EE) increased with speed in each trial. However, the Walk trial had a significantly higher EE than the Run trial at speeds exceeding 92 ± 2 % of the maximal walking speed (MWS, p < 0.01). Similarly, carbohydrate (CHO) oxidation was significantly higher in the Walk trial than in the Run trial at above 92 ± 2 %MWS in males (p < 0.001) and above 93 ± 1 %MWS in females (p < 0.05).[Conclusion]These findings suggest that EE and CHO oxidation during walking increase non-linearly with speed, and walking at a fast speed causes greater metabolic responses than running at the equivalent speed in young participants.     

Short-term, increasing dietary protein and fat moderately affect energy expenditure, substrate oxidation and uncoupling protein gene expression in rats

Macronutrient composition of diets can influence body-weight development and energy balance. We studied the short-term effects of high-protein (HP) and/or high-fat (HF) diets on energy expenditure (EE) and uncoupling protein (UCP1-3) gene expression. Adult male rats were fed ad libitum with diets containing different protein-fat ratios: adequate protein-normal fat (AP-NF): 20% casein, 5% fat; adequate protein-high fat (AP-HF): 20% casein, 17% fat; high protein-normal fat (HP-NF): 60% casein, 5% fat; high protein-high fat (HP-HF): 60% casein, 17% fat. Wheat starch was used for adjustment of energy content. After 4 days, overnight EE and oxygen consumption, as measured by indirect calorimetry, were higher and body-weight gain was lower in rats fed with HP diets as compared with rats fed diets with adequate protein content (P<.05). Exchanging carbohydrates by protein increased fat oxidation in HF diet fed groups. The UCP1 mRNA expression in brown adipose tissue was not significantly different in HP diet fed groups as compared with AP diet fed groups. Expression of different homologues of UCPs positively correlated with nighttime oxygen consumption and EE. Moreover, dietary protein and fat distinctly influenced liver UCP2 and skeletal muscle UCP3 mRNA expressions. These findings demonstrated that a 4-day ad libitum high dietary protein exposure influences energy balance in rats. A function of UCPs in energy balance and dissipating food energy was suggested. Future experiments are focused on the regulation of UCP gene expression by dietary protein, which could be important for body-weight management.     

An energy 'sources' and 'fractions' approach to the mechanical energy expenditure problem--III. Mechanical energy expenditure reduction during one link motion

Mechanical energy economy and transformation during one link motion are analyzed on the basis of the theory developed in the previous publications (parts I and II of this series, J. Biomechanics 19, 287-300). The 'compensation coefficient' characterizing mechanical energy economy is introduced. The attempts to estimate MEE using only energy curves and neglecting the powers of real sources of energy implicitly lead to replacement of real force and moment systems by the systems reduced to the centers of mass. But such an unintentional substitution of imaginary sources for real ones, specifically, the reduction of forces acting on the link to the equivalent system, changes estimates of mechanical energy expenditure (MEE). That is why the methods of calculating MEE economy based on the determination of so-called 'quasi-mechanical' work (the sum of the kinetic and potential energy increases per one cycle of motion) are not correct. There are two mechanisms to reduce the MEE using the antiphase fluctuations (corresponding to energy transformations) of the (a) rotational and translational fractions of the total energy (at the expense of the F-sources); (b) potential and kinetic energies (at the expense of the mg-source).     

Regulation of myocardial substrate metabolism during increased energy expenditure: insights from computational studies

In response to exercise, the heart increases its metabolic rate severalfold while maintaining energy species (e.g., ATP, ADP, and Pi) concentrations constant; however, the mechanisms that regulate this response are unclear. Limited experimental studies show that the classic regulatory species NADH and NAD+ are also maintained nearly constant with increased cardiac power generation, but current measurements lump the cytosol and mitochondria and do not provide dynamic information during the early phase of the transition from low to high work states. In the present study, we modified our previously published computational model of cardiac metabolism by incorporating parallel activation of ATP hydrolysis, glycolysis, mitochondrial dehydrogenases, the electron transport chain, and oxidative phosphorylation, and simulated the metabolic responses of the heart to an abrupt increase in energy expenditure. Model simulations showed that myocardial oxygen consumption, pyruvate oxidation, fatty acids oxidation, and ATP generation were all increased with increased energy expenditure, whereas ATP and ADP remained constant. Both cytosolic and mitochondrial NADH/NAD+ increased during the first minutes (by 40% and 20%, respectively) and returned to the resting values by 10-15 min. Furthermore, model simulations showed that an altered substrate selection, induced by either elevated arterial lactate or diabetic conditions, affected cytosolic NADH/NAD+ but had minimal effects on the mitochondrial NADH/NAD+, myocardial oxygen consumption, or ATP production. In conclusion, these results support the concept of parallel activation of metabolic processes generating reducing equivalents during an abrupt increase in cardiac energy expenditure and suggest there is a transient increase in the mitochondrial NADH/NAD+ ratio that is independent of substrate supply.     

The effects of movement velocity during squatting on energy expenditure and substrate utilization in whole-body vibration

The purpose of this study was to examine whether and how cycle time duration affects energy expenditure and substrate utilization during whole-body vibration (WBV). Nine men performed 3 squatting exercises in execution frequency cycles of 6, 4, and 2 seconds to 90 degrees knee flexion with vibration (Vb+) (frequency was set at 30 Hz and the amplitude of vibration was 4 mm) and without vibration (Vb-) during 3 minutes, each with an additional load of 30% of the subject's body weight. A 2-way analysis of variance for VO2 revealed a significant vibration condition main effect (p < 0.001) and a cycle time duration effect (p < 0.001). When differences were analyzed by Fisher's LSD test, cycle time duration of 2 seconds was significantly different from 4 and 6 seconds, both in Vb+ and Vb-. Total energy expenditure (EE(tot)), carbohydrate oxidation rate (EE(cho)), and fat oxidation rate (EE(fat)) demonstrated a significant vibration condition main effect (EE(tot): p < 0.01; EE(cho): p < 0.001; EE(fat): p < 0.001) and cycle time duration main effect (EE(tot) and EE(cho): p < 0.001; EE(fat): p < 0.01). EE(tot), EE(cho), and EE(fat) post hoc comparisons indicated that values for the 2-second test significantly differed from 4 and 6 seconds when compared in the same vibration condition. VO2 and EE values were greater in Vb+ than in Vb- conditions with the same cycle time duration. Our study confirms that squatting at a greater frequency helps to maximize energy expenditure during exercise with or without vibration. Therefore, cycle time duration must be controlled when vibration exercise is prescribed.     

Reduction in postprandial energy expenditure during pregnancy.

Energy expenditure was measured during pregnancy in seven primigravid women at 12-15, 25-28, and 34-36 weeks and after the cessation of lactation. On each occasion the resting metabolic rate and the increase in metabolic rate after ingestion of a liquid test meal were measured by indirect calorimetry. In absolute terms the resting metabolic rate increased steadily during pregnancy but when expressed per unit of body weight no change was found. The energetic response to a mixed constituent meal was significantly reduced by 28% in the middle trimester of pregnancy. These findings suggest a possible maternal adaptation to increase energetic efficiency at a time when the energy demands of the fetus are high.     

Effect of beta1- and beta2-adrenergic stimulation on energy expenditure,substrate oxidation,and UCP3 expression in humans

In humans, beta-adrenergic stimulation increases energy and fat metabolism. In the case of beta1-adrenergic stimulation, it is fueled by an increased lipolysis. We examined the effect of beta2-adrenergic stimulation, with and without a blocker of lipolysis, on thermogenesis and substrate oxidation. Furthermore, the effect of beta1-and beta2-adrenergic stimulation on uncoupling protein 3 (UCP3) mRNA expression was studied. Nine lean males received a 3-h infusion of dobutamine (DOB, beta1) or salbutamol (SAL, beta2). Also, we combined SAL with acipimox to block lipolysis (SAL+ACI). Energy and substrate metabolism were measured continuously, blood was sampled every 30 min, and muscle biopsies were taken before and after infusion. Energy expenditure significantly increased approximately 13% in all conditions. Fat oxidation increased 47 +/- 7% in the DOB group and 19 +/- 7% in the SAL group but remained unchanged in the SAL+ACI condition. Glucose oxidation decreased 40 +/- 9% upon DOB, remained unchanged during SAL, and increased 27 +/- 11% upon SAL+ACI. Plasma free fatty acid (FFA) levels were increased by SAL (57 +/- 11%) and DOB (47 +/- 16%), whereas SAL+ACI caused about fourfold lower FFA levels compared with basal levels. No change in UCP3 was found after DOB or SAL, whereas SAL+ACI downregulated skeletal muscle UCP3 mRNA levels 38 +/- 13%. In conclusion, beta2-adrenergic stimulation directly increased energy expenditure independently of plasma FFA levels. Furthermore, this is the first study to demonstrate a downregulation of skeletal muscle UCP3 mRNA expression after the lowering of plasma FFA concentrations in humans, despite an increase in energy expenditure upon beta2-adrenergic stimulation.     

An energy 'sources' and 'fractions' approach to the mechanical energy expenditure problem--V. The mechanical energy expenditure reduction during motion of the multi-link system

Mechanical energy economy during motion of the multi-link system is analyzed on the basis of the theory developed in the previous publications (parts I-IV of this series, J. Biomechanics 19, 287-309). The compensation coefficients for the F- and M-sources and also the absolute compensation coefficient reflecting the mechanical energy economy due to four possible resources are introduced. These resources are the antiphase fluctuations of (I) each link's total energy fractions involving energy transformations between (1) rotational and translational fractions by F-sources, (2) kinetic and potential fractions by mg-source; (II) the links' total energies involving energy transfers between (3) links by F-sources, (4) links by M-sources. The conditions of mechanical energy economy, particularly due to M-sources, are analyzed.     

Catecholamine release, growth hormone secretion, and energy expenditure during exercise vs. recovery in men.

We examined the relationship between energy expenditure (in kcal) and epinephrine (Epi), norepinephrine (NE), and growth hormone (GH) release. Ten men [age, 26 yr; height, 178 cm; weight, 81 kg; O(2) uptake at lactate threshold (LT), 36.3 ml. kg(-1). min(-1); peak O(2) uptake, 49.5 ml. kg(-1). min(-1)] were tested on six randomly ordered occasions [control, 5 exercise: at 25 and 75% of the difference between LT and rest (0.25LT, 0.75LT), at LT, and at 25 and 75% of the difference between LT and peak (1.25LT, 1.75LT) (0900-0930)]. From 0700 to 1300, blood was sampled and assayed for GH, Epi, and NE. Carbohydrate (CHO) expenditure during exercise and fat expenditure during recovery rose proportionately to increasing exercise intensity (P = 0.002). Fat expenditure during exercise and CHO expenditure during recovery were not affected by exercise intensity. The relationship between exercise intensity and CHO expenditure during exercise could not be explained by either Epi (P = 1.00) or NE (P = 0.922), whereas fat expenditure during recovery increased with Epi and GH independently of exercise intensity (P = 0. 028). When Epi and GH were regressed against fat expenditure during recovery, only GH remained statistically significant (P < 0.05). We conclude that a positive relationship exists between exercise intensity and both CHO expenditure during exercise and fat expenditure during recovery and that the increase in fat expenditure during recovery with higher exercise intensities is related to GH release.     

Field use of D2 18O to measure energy expenditure of soldiers at different energy intakes

To test the application of doubly labeled water under adverse field conditions, energy expenditures of 16 special operations soldiers were measured during a 28-day field training exercise. Subjects were matched by fat-free mass and divided equally between an ad libitum ready-to-eat meal diet and a 2,000 kcal/day lightweight ration. Subjects recorded intakes daily, and body composition was measured before and after the exercise. At the beginning of the study, subjects moved to a new northerly location and, therefore, a new water supply. To compensate for this, a group of soldiers who did not receive heavy water was followed to measure isotopic base-line changes. Energy expenditure by doubly labeled water was in agreement with intake/balance (3,400 +/- 260 vs. 3,230 +/- 520 kcal/day). The overall coefficient of variation of energy expenditure by doubly labeled water was half that of intake/balance (7.6 vs. 16.1%). The coefficient of variation of repeat measures with doubly labeled water was 7.3%. Energy expenditure of the ready-to-eat meal group, 3,540 +/- 180 kcal/day, was not significantly different from the lightweight ration group, 3,330 +/- 301 kcal/day. Doubly labeled water was valid under field conditions.     

Sensitivity of methods for calculating energy expenditure by use of doubly labeled water

Attempts to estimate human energy expenditure by use of doubly labeled water have produced three methods currently used for calculating carbon dioxide production from isotope disappearance data: 1) the two-point method, 2) the regression method, and 3) the integration method. An ideal data set was used to determine the error produced in the calculated energy expenditure for each method when specific variables were perturbed. The analysis indicates that some of the calculation methods are more susceptible to perturbations in certain variables than others. Results from an experiment on one adult human subject are used to illustrate the potential for error in actual data. Samples of second void urine, 24-h urine, and breath collected every other day for 21 days are used to calculate the average daily energy expenditure by three calculation methods. The difference between calculated energy expenditure and metabolizable energy on a weight-maintenance diet is used to estimate the error associated with the doubly labeled water method.     

Training, muscle volume, and energy expenditure in nonobese American girls

Little is known about the relationship among training,energy expenditure, muscle volume, and fitness in prepubertalgirls. Because physical activity is high in prepubertalchildren, we hypothesized that there would be no effect of training.Forty pre- and early pubertal (mean age 9.1 ± 0.1 yr) nonobesegirls enrolled in a 5 day/wk summer school program for 5 wk and were randomized to control (n = 20) or training groups(n = 20; 1.5 h/day, endurance-type exercise). Totalenergy expenditure (TEE) was measured using doubly labeled water, thighmuscle volume using magnetic resonance imaging, and peak O₂uptake (O_2 peak) using cycle ergometry.TEE was significantly greater (17%, P < 0.02) in thetraining girls. Training increased thigh muscle volume (+4.3 ± 0.9%, P < 0.005) andO_2 peak (+9.5 ± 6%,P < 0.05), effects surprisingly similar to thoseobserved in adolescent girls using the same protocol (Eliakim A,Barstow TJ, Brasel JA, Ajie H, Lee W-NP, Renslo R, Berman N, and CooperDM, J Pediatr 129: 537-543, 1996). We furthercompared these two sample populations: thigh muscle volume per weightwas much lower in adolescent compared with prepubertal girls (17.0 ± 0.3 vs. 27.8 ± 0.6 ml/kg body mass; P < 0.001), and allometric analysis revealed remarkably low scaling factorsrelating muscle volume (0.34 ± 0.05, P < 0.0001), TEE (0.24 ± 0.06, P < 0.0004), andO_2 peak (0.28 ± 0.07, P < 0.0001) to body mass in all subjects. Muscle andcardiorespiratory functions were quite responsive to brief training inprepubertal girls. Moreover, a retrospective, cross-sectional analysissuggests that increases in muscle mass andO_2 peak may be depressed in nonobeseAmerican girls as they mature.

     

Pten positively regulates brown adipose function, energy expenditure, and longevity

Aging in worms and flies is regulated by the PI3K/Akt/Foxo pathway. Here we extend this paradigm to mammals. Pten(tg) mice carrying additional genomic copies of Pten are protected from cancer and present a significant extension of life span that is independent of their lower cancer incidence. Interestingly, Pten(tg) mice have an increased energy expenditure and protection from metabolic pathologies. The brown adipose tissue (BAT) of Pten(tg) mice is hyperactive and presents high levels of the uncoupling protein Ucp1, which we show is a target of Foxo1. Importantly, a synthetic PI3K inhibitor also increases energy expenditure and hyperactivates the BAT in mice. These effects can be recapitulated in isolated brown adipocytes and, moreover, implants of Pten(tg) fibroblasts programmed with Prdm16 and Cebpβ form subcutaneous brown adipose pads more efficiently than wild-type fibroblasts. These observations uncover a role of Pten in promoting energy expenditure, thus decreasing nutrient storage and its associated damage.