Development and cross-validation of prediction equations for estimating resting energy expenditure in severely obese Caucasian children and adolescents

The objectives of the present study were to develop and cross-validate new equations for predicting resting energy expenditure (REE) in severely obese children and adolescents, and to determine the accuracy of new equations using the Bland–Altman method. The subjects of the study were 574 obese Caucasian children and adolescents (mean BMI z-score 3·3). REE was determined by indirect calorimetry and body composition by bioelectrical impedance analysis. Equations were derived by stepwise multiple regression analysis using a calibration cohort of 287 subjects and the equations were cross-validated in the remaining 287 subjects. Two new specific equations based on anthropometric parameters were generated as follows: (1) REE=(Sex×892·68)−(Age×115·93)+(Weight×54·96)+(Stature×1816·23)+1484·50 (R2 0·66; se 1028·97 kJ); (2) REE=(Sex×909·12)−(Age×107·48)+(fat-free mass×68·39)+(fat mass×55·19)+3631·23 (R2 0·66; se 1034·28 kJ). In the cross-validation group, mean predicted REE values were not significantly different from the mean measured REE for all children and adolescents, as well as for boys and for girls (difference <2 %) and the limits of agreement (±2 sd) were +2·06 and −1·77 MJ/d (NS). The new prediction equations allow an accurate estimation of REE in groups of severely obese children and adolescents. These equations might be useful for health care professionals and researchers when estimating REE in severely obese children and adolescents

benefits of aerobic exercise training with recommendations for healthy aging

The purpose of this article is to provide an overview on the importance of aerobic exercise and its characteristics for healthy aging. The first section briefly reviews the effects of aging on maximal aerobic power; Section 2 considers the effects of aerobic exercise training, and Section 3 summarizes the recommendations and some limitations of the current guidelines for aerobic exercise training. Physical activity cannot stop the biological aging processes; however, there is evidence that regular aerobic exercise can minimize the physiological effects of an otherwise sedentary lifestyle and increase active life expectancy by limiting the development and progression of chronic disease and disability conditions. The use of moderately standardized guidelines for exercise prescription resulted in safe and effective impact on health-related outcomes

Glucose pulse. A simple method to estimate the amount of glucose oxidized during exercise in type 1 diabetic patients

In type 1 diabetic patients, exercise contributes to enhance insulin sensitivity and may help, together with diet and insulin therapy, to achieve and maintain better metabolic control. Fat and carbohydrates are the main substrates for energy production in skeletal muscle during aerobic exercise in well-fed humans, with their relative contribution to total energy production being a function of exercise intensity. Below the anaerobic threshold, both oxygen consumption and heart rate during exercise increase linearly as a function of exercise intensity. On the basis of these relationships, the aim of the present study was to verify the possibility of using heart rate to estimate the amount of glucose oxidized during exercise in type 1 diabetic patients as well as in a control group of healthy subjects. This study shows that heart rate can be a useful physiological parameter to be used to estimate the amount of glucose oxidized during exercise

Skeletal muscle oxidative function in vivo and ex vivo in athletes with marked hypertrophy from resistance training

Oxidative function during exercise was evaluated in 11 young athletes with marked skeletal muscle hypertrophy induced by long-term resistance training (RTA, body mass 102.67.3 kg, meanSD) and 11 controls (CTRL, body mass 77.86.0). Pulmonary O2 uptake (V\u27O2) and vastus lateralis muscle fractional O2 extraction (by near-infrared spectroscopy) were determined during an incremental cycle ergometer (CE) and one-leg knee-extension (KE) exercise. Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in permeabilized vastus lateralis fibers obtained by biopsy. Quadriceps femoris muscle cross sectional area, volume (determined by magnetic resonance imaging) and strength were greater in RTA vs. CTRL (by ~40%, ~33% and ~20%, respectively). V\u27O2peak during CE was higher in RTA vs. CTRL (4.050.64 L min-1 vs. 3.560.30)no difference between groups was observed during KE. The O2 cost of CE exercise was not different between groups. When divided per muscle mass (for CE) or quadriceps muscle mass (for KE) V\u27O2peak was lower (by 15-20%) in RTA vs. CTRL. Vastus lateralis fractional O2 extraction was lower in RTA vs. CTRL at all work rates, both during CE and KE. RTA had higher ADP-stimulated mitochondrial respiration (56.723.7 pmolO2s-1mg-1 ww) vs. CTRL (35.710.2), and a tighter coupling of oxidative phosphorylation. In RTA the greater muscle mass and maximal force, and the enhanced mitochondrial respiration seem to compensate for the hypertrophy-induced impaired peripheral O2 diffusion. The net results are an enhanced whole body oxidative function at peak exercise, and unchanged efficiency and O2 cost at submaximal exercise, despite a much greater body mas

Tensiomyography detects early hallmarks of bed-rest-induced atrophy before changes in muscle architecture.

In young and older people skeletal muscle mass is reduced after as little as seven days of disuse. The declines in muscle mass after such short periods are of high clinical relevance, particularly in older people who show higher atrophy rate, and a slower, or even a complete lack of muscle mass recovery after disuse. Ten men (24.3± 2.6 years) underwent 35 days of 6° head-down tilt bed rest followed by 30 days of recovery. During bed rest, a neutral energy balance was maintained, with three weekly passive physiotherapy sessions to minimise muscle soreness and joint stiffness. All measurements were performed in a hospital at days 1-10 (BR1-BR10), day 16 (BR16), 28 (BR28) and 35 (BR35) of bed rest, and day 1 (R+1), 3 (R+3) and 30 (R+30) after reambulation. Vastus medialis obliquus (VMO), vastus medialis longus (VML) and biceps femoris (BF) thickness (d) and pennation angle (Θ) were assessed by ultrasonography, while twitch muscle belly displacement (Dm) and contraction time (Tc) were assessed with tensiomyography. After bed rest, d and Θ decreased by 13-17% in all muscles (P<.001) and had recovered at R+30. Dm was increased by 42.3-84.4% (P<.001) at BR35 and preceded the decrease in d by 7, 5 and 3 days in VMO, VML and BF, respectively. Tc increased only in BF (32.1%; P<.001) and was not recovered at R+30. Tensiomyography can detect early bed-rest-induced changes in muscle with higher sensitivity before overt architectural changes and atrophy can be detected

Computerized cognitive training and brain derived neurotrophic factor during bed rest: Mechanisms to protect individual during acute stress

Acute stress, as bed rest, was shown to increase plasma level of the neurotrophin brain-derived neurotrophic factor (BDNF) in older, but not in young adults. This increase might represent a protective mechanism towards acute insults in aging subjects. Since computerized cognitive training (CCT) is known to protect brain, herein we evaluated the effect of CCT during bed rest on BDNF, muscle mass, neuromuscular function and metabolic parameters. The subjects that underwent CCT did not show an increase of BDNF after bed rest, and showed an anti-insular modification pattern in metabolism. Neuromuscular function parameters, already shown to beneficiate from CCT, negatively correlated with BDNF in research participants undergoing CCT, while positively correlated in the control group. In conclusion, BDNF increase can be interpreted as a standardized protective mechanism taking place whenever an insult occurs; it gives low, but consistent preservation of neuromuscular function. CCT, acting as an external protective mechanism, seems to modify this standardized response, avoiding BDNF increase or possibly modifying its time course. Our results suggest the possibility of differential neuroprotective mechanisms among ill and healthy individuals, and the importance of timing in determining the effects of protective mechanism