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Low levels of physical activity and high levels of obesity among children in the US is a public health concern. Accurate methods to estimate physical activity are needed to determine the efficacy of intervention programs and to explore relationships between daily physical activity and health status in children. The purpose of this study was to compare the simultaneous use of the Tritrac-R3D accelerometer (Tritrac), Yamax SW-200 Digiwalker step-counter (Digiwalker) and the Self Administered Physical Activity Checklist (SAPAC) to assess physical activity (PA) and energy expenditure (EE) in African-American children aged 7 to 10 years, using the doubly-labeled water (DLW) as the criterion method. Physical activity and energy expenditure were measured over seven consecutive days under free-living conditions. Resting metabolic rate and peak VO(2) were measured before the experimental period. There was no difference in physical activity energy expenditure (PAEE) measured by Tritrac or DLW (p > 0.05). Tritrac activity counts were highly correlated with DLW-PAEE (r = 0.81). High correlations between Digiwalker and DLW were observed when body weight was considered. A low correlation (r = 0.49) was observed between the physical activity energy expenditure by SAPAC and DLW. In conclusion, with some limitations the Tritrac and Digiwalker can provide useful and accurate information about PA and EE in 7- to 10-year-old children.

This study assessed the ability of four different activity monitors to discriminate changes in treadmill walking velocity. The relationships between walking velocity and bodily movement and between bodily movement and energy expenditure determined by indirect calorimetry (IC-EE or METs) were determined. Twenty-eight subjects walked at 3.2, 4.0, 4.8, 5.6, and 6.4 km/h (0 % grade) for 30 min on separate occasions. The Tritrac-R3D (TT), Computer Science & Applications, Inc. (CSA), and Mini-Logger (ML) activity monitors that measure bodily acceleration in one or three planes, and a Yamax Digiwalker-500 (YX) that records footsteps, were secured at the waistline of each subject. CSA monitors were also worn at the wrist and ankle. Walking velocity and bodily movement were significantly related (r = 0.89 to 0.93) for TT, CSA, ML, and YX. Importantly, changing each walking velocity produced significant changes in bodily movement that was detected by each monitor. Bodily movement and IC-EE were significantly related for TT, CSA, ML, and YX (r = 0.47 to 0.94). Compared to IC-EE, and at all walking speeds, EE was significantly overestimated by the TT, and EE was significantly underestimated by the YX. These results indicate that the activity monitors can differentiate bodily movement associated with walking at slow speeds better than they can estimate energy expenditure associated with walking at slow speeds.

This study evaluated the ability of a commercially available accelerometer (Tritrac-R3 D) to measure energy expenditure in 16 subjects at rest (pre- and post-exercise) and during three different intensities of steady-state exercise (40-70% of peak oxygen consumption [VO2peak]) while ambulating on a treadmill (no grade). Oxygen consumption and the respiratory exchange ratio from indirect calorimetry and the vector magnitude of triaxial accelerations were used to estimate energy expenditure using the manufacturers' equations. There was a significant relationship between indirect calorimetry-derived energy expenditure and the energy expenditure derived from the accelerometer (r=0.96). Using analysis of variance, there was no difference in the energy expenditure derived by the two methods at rest before exercise and during the three different intensities of ambulatory exercise. There was a significant difference between energy expenditure derived via indirect calorimetry and with the accelerometer during rest after exercise, probably due to the failure of the accelerometer to accurately estimate the energy expenditure associated with the progressive decline in post-exercise oxygen consumption. Thus, this commercially available accelerometer appears to provide statistically acceptable estimates of energy expenditure at rest and during zero-grade treadmill ambulation up to about 70% VO2peak. This may indicate its acceptable utility for large-scale population studies of physical activity involving this mode of movement. The failure of the accelerometer to accurately estimate energy expenditure during recovery from exercise may contribute to an underestimation of energy expenditure in some physically active individuals.

The recently cloned obesity gene (ob) encodes a protein, leptin, which is secreted from adipose tissue and interacts with hypothalamic receptors to decrease appetite, increase energy expenditure, and reduce body lipid stores. The levels of ob mRNA are increased in several models of obesity, consistent with the hypothesis that obese animals may be resistant to the actions of leptin. The present study examined the impact of increased energy expenditure through exercise training on ob mRNA gene expression and body composition in the SHHF/Mc-fa(cp) male rat, a rodent model of obesity, insulin resistance, and type II diabetes. Six week old lean and obese animals were trained 8-12 weeks by treadmill running at 70% peak oxygen uptake, 5 days/wk, for 1.5 hr/day. After endurance training, exercised rats had significantly lower total body fat compared to sedentary rats of the same age, despite maintaining the same body weight. In the obese SHHF/Mcc-fa(cp) rat, the level of ob mRNA expression was markedly increased by four fold in subcutaneous adipose tissue compared to lean controls (p<0.05). In response to exercise training, there was a significant 85 % decrease in ob mRNA in exercised-training lean rats (p < 0.05) compared with non-exercised controls, while in obese-exercised rats, ob gene expression was significantly reduced only by 50% relative to non-exercised obese rats (p < 0.05). These results demonstrate that exercise training reduces fat mass and ob mRNA in lean and obese rats, and supports the hypothesis of a feedback loop between the adipocyte and hypothalamus that attempts to maintain body weight at a constant level by reducing ob gene expression in response to increased energy expenditure.

This study examined the effect of three exercise-diet regimens on muscle glycogen supercompensation and subsequent performance during a 20.9-km run. A diet containing 15% carbohydrate (CHO,L), 50% CHO (M), or 70% (CHO (H) was arranged in three trials as follows: trial A = 3 days L, 3 days H; trial B = 3 days M, 3 days H; trial C = 6 days M. For each trial a 5-day depletion-taper exercise sequence was conducted on the treadmill at 73% VO2 max. The runs were 90, 40, 40, 20, and 20 min, respectively. A day of rest preceded the 20.9-km performance run. Muscle biopsies were obtained from the gastrocnemius on days 4 and 7 (both prior to and after the performance run). Trials A, B, and C elevated muscle glycogen to 207, 203, and 159 mmol glucosyl units/kg wet tissue (mmG), respectively. The performance run in both trials A and B utilized significantly more glycogen than in trial C: 5.0 and 5.1 mmG/km vs. 3.1 mmG/km. There were, however, no differences in either performance run times or post-performance run glycogen levels between the trials. These data demonstrate that (1) muscle glycogen can be elevated to high levels with a moderate exercise-diet regimen; (2) initial muscle glycogen levels influence the amount subsequently utilized during exercise; (3) carbohydrate loading is of no benefit to performance for trained runners during a 20.9-km run.

This study examined the relationship between muscle glycogen and muscle water content. Exercise dietary manipulations were used to vary skeletal muscle glycogen levels in four groups of rodents: (1) eight animals were sedentary controls (SC); (2) ten animals were treadmill familiarized and allowed to recover 24 h before sacrifice (F); (3) ten animals were treadmill familiarized and exercised to exhaustion (E); (4) ten animals were treadmill familiarized, exercised to exhaustion, and allowed to recover with food and water ad libitum for 72 h (ER). All animals were sacrificed in a resting state to normalize intracellular, extracellular, and interstitial water compartments; thus, the E group was sacrificed 45 m in following their run. The treatments altered skeletal muscle glycogen to values ranging from 10.0 to 30.2 mumol glucosyl units/g wet tissue weight. Neither muscle triglyceride nor protein levels were affected by the treatments. Muscle water content expressed as mumol H2O lost/g wet tissue weight or made relative to protein content showed no consistent relationship to the glycogen content. These data, therefore, do not support the commonly accepted muscle glycogen-to-water ratio of 1.0:2.7 (g:g). Further work is necessary to quantify the exact amount of water that is actually associated with the glycogen complex.