Several rodent models of obesity have been shown to develop excessive adiposity only when voluntary cage ambulation is restricted. We have previously shown that mice lacking the sarco(endo)plasmic reticulum Ca2+-ATPase pump regulatory protein sarcolipin (Sln–/–), an uncoupler of Ca2+ uptake, develop excessive diet-induced obesity under standard housing conditions. However, it is unclear whether this phenotype is due, in part, to the sedentary housing environment in which these animals are kept. To address this, we allowed wild-type and Sln–/– animals ad libitum access to voluntary wheel running while consuming a standard chow or high-fat diet for 8 weeks. During this period, wheel revolutions were monitored along with weekly mass gain. Postdiet glucose tolerance and visceral adiposity were also taken. The volume of wheel running completed was similar between genotype, regardless of diet. Although voluntary activity reduced mass gain relative to sedentary controls within each diet (P < 0.05), visceral adiposity was surprisingly unaltered with activity. However, Sln–/– mice developed excessive obesity (P < 0.05) and glucose intolerance (P < 0.05) with high-fat feeding relative to wild-type controls. These findings indicate that the excessive diet-induced obese phenotype previously observed in Sln–/– mice is not the result of severely restricted daily ambulation, but in fact the inability to recruit uncoupling of the Ca2+-ATPase pump.

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This paper proposes a novel approach for gait analysis from wearable sensing, based on an adaptive periodic model of any gait signal. The proposed method learns a model of the gait cycle during online measurement, using a continuous representation that can adapt to inter and intra-personal variability by creating an individualized model. Once the algorithm has converged to the input signal, key gait events can be identified relative to the estimated gait phase; these events can then be used to calculate gait parameters. The approach is implemented and tested on a human motion dataset where heel impact and toe takeoff events are extracted with an average error of 0.04 cycles.

In mice, transgenic manipulation of Ca-handling proteins is sufficient to alter the metabolic phenotype of muscle. We have previously shown that ablation of sarcolipin (SLN), a regulatory protein and uncoupler of sarco(endo)plasmic reticulum Ca-ATPases, leads to excessive diet-induced obesity and glucose intolerance in mice. However, it is unclear how loss of SLN per se affects muscle oxidative capacity and the ability of mitochondria to adapt to physiological stimuli, such as exercise training or calorie overload. To address this question, and wild-type (WT) littermates were given access to voluntary running wheels or underwent a treadmill training protocol for 8 wk. Furthermore, a separate group of mice were given a high-fat diet (42% kcal from fat for 8 wk) to determine whether the excessively obese phenotype of mice is associated with altered oxidative capacity. While voluntary running was insufficient to elicit mitochondrial adaptations, treadmill-trained mice showed significant increases ( < 0.05) in the maximal activities of succinate dehydrogenase (+11%), citrate synthase (+12%), cytochrome oxidase (COX: +17%), along with increased protein expression of cytochrome (+34%) and COX IV (+28%), which were irrespective of SLN expression. Lastly, no changes in the activities of mitochondrial marker enzymes existed with high-fat feeding, regardless of genotype. Together, these findings indicate that SLN is not required for the regulation of oxidative capacity in response to physiological stress, namely exercise or caloric surfeit. Sarcolipin (SLN) has gained considerable attention for its uncoupling role of sarco(endo)plasmic reticulum Ca-ATPase (SERCA). Because of SLN's ability to alter both cellular energy use and cytosolic [Ca], the potential exists for a regulatory role of mitochondrial biogenesis. Herein, we show skeletal muscle oxidative capacity to be unaltered in mice lacking SLN following exercise training or high-fat feeding. Our results contrast with published studies of SLN-overexpressing mice, possibly owing to supraphysiological uncoupling of SERCA.

Objective: To investigate the relationship between the anteversion and retroversion of pelvic angles and the ability of the sit-to-stand movement. Design: Randomized controlled trial, Survey. Setting: Research units of rehabilitation hospitals. Participants: Thirty-two hemiparetic subjects, age 66. 7AE8.2 years and age-matched 50 healthy controls, age 64.2AE8.2 gave their informed consent to participate in the present experiment. Interventions: Not applicable. Main Outcome Measure(s): To measure the maximum anteversion and retroversion of pelvic angles and assess the ability of sit-to-stand movement, the subjects sat on a height-adjustable instrumented chair with keeping both arms crossed on the chest and their feet in parallel position. The pelvic angles were measured five times using a manual goniometer. The hemiparetic patients who could perform independently all three trials were classified into the possible group (18 persons). Remained patients were into the impossible group (14 persons). Results: The maximum anteversion of pelvic angle in control group was 91.6AE5.0. That in the impossible group (88.8AE2.8) was significant larger than that in the possible group (102.4AE6.1) (p<0.001). The border angle (95) between both hemiparetic was observed. The maximum retroversion of pelvic angle in each group was 117.6AE8.1 , 108.5AE5.6 , and 109.6AE4.6 in the control group, the possible group and the impossible group, respectively. Conclusions: The possible group has more large range of pelvic inclination, especially anteversion of pelvic angle, than the impossible group. Evidently, inclining more forwardly the pelvis than 95 is necessary to perform the sit-to-stand movement in hemiparetic patients.