Kinesiology
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Item Physical Activity and Brain Function in Older Adults at Increased Risk for Alzheimer’s Disease(MDPI, 2013-01-14) Smith, J. Carson; Nielson, Kristy A.; Woodard, John L.; Seidenberg, Michael; Rao, Stephen M.Leisure-time physical activity (PA) and exercise training are known to help maintain cognitive function in healthy older adults. However, relatively little is known about the effects of PA on cognitive function or brain function in those at increased risk for Alzheimer’s disease through the presence of the apolipoproteinE epsilon4 (APOE-ε4) allele, diagnosis of mild cognitive impairment (MCI), or the presence of metabolic disease. Here, we examine the question of whether PA and exercise interventions may differentially impact cognitive trajectory, clinical outcomes, and brain structure and function among individuals at the greatest risk for AD. The literature suggests that the protective effects of PA on risk for future dementia appear to be larger in those at increased genetic risk for AD. Exercise training is also effective at helping to promote stable cognitive function in MCI patients, and greater cardiorespiratory fitness is associated with greater brain volume in early-stage AD patients. In APOE-ε4 allele carriers compared to non-carriers, greater levels of PA may be more effective in reducing amyloid burden and are associated with greater activation of semantic memory-related neural circuits. A greater research emphasis should be placed on randomized clinical trials for exercise, with clinical, behavioral, and neuroimaging outcomes in people at increased risk for AD.Item The Influence of Family Dog Ownership and Parental Perceived Built Environment Measures on Children’s Physical Activity within the Washington, DC Area(MDPI, 2017-11-16) Roberts, Jennifer D.; Rodkey, Lindsey; Grisham, Cortney; Ray, RashawnSedentary behavior and physical inactivity are significant contributors to youth obesity in the United States. Neighborhood dog walking is an outlet for physical activity (PA). Therefore, understanding the relationship between built environment, dog ownership, and youth PA is essential. This study examined the influence of dog ownership and parental built environment perceptions on children’s PA in the Washington, D.C. area. In 2014, questionnaires were mailed to 2000 parents to assess family dog ownership; children’s outdoor dog walking or playing; and parental perceived built environment measures. Chi-square analyses examined differences in parental perceived built environment measures between children with and without family dogs. The sample included 144 children (50% female; average-age 9.7 years; 56.3% White; 23.7% African-American; 10.4% Asian-American; 29.9% owned dog). Only 13% and 5.6% of the children walked or played outdoors with the dog daily, respectively. A significantly greater proportion (p-value < 0.05) of parents who owned dogs recognized and observed some home built environment measures (e.g., traffic speed on most streets is 30 mph or less) that were PA -promoting for their children. Findings suggest that dog ownership may provide more positive parental perceptions of the neighborhood built environment, which supports children’s outdoor PA through dog walking and playing.Item Examining the Influence of a New Light Rail Line on the Health of a Demographically Diverse and Understudied Population within the Washington, D.C. Metropolitan Area: A Protocol for a Natural Experiment Study(MDPI, 2018-02-13) Roberts, Jennifer D.; Hu, Ming; Saksvig, Brit Irene; Brachman, Micah L.; Durand, Casey P.Approximately two-thirds of adults and youth in Prince George’s County, Maryland, a suburb of Washington, D.C. are overweight or obese and less than half are achieving daily physical activity recommendations. Active transportation (AT), such as walking, biking or using public transportation (PT), is a strategic pathway to improving physical activity levels and thus reducing excess weight. Utilizing an expansion of the Washington, D.C. area transportation system with a new light rail line, the Purple Line Outcomes on Transportation (PLOT) Study will exam pre- and post-Purple Line PT use, AT behaviors and attitudes and physical activity among Prince George’s County adults and youth. The PLOT Study will take advantage of this natural experiment in an area enduring significant racial/ethnic and gender-based overweight or obesity and physical inactivity disparities. While similar natural experiments on AT have been conducted in other U.S. cities, those studies lacked diverse and representative samples. To effectively evaluate these physical activity outcomes among this population, efforts will be used to recruit African American and Latino populations, the first and second most common racial/ethnic groups in Prince George’s County. Finally, the PLOT Study will also examine how contextual effects (e.g., neighborhood built environment) impact PT, AT and physical activity.Item Between Privilege and Oppression: An Intersectional Analysis of Active Transportation Experiences Among Washington D.C. Area Youth(MDPI, 2019-04-12) Roberts, Jennifer D.; Mandic, Sandra; Fryer, Craig S.; Brachman, Micah L.; Ray, RashawnThe use of active transportation (AT), such as walking, cycling, or even public transit, as a means of transport offers an opportunity to increase youth physical activity and improve health. Despite the well-known benefits of AT, there are environmental and social variables that converge on the AT experiences of low-income youth and youth of color (YOC) that have yet to be fully uncovered. This study uses an intersectional framework, largely focusing on the race-gender-class trinity, to examine youth AT within a context of transportation inequity. Theoretically guided by the Ecological Model of Active Transportation, focus groups were completed with two groups of girls (15 participants) and two groups of boys (nine participants) ranging between the ages of 12–15 years who lived within the Washington D.C. area. This research found race, gender, and class to be inhibitors of AT for both boys and girls, but with more pronounced negative influences on girls.Item The Color of Health: Residential Segregation, Light Rail Transit Developments, and Gentrification in the United States(MDPI, 2019-09-30) Tehrani, Shadi O.; Wu, Shuling J.; Roberts, Jennifer D.As the modern urban–suburban context becomes increasingly problematic with traffic congestion, air pollution, and increased cost of living, city planners are turning their attention to transit-oriented development as a strategy to promote healthy communities. Transit-oriented developments bring valuable resources and improvements in infrastructure, but they also may be reinforcing decades-old processes of residential segregation, gentrification, and displacement of low-income residents and communities of color. Careful consideration of zoning, neighborhood design, and affordability is vital to mitigating the impacts of transit-induced gentrification, a socioeconomic by-product of transit-oriented development whereby the provision of transit service “upscales” nearby neighborhood(s) and displaces existing community members with more affluent and often White residents. To date, the available research and, thus, overall understanding of transit-induced gentrification and the related social determinants of health are limited and mixed. In this review, an overview of racial residential segregation, light rail transit developments, and gentrification in the United States has been provided. Implications for future transit-oriented developments are also presented along with a discussion of possible solutions.Item Does visual feedback during walking result in similar improvements in trunk control for young and older healthy adults?(Springer Nature, 2013-11-26) Anson, Eric; Rosenberg, Russell; Agada, Peter; Kiemel, Tim; Jeka, JohnMost current applications of visual feedback to improve postural control are limited to a fixed base of support and produce mixed results regarding improved postural control and transfer to functional tasks. Currently there are few options available to provide visual feedback regarding trunk motion while walking. We have developed a low cost platform to provide visual feedback of trunk motion during walking. Here we investigated whether augmented visual position feedback would reduce trunk movement variability in both young and older healthy adults. The subjects who participated were 10 young and 10 older adults. Subjects walked on a treadmill under conditions of visual position feedback and no feedback. The visual feedback consisted of anterior-posterior (AP) and medial-lateral (ML) position of the subject’s trunk during treadmill walking. Fourier transforms of the AP and ML trunk kinematics were used to calculate power spectral densities which were integrated as frequency bins “below the gait cycle” and “gait cycle and above” for analysis purposes. Visual feedback reduced movement power at very low frequencies for lumbar and neck translation but not trunk angle in both age groups. At very low frequencies of body movement, older adults had equivalent levels of movement variability with feedback as young adults without feedback. Lower variability was specific to translational (not angular) trunk movement. Visual feedback did not affect any of the measured lower extremity gait pattern characteristics of either group, suggesting that changes were not invoked by a different gait pattern. Reduced translational variability while walking on the treadmill reflects more precise control maintaining a central position on the treadmill. Such feedback may provide an important technique to augment rehabilitation to minimize body translation while walking. Individuals with poor balance during walking may benefit from this type of training to enhance path consistency during over-ground locomotion.Item Mitochondrial oxygen consumption deficits in skeletal muscle isolated from an Alzheimer’s disease-relevant murine model(Springer Nature, 2014-02-13) Schuh, Rosemary A; Jackson, Kathryn C; Schlappal, Anna E; Spangenburg, Espen E; Ward, Christopher W; Park, Ji H; Dugger, Natalie; Shi, Guo Li; Fishman, Paul SAge is considered a primary risk factor for neurodegenerative diseases including Alzheimer’s disease (AD). It is also now well understood that mitochondrial function declines with age. Mitochondrial deficits have been previously assessed in brain from both human autopsy tissue and disease-relevant transgenic mice. Recently it has been recognized that abnormalities of muscle may be an intrinsic aspect of AD and might contribute to the pathophysiology. However, deficits in mitochondrial function have yet to be clearly assessed in tissues outside the central nervous system (CNS). In the present study, we utilized a well-characterized AD-relevant transgenic mouse strain to assess mitochondrial respiratory deficits in both brain and muscle. In addition to mitochondrial function, we assessed levels of transgene-derived amyloid precursor protein (APP) in homogenates isolated from brain and muscle of these AD-relevant animals. We now demonstrate that skeletal muscles isolated from these animals have differential levels of mutant full-length APP depending on muscle type. Additionally, isolated muscle fibers from young transgenic mice (3 months) have significantly decreased maximal mitochondrial oxygen consumption capacity compared to non-transgenic, age-matched mice, with similar deficits to those previously described in brain. This is the first study to directly examine mitochondrial function in skeletal muscle from an AD-relevant transgenic murine model. As with brain, these deficits in muscle are an early event, occurring prior to appearance of amyloid plaques.Item The SH3 and cysteine-rich domain 3 (Stac3) gene is important to growth, fiber composition, and calcium release from the sarcoplasmic reticulum in postnatal skeletal muscle(Springer Nature, 2016-04-11) Cong, Xiaofei; Doering, Jonathan; Mazala, Davi A. G.; Chin, Eva R.; Grange, Robert W.; Jiang, HonglinThe SH3 and cysteine-rich domain 3 (Stac3) gene is specifically expressed in the skeletal muscle. Stac3 knockout mice die perinatally. In this study, we determined the potential role of Stac3 in postnatal skeletal muscle growth, fiber composition, and contraction by generating conditional Stac3 knockout mice. We disrupted the Stac3 gene in 4-week-old male mice using the Flp-FRT and tamoxifen-inducible Cre-loxP systems. RT-qPCR and western blotting analyses of the limb muscles of target mice indicated that nearly all Stac3 mRNA and more than 70 % of STAC3 protein were deleted 4 weeks after tamoxifen injection. Postnatal Stac3 deletion inhibited body and limb muscle mass gains. Histological staining and gene expression analyses revealed that postnatal Stac3 deletion decreased the size of myofibers and increased the percentage of myofibers containing centralized nuclei, with no effect on the total myofiber number. Grip strength and grip time tests indicated that postnatal Stac3 deletion decreased limb muscle strength in mice. Muscle contractile tests revealed that postnatal Stac3 deletion reduced electrostimulation-induced but not the ryanodine receptor agonist caffeine-induced maximal force output in the limb muscles. Calcium imaging analysis of single flexor digitorum brevis myofibers indicated that postnatal Stac3 deletion reduced electrostimulation- but not caffeine-induced calcium release from the sarcoplasmic reticulum. This study demonstrates that STAC3 is important to myofiber hypertrophy, myofiber-type composition, contraction, and excitation-induced calcium release from the sarcoplasmic reticulum in the postnatal skeletal muscle.Item Calcium dysregulation, functional calpainopathy, and endoplasmic reticulum stress in sporadic inclusion body myositis(Springer Nature, 2017-03-22) Amici, David R.; Pinal-Fernandez, Iago; Mázala, Davi A. G.; Lloyd, Thomas E.; Corse, Andrea M.; Christopher-Stine, Lisa; Mammen, Andrew L.; Chin, Eva R.Sporadic inclusion body myositis (IBM) is the most common primary myopathy in the elderly, but its pathoetiology is still unclear. Perturbed myocellular calcium (Ca2+) homeostasis can exacerbate many of the factors proposed to mediate muscle degeneration in IBM, such as mitochondrial dysfunction, protein aggregation, and endoplasmic reticulum stress. Ca2+ dysregulation may plausibly be initiated in IBM by immune-mediated membrane damage and/or abnormally accumulating proteins, but no studies to date have investigated Ca2+ regulation in IBM patients. We first investigated protein expression via immunoblot in muscle biopsies from IBM, dermatomyositis, and non-myositis control patients, identifying several differentially expressed Ca2+-regulatory proteins in IBM. Next, we investigated the Ca2+-signaling transcriptome by RNA-seq, finding 54 of 183 (29.5%) genes from an unbiased list differentially expressed in IBM vs. controls. Using an established statistical approach to relate genes with causal transcription networks, Ca2+ abundance was considered a significant upstream regulator of observed whole-transcriptome changes. Post-hoc analyses of Ca2+-regulatory mRNA and protein data indicated a lower protein to transcript ratio in IBM vs. controls, which we hypothesized may relate to increased Ca2+-dependent proteolysis and decreased protein translation. Supporting this hypothesis, we observed robust (4-fold) elevation in the autolytic activation of a Ca2+-activated protease, calpain-1, as well as increased signaling for translational attenuation (eIF2α phosphorylation) downstream of the unfolded protein response. Finally, in IBM samples we observed mRNA and protein under-expression of calpain-3, the skeletal muscle-specific calpain, which broadly supports proper Ca2+ homeostasis. Together, these data provide novel insight into mechanisms by which intracellular Ca2+ regulation is perturbed in IBM and offer evidence of pathological downstream effects.Item Defects in sarcolemma repair and skeletal muscle function after injury in a mouse model of Niemann-Pick type A/B disease(Springer Nature, 2019-01-05) Michailowsky, V.; Li, H.; Mittra, B.; Iyer, S. R.; Mazála, D. A. G.; Corrotte, M.; Wang, Y.; Chin, E. R.; Lovering, R. M.; Andrews, N. W.Niemann-Pick disease type A (NPDA), a disease caused by mutations in acid sphingomyelinase (ASM), involves severe neurodegeneration and early death. Intracellular lipid accumulation and plasma membrane alterations are implicated in the pathology. ASM is also linked to the mechanism of plasma membrane repair, so we investigated the impact of ASM deficiency in skeletal muscle, a tissue that undergoes frequent cycles of injury and repair in vivo. Utilizing the NPDA/B mouse model ASM−/− and wild type (WT) littermates, we performed excitation-contraction coupling/Ca2+ mobilization and sarcolemma injury/repair assays with isolated flexor digitorum brevis fibers, proteomic analyses with quadriceps femoris, flexor digitorum brevis, and tibialis posterior muscle and in vivo tests of the contractile force (maximal isometric torque) of the quadriceps femoris muscle before and after eccentric contraction-induced muscle injury. ASM−/− flexor digitorum brevis fibers showed impaired excitation-contraction coupling compared to WT, a defect expressed as reduced tetanic [Ca2+]i in response to electrical stimulation and early failure in sustaining [Ca2+]i during repeated tetanic contractions. When injured mechanically by needle passage, ASM−/− flexor digitorum brevis fibers showed susceptibility to injury similar to WT, but a reduced ability to reseal the sarcolemma. Proteomic analyses revealed changes in a small group of skeletal muscle proteins as a consequence of ASM deficiency, with downregulation of calsequestrin occurring in the three different muscles analyzed. In vivo, the loss in maximal isometric torque of WT quadriceps femoris was similar immediately after and 2 min after injury. The loss in ASM−/− mice immediately after injury was similar to WT, but was markedly larger at 2 min after injury. Skeletal muscle fibers from ASM−/− mice have an impairment in intracellular Ca2+ handling that results in reduced Ca2+ mobilization and a more rapid decline in peak Ca2+ transients during repeated contraction-relaxation cycles. Isolated fibers show reduced ability to repair damage to the sarcolemma, and this is associated with an exaggerated deficit in force during recovery from an in vivo eccentric contraction-induced muscle injury. Our findings uncover the possibility that skeletal muscle functional defects may play a role in the pathology of NPDA/B disease.