My research addresses the impact of exercise on cardio-metabolic health outcomes across the lifespan. Most recently, I have been investigating the role of skeletal muscle adaptations and the impact of muscular fitness as an independent predictor of health status as it is linked to both premature mortality and several morbidities across the lifespan. We have recently reported that a simple clinical assessment of muscular strength is a powerful predictor of cardiometabolic risk in children and have identified low thresholds for strength that could be helpful for clinicians. Maintaining strength over time, as we have recently investigated, is critical to guard against the future development of cardiometabolic risk. We have also shown that the muscle’s response to strengthening activities initiates a series of immune system responses that promotes metabolic function indicating the alternative benefits of strengthening activities among those with metabolic dysfunction. I am also an ongoing member of the Genetics and Exercise Research Consortium, I continue to investigate the role that genes play on the adaptive responses to exercise and how these may contribute to a personalized prescriptive approach to optimal health outcomes.
My research interests include the role of exercise, diet and and obesity on risk factors for cardiovascular disease (CVD) and inflammation. More specifically, my research topics are focused on the effects of exercise and diet interventions on the responses of atherosclerotic and inflammatory biomarkers by examining plasma lipid and lipoprotein parameters, pro-/anti- inflammatory biomarkers, cell adhesion molecules (CAMs), matrix metalloproteinases (MMPs), and tissue inhibitors of MMPs (TIMPs). The current projects examine the effects of high-fat vs. high-carbohydrate on these atherosclerotic and inflammatory biomarkers in obesity.
My research focus is on skeletal and cardiac muscle biology, biochemistry, and metabolism. My lab investigates the molecular signaling pathways in the regulation of muscle size in pre-clinical models such as disuse, cancer cachexia, and obesity. Prior findings from my research have demonstrated that mitochondrial dysfunction can negatively impact muscle protein synthesis and protein degradation and therefore may be an important target in preventing muscle atrophy. Using a combination of molecular biology and genetic approaches, my lab continues to explore the relationship between mitochondrial function and muscle mass with a long term goal of generating targeted therapeutics to prevent muscle wasting in a variety of models.
My research interests lie in health promotion through physical activity behavior. Specifically, I am interested in the application, measurement, and evaluation of how theoretical constructs promote, explain, and predict physical activity behaviors; the translation of these applications and relationships into community-based settings; and subsequently, how physical activity impacts chronic disease, functionality, and quality of life across the lifespan. More recently, I have focused my efforts on better understanding the role of environmental support for physical activity in rural and worksite communities, measurement of this support, and implications for behavior change.
My research interests are focused on adverse health behaviors in collegiate student populations. To date I have examined risk factors and motivations associated the prescription medication misuse, energy drink consumption, and hazardous drinking. My primary area of research examines the risk factors and motivations associated with stimulant use (e.g. prescription stimulants, energy drinks) in undergraduate student samples. Currently my research is focused on examining neuroethical and spiritual issues related to stimulant misuse.
My research interests are focused on the promotion of quality nutritional intake, supplements, healthy body weight and composition. A near-term research project will investigate diet quality, body composition and food insecurity in college aged participants. I am also interested in exercise effects on body composition, both weight training and aerobic, coupled with quality nutritional intake including supplementation. My research questions are aimed at determining the beneficial effects of supplementation and exercise and the cumulative effects on body composition. A second project in the planning phase will focus on peri- and post-menopausal women and the effect of leucine and omega3 supplementation combined with a weight training program. The information from this study is designed to further develop hypotheses related to the influence of supplements and response of biomarkers such as cortisol and vitamin D and the role they play in transforming body composition. The overarching goal is to continue to identify the unique contributions of exercise, diet quality and supplementation in improving body composition with or without weight loss.
The focus of my laboratory is on elucidating the relationship between diet, the microbiome and colon cancer etiology. Our goal is to 1) delineate the dietary factors that modify the microbiome and its function, 2) develop microbial multi-omic classifiers that improve stratification of patients for colon cancer treatment, and 3) identify key functional pathways and mechanisms of the microbiota-host communication, including nucleic acid sensing cell receptors that control inflammation. Ultimately, our goal is to discover microbial and metabolic targets for the development of clinical tools to improve treatment and reduce mortality from colon cancer.
The overarching goal of my research laboratory is to identify mechanisms and potential therapeutic strategies for cancer cachexia. Cachexia, a muscle and adipose wasting syndrome, significantly decreases both quality and length of life in patients suffering from advanced cancers. Current projects are focused on identifying mechanisms of cardiac muscle dysfunction in cachexia and understanding how decreased cardiac performance may contribute to cachexia pathogenesis. We are particularly interested in the role of altered calcium handling and metabolic dysfunction in the heart during cachexia. We utilize an animal model of cachexia and employ techniques in physiology, molecular biology, and biochemistry to measure heart function and identify changes in protein and gene expression that contribute to functional changes.