Philip Michael Gallagher

Throughout my career I have been passionate about and have considerable experience in skeletal muscle physiology. My innovative personality has facilitated the design and execution of numerous research studies that are highlighted in my vitae. More recently, I am exploring the utilization of next-generation gene expression techniques to examine both genetic and epigenetic factors associated with health and disease as well as electron microscopy to examine morphological changes in muscle cells. Furthermore, I have experience with the testing of muscle function from the whole muscle to single fiber level. I also have considerable practice managing and participating in various working groups at the department, school and university level. In addition to my role as the Director of the Applied Physiology Laboratory, I have served as the department's Director of the Exercise Science programs for the past ten years. There are five faculty members in our Exercise Science group that I lead in determining program planning, designing student assessments, procedural issues, coordinating curricular changes, as well as spearhead efforts regarding student recruitment and retention. At the professional level I am active in the American College of Sports Medicine (ACSM), and am currently applying for Fellow status. I have served as President and as the Kansas State Representative for the Central States Chapter of ACSM and I am a member of the American Physiological Society and the National Strength and Conditioning Association, serving as an active contributor to their meetings.

I have performed both basic and clinical based investigations over the past fifteen years with emphasis in aging and muscle physiology. Currently, there are two primary lines of research that I am pursuing. The first line of my research involves the role of physiological and metabolic mechanisms related to skeletal muscle hypertrophy and atrophy, including the following: 1) the activation of signaling proteins in skeletal muscle in response to different forms of stress (e.g. metabolic, physical, etc.), and 2) examining the effects of supplements and resistance exercise on whole muscle and intracellular signaling proteins to attenuate and perhaps reverse muscle atrophy. The second line of research is on the etiology of disorders and disease, particularly associated with physical activity (or lack thereof) and its effects on immune function. My interests include: 1) the response of cytokines (myokines and adipokines) to various conditions such as physical stress, aging, lack of physical activity and disease cachexia, and 2) methods to reduce the cytokine response to stress.

My broad, long-term goal is to develop countermeasures to prevent muscle loss associated with aging and other disorders (e.g. cachexia). One of my more intriguing research findings is that resistance training induces an increase in fast-twitch fibers in the young, but older individuals display a further increase in the percentage of slow-twitch fibers. We have noted that cytokine levels at rest are higher in older individuals and that these levels remain elevated following a resistance-training program. These data have important implications for the study of physical fitness among older populations. These data also suggest that the field should focus future studies on how the regulation of muscle fibers differs between younger and older adults and on how we can attenuate the basal level of stress experienced by older individuals. Two major questions that remain to be answered are what role does activity plays in this fiber-type transformation, and how is the mitochondria involved in the reduction of fast-twitch fibers as humans age in response to exercise? I would like to develop a strategy to counteract the fiber-type specific atrophy associated with aging. Thus, I plan to compare markers of mitochondrial function and turnover in slow- and fast-twitch muscle fibers in younger and older adults. This research will also examine the efficacy of using resveratrol and other anti-oxidative/inflammatory agents as a countermeasure to oxidative stress in older adults. This research will hopefully help change the way treatments are prescribed to combat the loss of fast-twitch muscle fibers, resulting in reduced fatigue, increased activity, and improved ability to perform activities of daily living for the aging population.

I recently started working with physicians at the University of Kansas Medical Center to identify biomarkers and mechanisms of cachexia associated with severe burn trauma. There is a critical need to predict the onset of cachexia at the earliest stages as patients experiencing cachexia have poor long-term outcomes, including increased fatigability, weakness, and decreased quality of life. Severe burn trauma (total burn surface area >20%) patients suffer from hyper-metabolic conditions and inflammation that often leads to cachexia, defined as extreme skeletal muscle wasting and weakness. A strong relationship exists between cachexia and negative patient outcomes, but the mechanisms for this remain largely unstudied. Advances in transcriptomics allow for the generation of numerous candidate biomarkers with potential clinical value. However, there is remarkably little data on biomarkers and epigenetic changes associated with muscle cachexia in severe burn trauma.

Another interesting research area is the examination of mechanoreceptor transduction in skeletal muscle. This line of research has found that Acetaminophen appears to increase mechanoreceptor transduction in skeletal muscle. For this study, Acetaminophen was administered to rats for 8 weeks and this resulted in higher levels of the 70 kDa alpha7 integrin subunit, total Focal Adhesion Kinase, cSrc and s6k, independent of exercise status. The role that Acetaminophen and other potential COX enzyme inhibitors play in muscle hypertrophy is controversial, but this data suggests a possible mechanism of how Acetaminophen may cause hypertrophy. Considering the extensive use of NSAIDs with older individuals, this research may prove to be extremely relevant to this population. This data was presented at the Experimental Biology meeting in April 2015 and we are planning on submitting the manuscript concerning this study to the Journal of Applied Physiology soon. I am also in the early stages of preparing a proposal to NIH to examine the mechanisms of these findings.

We have also examined the role that heat-shock (prior exposure to high temperature 24-48 hours before exercise) may have in protecting against muscle damage during exercise. Previous study performed by other investigators found that heat shock attenuated damage from cryolesioning in various tissues of animals, but it is physiologically impossible to be exposed to that type of damage by exercise. My approach, then, allows for real-life applications in humans that have the potential of greatly improving the efficiency of treatments and possible prevention of muscle atrophy. In animals, we have shown increased JNK expression following muscle damage. JNK is a known regulator of Caspase-3, which is significantly up-regulated following muscle damage. However, our work in human skeletal muscle show that HSP induction is difficult under practical physiological conditions. However, there is potential for pharmacological interventions to induce the cytoprotective heat shock response.

I am also the Co-PI on a proposal that was awarded by the Office of Naval Research to study a dual stress model (martial arts) with US Marine stationed at Fort Leonard Wood. For this study, we will evaluate the physiological and psychological response to repeated bouts of Marine Corps Martial Arts Program (MCMAP) training. More specifically, we will increase the effectiveness of MCMAP by identifying optimal training intervals and/ or cognitive stimuli that will improve the training environment. In addition to being the Co-PI on the project, my particular role in this study involves the inflammatory/immune response that occurs during this high-stress environment. Acute bouts of moderate and high-intensity exercise induce transient shifts in physiologic systems resulting from the combined physical and psychological demands of the given effort. Within this context, exercise induced alterations of specific immune cell populations and hormonal concentrations are some of, if not the most, established effects of exercise on a physiological system. Thus, we are examining changes in the profile of stress hormones, circulating immune cells and immunomodulatory cytokines following dual stress challenge models.

Since my faculty appointment in September 2004, I have published 30 manuscripts in peer-reviewed journals, have four articles in review, and have co-authored two book chapters (one is in the final stages of being accepted). I have authored 47 published abstracts, and have given 19 peer-reviewed national scholarly presentations. I have submitted 23 research proposals as PI or Co-I to external organizations (ten of which were accepted for funding) and have obtained funding for approximately five million dollars and I have submitted seven internal research proposals, all of which were awarded. Finally, I was awarded the Promising Scholar Faculty Achievement Award from the School of Education at the University of Kansas in 2008.