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Vaughna Galvin,1 Dennis J Cheek,2 Yan Zhang,3 Gregory Collins,1 David Gaskin4 1School of Nurse Anesthesia, Texas Christian University, Fort Worth, TX, USA; 2School of Nursing, Texas Christian University, Fort Worth, TX, USA; 3Harris College of Nursing and Health Sciences, Texas Christian University, Fort Worth, TX, USA; 4Republic Pain Specialists, Physicians Centre Hospital, Bryan, TX, USACorrespondence: Vaughna Galvin, School of Nurse Anesthesia, Annie Richardson Bass Building, 2800 West Bowie Street, Suite 3101, Fort Worth, TX, 76109, USA, Tel +1 817-257-7887, Fax +1 817-257-5472, Email V.B.GALVIN@tcu.eduAbstract: One hundred ninety-five patients presenting with post-COVID symptomology, including parosmia and dysgeusia, underwent reversible stellate ganglion blockade. Stellate ganglion blockade was performed at an outpatient facility, and patients were evaluated via survey at seven days post-injection. Of the 195 participants, ages ranged from 18– 69 years of age with the breakdown of sexes being females n = 157 and males n = 38. The most significant finding was a reported improvement in olfaction post-injection in 87.4% of subjects. The effectiveness of this novel treatment for post-COVID is promising and warrants further investigation.Keywords: cervical sympathetic block, COVID, parosmia, dysgeusia, dysautonomia

High-sugar consumption is related to dyslipidemia. How acute exercise affects postprandial lipid and lipoprotein particle responses to a high-sugar meal (HSM) in postmenopausal women is unclear. We examined the effects of a late afternoon/early evening bout of aerobic exercise on postprandial lipid and lipoprotein particle responses to a HSM breakfast the following day in 22 postmenopausal women. Subjects underwent exercise (EX) and no exercise (NE) conditions in the evening 13-16 h before the HSM breakfast consumption, in a random order. During the EX condition, subjects performed supervised aerobic exercise for 60 min at 75% of age-predicted maximum heart rate. The HSM (75.6% carbohydrate and 33% energy needs) was consumed after a 12-h fast. Serum lipids and lipoproteins were assessed at baseline and postprandially (60, 120, 180 min). Repeated measures analysis showed significantly lower area under the curve (geometric means [95% CI]) for triglycerides (TG) (2.96[2.43, 3.61] vs. 3.24[2.70, 3.88] mmol/L*hr; p = 0.049) and very low density lipoprotein particles (VLDLP) (114.6[88.2, 148.9] vs. 134.3[108.1, 166.9] nmol/L*hr; p = 0.02) during the EX versus NE condition. There were no condition effects for other variables. In conclusion, the EX versus NE condition lowered postprandial AUC for TG and VLDLP following HSM consumption in postmenopausal women.

Winter is characterized by stressful conditions which compromise health and render animals more vulnerable to infection and illness than during other times of the year. Organisms are hypothesized to adapt to these seasonal stressors by increasing investment in immune function in response to diminished photoperiod duration. Here, we examined this hypothesis in a sample of healthy human participants. Using several functional immune assays in vitro, as well as by utilizing measures of in vivo proinflammatory cytokine levels, we predicted that shorter day length would be associated with greater investment in immunological function. Results revealed that shorter days predicted significant upregulation of several facets of immune function, including natural killer cell cytotoxicity, peripheral blood mononuclear cell proliferation (in response to, and in the absence of stimulation), and plasma levels of interleukin-6, as well as lower rates of Staphylococcus aureus growth in serum ex vivo. Further, consistent with the hypothesis that these trade-offs would be offset by decreased investment in mating effort, shorter day length also predicted lower levels of total testosterone in men. These results suggest that ambient photoperiod may be a powerful regulator of human immunological activity, providing some of the first evidence of seasonal changes in multiple facets of human immune function.

Early life stress increases one’s risk for health problems later in life, and many studies find that these effects are sex-differentiated. Here, we examined relationships between multiple sources of early life stress and adult immune function in humans across several functional assays. Adult participants provided retrospective information about their childhood (a) socioeconomic status, (b) household unpredictability, and (c) exposure to adverse experiences. Participants’ peripheral blood mononuclear cells (PBMCs) were then isolated for use in functional assays of immune performance: (a) tumor cell lysis by natural killer cells, (b) phagocytosis of Escherichia coli bioparticles, and (c) mitogen-induced leukocyte proliferation and cytokine release. In men, lower childhood socioeconomic status predicted decrements in immunological performance across functional assays, along with greater spontaneous cytokine release from PBMCs. These changes co-occurred with elevations in plasma testosterone levels. Similar effects were not observed for other sources of stress, nor were they found in women (with the exception of spontaneous cytokine release). These findings provide evidence that low childhood socioeconomic status has a lasting negative impact on multiple aspects of immune function, particularly in men.

Since the successful completion of the Human Genome Project in 2003, extensive genomic research has continued to alter pathophysiology at the molecular level. This research includes investigation of the specific receptors and metabolizing enzymes in drug pharmacodynamics and pharmacokinetics, specifically the cytochrome P450 system located primarily in the liver. In this article, pharmacogenomics and the role of the cytochrome P450 system in metabolism of various drugs are discussed. Specifically, drugs that are used in the critical care setting and are of clinical significance to the bedside critical care nurse are examined.

Here, we propose a novel theoretical model linking present-focused decision-making to the activities of the immune system. We tested our model by examining the relationship between inflammatory activity – in vivo and in vitro – and decision-making characterized by impulsivity, present focus, and an inability to delay gratification. Results support our model, revealing that inflammation predicts these outcomes even after controlling for factors that may contribute to a spurious linkage between them. Moreover, subsequent analyses revealed that our model was a better fit for the data than alternative models using present-focused decision-making and its health-harming behavioural sequelae (e.g., smoking, risky sexual behaviour) to predict inflammation, lending support for the proposed directionality of this relationship. Together, these results suggest that inflammation may contribute to decision-making patterns that can result in undesirable personal and societal outcomes.

High-sugar intake may cause endothelial dysfunction. It is unknown if a bout of aerobic exercise improves endothelial dysfunction caused by a high-sugar meal in postmenopausal women. This study evaluated if prior aerobic exercise attenuates postprandial endothelial dysfunction in postmenopausal women. Twenty-two postmenopausal women (age [mean±SD]: 60.4±6.5 years; % body fat: 40.3%±7.5%) underwent an exercise (EX) or no exercise (NE) condition, in a random order, 13–16 hours prior to the high-sugar meal consumption. The EX condition included a 60 min bout of supervised aerobic exercise at 75% of age-predicted maximum heart rate. The high-sugar meal, consumed after a 12-hour fast, contained 33% of the subjects’ daily energy needs, and 75.6% energy from carbohydrates. Flow-mediated dilation (FMD) and blood concentrations of glucose, insulin, endothelin-1 (ET-1), and nitric oxide (NO) were assessed at baseline and 60 min, 120 min, and 180 min postprandially. Repeated measures analysis test showed that there were no condition by time interaction or condition effects for FMD, glucose, insulin, or NO. There was a significant condition by time interaction but no condition effect for ET-1. Area under the curve was also not different by condition for insulin sensitivity or the above variables. In conclusion, prior aerobic exercise compared with NE did not affect FMD, blood glucose, insulin, ET-1 or NO concentrations, or insulin sensitivity following a high-sugar meal in postmenopausal women. Future studies should look at the effect of different EX intensities on meal-induced endothelial dysfunction in this population. Trial Registration: ClinicalTrials.gov Identifier: NCT02919488

The treatment of mental illness is often done on a trial-and-error basis and achieving therapeutic benefits from a medication is not always guaranteed. Pharmacogenomics explores the role of gene-gene interactions and interindividual responses to a drug and may be promising in the guidance of pharmacotherapeutic options. In the present study, the impact of pharmacogenomic testing in management of mental health medication was investigated. Participants were identified at a local outpatient mental health facility through convenience sampling. Retrospective chart review included medication history, adverse drug reactions, pharmacogenomic history, and demographic data including insurance coverage. Chart review focused on six months pre- and post-pharmacogenomic for a comparison with the patient serving as their own control. Results indicate a high incidence of alterations in two specific cytochrome enzymes, CYP2D6 and CYP2C19. In total, 82% of the sample had variations with CYP2D6, while 64% of individuals had variations with CYP2C19. In total, 91% of patients tested received Medicaid or Medicare. Post-pharmacogenomic testing, all patient drug regimens were modified, and all reported less adverse side effects. Moreover, advanced practice nurse providers educated patients about the availability of genetic testing, initiated testing and provided care based on findings. These results demonstrate the utility of genetic testing in the realm of mental health. Future directions involve further exploring the benefits of pharmacogenomic testing in this vulnerable population.

Lisa M Bashore, Glenda Daniels, Lori Borchers, Lynette L Howington, Dennis J Cheek Harris College of Nursing and Health Sciences, Texas Christian University, Fort Worth, TX, USA Background: This quasi-experimental study explored full-time nurse faculty competency in genomics and genetics using a validated measure prior to and following educational sessions during one academic semester. The findings represent the researchers’ efforts to educate nurse faculty and to support their competency in genomics and genetics as information shared with students is only as robust as faculty knowledge.Methods: Faculty who consented to participate completed the Genomic Nurse Concept Inventory (GNCI©) to measure their knowledge of the concepts surrounding genomics and genetics prior to the education intervention and then following all three education sessions. The education sessions were carried out over a semester using a lunch and learn forum.Results: Our first assumption was that 50% of faculty would score below 70% on the pretest. Eligible nurse faculty 29/48 (60%) completed the GNCI© and scores show they had limited knowledge in three areas: nomenclature of genes and gene function, inheritance patterns, and the clinical application of genomics to human disease. Over half of nurse faculty 17/29 (59%) scored less than 70% on the GNCI© supporting our first assumption. The second assumption that over 85% of faculty would score at least 70% on the GNCI© after the education was not supported. The education sessions improved scores on the GNCI© in the 12/29 (41%) faculty who completed the measures prior to and after the intervention.Conclusion: Despite the growing knowledge about genomics/genetics and the application to clinical practice, health professionals like nurses are not competent in these concepts. Nursing faculty require competency in genomics and genetics in order to integrate these concepts in nursing curricula. Outcomes of this project show the need to provide education and support for nurse faculty in genomics and genetics. Keywords: education, genetics, genomics, incorporation, knowledge, undergraduate bachelors program

Pharmacogenomics is one of the many "omics" fields of study (transcriptomics, lipidomics, metabolomics, and phenomics) that have risen as the result of the human genome project and the growing understanding of the science of genomics. Genomics, the study of the structure, content, function, and evolution of genomes, has become relevant to healthcare professionals largely due to the advances in molecular technologies, particularly DNA sequencing (Table 1). Genomics is changing the nature of medicine and delivery of health care and the ability to examine and ultimately comprehend the nature of disease and drug action at the molecular level. Obtaining this goal is the ultimate basis of "precision medicine": to characterize or individualize care for human disease (National Institutes of Health, 2015). Precision medicine, a recent term, includes not just the right drug for the right individual (formerly called personalized medicine), but also the right drug for the specific disease type afflicting the specific individual. Precision medicine will allow for much more specific and successful therapeutic interventions than are now possible (Collins & Varmus, 2015).Many of the differences observed in how individuals respond to drugs are inherited and, therefore, are at least in part due to the genetic makeup of the patient (Kalow, 2004). Pharmacogenetics was coined in 1959 by a German geneticist (Vogel, 1959) and has been an active area of research even before the genomic revolution. While the terms pharmacogenetics and pharmacogenomics are often used interchangeably, pharmacogenetics is generally used to refer to the role of single genes in drug response while pharmacogenomics is the broader term that encompasses the role of the entire genome, including gene-gene interactions in drug response. The selection of studies and web resources for this review was done using the authors' expertise in the study and practice in pharmacogenomics and pharmacogenetics. The resources and references have been selected based on their clear representation of the foci of this article.Pharmacogenomics has the ultimate aim of identifying the many underlying genetic factors that play a role in the efficacy or toxicity of all drugs. Pharmacogenomics is one of the most rapidly growing fields of biomedical science and is becoming integral to all aspects of drug discovery, design, and development. The basic proposition of pharmacogenomics is the knowledge of the specific genetic factors that affect drug response. As a result, it will be possible to adjust dosages or suggest alternative therapies to avoid toxicities in patients and yield optimal patient outcomes. The definitions of these terms can be found in Table 1.Pharmacogenetics is the study of genetic factors that explain the response of patients to correctly dosed drugs. However, it is crucial to recognize that many environmental factors, including age, lifestyle, diet, and concurrent drug therapies, will also determine how a patient will respond to a drug. These nongenetic factors often play a larger role in a patient's response to a given drug (Nebert, Zhang, & Vesell, 2008).One classic example of the role of environmental factors in shaping drug response is drug inducers and inhibitors of the cytochrome P450 (CYP 450) enzyme system. Many drugs may induce or inhibit the activity of the P450 (CYP 450) metabolizing enzyme system, resulting in drug-drug interactions with possible adverse reactions or therapeutic failures. For example, many statins (3-hydroxy-3-methyl-glutaryl-coenzyme A [HMG-CoA] reductase inhibitors) taken to lower plasma cholesterol levels are known inhibitors of specific cytochrome P450 enzymes (Transon, Leeman, & Dayer, 1996; Zhou, 2009). The cytochrome P450 gene, CYP2D6, is one member of this family of enzymes responsible for the metabolism of thousands of exogenous and endogenous compounds. CYP2D6 codes for an enzyme largely responsible for the conversion of codeine to morphine in the liver. …

The burden of orthostatic hypotension (OH) on public health is a universally recognized enigmatic clinical condition that is associated with significant increases on morbidity and mortality rates, and can take a major toll on one's quality of life. Orthostatic hypotension is predictive of vascular deaths from acute myocardial infarction, strokes in the middle aged population, and increases mortality rates when associated with diabetes, hypertension, Parkinson's disease, and patients receiving renal dialysis. The consensus definition for OH is a fall in systolic blood pressure of at least 20 mm Hg and/or diastolic blood pressure of at least 10 mm Hg within 3 minutes of quiet standing. Because neurogenic OH is often accompanied by supine hypertension, the treatment program should aim toward minimizing OH and the potential fall injuries related to cerebral hypoperfusion without exacerbating nocturnal hypertension that may lead to excessive cardiovascular complications.

Hospitals are under immense pressure to reduce heart failure readmissions that occur within 30 days of discharge, and to improve the quality of care for these patients. Penalties mandated by the Affordable Care Act decrease hospital reimbursement and ultimately the overall cost of caring for these patients increases if they are not well managed. Approximately 25% of patients hospitalized for heart failure are at high risk for readmission and these rates have not changed over the past decade. As a result of an aging population, the incidence of heart failure is expected to increase to one in five Americans over the age of 65. Pharmacologic management can reduce the risk of death and help prevent unnecessary hospitalizations. Healthcare providers who have knowledge of heart failure medications and drug interactions and share this information with their patients contribute to improved long-term survival and physical functioning as well as fewer hospitalizations and a delay of progressive worsening of heart failure.

AB Purpose: Aerobic exercise is frequently prescribed to reduce inflammatory-related disease (cardiovascular disease and diabetes) risk. Resistance training (RT), however, may be key to maximizing anti-inflammatory benefits of consistent exercise. We examined the influence of RT on inflammatory biomarkers in obese, postmenopausal women. Methods: Twenty-three women (65.6 +/- 2.6 yr; body mass index, 33 kg[middle dot]m-2) underwent 12 wk of RT (3 sets, 10 exercises, 3x per week, 8-12 repetition maximum (RM), resistance exercise (EX), N = 11) or social interaction intervention (SI, stretching, knitting, health lectures, 2x per week, control group (CON), N = 12). Both before (BT) and after (AT) RT or SI, blood was collected before (PR), immediately (PO), 2 h (2H), and 24 h (24H) after a single resistance exercise bout (RE) in EX and at the same time points in nonexercise, resting CON. For all time points, blood was analyzed for IL-6, leptin, and lipopolysaccharide (LPS)-stimulated tumor necrosis factor-[alpha] (TNF-[alpha]) (LPS-TNF) and IL-10 (LPS-IL10). PR samples were also examined for C-reactive protein, TNF-[alpha], and adiponectin, and mRNA expression of toll-like receptor 4 (TLR4) and MC1R. Subcutaneous adipose tissue was extracted BT and AT and analyzed for mRNA expression of monocyte chemotactic protein-1, leptin, CD68, and TLR4. Results: RT improved strength (44%) and reduced circulating C-reactive protein (-33%), leptin (-18%) and TNF-[alpha] (-29%) with no change in body composition. IL-6 decreased after SI in CON (-17%). LPS-TNF increased after SI or RT (CON +26%, EX +67%, respectively), whereas LPS-IL10 decreased in CON (-28%) but increased in EX (+20%). RT did not influence inflammatory biomarker gene expression in whole blood or subcutaneous adipose tissue. A single RE bout augmented LPS-TNF and LPS-IL10 at 24H in EX, particularly AT. Conclusion: RT reduced markers of subclinical inflammation in circulation in obese, postmenopausal women in the absence of changes in body composition. Chronic RT also enhanced response to endotoxin challenge both at rest (PR) and 24 h after an acute RE bout (24H). (C)2012The American College of Sports Medicine

Although awareness of cardiovascular disease (CVD) as the leading cause of death among U.S. women has improved over the past decade, factors such as obesity, untreated hypertension, diabetes and the lack of access to healthcare services prevent healthcare providers from making additional gains in the fight against heart disease. Due to demographic changes in the U.S., healthcare providers are beginning to acknowledge the challenge of providing quality care to a diverse population. Root causes of health care disparities include variations and lack of provider understanding of health beliefs, cultural values and preferences, and patients’ inability to communicate symptoms in multiple languages. Barriers related to the patient, care provider and the healthcare system are discussed as well as ideas that will help address the challenges we face going forward.

Hospitalization for heart failure accounts for a substantial portion of the overall cost of caring for these patients and is a predictor of shortened survival in patients with chronic HF. Avoidance of readmission is critical as those hospitalized with HF face a 50% rate of readmission within 6 months and 25%-35% incidence of mortality within a year.Knowledge of this syndrome is important in order to deliver comprehensive supportive care to these patients and reduce readmissions Intravenous drug therapy is an important adjunct in this effort. This article focuses on the syndrome as it relates to intravenous agents prescribed for the patient in the home setting.

Find out about the latest guidelines for unstable angina and non-ST-segment-elevation myocardial infarction.

This article aims to introduce the nurse to pharmacogenomics and its implications for clinical practice with regard to drug therapy.Pharmacogenomics is discussed with regard to the basic tenets, relationships to common health conditions, education and practice resources, and implications for nursing practice.Peer-reviewed literature, websites, and expert professional guidelines were reviewed with relation to pharmacogenomics and nursing practice.The genetic-genomic literature has grown significantly since the completion of the Human Genome Project in 2003. This information is now being translated into practice with regard to the patient's genetic profile and the impact on drug therapy, which is pharmacogenomics.The utilization of the patient genetic-genomic profile is beginning to have an impact on patient drug therapy in clinical practice.Nurses are in the position to make sure, with the increased translation of pharmacogenomics into clinical practice, that adverse drug reactions are avoided and doses are optimized.

This single layer of cells lining the vasculature plays an important role in cardiovascular disease, diabetes, and many other disorders. Here's what you need to know.

Heart disease in men is declining steadily, but it remains the number one killer of men in the United States. CLRD, influenza/pneumonia, and lung cancer are three more causes of top 10 mortalities in men. Epidemiological and clinical studies conclude that CVD is largely preventable through lifestyle modification. CHD, COPD, occupational lung disease, and lung cancer are all preventable by primary prevention (ie, no cigarette smoking). All men should be counseled about the grave significance of heart and lung disease as a cause of illness and death, the importance of primary prevention, and the great variability in symptom presentation. Nurses are in the ideal position to educate patients, families, and colleagues about heart and lung disease.

The pace of knowledge development related to genetics continues to progress exponentially. Knowledge gained through the Human Genome Project will have a profound impact on the practice of nursing, and the widespread integration of genetics into nursing education, clinical practice, and research will be essential. Many nurses continue to view genetic services as relegated to a specialist in a tertiary center and not relevant to their practice. This is certainly about to change. This article reviews the major implications of Human Genome Project for changing the landscape of health care and nursing, discusses several specific examples of genetic testing, and describes strategies under way to help prepare nurses to meet these new demands. Understanding new DNA-based genetic-testing technologies will be important for nurses as these tests become more available and nurses assist clients in the management of their genetic health. Nurses must become active participants in embracing the challenges and opportunities related to this genetic revolution, which over the next 5 to 10 years will reach nurses in every specialty and in every practice setting.

Angiostatin blocks tumor angiogenesis in vivo , almost certainly through its demonstrated ability to block endothelial cell migration and proliferation. Although the mechanism of angiostatin action remains unknown, identification of F 1 -F O ATP synthase as the major angiostatin-binding site on the endothelial cell surface suggests that ATP metabolism may play a role in the angiostatin response. Previous studies noting the presence of F 1 ATP synthase subunits on endothelial cells and certain cancer cells did not determine whether this enzyme was functional in ATP synthesis. We now demonstrate that all components of the F 1 ATP synthase catalytic core are present on the endothelial cell surface, where they colocalize into discrete punctate structures. The surface-associated enzyme is active in ATP synthesis as shown by dual-label TLC and bioluminescence assays. Both ATP synthase and ATPase activities of the enzyme are inhibited by angiostatin as well as by antibodies directed against the α- and β-subunits of ATP synthase in cell-based and biochemical assays. Our data suggest that angiostatin inhibits vascularization by suppression of endothelial-surface ATP metabolism, which, in turn, may regulate vascular physiology by established mechanisms. We now have shown that antibodies directed against subunits of ATP synthase exhibit endothelial cell-inhibitory activities comparable to that of angiostatin, indicating that these antibodies function as angiostatin mimetics.

In 1929, Drury and Szent-Gyorgyi described the effects of a simple extract of heart muscle and other tissues on the mammalian heart. This extract was identified as adenylic acid and found to have profound effects on the cardiovascular system. The discovery and identification of adenyl purines and their effects on the cardiovascular system has now extended to other biological functions such as neurotransmission, neuromodulation, and endocrine/exocrine secretory functions and beyond. This review examines the history of the discovery and identification of the many roles played by adenyl purines in regulation of physiological homeostasis.

The endothelial cells of the vascular system are responsible for many biological activities that maintain vascular homeostasis. Responding to a variety of chemical and physical stimuli, the endothelium elaborates a host of vasoactive agents. One of these agents, endothelium-derived relaxing factor, now accepted as nitric oxide, influences both cellular constituents of the blood and vascular smooth muscle. A principal intracellular target for nitric oxide is guanylate cyclase, which, when activated, increases the intracellular concentration of cyclic guanosine monophosphate, which in turn activates protein kinase G. Acting by this pathway, nitric oxide induces relaxation of vascular smooth muscle and inhibits platelet activation and aggregation. Derangements in endothelial production of nitric oxide are implicated as both cause and consequence of vascular diseases, including hypertension, atherosclerosis, and coronary artery disease.

The implications of genetics and genomics for critical care nurses are becoming more evident, not only in the care provided but also in the numerous medications administered. Genetic causes are being discovered for an increasing number of chronic illnesses and diseases, such as Huntington disease. Because of the scientific and pharmacological advances, leading nursing organizations, such as the American Nurses Association, have established competencies in genetic knowledge for nurses. Such competencies help ensure quality care. Recent advances in the pharmacogenomics of therapy for human immunodeficiency virus disease, cancer, cardiovascular disease, and malignant hyperthermia have indicated a genetic linkage; therefore treatments are targeted toward the genetic aspect of the abnormality. Critical care nurses need knowledge of these genetic conditions and of medications affected by genetic factors.

The use of clinical simulation in graduate level nursing education provides the opportunity for students to learn and apply theoretical practices of nursing care in a safe and controlled environment. It was postulated that laboratory simulation would mimic the stress levels of a real clinical situation as measured by the stress hormone cortisol. The purpose of this study was to determine whether high-fidelity simulation approximates the stress experienced by nurse anesthesia students in the operating room. Participants (n = 21) were recruited from an accredited nurse anesthesia program in the southern U.S. Saliva was collected for 3 days under controlled conditions for baseline data. Next, saliva was collected for 3 days: the day before, the day of, and the day after simulation. The same process was repeated for the first clinical day in the operating room. The participants acted as their own control. There was a significant (p< 0.05) increase in cortisol levels during laboratory simulation as compared to baseline values. Although levels of cortisol were higher during clinical time than baseline, this increase was not significant (p> 0.05), and levels were lower than levels during simulation. Laboratory simulation of patient scenarios raised the stress hormone cortisol level threefold above baseline levels in nurse anesthesia students, while actual clinical experience did not.

The purpose of this study was to determine whether resistance exercise training-induced reductions in inflammation are mediated via melanocortin 3 receptor expression in obese (BMI 3 2 . 7 ± 3 . 7 ) women ( 6 5 . 6 ± 2 . 8 yrs) randomized to either a control ( 𝑁 = 1 1 ) or resistance training group ( 𝑁 = 1 2 ). The resistance trained group performed resistance training 3 days/week for 12 weeks. Resting blood samples were collected before and after the training intervention in both resistance trained and control groups. Resistance training upregulated melanocortin 3 receptor mRNA by 16-fold ( 𝑃 = . 0 3 5 ) and decreased monocyte count, without changing leukocyte number, body composition, or body weight. Resistance trained individuals exhibited increased sensitivity to inflammatory stimuli, whereas control individuals exhibited no change. While there was no change in whole blood tumor necrosis factor alpha mRNA between the groups, whole blood interleukin 10 mRNA was higher in the resistance trained group following the intervention period. In summary, it appears that resistance training may modulate melanocortin 3 receptor expression, providing a possible mechanism for the anti-inflammatory effects of exercise training.

Endothelial dysfunction increases the risk of cardiovascular disease, and regular exercise has been shown to increase endothelial function (EF); however, single bouts of exercise may also produce b...