scholarly journals Effects of Exercise Training on the Paracrine Function of Circulating Angiogenic Cells

Author(s):  
William S. Evans ◽  
Ryan M. Sapp ◽  
Katherine I. Kim ◽  
James M. Heilman ◽  
James Hagberg ◽  
...  

AbstractExercise training has various benefits on cardiovascular health, and circulating angiogenic cells have been proposed as executing these changes. Work from the late 1990s supported an important role of these circulating post-natal cells in contributing to the maintenance and repair of the endothelium and vasculature. It was later found that circulating angiogenic cells were a heterogenous population of cells and primarily functioned in a paracrine manner by adhering to damaged endothelium and releasing growth factors. Many studies have discovered novel circulating angiogenic cell secreted proteins, microRNA and extracellular vesicles that mediate their angiogenic potential, and some studies have shown that both acute and chronic aerobic exercise training have distinct benefits. This review highlights work establishing an essential role of secreted factors from circulating angiogenic cells and summarizes studies regarding the effects of exercise training on these factors. Finally, we highlight the various gaps in the literature in hopes of guiding future work.

2014 ◽  
Vol 117 (5) ◽  
pp. 500-506 ◽  
Author(s):  
Gayatri Guhanarayan ◽  
Julianne Jablonski ◽  
Sarah Witkowski

Circulating angiogenic cells (CACs) are a diverse group that have been identified as predictors of cardiovascular health and are inversely proportional to cardiovascular disease (CVD) outcomes. Inactivity is a growing concern in industrialized nations and is an independent risk factor for CVD. There is limited evidence regarding the impact of reduced physical activity (rPA) on different CAC populations. The purpose of this study was to evaluate the effect of objectively monitored rPA with maintained energy balance on two CAC populations (CFU and CD34+cells), intracellular nitric oxide (NOi), and genes related to NO production in active, healthy men. Participants (age 25 ± 2.9 yr) refrained from structured physical activity for 10 days, which was reflected by a significant reduction in time in vigorous + very vigorous intensity activity ( P = 0.03). Sedentary time tended to increase ( P = 0.06) with rPA. CFU CACs have been characterized as mainly monocytic and lymphocytic cells. We found significant reductions in both the number of CFU CACs (−35.69%, P = 0.01) and CFU CAC NOi (−33.84%, P = 0.03). Neither NOi nor the number of CD34+cells, which are hematopoietic and endothelial progenitors, changed with rPA. We found no significant differences in NO-related gene expression or oxidative stress-related gene expression with rPA in either CAC type. Therefore, we conclude that although various CAC populations have been related to vascular health, regular physical activity is necessary to maintain CAC NOi and the vulnerability of CACs to short-term reductions in physical activity is population specific.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 533-533
Author(s):  
Tyler Marx ◽  
Anastasiia Vasileva ◽  
Stephen Hutchison ◽  
Jennifer Stern

Abstract Aerobic exercise training is a potent intervention for the treatment and prevention of age-related disease, such as heart disease, obesity, and Type 2 Diabetes. Insulin resistance, a hallmark of Type 2 Diabetes, is reversed in response to aerobic exercise training. However, the effect of aerobic exercise training on glucagon sensitivity is unclear. Glucagon signaling at the liver promotes fatty acid oxidation, inhibits De novo lipogenesis, and activates AMP Kinase, a key mediator of healthy aging. Like humans, aging in mice age leads to a decline in physical and metabolic function. To understand the role of glucagon signaling in exercise-induced improvements in physical and metabolic function in the mouse, we implemented a 16-week aerobic exercise training protocol in young and aged mice. 16 weeks of exercise training initiated at 6 months of age increased markers of physical function (P<0.01) and attenuated age-related weight gain (P<0.05) and fat mass (P<0.0001). Additionally, exercise training improved glucose clearance (P<0.01), enhanced glucose-stimulated insulin secretion (P<0.01) and decreased hepatic lipid accumulation (P<0.05). Importantly, exercise training decreased hypoglycemia stimulated glucagon secretion (P<0.01), with no effect on hepatic glucagon receptor mRNA expression or serum glucagon. Thus, we propose that aerobic exercise training enhances glucagon sensitivity at the liver, implicating glucagon as a potential mediator of exercise-induced improvements in aging. Studies initiating the same aerobic exercise training intervention at 18 months of age in the mouse are currently underway to establish the role of glucagon receptor signaling in exercise-induced improvements in aging.


2017 ◽  
Vol 54 (5) ◽  
pp. 272-279 ◽  
Author(s):  
Koichiro Tanahashi ◽  
Keisei Kosaki ◽  
Yuriko Sawano ◽  
Toru Yoshikawa ◽  
Kaname Tagawa ◽  
...  

2016 ◽  
Vol 41 (8) ◽  
pp. 832-841 ◽  
Author(s):  
Rian Q. Landers-Ramos ◽  
Kelsey J. Corrigan ◽  
Lisa M. Guth ◽  
Christine N. Altom ◽  
Espen E. Spangenburg ◽  
...  

Cardiovascular disease risk increases with age due, in part, to impaired endothelial function and decreased circulating angiogenic cell (CAC) number and function. We sought to determine if 10 days of aerobic exercise training improves endothelial function, CAC number, and intracellular redox balance in older sedentary adults. Eleven healthy subjects (4 men, 7 women), 61 ± 2 years of age participated in 60 min of aerobic exercise at 70% maximal oxygen consumption for 10 consecutive days while maintaining body weight. Before and after training, endothelial function was measured as flow-mediated dilation of the brachial artery and fasting blood was drawn to enumerate 3 CAC subtypes. Intracellular reactive oxygen species (ROS) and nitric oxide (NO) in CD34+ CACs were measured using fluorescent probes and reinforced via real-time quantitative polymerase chain reaction. Flow-mediated dilation improved significantly following training (10% ± 1.3% before vs. 16% ± 1.4% after training; P < 0.05). Likewise, CD34+/KDR+ number increased 104% and KDR+ number increased 151% (P < 0.05 for both), although CD34+ number was not significantly altered (P > 0.05). Intracellular NO and ROS levels in CD34+ CACs were not different after training (P > 0.05 for both). Messenger RNA expression of SOD1, endothelial nitric oxide synthase, and NADPH oxidase 2 and neutrophil cytosolic factor 1 in CD34+ CACs was not significantly altered with training (P > 0.05). In conclusion, 10 consecutive days of aerobic exercise increased flow-mediated dilation and CAC number in older, previously sedentary adults, but did not affect intracellular redox balance in CD34+ CACs. Overall, these data indicate that even short-term aerobic exercise training can have a significant impact on cardiovascular disease risk factors.


Author(s):  
Renata Kelly Da Palma ◽  
Christiane Malfitano ◽  
Guilherme Lemos Shimojo ◽  
Iris Callado Sanches ◽  
Kátia De Angelis

Background: Hypertension is one of the leading causes of death due to stroke, heart attack and kidney failure. The understanding of the pathophysiological mechanisms involved in its development and maintenance is critical to potential therapeutic interventions. Thus, animal models of hypertension have been used in the study of this disease for many years. Objective: To investigated the effects of dynamic aerobic exercise training as a non-pharmacological approach for the management of hypertension in animal models. Method/Design: This study is a literature review conducted in the Medline database. Results: The results demonstrated that aerobic exercise training may reduce blood pressure in different rat models of hypertension. Conclusions: The dynamic aerobic exercise can reduced blood pressure in different animal models of hypertension by mechanisms that involving neurohumoral changes, reinforcing the important role of this approach in the treatment of hypertension and its associated disorders


Metabolism ◽  
2013 ◽  
Vol 62 (10) ◽  
pp. 1485-1494 ◽  
Author(s):  
Katharine E. Hall ◽  
Matthew W. McDonald ◽  
Kenneth N. Grisé ◽  
Oscar A. Campos ◽  
Earl G. Noble ◽  
...  

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Anna Laura Viacava Américo ◽  
Cynthia Rodrigues Muller ◽  
Miriam Helena Fonseca‐Alaniz ◽  
Fabiana Sant'Anna Evangelista

2015 ◽  
Vol 309 (4) ◽  
pp. H543-H552 ◽  
Author(s):  
Tiago Fernandes ◽  
Valério G. Baraúna ◽  
Carlos E. Negrão ◽  
M. Ian Phillips ◽  
Edilamar M. Oliveira

Left ventricular (LV) hypertrophy is an important physiological compensatory mechanism in response to chronic increase in hemodynamic overload. There are two different forms of LV hypertrophy, one physiological and another pathological. Aerobic exercise induces beneficial physiological LV remodeling. The molecular/cellular mechanisms for this effect are not totally known, and here we review various mechanisms including the role of microRNA (miRNA). Studies in the heart, have identified antihypertrophic miRNA-1, -133, -26, -9, -98, -29, -378, and -145 and prohypertrophic miRNA-143, -103, -130a, -146a, -21, -210, -221, -222, -27a/b, -199a/b, -208, -195, -499, -34a/b/c, -497, -23a, and -15a/b. Four miRNAs are recognized as cardiac-specific: miRNA-1, -133a/b, -208a/b, and -499 and called myomiRs. In our studies we have shown that miRNAs respond to swimming aerobic exercise by 1) decreasing cardiac fibrosis through miRNA-29 increasing and inhibiting collagen, 2) increasing angiogenesis through miRNA-126 by inhibiting negative regulators of the VEGF pathway, and 3) modulating the renin-angiotensin system through the miRNAs-27a/b and -143. Exercise training also increases cardiomyocyte growth and survival by swimming-regulated miRNA-1, -21, -27a/b, -29a/c, -30e, -99b, -100, -124, -126, -133a/b, -143, -144, -145, -208a, and -222 and running-regulated miRNA-1, -26, -27a, -133, -143, -150, and -222, which influence genes associated with the heart remodeling and angiogenesis. We conclude that there is a potential role of these miRNAs in promoting cardioprotective effects on physiological growth.


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