Impact of Age and Aerobic Exercise Training on Conduit Artery Wall Thickness: Role of the Shear Pattern

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


2003 ◽  
Vol 94 (2) ◽  
pp. 549-554 ◽  
Author(s):  
Phillip E. Gates ◽  
Keith P. George ◽  
Ian G. Campbell

Upper body exercise has many applications to the rehabilitation and maintenance of cardiovascular health of individuals who are unable to exercise their lower body. The hemodynamic loads of upper body aerobic exercise are characterized by relatively high blood pressure and relatively low venous return. It is not clear how the left ventricle adapts to the specific hemodynamic loads associated with this form of exercise training. The purpose of this study was to measure left ventricular structure and function in previously sedentary men by using echocardiography before and after 12 wk of aerobic arm-crank exercise training ( n = 22) or a time control period ( n = 22). Arm-crank peak oxygen consumption (in ml · kg−1 · min−1) increased by 16% ( P < 0.05) after training, and significant differences ( P < 0.05) were found in wall thickness (from 0.86 to 0.99 cm) but not in left ventricular internal dimension in diastole or systole. This suggested a concentric pattern of left ventricular hypertrophy that persisted after scaling to changes in anthropometric characteristics. No differences ( P < 0.05) were found for any measurements of resting left ventricular function. We conclude that upper body aerobic exercise training results in a specific left ventricular adaptation that is characterized by increased left ventricular wall thickness but no change in chamber dimension.


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


2011 ◽  
Vol 111 (3) ◽  
pp. 657-664 ◽  
Author(s):  
Catherine R. Mikus ◽  
Seth T. Fairfax ◽  
Jessica L. Libla ◽  
Leryn J. Boyle ◽  
Lauro C. Vianna ◽  
...  

The vasodilatory effects of insulin account for up to 40% of insulin-mediated glucose disposal; however, insulin-stimulated vasodilation is impaired in individuals with type 2 diabetes, limiting perfusion and delivery of glucose and insulin to target tissues. To determine whether exercise training improves conduit artery blood flow following glucose ingestion, a stimulus for increasing circulating insulin, we assessed femoral blood flow (FBF; Doppler ultrasound) during an oral glucose tolerance test (OGTT; 75 g glucose) in 11 overweight or obese (body mass index, 34 ± 1 kg/m2), sedentary (peak oxygen consumption, 23 ± 1 ml·kg−1·min−1) individuals (53 ± 2 yr) with non-insulin-dependent type 2 diabetes (HbA1c, 6.63 ± 0.18%) before and after 7 days of supervised treadmill and cycling exercise (60 min/day, 60–75% heart rate reserve). Fasting glucose, insulin, and FBF were not significantly different after 7 days of exercise, nor were glucose or insulin responses to the OGTT. However, estimates of whole body insulin sensitivity (Matsuda insulin sensitivity index) increased ( P < 0.05). Before exercise training, FBF did not change significantly during the OGTT (1 ± 7, −7 ± 5, 0 ± 6, and 0 ± 5% of fasting FBF at 75, 90, 105, and 120 min, respectively). In contrast, after exercise training, FBF increased by 33 ± 9, 39 ± 14, 34 ± 7, and 48 ± 18% above fasting levels at 75, 90, 105, and 120 min, respectively ( P < 0.05 vs. corresponding preexercise time points). Additionally, postprandial glucose responses to a standardized breakfast meal consumed under “free-living” conditions decreased during the final 3 days of exercise ( P < 0.05). In conclusion, 7 days of aerobic exercise training improves conduit artery blood flow during an OGTT in individuals with type 2 diabetes.


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.


2021 ◽  
Vol 32 (1) ◽  
pp. 11-19
Author(s):  
Liana C. Wooten ◽  
Brian T. Neville ◽  
Andrew A. Guccione ◽  
Lisa M.K. Chin ◽  
Randall E. Keyser

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