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How to Lower Your Heart Rate. Trending Topics. What Parents Need to Know. Share this article via email with one or more people using the form below. Additionally, exercise improves oxygen delivery throughout the body through vasodilation and angiogenesis — , protecting against ischemia-reperfusion injury in the heart , Further, exercise causes a long-term anti-inflammatory effect which is inversely related to the increased inflammation typically seen in CVD and obesity Many of the benefits sustained by exercise are due to mitochondrial adaptations throughout the body.
For example, exercise improves long-term cardiorespiratory fitness VO 2 by increasing the mitochondrial content and desaturation of myoglobin in skeletal muscle tissue, improving the oxidative capacity of skeletal muscle , , The increase of oxygen uptake and utilization by skeletal muscle as indicated by arteriovenous oxygen difference; a-vO 2 in response to regular exercise is protective against a decrease in obesity-related a-vO2, resulting in individuals to require more blood to receive the same amount of oxygen Mitochondrial biogenesis is augmented in cardiomyocytes in response to exercise 14 , , , These exercise-induced enhancements of mitochondrial function are important in preventing cardiovascular dysfunctions often caused by obesity.
Obesity is associated with defective mitochondrial biogenesis in the myocardium and reduced mitochondrial capacity for oxidative phosphorylation and ATP synthesis , In heart failure, fatty acid uptake, and utilization is decreased , likely causing the heart failure associated shift toward glucose metabolism in order to preserve cardiovascular function , , However, in advanced heart failure, diabetes, or obesity, myocardial insulin resistance may develop, impairing glucose uptake and accelerating cardiovascular dysfunction — Importantly, insulin sensitivity is improved in response to regular exercise which is vital in reducing the risk of obesity-related insulin resistance.
Insulin has also been indicated to directly regulate mitochondrial metabolism by promoting induction of OPA1, a GTPase that controls mitochondrial cristae integrity, energetics and mitochondrial DNA maintenance , , thus indicating another potential mechanism of exercise-induced improvements in cardiovascular health through mitochondrial function enhancement.
Reactive oxygen species ROS are physiological byproducts of aerobic mitochondrial metabolism and while necessary for initiating cellular repair or apoptosis, increased levels of ROS are associated with inflammation and several forms of CVD While exercise increases the direct production of ROS by mitochondria, the net cellular ROS load is reduced by exercise due to increased action of antioxidant systems By increasing the ability of mitochondria to prevent oxidative damage, exercise-induced modifications to mitochondria protect against ischemia-reperfusion damage to the heart.
During ischemia, the absence of oxygen from the heart creates an environment in which the return of oxygenated blood flow leads to the induction of inflammation and oxidative stress rather than restoration of normal function In contrast, exercise-induced adaptations to cardiomyocyte mitochondria dampen oxidative damage caused by ischemia-reperfusion, resulting in reduced cardiac injury and decreasing the risk of ischemia-related cardiac dysfunction or death — Exercise training induces vascular adaptations to several tissues , In the heart, the increase in vascularization protects against vascular stress and reduces the likelihood of a cardiac event 24 — These adaptations are mediated through increased expression of vascular endothelial nitric oxide synthase eNOS.
Exercise increases the intensity of physiological shear stress, inducing the shear stress-dependent activity of c-Src in endothelial cells and increasing expression of eNOS 27 , In the vascular endothelium, eNOS catalyzes the production of nitric oxide NO which causes vasodilation, inhibits platelet aggregation and prevents leukocyte adhesion to vessel walls, thus reducing the onset of atherosclerosis, thrombosis, ischemia, or other cardiac events , Exercise also induces angiogenesis, however the mechanisms regulating this process are unclear.
It has been hypothesized that the increase in nitric oxide NO production after exercise upregulates pro-angiogenic factors, particularly vascular endothelial growth factor VEGF One recent study determined that male rats who underwent exercise training for 10 weeks after MI had increased Akt phosphorylation of eNOS, and reactivation of cardiac VEGF pathway activity, resulting in increased angiogenesis While the mechanisms are not completely defined, it is clear that exercise induces arteriogenesis, increases angiogenesis and protects against vascular stress, thus decreasing the possibility of a cardiac event — , , Inflammation is a complex yet normal biological reaction to damaging stimuli Exercise, however, results in a long-term anti-inflammatory effect , Excess immune activation caused by obesity is of particular concern for vascular health, as activation of TLR4 causes monocyte recruitment and conversion to foam cells, driving the progression of atherosclerosis 67 , Exercise prevents the development of atherosclerosis by reducing expression of TLRs on monocytes and macrophages, which subsequently decreases the availability of TLR4 ligands and inhibiting pro-inflammatory cytokine production , , Exercise also decreases pro-inflammatory N-terminal pro b-type natriuretic NT-proBNP and high-sensitivity C-reactive protein hsCRP within the heart, both of which are predictors of heart failure in atherosclerosis , Skeletal muscle can act as a secretory organ by stimulating the production, secretion, and expression of specific myokines after contraction — Myokines are chemical messengers that function in an autocrine, paracrine, or endocrine manner to influence crosstalk between different organs including skeletal muscle, liver, and adipose tissue — They are of great interest with regards to cardiovascular health because the well-known protective actions of exercise on cardiovascular function are at least partially mediated by increased secretion of myokines Figure 2 Figure 2.
Exercise-induced myokines mediate organ cross-talk and improve cardiometabolic health. C Myonectin MyoN increases fatty acid uptake in adipocytes and hepatocytes , and promotes protects against ischemic injury in the heart, possibly through Akt activation IL-6 was introduced as the first myokine over a decade ago Circulating levels of IL-6 are increased in response an acute bout of aerobic exercise , and can act in an endocrine fashion to improve metabolic and cardiovascular health.
IL-6 also increases lipolysis and fatty acid oxidation in adipose tissue and can increase glucose uptake through stimulation of the AMP-activated protein kinase AMPK signaling pathway , More investigation is required to determine the direct effects of IL-6 action on cardiovascular health. Myonectin or CTRP15 is abundantly expressed in skeletal muscle and is increased in response to chronic aerobic exercise Importantly, injection of myonectin into wild-type mice decreases circulating free fatty acids levels by increasing fatty acid uptake in adipocytes and hepatocytes Myonectin has also been identified to have protective effects on cardiovascular health; mice deficient in Myonectin had enhanced ischemic injury in response to MI while systemic delivery of myonectin attenuated ischemic injury Further work is needed to determine whether these benefits are observed in response to an increase in myonectin after exercise.
Fstl1, also referred to as TSC, is a secreted glycoprotein that belongs to the follistatin family of proteins and is upregulated in skeletal muscle in response to exercise , , Expression of Fstl1 is also increased in ischemic and hypertrophic hearts of mice and functions in a protective manner Systemic administration of Fstl1 in both mouse and swine models led to reduced apoptosis, inflammation and injury size following ischemia-reperfusion , In vitro , treatment of cultured cardiomyocytes with Fstl1 reduces apoptosis in response to hypoxia-reoxygenation by activating Akt and AMPK , One recent study demonstrated that Fstl1 stimulates early fibroblast activation, which is required for acute repair and protects the heart from rupture after ischemia-reperfusion While the exact role of an exercise-induced increase in Flst1 on cardiovascular function has not been defined, these data indicate that Fstl1 is increased in response to exercise, and an increase in circulating Fstl1 functions to repair cardiovascular damage and improve cardiovascular function NDNF is a glycosylated protein secreted from the endothelial cells of skeletal muscle This pro-angiogenic affect is an important component in the recovery from MI; intramuscular administration of NDNF using an adenoviral vector improved systolic function in a mouse model after MI Additionally, increased levels of NDNF released from skeletal muscle in response to exercise enhance fatty acid oxidation through activation of AMPK These data demonstrate the importance of NDNF as an endogenous ischemia- and exercise inducible factor that can enhance revascularization and therefore have a cardiovascular protective effect.
The rate of obesity-related cardiovascular disease is rapidly increasing, and often associated with additional co-morbidities including type 2 diabetes 3 , 6 , 8. It is clear that exercise reduces cardiovascular risk factors, and this reduction in risk factors is independent of changes to body weight or incidence of type 2 diabetes 75 — 77 , 79 , , Exercise is also an important therapeutic treatment for patients who have cardiovascular diseases 14 , further demonstrating the protective and restorative properties of exercise.
In patients with CVD, exercise improved endothelium-dependent vasodilatation, increased ejection fraction and exercise tolerance, improved quality of life, and reduced CVD-related mortality 10 , 91 , 92 , , , — Exercise improves cardiovascular health by several mechanisms including increased mitochondrial biogenesis and fatty acid oxidation 14 , , , — dilation of blood vessels causing improved myocardial perfusion 9 — 11 , and reduction of inflammation providing protection against the development of atherosclerosis 67 , , Myokines released from skeletal muscle during exercise also mediate systemic and cardiovascular health benefits through an anti-inflammatory action, increased fatty acid oxidation, increased glucose uptake, and improved insulin secretion and sensitivity , , , , — Importantly, several myokines IL-6, Myonectin, Fstl1, and NDNF have also been shown to have cardiovascular protective effects in response to ischemia-reperfusion injury — , , While it is clear that exercise is important, the mechanistic pathways behind exercise-induced benefits on cardiovascular health are still being identified.
Further understanding of the molecular mechanisms through which exercise improves cardiovascular function will lead to the development of therapeutics which can act in conjunction with exercise programs, and for individuals whom are unable or unwilling to exercise to amplify the beneficial effects of exercise. Future research will investigate the effects of cardiac specific proteins on cardiovascular health, expanding research into the areas of system cross-talk will help delineate how other tissues, skeletal muscle in particular, can mediate cardiovascular improvements via myokine release.
How these myokines affect cardiovascular function, including adaptations to mitochondrial activity, angiogenesis and inflammatory responses will provide insight into new mechanisms for the beneficial effects of exercise on cardiovascular function.
Accordingly, myokines may act as potential targets for heart disease prevention and therapies. Recent studies have investigated the use of gene therapies, including the use of adeno-associated virus, on cardiovascular function.
While these therapies have not been fully optimized with remaining issues in immunogenicity, efficacy and genotoxicity , their development provides excitement for the potential therapies focused on exercise-induced myokines that improve cardiovascular function as a treatment for patients who are unable, or perhaps unwilling, to exercise. Together these data highlight the importance of exercise and exercise-related therapies to both prevents the development of cardiovascular disease and promotes recovery and improved health in patients with CVD.
All authors approved the final version of the manuscript. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. PubMed Abstract Google Scholar. Body mass index and the prevalence of hypertension and dyslipidemia. Obes Res.
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Fontana L. Interventions to promote cardiometabolic health and slow cardiovascular ageing. Nat Rev Cardiol. Regulation of coronary blood flow during exercise. Physiol Rev. The more you exercise, the more these things will continue to improve. There are some unseen benefits of long-term exercise as well that you may not have realized. These are the three main benefits:. These three benefits come together to help your body even more by increasing your energy, improving your breathing and even lowering blood pressure.
Additionally, you may have other benefits that you notice that are in direct relation to your exercise. At Warner Family Practice, our physicians conduct thousands of annual comprehensive physicals, also known as executive physicals, and actually chart the short and long term impact of exercise.
If you have not been active for a significant stretch of time, just starting any exercise program may seem like an impossible task.
There are some easy exercises that you can do to ease into exercising. Insulin sensitivity The association between blood lipids and cardiovascular health is highly influenced by systemic insulin sensitivity, and resistance to insulin signaling is known to promote the development of heart disease, in part by altering the blood lipid profile Blood pressure During exercise, increases in cardiac stroke volume and heart rate raise cardiac output, which coupled with a transient increase in systemic vascular resistance, elevate mean arterial blood pressure Cardiac adaptations During exercise, the heart is subjected to intermittent hemodynamic stresses of pressure overload, volume overload, or both.
Blood and vasculature The oxygen carrying capacity of blood, determined by the number of circulating erythrocytes and their associated intracellular hemoglobin concentration, is an important determinant of exercise performance and resistance to fatigue Concluding remarks and remaining questions to be addressed Despite the extensive body of knowledge documenting the unequivocal health benefits of exercise, a vast majority of Americans do not engage in sufficient physical activity Open in a separate window.
Figure 1. Author contributions All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication. Conflict of interest statement The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Footnotes Funding. References 1. CDC N Heart disease and stroke statistics update: a report from the American Heart Association.
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Adipocyte insulin resistance: effects of aging, obesity, exercise, and food restriction.
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