Effects of exercise training on arterial function in type 2 diabetes mellitus,t s line tracking,glycemic management of type 2 diabetes mellitus pdf oms - Good Point


Large-conductance Ca2+-activated K+ (BKCa) channels play a critical role in regulating cellular excitability and vascular tone. ReferencesAlbarwani S, Al-Siyabi S, Baomar H, Hassan MO (2010) Exercise training attenuates ageing-induced BKCa channel downregulation in rat coronary arteries. JavaScript is currently disabled, this site works much better if you enable JavaScript in your browser. Science, Technology and Medicine open access publisher.Publish, read and share novel research. During muscular contraction the bloodflow is blocked, and the O2 tissue tension falls drastically. Ophtalmoscopy for hypertonic changes of the retina also provides the diagnosis hypertension.
In some cases of hypertension there is a clear relation to the renin-angiotensin-aldosterone cascade (Chapter 24).
Introduction Individuals with type 2 diabetes have a risk of heart failure 2-5 times greater than age matched controls, and the risk is greater for women compared to men. The aim of the study is to determine the effects of short-term high-intensity exercise on arterial function and glucose tolerance in obese individuals with and without the metabolic syndrome (MetSyn). ReferencesAkbari CM, Saouaf R, Barnhill DF, Newman PA, LoGerfo FW, Veves A (1998) Endothelium-dependent vasodilatation is impaired in both microcirculation and macrocirculation during acute hyperglycemia. CrossRefCononie CC, Goldberg AP, Rogus E, Hagberg JM (1994) Seven consecutive days of exercise lowers plasma insulin responses to an oral glucose challenge in sedentary elderly. CrossRefTesfamariam B, Cohen RA (1992) Free radicals mediate endothelial cell dysfunction caused by elevated glucose. Department of Kinesiology and Community Health, University of Illinois at Urbana-Champaign, 906 S. Exercise training showed reversible beneficial effects on cardiovascular systems with an improvement of vascular functions. Myoglobin is important as a dynamic O2 store in muscle cells, although myoglobin is not totally saturated with O2.
Prior to the onset of heart failure, individuals with type 2 diabetes exhibit structural and functional abnormalities of the myocardium. Exp Diabetes Res 2008:672021, 6 pMancini GB, Yeoh E, Abbott D, Chan S (2002) Validation of an automated method for assessing brachial artery endothelial dysfunction. Although exercise training improves myocardial function in animal models of type 2 diabetes, data is in humans is limited. Changes in aerobic capacity, flow-mediated dilation (FMD), and arterial stiffness using central and peripheral pulse wave velocity (PWV) measurements were assessed pre- and post-training. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.AbstractThis study measured cognitive and vascular responses to aerobic training in sedentary young adults. Harold Laughlin1[1] Department of Biomedical Sciences, University of Missouri, Columbia Missouri and Morningside College, Sioux City, Iowa,, United States of America1. Division of Diabetes and Cardiovascular Research Leeds Institute for Genetics Health and Therapeutics (LIGHT) Laboratories, University of Leeds, Leeds, United Kingdom.
This study aimed to investigate the effect of moderate intensity exercise training upon cardiac function in overweight and obese postmenopausal women with type 2 diabetes (T2) compared to BMI matched, healthy controls (ND).
These measurements were obtained fasting and 1-h post-test meal while the subjects were hyperglycemic. Since intensity and duration of exercise were identical between training groups, the training volume was higher in EX2 than in EX1.
IntroductionThe endothelium, the innermost layer of blood vessels, has many important biological functions which are responsible for regulating vascular tone and structure.
Dessy, 2009eNOS activation by physical forces: from short-term regulation of contraction to chronic remodeling of cardiovascular tissues. Manson, 2005Epidemiological evidence for the role of physical activity in reducing risk of type 2 diabetes and cardiovascular disease. Laughlin, 2010Influence of exercise and perivascular adipose tissue on coronary artery vasomotor function in a familial hypercholesterolemic porcine atherosclerosis model. Exercise training not only decreased heart rate, but also attenuated pressor responses induced by angiotensin II or norepinephrine (NE).
One of the major functions of a healthy endothelium is to ensure adequate blood supply to the different tissues.
Fielding, 1997Two sterol regulatory element-like sequences mediate up-regulation of caveolin gene transcription in response to low density lipoprotein free cholesterol. Prior to and following 6 months of moderate intensity exercise training (55-75% heart rate reserve), participants completed a modified Bruce cardiopulmonary exercise test to assess VO 2peak. The maximal vascular contraction induced by 10?5 M NE was significantly decreased after training. This particular process is regulated by the release and interaction of different vasoactive substances (i.e. Montani, 1990Growth regulation of the vascular system: evidence for a metabolic hypothesis.
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In precontracted thoracic aorta with NE (10?5 M), activation of the BKCa channels by NS1619 significantly decreased the tension. Anthropometry (body mass, height, waist and hip circumferences) and a fasting venous blood sample (for insulin, glucose, HbA1c) were also assessed. Inside-out patch clamp recording on aortic SMCs showed that exercise training significantly increased the open probability, decreased the mean closed time and increased the mean open time of BKCa channels.
Motz, 2002Evidence for an independent and cumulative effect of postprandial hypertriglyceridemia and hyperglycemia on endothelial dysfunction and oxidative stress generation: effects of short- and long-term simvastatin treatment. Two-way mixed mode ANOVA with repeated measures tested the interaction between time (0 Vs 6 months) and group (T2 Vs ND).
Type 2 diabetes mellitus (T2DM) is among those chronic diseases that are associated with endothelial dysfunction which may contribute to limited glucose uptake in skeletal muscle.
Panza, 2004Insulin impairs endothelium-dependent vasodilation independent of insulin sensitivity or lipid profile.
Giugliano, 2008Oscillating glucose is more deleterious to endothelial function and oxidative stress than mean glucose in normal and type 2 diabetic patients. Shaw, 2008Improved endothelial function following a 14-month resistance exercise training program in adults with type 2 diabetes. Central and peripheral PWV were not altered with training for either group (MetSyn, n = 13; Non-MetSyn, n = 13). These data suggest that there is a dose effect for exercise training volume for the activation of BKCa channels in vascular SMCs, which contributes to improvement of the arterial function in thoracic aortas. Acta Physica Hungarica 87:127–138Duncker DJ, Bache RJ (2008) Regulation of coronary blood flow during exercise. In fact, diabetes-related endothelial dysfunction has been reported to lead to morphologic and structural vascular changes present throughout the course of diabetes (Taylor and Poston, 1994).


Luscher, 1992Oxidized low density lipoproteins induce mRNA expression and release of endothelin from human and porcine endothelium. A 10-day high-intensity exercise program in obese individuals improved aerobic capacity and glucose tolerance but no change in arterial function was observed. There are around 17 million people in the United States who have diabetes, of whom close to 95% have T2DM.
Creager, 2003Oral antioxidant therapy improves endothelial function in Type 1 but not Type 2 diabetes mellitus. Laughlin, 2010Physical activity maintains aortic endothelium-dependent relaxation in the obese type 2 diabetic OLETF rat. Acute hyperglycemia had a deleterious effect on arterial function, suggesting that persons with impaired glucose homeostasis may experience more opportunities for attenuated arterial function on a daily basis which could contribute to increased cardiovascular risk. Cardiovascular disease (CVD) is the major cause of morbidity and mortality in people with T2DM (Ness et al., 1999), and coronary heart disease is the most common cause of death among those individuals. Thus the primary purpose of this chapter is to summarize the current available literature concerning the effects of T2DM on arterial endothelium. Yeung, et al.1995Close relation of endothelial function in the human coronary and peripheral circulations. Liu, 2010The lack of utility of circulating biomarkers of inflammation and endothelial dysfunction for type 2 diabetes risk prediction among postmenopausal women: the Women’s Health Initiative Observational Study. Conclusion Compared to ND women, the cardiac function of T2 women in response to moderate intensity exercise training is impaired. This appears to be a function of a lack of plasticity of the flow generating capacity of the heart. Role of the endothelium in vasoregulation All blood vessels in the systemic and pulmonary circulations are lined by a continuous single cell layer of endothelium. Weintraub, 2009Proinflammatory phenotype of perivascular adipocytes: influence of high-fat feeding. As a result of research over the past 30 years it is established that the endothelium constitutes a very important and exciting organ. The endothelium plays an important role in hemostasis, inflammation, lipid metabolism, vascular growth, cell migration, formation of (and interactions with) extracellular matrix molecules, as well as control of vascular permeability and vascular resistance (both vasodilator and vasoconstrictor responses) (Furchgott and Vanhoutte, 1989; Ganz and Vita, 2003). The endothelium can detect chemical substances within the blood and physical forces imparted to blood vessel walls (i.e.
The vascular endothelium releases a variety of vasoactive substances, including vasodilator and vasoconstrictor substances such as endothelin, which contribute to vasomotor control in tissues throughout the body. As described below, the most common measure of the functional capacity of the endothelium is to measure endothelium-dependent dilation (EDD) primarily because of the potential to assess the health of the endothelium non-invasively. The relative importance of endothelium-dependent control differs among the tissues of the body at least in part because the endothelial lining is not a homogeneous compartment.
Sports Med 33:585–598Wang HD, Hope S, Du Y, Quinn MT, Cayatte A, Pagano PJ, Cohen RA (1999) Paracrine role of adventitial superoxide anion in mediating spontaneous tone of the isolated rat aorta in angiotensin II-Induced hypertension.
In its role in vascular control, NO diffuses to the underlying smooth muscle cells, where it activates soluble guanylyl cyclase, resulting in production of cyclic guanosine monophosphate (cGMP) and activation of protein kinase G (PKG), which leads to vasodilation.
The weight of evidence suggests that an increase in wall shear stress, secondary to the increased flow, is the physical force that initiates dilation (Pohl et al., 1991).
Prostanoid EDRFs are metabolites of arachidonic acid produced by the cyclooxygenase pathway.
Endothelins are vasoactive peptides produced by vascular endothelial cells (Korth et al., 1999). Three different isoforms of endothelins (ET) have been identified, namely, ET-1, ET-2 and ET-3 (Haynes and Webb, 1998; Masaki, 2004). ET-1 is the most abundant isoform expressed and secreted in endothelial cells and it is one of the most potent vasoconstrictor agents described to date (Haynes and Webb, 1998).
ET-1 is constitutively released by endothelial cells with the majority (~80%) released luminally towards vascular smooth muscle (Wagner et al., 1992). Thus ET-1 appears to act primarily in a local paracrine, rather than circulating endocrine, manner.
ET receptors are expressed on endothelial and vascular smooth muscle cells of both arteries and veins throughout the pulmonary and systemic vascular trees (Loesch, 2005; Rubanyi and Polokoff, 1994).
For instance, flow-mediated vasodilation (FMD), using ultrasonography, is the classic technique used to detect changes in superficial arteries (e.g.
The vasodilatory response, after a period of transient ischemia (~ 5 min), is dependent upon a series of neurologic, myogenic and chemical intermediates, which includes the release of NO. There is a good correlation between this post-ischemic vasodilation observed in the forearm (i.e. Invasive in vivo techniquesThese techniques are used to evaluate endothelial function of arteries and to determine the probable changes in their diameter, by ultrasonograhpy, or blood flow, by plethysmography, after cardiac catheterization to access the coronary circulation. Vascular inflammationEndothelial dysfunction is characterized by a chronic, systemic pro-inflammatory state, reduced vasodilation (reduction in relaxing factors and an increase in contracting factors), and a pro-thrombotic state. In fact, it has been suggested that endothelial dysfunction is an important factor in the pathogenesis of vascular disease observed in patients with diabetes (De Caterina, 2000; Schalkwijk and Stehouwer, 2005). Interestingly, the increased levels of CRP would mediate opposite actions on the vasculature. Insulin exerts anti-inflammatory effects at the cellular and molecular levels in vitro and in vivo. It has been shown that low-dose infusion of insulin reduces reactive oxygen species generation, and suppresses NADPH oxidase expression and plasma ICAM-1 and MCP-1 concentrations. The metabolic syndrome: Obesity and cardiovascular diseaseThe metabolic syndrome is a collection of risk factors for CVD, typically characterized by endothelial dysfunction. It is also well established that metabolic syndrome and obesity linked with metabolic syndrome promote endothelial dysfunction in adults and children (Aggoun, 2007; Singhal, 2005).
Insulin resistance is typically defined as decreased responsiveness to insulin’s actions that stimulate glucose uptake in the tissues (Lebovitz, 2001). The WHIOS involved 1,584 incident T2DM cases and 2,198 matched controls to evaluate the utility of plasma markers of inflammation and endothelial dysfunction for T2DM risk prediction. Results indicated that none of the inflammatory and endothelial dysfunction markers improved T2DM prediction in a multiethnic cohort of postmenopausal women.
It was also demonstrated recently in rat model of T2DM that insulin resistance manifested prior to a dramatic (20-35%) progressive decline in endothelial function concurrent with T2DM disease development (Bunker et al., 2010). HyperglycemiaGenerally speaking, hyperglycemia can be divided into two broad categories; a) impaired fasting glucose, and b) impaired glucose tolerance. Indeed, hyperglycemia is the major causal factor in the development of endothelial dysfunction in diabetes. In T2DM, the endothelium, due to glucose oxidation, promotes the increase of free radicals (e.g. In addition, there is evidence that indicates that increased ROS plays an important role in the development of diabetic complications. Furthermore, endothelial cells in patients with T2DM are not able to produce sufficient amount of NO and therefore fail to vasodilate in response to vasodilators (e.g.


The increased glucose levels (“hyperglycemia”) also promote mitochondrial formation of ROS. It has been reported that in aortic endothelial cells hyperglycemia induced increased superoxide production which prevents eNOS activity and expression (Srinivasan et al., 2004). The formation of peroxynitrite (superoxide and NO interaction) promotes blunted NO-mediated vasodilatory response and further induces cellular damage through depletion of tetrahydrobiopterin (BH4), an important co-factor for eNOS activity (Pannirselvam et al., 2002).
Dyslipidemia T2DM promotes elevated total cholesterol, high levels of oxidized lipoproteins, especially low density lipoptotein (LDL), high triglycerides levels, and decreased high-density lipoprotein (HDL) (Watkins, 2003). It has been suggested that abnormal lipids and lipoproteins play a role in endothelial dysfunction in T2DM (McVeigh et al., 1992). For instance, endothelium-dependent vasodilation was negatively and significantly correlated with elevated triglyceride, LDL and low HDL cholesterol concentrations (Watts et al., 1996). In the same manner, it has been shown that only LDL size was inversely correlated with the acetylcholine-induced brachial EDD (Makimattila et al., 1999).
Clearly, we can infer from the above studies that LDL is one of the chief factors involved in endothelial dysfunction. LDL and other lipoproteins are able to cross the endothelial cells layer by vascular transport, and later they are oxidatively modified at the sub-endothelial space into reactive oxygen species generated by macrophages, endothelial cells and smooth muscles (Steinberg, 1997). Oxidized-LDL decreases NO production by reduction of NOS (Tribe and Poston, 1996) or by stimulating the synthesis of caveolin-I (Bist et al., 1997), consequently contributing to defective vasodilatation. In addition, there are indications that oxidized-LDL could also enhance the release of ET-1, a main endothelial constrictor peptide (Boulanger et al., 1992).
Type 1 diabetes is characterized by an absence of insulin while T2DM is characterized by insulin resistance followed in time with decreased plasma insulin.
The vascular complications of T2DM take two major forms; a) atherosclerosis in conduit arteries and b) microvascular dysfunction in skeletal muscle vascular beds. The vasodilatory effects of insulin account for up to 40% of insulin-mediated glucose disposal in skeletal muscle following a meal.
Insulin-stimulated NO production via the insulin-receptor substrate-1 (IRS-1) pathway is diminished, while vasoconstriction through the mitogen-activated protein kinase (MAPK) pathway, endothelin-converting enzyme (ECE) and subsequent secretion of the vasoconstrictor ET-1 may be augmented. As a result, microvascular blood flow and delivery of glucose to muscle tissue are diminished, contributing to reduced skeletal muscle glucose uptake and peripheral insulin resistance.
Insulin resistance in T2DM appears to be the result of abnormal insulin-induced glucose uptake by skeletal muscle and microvascular dysfunction in skeletal muscle (blunted insulin-induced vasodilation). Local metabolic control of blood flow is abnormal and myogenic control of vascular smooth muscle tone is affected in diabetes as well. For instance, arterioles isolated from obese Zucker rat skeletal muscle exhibit increased spontaneous tone due to changes in vascular smooth muscle and to changes in an endothelium-derived factor (Frisbee et al., 2006). The endothelium of both conduit arteries and resistance arteries is dysfunctional in diabetes (Hodnett and Hester, 2007). Endothelial dysfunction in conduit arteries appears to be associated with decreased bio-availability of NO with sustained (or normal) eNOS content, decreased phospho-eNOS, deceased BH4 and cytochrome P450 expression as well as increased thromboxane (TXA2) content.
In the conduit arteries, endothelial dysfunction is believed to contribute to development of atherosclerosis while in the resistance arteries endothelial dysfunction leads to disruptions in the control of blood flow as well as blunted angiogenesis and structural vascular remodeling (rarefaction)(Frisbee et al., 2006).
In normal skeletal muscle insulin-mediated EDD-induced increases in blood flow are responsible for 25-50 % of the increase in glucose clearance stimulated by insulin administration (Kim et al., 2006). Thus, it appears that endothelial dysfunction of resistance arteries in muscle tissue includes blunted insulin-stimulated vasodilation (Mikus et al., 2010). Endothelial dysfunction in T2DM is associated with glucotoxicity, lipotoxicity, and inflammation which impair insulin signaling (i.e.
Evidence indicates that T2DM produces an imbalance in the production of NO and ET-1 in response to insulin so that ET-1 release is up-regulated (Kim et al., 2006).
Benefits of physical activityPhysical activity may be beneficial in slowing the initiation and progression of T2DM and its cardiovascular sequelae through favorable effects on body weight, insulin sensitivity, glycemic control, blood pressure, lipid profile, fibrinolysis, inflammatory defense systems, and endothelial function.
The following section is intended to present the available evidence of the beneficial effects of physical activity focusing on endothelial function. Aerobic exerciseStudies examining the acute effects of aerobic exercise training on endothelial function in T2DM are somewhat limited. Resistance exerciseEven more limited are studies examining the acute effects of resistance exercise training on endothelial function in T2DM. Currently only one study has examined the acute effects of resistance exercise training on endothelial function in subjects with T2DM. Their results indicated that resistance exercise training does not significantly affect cutaneous perfusion, either at baseline or following local heating. More studies are needed in this area for a better understanding of how resistance exercise training affects the endothelium in T2DM. Aerobic exerciseVery few studies exist examining the effects of chronic aerobic exercise training alone on endothelial function in T2DM. Several human studies exist examining the combined effects of chronic aerobic and resistance exercise training on endothelial function in T2DM, but yield conflicting results. Further studies in humans are needed at this time to know whether chronic aerobic exercise training alone exerts beneficial effects on endothelial function during T2DM. Current studies using the Otsuka Long-Evans Tokushima Fatty (OLETF) rat model of T2DM and obesity have revealed that chronic aerobic exercise training alone maintains endothelial function in conduit (i.e. It is worth noting that the experimental design of the OLETF studies was such that aerobic exercise training served as a preventative measure for endothelial dysfunction associated with T2DM, whereas in the human studies discussed above it served as an interventional measure for endothelial dysfunction associated with T2DM.
Resistance exerciseThe effects of chronic resistance exercise training on endothelial function are equally unclear at present.
Chronic resistance exercise training alone has been shown to have little to no effect on skin blood flow and endothelial function in patients with T2DM (Colberg et al., 2006a).
This study observed in ten individuals with T2DM and nine similar non-diabetic controls that 8 weeks of moderate-intensity resistance training did not enhance baseline skin blood perfusion or interstitial NO levels. Physical activity: Mechanisms for its vascular benefitsThe mechanisms responsible for the beneficial effects of physical activity on endothelium in T2DM are under intense investigation at this time. As for other forms of CVD, it is possible that exercise has beneficial effects on endothelial function directly due to the effects of shear stress or other hemodynamic effects of each exercise bout on the vascular wall or through effects of physical activity on systemic risk factors.
For instance, exercise bouts influence circulating cytokines released by skeletal muscle and adipose tissues and can alter circulating lipid profiles. Beneficial effects could also be the result of exercise-induced improvements in antioxidant systems in the vascular cells of the arteries, either endothelium or smooth muscle. It is important for research to establish the exact mechanisms so that exercise protocols can be designed to maximize these benefits.
However, the relationship of endothelial dysfunction and the many independent factors associated with T2DM (e.g. Furthermore, the precise mechanisms responsible for the beneficial effects of physical activity on the endothelium of individuals with T2DM are still under intense investigation.



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