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Exercise for Prevention and Relief of Cardiovascular Disease: Prognoses, Mechanisms, and Approaches



This review is aimed at summarizing the new findings about the multiple benefits of exercise on cardiovascular disease (CVD). We pay attention to the prevalence and risk factors of CVD and mechanisms and recommendations of physical activity. Physical activity can improve insulin sensitivity, alleviate plasma dyslipidemia, normalize elevated blood pressure, decrease blood viscosity, promote endothelial nitric oxide production, and improve leptin sensitivity to protect the heart and vessels. Besides, the protective role of exercise on the body involves not only animal models in the laboratory but also clinical studies which is demonstrated by WHO recommendations. The general exercise intensity for humans recommended by the American Heart Association to prevent CVD is moderate exercise of 30 minutes, 5 times a week. However, even the easiest activity is better than nothing. What is more, owing to the different physical fitness of individuals, a standard exercise training cannot provide the exact treatment for everyone. So personalization of exercise will be an irresistible trend and bring more beneficial effects with less inefficient physical activities. This paper reviews the benefits of exercise contributing to the body especially in CVD through the recent mechanism studies.
Review Article
Exercise for Prevention and Relief of Cardiovascular Disease:
Prognoses, Mechanisms, and Approaches
Danyang Tian
and Jinqi Meng
Department of Physiology, Hebei Medical University, Shijiazhuang, China
Department of Sports, Hebei Medical University, Shijiazhuang, China
Correspondence should be addressed to Jinqi Meng;
Received 10 December 2018; Revised 1 February 2019; Accepted 19 March 2019; Published 9 April 2019
Guest Editor: Fiammetta Monacelli
Copyright © 2019 Danyang Tian and Jinqi Meng. 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.
This review is aimed at summarizing the new ndings about the multiple benets of exercise on cardiovascular disease (CVD). We
pay attention to the prevalence and risk factors of CVD and mechanisms and recommendations of physical activity. Physical
activity can improve insulin sensitivity, alleviate plasma dyslipidemia, normalize elevated blood pressure, decrease blood
viscosity, promote endothelial nitric oxide production, and improve leptin sensitivity to protect the heart and vessels. Besides,
the protective role of exercise on the body involves not only animal models in the laboratory but also clinical studies which is
demonstrated by WHO recommendations. The general exercise intensity for humans recommended by the American Heart
Association to prevent CVD is moderate exercise of 30 minutes, 5 times a week. However, even the easiest activity is better than
nothing. What is more, owing to the dierent physical tness of individuals, a standard exercise training cannot provide the
exact treatment for everyone. So personalization of exercise will be an irresistible trend and bring more benecial eects with
less inecient physical activities. This paper reviews the benets of exercise contributing to the body especially in CVD through
the recent mechanism studies.
1. Cardiovascular Diseases: Prevalence and
Risk Factors
CVD is a class of diseases which are related to the heart or
blood vessels including stroke, heart failure, hypertension,
coronary artery diseases, heart arrhythmia, peripheral artery
disease, and atherosclerosis [1]. Individuals with CVD are
found to have the accompanying raised blood pressure, ele-
vated glucose, smoking, obesity, lack of exercise, excessive
alcohol consumption, and dyslipidemia. Fortunately, CVD
can be properly managed and prevented by controlling blood
pressure, glucose, lipid, smoking, and alcohol drinking and
through lifestyle modications for sleep, emotion, exercise,
and diet, which are called SEED intervention [2]. With the
aging of population in the world, CVD has become the
leading cause of death globally. Approximately 17.9 mil-
lion deaths in 2015 were caused by CVD in the world
[3]. The percentage of Chinese older than 60 has increased
to 16% in 2015 which directly leads to a consequence that
cardiovascular disease is becoming the leading cause of
death in China [4]. Multiple risk factors contributing to
CVD include obesity, high blood pressure, diabetes, aging,
male sex, metabolic syndrome, and physical inactivity.
Determined by body mass index (BMI), obesity refers to
the condition of those who have over 30 BMI and overweight
includes persons with BMI more than 25. The prevalence
among people of obesity has exceeded 50% in most countries
and is increasing in both adults and children over the past
few decades worldwide [5]. Obesity is found to increase
blood volume, CRP, and TNFαwhich cause cardiac remodel-
ing and inammation. Obesity also aggravates the risks of
high blood pressure, stroke, myocardial infarction (MI),
and insulin resistance, which are all risk factors of CVD [6].
Furthermore, mortality and morbidity of CVD have been
shown increasing in overweight populations, especially in
those with abdominal obesity [7].
As the most common form of diabetes, type 2 diabetes is
a chronic metabolic disease which is characterized by high
Oxidative Medicine and Cellular Longevity
Volume 2019, Article ID 3756750, 11 pages
blood glucose, low insulin sensitivity. With the incidence of
diabetes continuing to rise, the number of patients diagnosed
with diabetes has swelled from 30 million in 1985 to 382 mil-
lion in 2014, and scientists predict 592 million people will
have diabetes by 2035, almost 1 in 10 persons suering from
this disease [8]. Besides aecting aging people, this disease
also inuences an increasing number of young populations
and even children [9]. Lots of evidences and studies demon-
strate that type 2 diabetes acts as an independent risk factor
for CVD. The patients who are diagnosed with type 2 diabe-
tes have a worse prognosis and therapeutic eects of CVD
compared with those without diabetes. CVD death rates with
diabetes in the United States adults are 1.7 times higher than
those without diabetes [10]. The huge medical care burden of
type 2 diabetes generally attributes to vascular complications
like MI, hypertension, peripheral vascular disease, and
coronary artery disease [11].
Aging is a gradual, systematic, irreversible, degenerative
process in the body, which results in weakness, disease, and
even death. As there is an average increasing lifespan for
humans, there will be approximately 20% of the population
over 65 by 2030. Aging is an inevitable and important deter-
minant for CVD which leads to the decline of mitochondrial
functions, excess reactive oxygen species (ROS) production,
and disorder of Ca
levels [12]. Aging is relevant to the
progressive damage in various physiological processes and
increases incidence of atherosclerosis, hypertension, and
stroke [13], thus inducing an elevating risk of cardiac and
arterial systematic disorders. Studies show parts of the key
genes regulating lifespan including AMPK, m-TOR, and
IGF-1; sirtuins are closely related to CVD progress [14].
Epidemiologists demonstrate the dierent CVD occur-
rence rates between males and females. Clinical studies show
that the onset of heart attack is delayed 9 years in women
compared with men [15]. In a cross-sectional survey on
hospitalized patients with coronary artery disease, women
were found 3.1 years older than men [16]. It is widely
believed that estrogen is the prominent protective element
for females [17]. Besides, women tend to have a better aware-
ness of weight measurement and their waist circumference if
they have central obesity, which would lower the risk of
adiposity and dyslipidemia. Smoking and alcohol drinking
are severe risk factors for CVD, which are more common
lifestyle behaviors in men compared to women [18].
Metabolic syndrome is a condition characterized by low
high-density lipoprotein (HDL), high triglycerides (TG),
high blood pressure, high blood glucose, and central obesity,
associating with the risks of developing to CVD and type 2
diabetes. Studies show that metabolic syndrome aects
30-40% of people older than 65 by doubling the risk of
getting CVD [19]. Low HDL and high TG are associated with
elevated levels of low-density lipoprotein (LDL), which
increase the risk of having atherosclerosis [20]. High glucose
links to dysfunctions of glucose uptake and catabolism and
induces high oxidative stress, dysfunction of endothelial cells.
High blood pressure leads to cardiac and vascular injury.
Central obesity is related to maldistribution of free fatty
acid, overproduction of inammatory molecules, and leptin
resistance [21].
Physical inactivity has been identied as the fourth risk
factor of death worldwide, leading to approximately 3.2
million deaths annually. Various studies show an obvious
dose-response relationship between increased physical activ-
ity and decreased occurrence rate of CVD including reduced
blood pressure, body weight, ox-LDL, and elevated glucose
tolerance. A systematic review estimates that the lack of
exercise leads to 6% of coronary heart disease occurrence
worldwide. Deciency in physical activity leads to obesity,
increasing endogenous inammatory molecules and coagula-
tion factors. In addition, there is coordinated protective
eects to decrease the overall risk of incident CVD by exer-
cise [22, 23]. So having a healthy diet, avoiding smoking,
and keeping regular physical activity are the three pieces of
advice the WHO recommend to avoid CVD.
2. Mechanisms of Action for Physical Exercise
Many considerable evidences support the therapeutic and
protective eects of exercise on the body, including improve-
ment of insulin sensitivity of diabetic mice, attenuating sym-
pathetic activity, arterial pressure, and heart rate in the
spontaneously hypertensive rats [24]. Mitochondrial bio-
genic response, components of the electron transport chain,
mtDNA, and related lipid metabolic pathways are all
increased after exercise training [25]. Here, we talk about
the benets of exercise on cardiovascular disease from the
following aspects.
2.1. Insulin Sensitivity and Blood Glucose Control. Type 2
diabetes mellitus is a kind of chronic disease characterized
by obesity, hyperglycemia, impaired insulin secretion, and
insulin resistance [26]. Studies show that diabetic rats with
exercise training present reduced body weight, decreased
TG levels, and diminished blood glucose levels compared
with those sedentary rats [27, 28]. PPARγknown as
energy-balanced receptor,is well studied in metabolic dis-
orders. Carnitine palmitoyl transferase-1 (CPT-1) mainly
transports fatty acids into mitochondria for medium-chain
acyl-CoA dehydrogenase (MCAD) catalyzing β-oxidation.
Through upregulating PPARγand its target genes, CPT-1
and MCAD, exercise alleviates hepatic steatosis, promotes
glucose uptake, and improves insulin sensitivity in nonalco-
holic fatty liver disease mice [29]. Exercise stimulates the
translocation of glucose transporter type 4 (GLUT4) from
the cytoplasm to the cell membrane, thus promoting glucose
uptake and improving insulin resistance [30]. Besides,
improved insulin sensitivity is independent with exercise
modality. High or low intensity of exercise and aerobic or
anaerobic training lead to improvement in glucose clearance
curve and insulin sensitivity [31].
Besides improving insulin sensitivity, exercise facilitates
glucose uptake and usage via insulin-independent mecha-
nisms. Once glucose enters muscular and adipose cells, it will
be phosphorylated by hexokinase which is an irreversible
catalytic reaction to form glucose 6-phosphate (G-6-P) that
cannot diuse back out of cells. Glycolysis and glycogenesis
started from G-6-P and promote glucose uptake by cells
and usage in cells to aect blood glucose. Exercise increases
2 Oxidative Medicine and Cellular Longevity
G-6-P level in the skeletal muscles accompanying increased
GLUT4, hexokinase level, and glycogen synthase activity,
which nally improve glucose tolerance and decrease blood
glucose level [32].
2.2. Lipid Prole. Cholesterol is a soft waxy fat that our body
needs to function well. But too much cholesterol will become
risk factors for human diseases like heart disease, stroke, and
atherosclerosis [33]. For those who have been diagnosed with
diabetes, heart disease, and stroke or people who are taking
medicine to control cholesterol level, taking cholesterol test
every year is necessary [34]. Generally, a cholesterol test
includes total cholesterol, LDL, HDL, and TG [35]. Standard
management strategies like drug therapy and diet control are
generally used to lower serum cholesterol to prevent heart
disease. However, some people are insensitive to statins or
cannot tolerate statins. Hence, other ways need to replace
or be used together with statins. More and more evidences
support aerobic exercise as a positive method for alleviating
plasma dyslipidemia and improving the prognosis of cardio-
vascular diseases [36]. Through using meta-analyses to inves-
tigate exercise and lipid proles, Pedersen et al. concluded
that exercise led to benets of physical health [37]. A pro-
spective cohort study lasting for 10 years about exercise and
lipid metabolism shows that the risk of mortality is signi-
cantly reduced by combining statins with exercise, especially
compared to other therapy alone [38]. Comparing with LDL
and TG, HDL is more sensitive to exercise. Studies indicate
that HDL is increasing more or less both in humans and rats
after exercise [39, 40]. For the badcholesterol LDL, the
eects of exercise reduce the serum levels signicantly in rats
[40]. However, the eects are not consistent in humans,
which may be due to the dierent dietary habits and living
conditions [41, 42]. It is strongly accepted and reported that
exercise leads a high requirement of energy which induces
decreasing of plasma TG concentrations [43].
2.3. Blood Pressure. Blood pressure is elicited by the force
exerted by the blood against the blood vessels, which depends
on the ejection of the heart and resistance of the blood ves-
sels. Hypertension is another name of high blood pressure,
a disease related to heart attack, stroke, heart failure, and
other problems [44]. Exercise always leads to a postexercise
hypotension, and both normotensive and hypertensive
persons experience a transient reduction in blood pressure.
The reduced magnitude may achieve the point wherein
patients with hypertension recover to the normal blood pres-
sure levels. In a meta-analysis, they investigated the eects of
acute exercise on blood pressure response. There were signif-
icant changes, reduction of 4.8 mmHg for systolic blood pres-
sure (SBP) and 3.2 mmHg for diastolic blood pressure (DBP).
The epidemiological study demonstrates that 2 mmHg
decline in SBP leads to 6% reduction of stroke mortality
and 4% reduction of coronary heart disease mortality, and a
decrease of 5 mmHg causes the reduction of mortality of
these diseases by 14% and 9%, respectively [45]. So the
meta-analysis results conrm the undoubted place of nonin-
vasive therapy method, acute exercise.
The transient reduction only lasts for a few hours and
would recover after rest. However, the benets of physical
activity cannot be ignored because of chronic treatment of
exercise showing signicant changes among subjects. The
vasodilator activity leads to the decrease of blood pressure.
On the contrary, increased blood pressure is caused by
vasoconstriction. Moderate-intensity exercise causes a vaso-
dilatory response and decreases the vasoconstricting response
and lipid in rat aortas, which exhibits a decrease in diastolic
blood pressure [46, 47]. In addition to the vascular tone, exer-
cise decreases blood pressure through lowering oxidative
stress and inammation levels. In the spontaneous hyperten-
sion rats (SHR), exercise normalizes the increased collagen
deposition and diminished fenestra size in the internal elastic
lamina, meaning that exercise shows the benet roles in
normalizing the increased vascular stiness and decreased
vascular distensibility in both small mesenteric arteries and
coronary arteries [48]. However, high-intensity exercise leads
to the opposite eects that increased oxidative stress, elevated
blood pressure, and high vasoconstrictor activity are found
[49]. Some studies report that males tend to achieve greater
reductions than females from the exercise training [50]. How-
ever, the authors ignore the factors of menstrual cycle in the
female subjects which aect the regulation of the autonomic
nervous system [51]. Studying the eects of exercise on circa-
dian rhythms using ambulatory blood pressure monitoring,
there are signicant reductions of daytime BP, but no obvious
changes are observed at nighttime BP [44].
2.4. Blood Viscosity, Platelet Aggregation, and Thrombosis
Prole. Blood viscosity in normal conditions is like a Newto-
nian uid which is inuenced by hematocrit, shear rate of
blood ow, vascular caliber, and temperature. Elevated blood
viscosity which is associated with blood resistance increases
risks of cardiovascular complications. Blood viscosity is
decreasing during exercise accompanied by decreased sys-
temic vascular resistance [52]. More nitric oxide (NO) is
produced attributed to greater shear stress in exercise and
promote vasodilation [53, 54]. During exercise, erythrocyte
volume is slightly increased; however, a much higher increase
of plasma volume is generated which nally results in
lower blood viscosity. Decline in plasma brinogen level
is observed under the eect of exercise which plays important
roles in declining erythrocyte aggregation and decreasing
blood viscosity [55].
Platelet is a small volume component in blood which has
no cell nucleus generated from megakaryocytes. Through
forming thrombus, the platelets exert primary function of
maintaining hemostasis of blood ow. Once an injury occurs,
the platelets in the circulation will be activated and aggre-
gated to the interrupted endothelial site to plug the hole
[56]. So abnormality in platelet activation leads to a variety
of atherosclerotic diseases mainly through excess thrombosis
in small arteries like coronary arteries and blood vessels of
the brain [57]. Exercise training presents an antithrombotic
manner through platelet functional regulation. Through
enhancing blood ow, exercise enhances endothelial NO
production which counteracts platelet activation [58]. The
moderate physical activity decreases both platelet adhesion
3Oxidative Medicine and Cellular Longevity
and aggregation through downregulating intracellular cal-
cium levels and increasing cGMP levels [59]. It is recom-
mended by government guidelines that physical activity is
an eective way to prevent thrombosis [60]. Exercise is also
used to improve chronic complications of deep venous
thrombosis, postthrombotic syndrome. A six-month exercise
training markedly increases leg strength, hamstring and
gastrocnemius exibility, and overall tness [61]. However,
studies showed that the strenuous short-term exercise acti-
vated platelets and promoted aggregation of platelets, thus
increasing the risk of MI or cardiac arrest. This suggests that
acute exhausting exercise may trigger clot formation, but the
mechanisms remain to be claried [62].
2.5. Endothelial NO Production. NO is a gaseous signaling
molecule playing an irreplaceable role in a variety of biolog-
ical processes. It is catalyzed by various nitric oxide synthase
(NOS) enzymes by using substrate L-arginine. Known as an
endothelial-derived relaxing factor, NO contributes to not
only endothelial-dependent relaxation (EDR) but also to
the maintenance of endothelial function [63]. The endothe-
lium is a single layer of cells in the intima of vessels separat-
ing blood from the tissue. The functions of the endothelium
involve regulating angiogenesis, balancing vasoconstriction
and vasodilation, adjusting smooth muscle cell proliferation,
and excreting endocrine. The intact endothelium acts an
indispensable role in vessel homeostasis [64]. In a cross-
sectional study with 184 healthy individuals, L-arginine was
reduced and production of NO was increased after exercise
training [46]. The mechanisms may be partial that exercise
training leads to increased blood ow and shear stress, con-
tributing to endothelial NOS (eNOS) expression, NO release,
and artery relaxation. NO activates soluble guanylate cyclase
which increases cGMP and therefore activates protein kinase
G (PKG). In blood vessels, PKG activation always induces
relaxation and regulates blood pressure. In the heart, PKG
works as a brake on stress response signaling [65]. Through
increasing vascular AMPK/PPARδ, exercise suppresses
endoplasmic reticulum stress, thus increasing endothelial
NO bioavailability. Exercise shows preserved EDR in the
aorta and mesenteric artery in high-fat diet rats and db/db
mice [66]. In the aging-induced downregulation of VEGF
signaling cascade in the heart, exercise upregulates VEGF,
its receptors Flt-1 and Flk-1, and the downstream signaling
pathway Akt/eNOS [67]. Increased NO production usually
facilitates angiogenesis and vascular permeability.
Dysfunction of EDR and decrease of cGMP in both
plasma and vascular tissue are found in diabetic rats. How-
ever, chronic exercise improves endothelial function through
releasing NO in the aorta. Interestingly, exercise does not
aect the vascular function in normal rats administrated with
L-arginine but improves vascular function in the aortas from
diabetic rats [68]. In the high fat-induced obese mice,
impaired EDR, reduced NO bioavailability, and decreased
phosphorylation of eNOS are found in the coronary arteries
which can be normalized by exercise. Through injecting
β-adrenoceptor agonists, isoproterenol for 8 days, Yang
recapitulated cardiac hypertrophy which was regarded as
the primary risk factor for heart failure. After 4 weeks of
exercise training, the eNOS expression did not change, but
the phosphorylation of serine residue 1177 with an activating
impact on eNOS was increased and the phosphorylation at
threonine residue 495 with an inhibitory impact on eNOS
was decreased. As a result, exercise promoted NO production
and attenuated cardiac remodeling, echocardiographic and
hemodynamic changes after β-adrenergic overload [69].
2.6. Leptin Sensitivity. Leptin is a 16 kDa circulating hormone
which is predominantly released by adipocytes to exert
regulation of food intake and energy metabolism. Through
binding to leptin receptors on hypothalamic cells, leptin
inhibits hunger, prevents weight gain, and promotes positive
energy balance [70]. So leptin deciency or leptin resistance
promote diabetes, obesity, and other metabolic disorders.
Exercise improves leptin resistance and sensitivity, attenuates
body weight, and promotes homeostatic control of energy
balance through inuencing the leptin receptor in the ventro-
medial hypothalamic nucleus of obese mice [71, 72]. It also
directly works on leptin receptors to induce NO-dependent
vasodilation expressed in endothelial cells [73]. A decreased
leptin sensitivity and hyperleptinaemia are found in obese
mice coronary arteries, demonstrating leptin resistance and
low leptin sensitivity. Exercise maintains leptin sensitivity
of obese mice and preserves leptin receptor, thus exerting
endothelial protection [74]. Exercise facilitates SOCS3
expression and improves leptin resistance in the liver and
muscle of high-fat diet-induced rats [75]. Leptin sensitivity
is restored by exercise manifested as facilitating fatty acid
toward oxidation and away from triacylglycerol stores [76].
Through activating leptin, exercise also initiates the down-
stream JAK/STAT signal transduction pathway in obese mice
to protect against myocardial ischemia-reperfusion injury
[77]. Shapiro et al. found that leptin overexpression failed
to reduce body weight in obese rats, and chronic leptin treat-
ment aggravated the diet-induced obesity. Besides, wheel
running for obese rats was insucient to lower body weight.
However, combinational administration of exercise and
exogenous leptin dramatically induced weight loss and
improved leptin sensitivity [78]. That means exercise may
directly activate leptin signaling pathway or improve leptin
sensitivity via coordinating with other therapeutic methods.
2.7. Modulation of Autonomic Function. The autonomic
nervous system, regulated by the hypothalamus, consists of
sympathetic nervous system, parasympathetic nervous sys-
tem, and enteric nervous system. The primary autonomic
functions include cardiac regulation, control of respiration,
and vasomotor activity, which act largely unconsciously
[79]. Exercise training has benecial roles in autonomic func-
tion, as indicated by improved heart rate recovery (HRR) and
heart rate variability (HRV) in various populations, such as
in sedentary individuals and chronic heart failure patients
[80]. HRR refers to the declining rate of heart rate and is rec-
ognized as an indicator of cardiac prognosis [81]. HRV is
dened as consecutive heart beat variations in heart rate of
sinus rhythm. Reduced HRV represents attenuation of auto-
nomic regulation of sinoatrial node [82]. Exercise works as
an intervention for autonomic dysfunction in type 2 diabetes
4 Oxidative Medicine and Cellular Longevity
by preserving HRV, HRR, and baroreex sensitivity (BRS).
BRS is regulated by sympathetic and parasympathetic auto-
nomic nerves and is downregulated when there is cardiac
autonomic neuropathy [83].
Electrocardiogram is a noninvasive way to determine
cardiac conditions. Elevated R wave amplitudes and widened
QT intervals are reliable predictors of autonomic neuropa-
thy. Exercise training lowers heart rate and reduces QT inter-
val and R wave amplitudes on electrocardiogram in the
diabetic fatty rat model [84]. In myocardial-infarcted rats,
structural remodeling leads to heterogeneity which causes
slow conduction and creates the generation of arrhythmias.
However, exercise training increases ratio of parasympathetic
over sympathetic tones and decreases probability of ventric-
ular arrhythmias of the MI rats [85]. The mechanism of
exercise-induced improvement of arrhythmia might be
related to intrinsic electrophysiological cardioadaptive mech-
anisms because of decreased action potential duration
gradient between epicardial and endocardial cells in the
exercise-trained rats [86]. The mechanisms by which exercise
improves autonomic function and preserves neurovascular
perfusion might be related to increasing NO bioavailability,
lowering angiotensin II (AngII) levels, and suppressing
chronic inammation [8790]. It is controversial that some
studies show that MI, stroke, ventricular tachycardia, or
brillation can be elevated during the progress of physical
activity, so further studies about the duration, frequency,
and intensity need to be specically investigated.
2.8. Antioxidant Defense. ROS of physiological levels are
responsible for signaling molecules to regulate normal
physical activities. On the contrary, excessively generated
ROS plays a crucial role in the initiation and progression
of CVD [91]. ROS overproduction, decreased antioxidant
enzymes, and the downstream targets damage the subcel-
lular organelles, thus impairing the cardiovascular system.
Excessive ROS may decrease NO bioavailability and
NO/cGMP-dependent pathway which result in pathological
vasoconstriction and hypertension [92]. ROS also initiates
inammation with the activation of redox-sensitive tran-
scription factors and promotes expression of inammatory
molecules [93]. DNA is oxidized by ROS to form 8-oxo-dG
which can be detected in plasma and urine [94]. AngII-
induced insulin resistance is relevant to ROS, which can
impair insulin signaling by decreasing phosphorylation of
IRS1 and Akt and translocation of GLUT4 to the plasma
membrane [24].
Exercise attenuates oxidative damage in the blood vessel,
heart, brain, liver, skeletal muscle, and other organs. Exercise
reduces age-related mitochondrial oxidative damage and
increases mitochondrial NADH-cytochrome C reductase
activity in the heart of aged rats [95]. By improving the antiox-
idant enzymes and redox status in many organs and patholo-
gies, the chronic treadmill exercise has an anti-inammatory
eect. Exercise alleviates oxidative stress through inactivating
ERK/AMPK signaling pathway and decreases expression of
inammatory factors like IL-6, high-sensitivity CRP, TNFα,
and leucocyte dierentiation antigens in diabetes [96]. In
renovascular hypertensive rats, ROS released by vascular
endothelial cells impairs EDR by decreasing NO production
and facilitating vasoconstriction. Evidences indicate that
exercise reduces ROS, improves endothelial function, and
increases levels of elastin, brillin, and NO. The elevated
cardiac MDA levels and MPO activity and depleted GSH
and catalase expression in hypertensive rats are totally
reversed by exercise training [97]. BRS is improved by physi-
cal activity through reducing oxidative stress in the rostral
ventrolateral medulla to inhibit the sympathetic nerve
[98, 99]. In diabetic rats, the overproduction of ROS leads to
the abnormal aortic function and metabolic disorder.
Through exercise training, enzymes producing ROS such as
p67phox protein decrease and the enzymes taking part in
scavenging oxygen-free radicals, like superoxide dismutase
(SOD) 1, SOD2, catalase, and glutathione peroxidase (GPX),
are normalized, even increased [48, 100]. That means, all the
proteins taking part in oxidative stress tend to recover to
normal levels after exercise treatment [101].
Exercise upregulates the antioxidant defense mechanisms
through redox-sensitive transcription factors, NF-κB and
activator protein-1, and peroxisome proliferator-activated
receptor gamma coactivator 1-alpha (PGC-1α). Exercise nor-
malizes the aging-induced decline in mitochondrial oxidative
capacity through upregulating PGC-1α, redox-sensitive tran-
scription factors PPARγ, and the target antioxidant genes like
GPX and SOD2 [46, 102]. Through elevating laminar shear
stress, exercise upregulates SOD and downregulates NADPH
oxidase and VCAM-1. Through activating AMPK, exercise
training increases sirt3 and PPARγand the targets SOD1,
SOD2, GPX1, and catalase, thus resulting in less ROS produc-
tion and more ROS clearance in skeletal muscles [103].
Exercise increases thioredoxin reductase 1 and decreases
thioredoxin-interacting protein (TXNIP) in blood mononu-
clear cells and skeletal muscles, which promote antioxidant
ability and eliminate free radical [104, 105]. TXNIP is a regu-
lator of cellular redox signaling by binding thioredoxin to
inhibit the neutralization of ROS, indirectly enhancing the
oxidative stress [106]. Nuclear factor erythroid 2-like factor
2 (Nrf2) is reported to be an important transcription factor
that performs antioxidant defense mechanisms through
Nrf2-ARE signaling to activate antioxidant gene expression
[107]. Mounting evidences demonstrate that the Nrf2-ARE
signaling is downregulated in the aging heart, ischemia/reper-
fusion injury, and MI. Researchers nd that through chronic
exercise treatment, Nrf2 is upregulated and consequently
activates the key antioxidant enzyme expression such
as hemoxygenase-1, NADPH quinone oxidase-1, GPX1,
GPX2, glutathione reductase, γ-glutamyl cysteine ligase-
catalytic, γ-glutamyl cysteine ligase-modulatory, glucose-6-
phosphate dehydrogenase (G6PD), and catalase in the heart
[108, 109]. Based on these risk factors and studies, all major
cardiovascular societies recommend that a minimum of 5 days
a week of exercise, with at least 30 minutes of moderate-
intensity aerobic activity, is needed to prevent CVD [110].
3. The Recommendations for Physical Activity
Because of low-cost, low-risk, and nondrug intervention, the
European Society of Cardiology recommended that exercise
5Oxidative Medicine and Cellular Longevity
training should be provided by cardiac rehabilitation pro-
grams in patients with non-ST elevation acute coronary syn-
drome in 2015 [111]. Physical activity is a part of everybodys
life. However, the exercise intensity diers between people
depending on the physical condition of individuals [112].
Although lots of studies show a positive correlation between
exercise and good health, a thorough physical evaluation is
necessary before an intensive exercise training program.
The intensity, mode, duration, and frequency of exercise
can strongly aect outcome.
Aerobic exercise is dened as using aerobic metabolism
to extract energy in muscles, mainly referring to low- to
moderate-intensity physical activities. As discussed above,
aerobic exercise has favorable eects on lipid metabolism,
cardiac remodeling, post-MI heart failure, insulin resistance,
and endothelial function. Anaerobic exercise is an activity
that synthesize energy sources without using oxygen as
energy sources but glycolysis and fermentation. Anaerobic
exercise usually refers to high-intensity training, including
sprinting and power lifting. In several studies, high-
intensity exercise is recommended to lower TG and LDL.
Similar to aerobic exercise, anaerobic exercise also shows
positive inuences on body mass index and blood pressure
[113]. In some cases, high-intensity training shows more
benecial eects on the cardiovascular system and EDR
compared to low-intensity training [114]. The advantages
of high-intensity intermittent exercise refer to the fact that
the shorter time as 3-4 sessions/week will produce signicant
changes [115]. However, there is a paradox of disadvantages
about anaerobic exercise training that the elevated mortality
and sudden death are brought by high-intensity activity. A
well-recognized viewpoint is that acute strenuous exercise
increases the risks for cardiovascular diseases, like MI, by
upregulating blood pressure [57]. In conclusion, intensive
exercise should be intermittent especially for a long-term
program. Professional supervision and guidance are indis-
pensable when you conduct high-intensity exercise.
The general recommended exercise intensity for humans
from the American Heart Association to prevent CVD is 30
minutes, 5 times a week to reach at least 150 minutes per
week of moderate exercise, or 25 minutes, 3 times a week to
reach at least 75 minutes per week of vigorous activity. Indi-
viduals can choose one way of physical activity or combine
moderate and vigorous activities. They will also be beneted
even if they divide the entire time into several parts of 10 to
15 minutes per day. For those who want to lower the risk
for heart attack and stroke, 40 minutes of moderate to vigor-
ous intensity aerobic activity, 3 or 4 times a week, is recom-
mended [116]. Moderate-intensity exercise is more widely
performed among people who are interested in exercise and
enjoy rest time. Various studies show that the duration of
physical activity but not intensity is the primary factor lead-
ing to benets for humans [117].
Physical activity is regarded as an ecient way to prevent
and counteract age-related changes in muscle and organic
function [118]. As we know, any activity is better than none
and it is never too late to start for the elders [119]. The
American College of Sports Medicine and the American
Heart Association recommend detailed description for elder
people that 30 minutes, 5 times a week, of moderate intensity,
or 20 minutes, 3 times a week, of vigorous intensity activity is
good for aging-related diseases. Strength training should
be included to enhance muscle groups and prevent falls
as 8-10 exercises with 10-15 repetitions, twice a week [120].
For the elders, joining exercise classes to improve balance
and prevent falls are strongly suggested [121]. Exercise is
generally safe for older people unless for those elders
who already suered from health problems doing resistance
training [122].
Examples of aerobic exercise include cycling, dancing,
hiking, treadmill, climbing stairs, swimming, walking, and
any activities (the criterion is that you can talk without
breathing too hard). Anaerobic exercise refers to sprinting
and power lifting accompanied by accumulation of lactic acid
causing muscular fatigue [123]. However, the denition of
moderate and vigorous exercise varies between individuals
because the indispensability to measure the level of intensity
bases on your tness and overall health.
4. Future Perspectives
Many people are robbed by the thinking all-or-nothing when
doing exercise. However, the low-level intensity training pro-
gram could benet you as long as you begin to change. Even
the easiest activity is better than nothing and whenever you
start is not too late [124].
There are also some limits for the exercise training when
applied to real patientstreatment. The existing studies do
not provide an exact guidance on the diverse intensity, dura-
tion, and frequency of exercise that may be suitable for the
dierent kinds of diseases. In the future, personalization of
exercise will be an irresistible trend. For those young and in
healthy condition, it may be optional to consult a doctor
before they start an exercise program. However, personalized
exercise enables you to perform more specically based on
your present tness level, interest, age, and gender [125].
For those old who have been inactive for a long period, it is
necessary to consult physicians who will measure some
indexes, like cardiorespiratory endurance, muscular strength,
muscular endurance, and exibility, and make graded exer-
cise tests for individuals [126]. Also, for someone who has a
baseline disease, the extreme exercise training seems to trig-
ger the progression of disease. So tailored exercise would
bring benets not only for healthy humans but also for the
patients with chronic disease [127]. For slow disease-related
declines of muscle strength, tailored exercise may focus on
the training to improve muscle strength and reduce the risk
of falls. For those who has type 2 diabetes, body weight con-
trol and enhancement of peripheral circulation are the rst
two goals to realize. For people with arthritis, tailored exer-
cise helps reduce joint stiness and enhances muscle strength
[125, 128]. The systematical and overall exercise guidance
from a professional instructor is totally necessary. Personali-
zation of exercise training will be a huge demand and replace
the random mode of exercise today.
Although we get to know that exercise protects against
CVD through attenuating sympathetic activity, arterial pres-
sure, and heart rate, increasing blood ow and endothelial
6 Oxidative Medicine and Cellular Longevity
NO production, causing vessel dilation, decreasing inam-
matory cytokine and reactive oxygen species formation, the
exact mechanisms leading to transcriptional factor changes
or transcriptional modications are not studied. So future
studies may be applied to the mechanisms of protective
eects of exercise on the heart and vessels.
Conflicts of Interest
The authors declare that there is no conict of interests
regarding the publication of this paper.
This work was supported by the grant from the Postgraduate
Innovational Funding Project of Hebei Provincial Education
Oce (Grant CXZZBS2018064) and the Youth Fund for
Humanities and Social Sciences Research Projects in Higher
Institutions of Hebei Province (Grant SQ181136).
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11Oxidative Medicine and Cellular Longevity
... Cardiovascular diseases (CVDs) remain the leading cause of rising health costs 1 and mortality among the elderly. 1 2 Sedentary behaviour and physical inactivity are particularly emphasised as major modifiable cardiometabolic markers, 3 which are reflected by the increased prevalence of hypertension, diabetes and dyslipidaemia in older adults. 2 CVDs can be prevented by controlling key determinants of cardiometabolic markers, such as blood pressure (BP), blood glucose (BG) and lipids, through lifestyle modifications like exercise. 1 Acute aerobic exercise (AE) on lipid profile, BP and BG has been shown to reduce cardiometabolic markers and improve cardiovascular health. [4][5][6][7][8][9][10][11] However, most related studies have been restricted to younger individuals in clinical trials with an acute bout of exercise lasting 30-60 min at moderate to high intensity (VO2max 40%-75%) exercise. ...
... Cardiovascular diseases (CVDs) remain the leading cause of rising health costs 1 and mortality among the elderly. 1 2 Sedentary behaviour and physical inactivity are particularly emphasised as major modifiable cardiometabolic markers, 3 which are reflected by the increased prevalence of hypertension, diabetes and dyslipidaemia in older adults. 2 CVDs can be prevented by controlling key determinants of cardiometabolic markers, such as blood pressure (BP), blood glucose (BG) and lipids, through lifestyle modifications like exercise. 1 Acute aerobic exercise (AE) on lipid profile, BP and BG has been shown to reduce cardiometabolic markers and improve cardiovascular health. [4][5][6][7][8][9][10][11] However, most related studies have been restricted to younger individuals in clinical trials with an acute bout of exercise lasting 30-60 min at moderate to high intensity (VO2max 40%-75%) exercise. ...
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Objectives The acute effects of aerobic exercise on cardiometabolic markers are well documented in younger healthy individuals, but the same effects in older adults have not been elucidated. As such, this study compares the acute effects of three different types of age-appropriate aerobic exercises on cardiometabolic markers. Methods Healthy older golfers (n=25, 16 male and 9 female, 68±4 years) were enrolled in a randomised cross-over experiment. We compared the effects of three different acute aerobic exercises (18-hole golf, 6 km Nordic walk, 6 km walk) on blood pressure, blood glucose and blood lipid profile in a real-life environment. Results In the between-group comparison, playing golf resulted in a difference in blood glucose (golf: 0.01±1.0 mmol/L, walk: 1.3±0.9 mmol/L, p<0.001) compared with walking and triglycerides (golf: 0.13±0.2 mmol/L, Nordic walk: 0.31±0.2 mmol/L, walk: 0.23±0.2 mmol, p=0.012) and high-density lipoprotein cholesterol (golf: 0.04±0.06 mmol/L, Nordic walk: −0.02±0.06 mmol/L, walk: −0.02±0.07 mmol/L, p=0.002) compared with Nordic walking and walking. In addition, all groups had significant decreases (p<0.001) in systolic blood pressure, and Nordic walking and walking also demonstrated a decrease in diastolic blood pressure (p<0.05). Conclusion Acute bouts of aerobic exercise improved cardiovascular profile in healthy older adults. Despite the lower exercise intensity of golf, the longer duration and higher energy expenditure appeared to have a more positive effect on lipid profile and glucose metabolism compared with Nordic walking and walking. Trial registration number ISRCTN10007294 .
... Owing to its well-known benefits, the American Heart Association and the World Health Organization recommend at least 150 min per week of accumulated moderate-intensity or 75 min per week of vigorous-intensity aerobic physical activity [6,7]. The mechanism of action underlying the benefit of exercise is thought to involve decreasing sympathetic activation, arterial pressure, and heart rate; decreasing reactive oxygen species and inflammatory cytokines; and enhancing blood flow and endothelial NO production, which causes dilation of vessels [8]. However, many aspects of this mechanism are unknown and require further elucidation [9]. ...
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Background: Increased coronary artery calcification (CAC) has been reported in individuals with high levels of physical activity (PA). However, the association between increased CAC in a physically active population and cardiovascular mortality has not yet been well-established. This study aimed to investigate the association between PA levels and the presence or absence of CAC and cardiovascular mortality. Methods: A cohort study was conducted from 1 January 2011 to 30 December 2019. Mortality data were updated until 30 December 2020. The study population comprised 56,469 individuals who had completed the International Physical Activity Short Form Questionnaire and had undergone CAC score evaluation using a CT scan. We divided the participants into four groups: physically inactive individuals without CAC, physically inactive individuals with CAC, moderately active and health-enhancing physically active (HEPA) individuals without CAC, and moderately active and HEPA individuals with CAC. The primary outcome was cardiovascular mortality. The Cox proportional hazard model with confounding factor adjustment was conducted. Inverse probability of treatment weighting-based marginal-structural modelling was conducted. Results: The median follow-up duration was 6.60 years. The mean (SD) age of the study participants was 41.67 (±10.91) years, with 76.78% (n = 43,359) men. Compared with individuals without CAC, individuals with CAC demonstrated higher cardiovascular disease mortality regardless of PA level (Inactive and CAC > 0, HR 2.81, 95% CI: 1.76–19.19; moderately active and HEPA HR 3.27, 95% CI: 1.14–9.38). Conclusions: The presence of CAC might be associated with cardiovascular mortality regardless of PA level.
... Physical effort is considered by practitioners the basis of the concept of healthy lifestyle, to which is added the nutrition factor and integrative concept called leisure nontoxicity. Numerous experimental studies suggest that regular aerobic exercise reduces the risk of cardiovascular disease, prevents acute and chronic stress, inflammation of soft connective tissue and even the tumor process aspect mentioned in the introduction to the article (18,19). A noticeable and rarely mentioned aspect in the literature is that there are clear biochemical and physiological differences between the two sexes. ...
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In the case of pathologies with a slow onset, physical effort can correct certain molecular signaling pathways, but the primary factors that are often genetic, environmental or nutritional remain decisive. Blood glucose fluctuation is a primary indicator of a slow-onset pathology. The integration of the adaptive physiological response to physical effort in terms of carbohydrate metabolism is related to the functional humoral connection between skeletal muscle, adipose tissue, pancreas and liver. Physical effort is associated with a series of physiological changes, the intensity of which is influenced by the duration and intensity of physical effort. Physical effort, through the synthesis of specific molecular signals activates in the skeletal muscle the insulin-dependent and independent mechanisms that facilitate glucose absorption. In the case of our experimental model, the statistically significant increase in blood glucose levels during the training period is based on the activation of the central neuroendocrine axis with the release of hormones that remove glucose from stores or increase the degree of glucose conversion from glucoforming (glucose forming) molecules.
... Many studies have found that vitamin D deficiency is evident in most patients with CVD [52][53][54][55][56]. Although aerobic exercise training is an effective therapy for the prevention and treatment of CVD [57][58][59][60], its effects are not clear when the body is vitamin D deficient. One study found that aerobic exercise training while vitamin D deficient failed to counter certain metabolic syndrome indicators [61], suggesting that adequate vitamin D status is required to enable the beneficial effects of exercise. ...
Full-text available
Myocardial fibrosis is a pathological phenomenon associated with cardiovascular disease (CVD) that plays a crucial role in the development of heart diseases. Vitamin D deficiency can promote the development of CVD and exercise plays a role in the treatment of CVD. This study aimed to explore the effects of 12-week aerobic exercise training on myocardial fibrosis in vitamin D-deficient mice. A vitamin D-deficient mouse model was induced by a vitamin D-deficient (0 IU Vitamin D3/kg) diet. Twenty-four C57BL/6J male mice were randomly divided into three groups: a control sedentary group (CONS, n = 8), a vitamin D-deficient sedentary group (VDDS, n = 8), and a vitamin D-deficient exercise group (VDDE, n = 8) which was aerobically trained for 12 weeks. The results showed that the serum 25-hydroxyvitamin D [25(OH)D] levels of the VDDS group were <50 nmol/L, which was significantly lower than that of the CONS group. Compared with the CONS group, the VDDS group showed cardiac dysfunction and significant fibrosis, together with lower vitamin D receptor (VDR) mRNA and protein expression levels, higher mRNA expression levels of profibrotic and inflammatory factors, and higher transforming growth factor-β1 (TGF-β1) and phospho-Smad2/3 (P-Smad2/3) protein expression levels. Serum 25(OH)D levels in the VDDE group were significantly higher than those in the VDDS group. Compared with the VDDS group, the VDDE group showed improved cardiac function and alleviated myocardial fibrosis. Meanwhile, the VDDE group had significantly higher VDR mRNA and protein expression levels; lower mRNA expression levels of profibrotic and inflammatory factors; and lower TGF-β1 and P-Smad2/3 protein expression levels. In conclusion, aerobic exercise training remains a promising intervention for treating myocardial fibrosis in vitamin D deficiency.
... If you spend your life lying on a cot without physical activity, you will be more likely to move towards heart disease with stroke [83]. ...
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Too much of anything is bad for health. In recent years we have been familiar with “Binge”. It may be in the case of eating, drinking, or watching movies. Generation Z is very much affected by this way of living. This habit comes from indulgence. These indulgences come mainly from heredity factors, psychological conditions, dieting, peer pressure, etc. Studies show that some important features can be shared, including personality and emotional features such as neuroticism and urgency. Excessive indulgence can lead to physical and mental breakdowns. Interpersonal psychotherapy (IPT) is an effective specialty treatment for different disorders that leads to a healthy life. A continuous effort to identify the consequences of binge behaviours will also aid the development of the research field. We have to build a society free from excessive indulgence.
... 24 Hal yang perlu menjadi perhatian, terkhususnya selama pandemi COVID-19 yaitu manfaat kesehatan dari olahraga dapat diperoleh jika telah dilakukan dengan durasi 150 menit dalam satu minggu. 26,28,29 Pada penelitian ini didapatkan bahwa kelompok sampel dengan kebiasaan olahraga cenderung memiliki kadar IgG tinggi (52%), sedangkan kelompok sampel yang tidak memiliki kebiasaan olahraga cenderung memiliki kadar IgG rendah (60,7%). Akan tetapi, setelah dilakukan pengujian didapatkan hasil yang tidak signifikan (p value >0,05) sehingga secara statistik dapat dikatakan tidak terdapat hubungan signifikan antara respon imun pasca vaksinasi COVID-19 dengan kebiasaan olahraga. ...
Importance: Higher physical activity levels are associated with lower risks of cancer, cardiovascular disease, and diabetes, but associations with many common and less severe health conditions are not known. These conditions impose large health care burdens and reduce quality of life. Objectives: To investigate the association between accelerometer-measured physical activity and the subsequent risk of hospitalization for 25 common reasons for hospitalization and to estimate the proportion of these hospitalizations that might have been prevented if participants had higher levels of physical activity. Design, setting, and participants: This prospective cohort study used data from a subset of 81 717 UK Biobank participants aged 42 to 78 years. Participants wore an accelerometer for 1 week (between June 1, 2013, and December 23, 2015) and were followed up over a median (IQR) of 6.8 (6.2-7.3) years; follow-up for the current study ended in 2021 (exact date varied by location). Exposures: Mean total and intensity-specific accelerometer-measured physical activity. Main outcomes and measures: Hospitalization for the most common health conditions. Cox proportional hazards regression analysis was used to estimate hazard ratios (HRs) and 95% CIs for mean accelerometer-measured physical activity (per 1-SD increment) and risks of hospitalization for 25 conditions. Population-attributable risks were used to estimate the proportion of hospitalizations for each condition that might be prevented if participants increased their moderate to vigorous physical activity (MVPA) by 20 minutes per day. Results: Among 81 717 participants, the mean (SD) age at accelerometer assessment was 61.5 (7.9) years; 56.4% were female, and 97.0% self-identified as White. Higher levels of accelerometer-measured physical activity were associated with lower risks of hospitalization for 9 conditions: gallbladder disease (HR per 1 SD, 0.74; 95% CI, 0.69-0.79), urinary tract infections (HR per 1 SD, 0.76; 95% CI, 0.69-0.84), diabetes (HR per 1 SD, 0.79; 95% CI, 0.74-0.84), venous thromboembolism (HR per 1 SD, 0.82; 95% CI, 0.75-0.90), pneumonia (HR per 1 SD, 0.83; 95% CI, 0.77-0.89), ischemic stroke (HR per 1 SD, 0.85; 95% CI, 0.76-0.95), iron deficiency anemia (HR per 1 SD, 0.91; 95% CI, 0.84-0.98), diverticular disease (HR per 1 SD, 0.94; 95% CI, 0.90-0.99), and colon polyps (HR per 1 SD, 0.96; 95% CI, 0.94-0.99). Positive associations were observed between overall physical activity and carpal tunnel syndrome (HR per 1 SD, 1.28; 95% CI, 1.18-1.40), osteoarthritis (HR per 1 SD, 1.15; 95% CI, 1.10-1.19), and inguinal hernia (HR per 1 SD, 1.13; 95% CI, 1.07-1.19), which were primarily induced by light physical activity. Increasing MVPA by 20 minutes per day was associated with reductions in hospitalization ranging from 3.8% (95% CI, 1.8%-5.7%) for colon polyps to 23.0% (95% CI, 17.1%-28.9%) for diabetes. Conclusions and relevance: In this cohort study of UK Biobank participants, those with higher physical activity levels had lower risks of hospitalization across a broad range of health conditions. These findings suggest that aiming to increase MVPA by 20 minutes per day may be a useful nonpharmaceutical intervention to reduce health care burdens and improve quality of life.
Conference Paper
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Coronavirus is a new virus that was first identified in Wuhan, China. It is called COVID- 19. Older versions of the virus, such as SARS, also became somewhat prevalent in China and other countries, including Iran. The corona virus is now infecting millions of people around the world. On the other hand, fear of this virus has caused many people to stay at home and quarantine themselves. The reason for the spread of the corona virus. The aim of the present study is to investigate the relationship between physical activity and the progression of coronavirus.
The purpose of this study was to differences in cardiovascular risk factors and upper and lower limb muscle function according to the WHR classification in women with obese. Eighty-three obese women with over 30% body fat who aged between 20- and 30-years were divided into 3 groups: normal control group (NCG, n=6), obese women with low WHR group (WHR 0.85 or less<sup>+</sup> more than 30% body fat, OLW, n=64), obese women with high WHR group (WHR 0.85 or more<sup>+</sup> more than 30% body fat, OHW, n=13). We performed measurements to determine cardiovascular risk factors, basic physical fitness, isokinetic knee and trunk muscle functions according to WHR classification.As the result of this study, the knee flexor peak torque and hamstring to quadriceps torque ratio (H:Q ratio) as well as isokinetic endurance capacity of the right and left knee flexors were significantly higher in the NCG compared to the OLW and OHW. In addition, sergeant jump was significantly higher in the NCG compared to the OLW and OHW. But other basic physical fitness factors and cardiovascular disease risk factors were no significant difference between all groups. Our findings confirmed that WHR risk level may be an important predictor of lower extremity muscle function in obese women.
It is well known that exercise is beneficial for cardiovascular health. Oxidative stress is the common pathological basis of many cardiovascular diseases. The overproduction of free radicals, both reactive oxygen species and reactive nitrogen species, can lead to redox imbalance and exacerbate oxidative damage to the cardiovascular system. Maintaining redox homeostasis and enhancing anti‐oxidative capacity are critical mechanisms by which exercise protects against cardiovascular diseases. Moderate‐intensity exercise is an effective means to maintain cardiovascular redox homeostasis. Moderate‐intensity exercise reduces the risk of cardiovascular disease by improving mitochondrial function and anti‐oxidative capacity. It also attenuates adverse cardiac remodeling and enhances cardiac function. This paper reviews the primary mechanisms of moderate‐intensity exercise‐mediated redox homeostasis in the cardiovascular system. Exploring the role of exercise‐mediated redox homeostasis in the cardiovascular system is of great significance to the prevention and treatment of cardiovascular diseases. Exercise reduces the risk of cardiovascular diseases. Maintaining redox homeostasis is one of the important mechanisms by which moderate‐intensity exercise protects the heart. Moderate‐intensity exercise improves the body's antioxidant capacity, which helps maintain a relatively stable redox state in the cardiovascular system. Moderate‐intensity exercise is a potential approach to prevent and treat cardiovascular diseases, such as myocardial infarction, heart failure, cardiomyopathy, etc.
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Objective To emphasize the mechanism of concurrent exercise effect on lipid disorders in insulin resistance (IR) and nonalcoholic fatty liver disease (NAFLD). Materials and methods Twenty male ApoE knockout mice were randomly divided into two groups: HFD group (n = 10) fed a high fat diet, and HFDE group (n = 10) with high-fat diet intervention for 12 weeks and swimming exercise. Other ten healthy male C57BL/6 J mice were fed a normal diet, and included as control group. Retro-orbital blood samples were collected for biochemical analysis. Oil red O staining of liver tissues was performed to confirm the exercise effect. Western blotting was performed to evaluate the expressions of PPAR-γ, CPT-1, MCAD. Results The levels of TG, TC, LDL, FFA, FIN, FPG and Homa-IRI in the HFD group were significantly higher than ND group, while these were markedly decreased in the HFDE group compared with HFD group. The Oil Red O staining of liver samples further confirmed the exercise effect on the change of lipid deposition in the liver. Western blotting showed increased expressions of PPAR-γ, CPT-1, MCAD induced by high fat diet were significantly downregulated by exercise. Conclusion A concurrent 12-week exercise protocol alleviated the lipid metabolism disorders of IR and NAFLD, probably via PPAR-γ/CPT-1/MCAD signaling.
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Background The global prevalence of type 2 diabetes-related complications is not well described. We assessed prevalence of vascular complications at baseline in DISCOVER (NCT02322762; NCT02226822), a global, prospective, observational study program of 15,992 patients with type 2 diabetes initiating second-line therapy, conducted across 38 countries. Methods Patients were recruited from primary and specialist healthcare settings. Data were collected using a standardized case report form. Prevalence estimates of microvascular and macrovascular complications at baseline were assessed overall and by country and region, and were standardized for age and sex. Modified Poisson regression was used to assess factors associated with the prevalence of complications. Results The median duration of type 2 diabetes was 4.1 years (interquartile range [IQR]: 1.9–7.9 years), and the median glycated hemoglobin (HbA1c) level was 8.0% (IQR: 7.2–9.1%). The crude prevalences of microvascular and macrovascular complications were 18.8% and 12.7%, respectively. Common microvascular complications were peripheral neuropathy (7.7%), chronic kidney disease (5.0%), and albuminuria (4.3%). Common macrovascular complications were coronary artery disease (8.2%), heart failure (3.3%) and stroke (2.2%). The age- and sex-standardized prevalence of microvascular complications was 17.9% (95% confidence interval [CI] 17.3–18.6%), ranging from 14.2% in the Americas to 20.4% in Europe. The age- and sex-standardized prevalence of macrovascular complications was 9.2% (95% CI 8.7–9.7%), ranging from 4.1% in South-East Asia to 18.8% in Europe. Factors positively associated with vascular complications included age (per 10-year increment), male sex, diabetes duration (per 1-year increment), and history of hypoglycemia, with rate ratios (95% CIs) for microvascular complications of 1.14 (1.09–1.19), 1.30 (1.20–1.42), 1.03 (1.02–1.04) and 1.45 (1.25–1.69), respectively, and for macrovascular complications of 1.41 (1.34–1.48), 1.29 (1.16–1.45), 1.02 (1.01–1.02) and 1.24 (1.04–1.48), respectively. HbA1c levels (per 1.0% increment) were positively associated with microvascular (1.05 [1.02–1.08]) but not macrovascular (1.00 [0.97–1.04]) complications. Conclusions The global burden of microvascular and macrovascular complications is substantial in these patients with type 2 diabetes who are relatively early in the disease process. These findings highlight an opportunity for aggressive early risk factor modification, particularly in regions with a high prevalence of complications. Trial registration; NCT02322762. Registered 23 December 2014.; NCT02226822. Registered 27 August 2014. Electronic supplementary material The online version of this article (10.1186/s12933-018-0787-8) contains supplementary material, which is available to authorized users.
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Prevention of deadly diseases like heart attack or stroke is more effective than treating patients with already progressed disease. Epidemiologic studies raised the possibility that eating healthy food and doing physical exercise may prevent thrombotic diseases. To create an ‘antithrombotic diet’, fruits and vegetables should be selected and the benefit of diet and exercise should be monitored in people. We found that the Global Thrombosis Tests are useful for both selection of antithrombotic diet components and monitoring thrombotic status of individuals.
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Background: Cardiovascular disease (CVD) is not only the primary cause of death in developed western countries, but also its disease burden is increasing in China. The purpose of constructing population cardiovascular health index is to monitor, compare and evaluate disease burden, influencing factors and prevention and control levels of Chinese population cardiovascular disease in order to provide evidence to improve population cardiovascular health. Methods: This study collected multi-source data and constructed China Cardiovascular Health Index (CHI) using literature review, questionnaire surveys, Delphi method and Analytical Hierarchy Process (AHP) model. Results: China CHI system included 52 indices of 5 dimensions, which were prevalence status of CVD, exposure of risk factors, prevention and control of risk factors, treatment situation and public health policy and service ability. The weights of 5 dimensions from high to low were successively prevention and control of risk factors 0.3656, prevalence status of CVD 0.2070, treatment situation 0.1812, public health policy and service ability 0.1458, and exposure of risk factors 0.1004. Conclusion: China CHI is a comprehensive evaluation system raised to effectively control the prevalence of CVD. In the future, we should strengthen and improve CVD monitoring and big data usage, to ensure these indices to reflect the practical situations and to become utility of controlling CVD.
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The current study examined the effect of aging and long-term wheel-running on the expression of heat shock protein (HSP), redox regulation, and endoplasmic reticulum (ER) stress markers in tibialis anterior (T.A.) and soleus muscle of mice. Male mice were divided into young (Y, 3-month-old), old-sedentary (OS, 24-month-old), and old-exercise (OE, 24-month-old) groups. The OE group started voluntary wheel-running at 3 months and continued until 24 months of age. Aging was associated with a higher thioredoxin-interacting protein (TxNiP) level, lower thioredoxin-1 (TRX-1) to TxNiP ratio-a determinant of redox regulation and increased CHOP, an indicator of ER stress-related apoptosis signaling in both muscles. Notably, GRP78, a key indicator of ER stress, was selectively elevated in T.A. Long-term exercise decreased TxNiP in T.A. and soleus muscles and increased the TRX-1/TxNiP ratio in soleus muscle of aged mice. Inducible HSP70 and constituent HSC70 were upregulated, whereas CHOP was reduced after exercise in soleus muscle. Thus, our data demonstrated that aging induced oxidative stress and activated ER stress-related apoptosis signaling in skeletal muscle, whereas long-term wheel-running improved redox regulation, ER stress adaptation and attenuated ER stress-related apoptosis signaling. These findings suggest that lifelong exercise can protect against age-related cellular stress.
The past 2 decades have witnessed a growing body of work investigating the feasibility and efficacy of exercise therapy on a broad array of outcomes in many different oncology scenarios. Despite this heterogeneity, the exercise therapy prescription approach and the dose tested has been largely similar. Thus, current exercise therapy prescriptions in the oncology setting adopt a one-size-fits-all approach. In this article, we provide an overview of personalization of exercise therapy in cancer using the principles of training as an overarching framework. Specifically, we first review the fundamentals of exercise prescription in chronic disease before focusing attention on application of these principles to optimize the safety and efficacy of exercise therapy on (1) cancer treatment-induced cardiovascular toxicity and (2) tumor progression and metastasis.
Regular exercise may reduce the risk of major cardiovascular thrombotic events. However, previous studies suggest that the risk of myocardial infarction or primary cardiac arrest is transiently increased during exercise. Thus, on the one hand, exercise seems to be able to protect against cardiovascular disease, but on the other hand, it seems to provoke sudden cardiac death. As platelets play a key role in arterial thromboembolic disease, the effect of exercise on platelet function is of special interest. This systematic review summarizes the evidence of the influence of exercise on platelet function in patients with coronary artery disease, angina pectoris, hypertension, or peripheral arterial disease. We specifically investigated, (1) if platelet function was increased in patients prior to exercise compared with healthy controls, (2) if exercise influenced platelet function differently in patients compared with healthy controls, and finally (3) if exercise reduced the effect of aspirin (acetylsalicylic acid). We performed a literature search in PubMed, Embase, Scopus, and Cochrane Library. In total, 18 articles were included and grouped into studies including patients with coronary artery disease (n = 7), angina pectoris (n = 5), hypertension (n = 5), and patients with peripheral arterial disease (n = 2). One study included both patients with coronary artery disease and patients with hypertension, and this study was therefore included in both groups. All studies performed short-term exercise either using treadmill (n = 12), primarily following the Bruce protocol, or bicycle ergometer test (n = 6). Overall, patients did not differ from healthy controls in platelet aggregation or activation prior to exercise. After exercise, conflicting results were reported with some studies reporting intensified platelet aggregation and/or platelet activation, some studies found no difference, whereas a few studies reported a reduction in platelet aggregation after exercise when compared with controls. Exercise seemed to impair the effect of aspirin during or shortly after exercise. In conclusion, the studies reported contradictive results. However, this review indicates that strenuous short-term exercise induces increased platelet activation also implying a reduced effect of aspirin during short-term exercise. Controlled studies on the effect of regular long-term low-intensity exercise are needed to further clarify the influence of long-term exercise on platelet function.
Background--It is unclear whether the greater benefits of moderate-to-vigorous physical activity (PA) over light PA are attributed to the higher-intensity PA or simply the greater volume of PA accumulated per unit time for moderate-to-vigorous PA. We examined this question using estimates of the volume of light and moderate-to-vigorous PA in relation to all-cause mortality. Methods and Results--We used National Health and Nutrition Examination Survey 2003-2006 accelerometer records in adults (≥40 years; n=4840) and mortality data collected through 2011 (n=700 deaths). We estimated intensity-specific PA volume using activity counts (AC) accumulated in light (100-759 AC/min), moderate-to-vigorous PA (≥760 AC/min), and total PA (≥100 AC/ min). We examined quartiles of each exposure using Cox proportional hazard models (hazard ratios [95% confidence interval) adjusted for demographic and behavioral risk factors, health status, and body mass index. Mortality risk was less across increasing quartiles of light PA volume (AC × 1000) when compared with the least quartile (AC ≤61.8); the least risk occurred in the upper quartile of light PA, AC > 98.5 (hazard ratios=0.69, 95% confidence interval: 0.47, 1.00, P trend ≤0.05). The benefits for mortality risk were greater across quartiles of moderate-to-vigorous PA and reached a hazard ratio of 0.28 (95% confidence interval: 0.17, 0.46, P trend ≤0.05) for AC > 187.9, when compared with the referent group (AC ≤50.8). Results examining various combinations of light and moderate-to-vigorous intensity-specific volumes demonstrated the strong influence of total activity on mortality risk. Conclusions--In this population, increasing light PA was associated with less mortality, but at an approximately equal volume of PA, moderate-to-vigorous PA appeared to have greater benefits.
Diabetes mellitus is a complicated metabolic disease with symptoms of hyperglycemia, insulin resistance, chronic damage and dysfunction of tissues, and metabolic syndrome for insufficient insulin production. Evidence has indicated that exercise treatments are essential in the progression of type‑ІІ diabetes mellitus, and affect insulin resistance and activity of islet β‑cells. In the present study, the efficacy and signaling mechanism of aerobic exercise on blood lipids and insulin resistance were investigated in the progression of type‑ІІ diabetes mellitus. Body weight, glucose metabolism and insulin serum levels were investigated in mouse models of type‑ІІ diabetes mellitus following experienced aerobic exercise. Expression levels of inflammatory factors, interleukin (IL)‑6, high‑sensitivity C‑reactive protein, tumor necrosis factor‑α and leucocyte differentiation antigens, soluble CD40 ligand in the serum were analyzed in the experimental mice. In addition, expression levels of toll‑like receptor 4 (TLR‑4) were analyzed in the liver cells of experimental mice. Changes of oxidative stress indicators, including reactive oxygen species, superoxide dismutase, glutathione and catalase were examined in the liver cells of experimental mice treated by aerobic exercise. Expression levels and activity of extracellular signal‑regulated kinases (ERK) and AMP‑activated protein kinase (AMPK) signaling pathways were investigated in the liver cells of mouse models of type‑ІІ diabetes mellitus after undergoing aerobic exercise. Aerobic exercise decreased the expression levels of inflammatory factors in the serum of mouse models of type‑ІІ diabetes mellitus. The results indicated that aerobic exercise downregulated oxidative stress indicators in liver cells from mouse models of type‑ІІ diabetes mellitus. In addition, the ERK and AMPK signaling pathways were inactivated by aerobic exercise in liver cells in mouse models of type‑ІІ diabetes mellitus. The activity of ERK and AMPK, and the function of islet β‑cells were observed to be improved in experimental mice treated with aerobic exercise. Furthermore, blood lipid metabolism and insulin resistance were improved by treatment with aerobic exercise. Body weight and glucose concentration of serology was markedly improved in mouse models of type‑ІІ diabetes mellitus. Furthermore, TLR‑4 inhibition markedly promoted ERK and AMPK expression levels and activity. Thus, these results indicate that aerobic exercise may improve blood lipid metabolism, insulin resistance and glucose plasma concentration in mouse models of type‑ІІ diabetes mellitus. Thus indicating aerobic exercise is beneficial for improvement of blood lipid and insulin resistance via the TLR‑4‑mediated ERK/AMPK signaling pathway in the progression of type‑ІІ diabetes mellitus.
Physical inactivity is one of the most prevalent major health risk factors, with 8 in 10 US adults not meeting aerobic and muscle-strengthening guidelines, and is associated with a high burden of cardiovascular disease. Improving and maintaining recommended levels of physical activity leads to reductions in metabolic, hemodynamic, functional, body composition, and epigenetic risk factors for noncommunicable chronic diseases. Physical activity also has a significant role, in many cases comparable or superior to drug interventions, in the prevention and management of >40 conditions such as diabetes mellitus, cancer, cardiovascular disease, obesity, depression, Alzheimer disease, and arthritis. Whereas most of the modifiable cardiovascular disease risk factors included in the American Heart Association's My Life Check - Life's Simple 7 are evaluated routinely in clinical practice (glucose and lipid profiles, blood pressure, obesity, and smoking), physical activity is typically not assessed. The purpose of this statement is to provide a comprehensive review of the evidence on the feasibility, validity, and effectiveness of assessing and promoting physical activity in healthcare settings for adult patients. It also adds concrete recommendations for healthcare systems, clinical and community care providers, fitness professionals, the technology industry, and other stakeholders in order to catalyze increased adoption of physical activity assessment and promotion in healthcare settings and to contribute to meeting the American Heart Association's 2020 Impact Goals.