CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 2, March/April 2017
AFRICA
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dysregulation may be key aspects in the pathogenesis of
CHD.
5,10,16,23,32-34
These aspects decrease during exercise and may
therefore play a part in the 1.33-fold decreased risk for CHD.
Based on the evidence, it is believed that the CHD benefit
associated with exercise is substantial and should garner a similar
level of public interest as do other risk factors such as smoking,
high cholesterol levels and treatments such as statin therapy.
However, while exercise is frequently advised for healthy living,
36
it is unfortunate that only 48.9% of Americans meet the physical
activity guidelines. It follows from this that 51.1% of Americans
do not meet the minimum physical activity guidelines, which
results in 162.8 million Americans at a greater risk of CHD due
to physical inactivity.
37
The individual studies selected unfortunately represent only
the risk associated with the cohort studied and cannot accurately
be extrapolated to other populations without further research.
Conclusion
Although it is well known that moderate exercise is associated
with a lower risk of CHD, all the positive effects on CHD
pathogenesis were not available in a detailed integrated model.
Such a model would help provide further insight. A high-level
conceptual model was therefore developed, which links moderate
exercise with the pathogenesis, hallmarks and biomarkers of
CHD.
The novel connection graph developed from this model
shows, at a glance, the positive effect of moderate exercise on
certain important aspects of the pathogenesis of CHD. It helps
to graphically explain why moderate exercise is associated with
lower CHD risk. From this it is apparent that exercise has a wide-
ranging impact on the pathogenesis of CHD, with these effects
notable in changes in CHD biomarkers.
The integrated high-level CHD model and simplified
connection graph provide a summary of evidence for a causal
relationship between CHD risk and moderate exercise. We
acknowledge the fact that the integrated view is relevant to
other lifestyle issues and for full comprehension will have to be
replicated in other articles describing these factors.
The angel investor was Dr Arnold van Dyk and the research was later self-
funded. Prof Leon Liebenberg was involved in the initial research.
References
1.
Mathers CD, Boerma T, Fat DM. Global and regional causes of death.
Br Med Bull
2009;
92
(1): 7–32.
2.
Mora S, Cook N, Buring JE, Ridker PM, Lee I-M. Physical activity and
reduced risk of cardiovascular events potential mediating mechanisms.
Circulation
2007;
116
(19): 2110–2118.
3.
Green DJ, Spence A, Halliwill JR, Cable NT, Thijssen DH. Exercise
and vascular adaptation in asymptomatic humans.
Exp Physiol
2011;
96
(2): 57–70.
4.
Thompson PD, Buchner D, Piña IL, Balady GJ, Williams MA, Marcus
BH,
et al
. Exercise and physical activity in the prevention and treatment
of atherosclerotic cardiovascular disease: A statement from the Council
on Clinical Cardiology (Subcommittee on Exercise, Rehabilitation,
and Prevention) and the Council on Nutrition, Physical Activity, and
Metabolism (Subcommittee on Physical Activity).
Circulation
2003;
107
(24): 3109–3116.
5.
Gleeson M, Bishop NC, Stensel DJ, Lindley MR, Mastana SS, Nimmo
MA. The anti-inflammatory effects of exercise: mechanisms and impli-
cations for the prevention and treatment of disease.
Nat Rev Immunol
2011;
11
(9): 607–615.
6.
Mathews MJ. A systems engineering approach to coronary heart disease
[PhD dissertation]. Potchefstroom: North-West University, 2016.
7.
Mathews MJ, Liebenberg L, Mathews EH. How do high glycemic load
diets influence coronary heart disease?
Nutr Metab
2015; 12(1): 6.
8.
Mathews MJ, Liebenberg L, Mathews EH. The mechanism by which
moderate alcohol consumption influences coronary heart disease.
Nutr
J
. 2015;
14
(1): 33.
9.
Mathews MJ, Mathews EH, Liebenberg L. The mechanisms by which
antidepressants may reduce coronary heart disease risk.
BMCCardiovasc
Disord
2015;
15
(1): 82.
10. Strasser B. Physical activity in obesity and metabolic syndrome.
Ann NY
Acad Sci
2013;
1281
(1): 141–159.
11. Warburton DE, Nicol CW, Bredin SS. Health benefits of physical activ-
ity: the evidence.
Can Med Assoc J
2006;
174
(6): 801–809.
12. Reaven GM. Role of insulin resistance in human disease.
Diabetes
1988;
37
(12): 1595–1607.
13. Dandona P, Aljada A, Chaudhuri A, Mohanty P, Garg R. Metabolic
syndrome: A comprehensive perspective based on interactions between
obesity, diabetes, and inflammation.
Circulation
2005;
111
(11): 1448–
1454.
14. Hotamisligil GS, Shargill NS, Spiegelman BM. Adipose expression of
tumor necrosis factor-alpha: direct role in obesity-linked insulin resist-
ance.
Science
1993;
259
(5091): 87–91.
15. Xu H, Barnes GT, Yang Q, Tan G, Yang D, Chou CJ, et al. Chronic
inflammation in fat plays a crucial role in the development of obesity-
related insulin resistance.
J Clin Invest
2003;
112
(12): 1821–1830.
16. Petersen AMW, Pedersen BK. The anti-inflammatory effect of exercise.
J Appl Physiol
2005;
98
(4): 1154–1162.
17. Libby P. Inflammation in atherosclerosis.
Arterioscler Thromb Vasc Biol
2012;
32
(9): 2045–2051.
18. Pischon T, Girman CJ, Hotamisligil GS, Rifai N, Hu FB, Rimm EB.
Plasma adiponectin levels and risk of myocardial infarction in men.
J
Am Med Assoc
2004;
291
(14): 1730–1737.
19. Pedersen BK, Saltin B. Evidence for prescribing exercise as therapy in
chronic disease.
Scand J Med Sci Sports
2006;
16
(S1): 3–63.
20. Brown NJ, Agirbasli MA, Williams GH, Litchfield WR, Vaughan DE.
Effect of activation and inhibition of the renin-angiotensin system on
plasma PAI-1.
Hypertension
1998;
32
(6): 965–971.
21. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA,
Izzo JL,
et al
. Seventh report of the joint National Committee on
Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure.
Hypertension
2003;
42
(6): 1206–1252.
22. Klein S, Burke LE, Bray GA, Blair S, Allison DB, Pi-Sunyer X,
et al
.
Clinical implications of obesity with specific focus on cardiovascu-
lar disease. A statement for professionals from the American Heart
Association Council on Nutrition, Physical Activity, and Metabolism:
endorsed by the American College of Cardiology Foundation.
Circulation
2004;
110
(18): 2952–2967.
23. Rose AJ, Richter EA. Skeletal muscle glucose uptake during exercise:
how is it regulated?
Physiology
2005;
20
(4): 260–270.
24. Cimenti C, Schlagenhauf A, Leschnik B, Schretter M, Tschakert
G, Gröschl W,
et al.
Low endogenous thrombin potential in trained
subjects.
Thromb Res
2013;
131
(6): e281–e285.
25. Rauramaa R, Salonen JT, Seppänen K, Salonen R, Venäläinen J,
Ihanainen M,
et al
. Inhibition of platelet aggregability by moderate-
intensity physical exercise: a randomized clinical trial in overweight men.