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cardiovascular diseases [ 2 – 4 ]. Mechanisms of maintaining this cardioprotective
phenotype are less known and here we want to elucidate some of the physiological
processes behind it.
2 Neoangiogenesis in Healthy Heart
First, it is necessary to tell, that information about neoangiogenesis in the physio-
logical terrain of healthy myocardium is scarce. Most of the papers are not dealing
with endothelium in myocardium (thus we are pushed only to prudently extrapolate
the results for the myocardium) or study the neoangiogenesis in infarction region
within the heart wall [ 5 ]. Transferring results obtained from skeletal muscle and
hypothesize similar results for the heart is therefore speculative and questionable
and further works are needed to get a foothold in near future. Other studies e.g [ 6 , 7 ].
are proving functionality of several pathways with direct positive effect on neoan-
giogenesis, but they bear no relation to exercise. Recent studies have shown that
angiogenesis in coronary microvasculature is caused by endogenous stem cell/
progenitor mobilization and participation, and its paracrine effects on endothelial
cells function and microvascular distribution. Exercise could mobilize and activate
the expression and secretion of endogenous stem cell and angiogenic factors, and
affect the cardiac angiogenesis in epigenetics [ 8 ].
In this chapter, we are focusing on aerobic, endurance-based exercise (walking,jogging, swimming, skiing, or cycling 3 to 4 times a week or analogous physical
activity in animal model [ 9 ]) and its role in coronary neoangiogenesis. It is sug-
gested that heavy resistance training in contrast to endurance training does not result
in increased capillary density in skeletal muscle [ 10 , 11 ]. The response of the heart
is not dependent on the type of exercise applied, but rather on the duration and
intensity at which the exercise is performed [ 12 ]. After regular exercise performed
for longer period of time, typical functional and even morphological signs of adap-
tation in vasculature can be monitored. Without these, other morphological signs of
adaptation of heart wall as physiological hyperthrophy of cardiomyocytes [ 13 ]
could be counterproductive. Hyperthrophy (and even hyperplasia [ 14 , 15 ]), together
with neoangiogenesis has a protective effect against cardiovascular diseases [ 16 ].
Several cell populations play its role in neoangiogenesis – endothelial cells,endothelial stem cells, pericytes, endocardial cells [ 17 ], telocytes [ 15 , 18 ], partially
fibroblasts, vascular smooth muscle cells [ 19 ] and cardiomyocytes [ 20 ].
Correct structural association between (hypertrophied) cardiomyocyte and newlyformed capillaries after exercise is important for maintaining proper function of the
myocardium. Each cardiomyocyte possess its own capillary, what can be seen in
electron micrographs from scanning electron microscope as well after imunolabel-
ing of endothelial cells around (Figs. 7.1 and 7.2).
M. Miko and I. Varga