CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 8, September 2012
454
AFRICA
injury.
The main findings of the present study were that four weeks
of resistance training: (1) increased the weight-lifting ability,
(2)
induced cardiac hypertrophy without any significant change
in cardiac function, and (3) did not preserve the heart against
IR-induced injuries, as evidenced by no change in the infarct size
and apoptosis rate.
Weight loss, cardiac hypertrophy and work performed are
some of the indices to characterise training efficiency. Previously,
Barauna
et al
.
reported that four weeks of resistance training in
rats increased their weight-lifting ability and induced cardiac
hypertrophy with no change in cardiac function.
4
Progression in
weight-lifting ability indicates training efficacy and development.
While maximum heart rate or VO
2
max
are used to prescribe
endurance exercise training,
5
work performed may be a good
indicator of resistance-training efficacy. Moritany and Vries
showed that neuronal and muscular adaptations were involved
in training-induced enhancement of the rat’s muscular strength.
12
Resistance training is a known stimulus for cardiac
hypertrophy due to pressure overload imposed on the heart
during training.
13
Our results are in agreement with pervious
research.
4,13
The precise underlying mechanism of resistance
training-induced cardiac hypertrophy needs to be elucidated. In
this regard it has been suggested that induction of angiotensin
receptor type 1 (AT
1
)
expression in the heart and elevation of
circulating anabolic hormones may be involved.
13,14
In this study, coronary flow, left ventricular developed
pressure and diastolic pressure did not differ significantly
between the trained and untrained rats. There are several
published reports on the beneficial effect of resistance exercise
on cardiac performance in patients with heart failure.
15-17
In this
regard it has been proposed that resistance training could improve
stroke volume and ejection fraction without enhancement of
cardiomegaly or cardiac deterioration.
15-17
Few studies have investigated the effect of this type of
exercise on cardiac function in healthy individuals and most
did not report on changes in heart function after resistance
training.
18-20
Moreover, Barauna
et al
.
reported that four weeks of
resistance training did not change cardiac function in rats. Our
results are in agreement with the results of these studies.
4
Growing evidence indicates that IR-induced myocardial cell
death is not limited to necrosis but also includes apoptotic cell
death.
21
For this reason, we measured ventricular apoptosis rate
and infarct size in our study. The results show that short-term
resistance training neither induces excessive damage to the heart
nor preserves it against IR-induced injury, because apoptosis rate
and infarct size did not change between our trained and control
animal hearts.
While it has been shown that short- to long-term endurance
exercise can protect the heart against IR-induced injury,
3
some
investigations did not report the beneficial effects of endurance
exercise (up to 12 weeks) on cardiac performance, anti-oxidant
defense and cell death rate.
10,22
It has been proposed that these
controversial results could have resulted from methological
differences, such as type and duration of endurance exercise
(
swimming, treadmill or wheel running), time between the end of
the training programme and sacrifice of the animals.
23
Conclusion
Previously we saw that 12-week resistance exercise training
preserved the heart against IR-induced injury but the results of
this study showed that four-week resistance training was unable
to achieve this. Nevertheless, this is the first study with this
purpose and a precise conclusion about this issue needs more
investigation.
We appreciate the support provided by the Scientific Association of the
Islamic Azad University, Tabriz branch, in the form of a study grant.
References
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Fig. 3. Effect of resistance exercise on the heart infarct
size. Top: representative digital images of the stained
heart. Non-necrotic viable tissue is dark, and infracted
tissue is light. Bottom: quantification of average infarct
size expressed as a percentage of ischaemic ZAR (zone
at risk). Values are mean
±
SD (
n
=
6
rats); Sed: sedentary
and EXT: exercise-trained rats.
50
40
30
20
10
0
Sed
EXT
Infarct size (% ZAR)
Fig. 4. Effect of resistance exercise on the heart apopto-
sis rate. Top: cell death determined by the TUNEL method
at
×
40
magnification (black nuclei are the apoptotic
cells). Bottom: comparison of apoptotic cell ratios in the
two groups. Sed: sedentary and EXT: exercise trained
rats. Values are mean
±
SD (
▲
=
6
for trained and
▲
=
5
for sedentary rats).
8
6
4
2
0
Sed
EXT
Apoptosis cells (%)
