pre- and post-MI are lacking, there have been several published animal
studies. Studies using rat models have shown a definite benefit to
swimming before an MI. In rats, a pre-MI swimming regimen, which
consisted of a 7-week program,was subsequently shown to significantly
reduce scar size after the MI. In addition, swimming pre-MI was
shown to increase the rate of expression of key beneficial genes
involved in LV remodeling [75]. Gaudren et al. evaluated swimming as
an endurance exercise after anMI in rats. Data did not showa mortality
or remodeling benefit or harm after a small infarction. However, swimming
was actually shown to cause harm in rats that had a large infarction
area. The harm was caused whether the swimming was initiated
early or late after an MI, but more profound in exercise regimens initiated
early after anMI.Deathwas a result of aggravated LV remodeling and
wall stress caused by endurance exercises, and was postulated as a
caveat to starting any type of endurance exercising after an MI causing
LV dysfunction [76]. Extrapolation of results is difficult because of differences
in species, and due to difficulty in standardizing the extent of
infarct and intensity of exercise. However, results indicate that swimming
rehabilitation programs should not be initiated immediately
after an MI, and that further research is needed on the optimal time
after an MI to start a program.
Needless to say, the results of swimming in patients with CAD
have had varied results. The difference may lie in the stability of the
CAD, as prior investigations have shown that sudden death that
occurs in men with severe CAD is a result of plaque rupture [77].
However, it appears that swimming can be tolerated well in patients
with stable disease, and should be used following physician screening
in those patients in cardiac rehabilitation. Specifically, heart rate
monitoring with specific exercise prescriptions may be needed in
such patients to ensure safety during water exercises.
7. Swimming and congestive heart failure
A greater percentage of patients with chronic, stable CHF are being
referred to cardiac rehabilitation programs and concern remains as to
whether swim exercise can be tolerated without adverse effects in
this population. Traditionally, it was thought that swimming could
pose risks to patients with diastolic or systolic heart failure due to
hydrostatically induced volume shifts causing ventricular decompensation.
As previously mentioned, hydrostatic pressure causes blood to
shift into the intrathoracic cavity, resulting in increased venous return.
It was feared that in patients with decreased myocardial contractility,
compensatory mechanisms such as an increase in end-diastolic LV
volume would become overburdened. This could result in increased LV
end-diastolic pressure followed by pulmonary congestion and a decrease
in stroke volume. This was demonstrated in one study, which showed
evidence of increased preload and increased pulmonary capillary and
artery pressures, in swimming as compared to supine cycle ergometry
in patients with moderate to severe compensated CHF [78]. In addition,
in patients with severe CHF, there was evidence of ventricular wall dyskinesia
and overload with water immersion. Of note, patients did not exhibit
any symptoms of LV or fluid overload. Another concern is whether
patients with CHF can tolerate swimming exercises. One study, which
investigated 25 patients with coronary heart disease found 50% of
patients with depressed LV systolic function (mean LV ejection fraction
[LVEF] 44%) were unable to complete the swimming protocol as compared
to 23% of patients with preserved systolic function (mean LVEF
54%) [9]. However, in contrast to these results, the majority of newer
studies indicate that swimming exercises can be well tolerated. Recent
studies show that patients with depressed LVEFs, but stable symptoms,
are able to increase cardiac index adequately to support swimming exercises;
however the increase in VO2 and cardiac index, and the decrease in
systemic vascular resistance trends were lower in patients with systolic
dysfunction compared to those with CAD, or a preserved LVEF [79]. The
role of water exercises versus land exercises was again examined with
respect to cardiac rehabilitation programs in patients with CADwith preserved
LVEF or patients with CHF. Interestingly, water based exercises
were shown to be tolerated well and showed a statistically significant
increase in LVEF after the 3 week program. In addition, after just
3 weeks of water-based exercises, statistically significant changes were
seen including an increase in calculated stroke volume and a decrease
in heart rate. Results of land exercises were comparable to those of
water based exercising, with a trend towards greater improvement in
LVEF with water based exercising [80]. These results were repeated in
a 3 week cardiac rehabilitation program. After 3 weeks of water based
exercising, natural responses to water immersion were restored in
heart failure patients. Increases in stroke volume and cardiac output
were noted after the program when they were not present before