International Journal of Cardiology 168 (2013) 19–26

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International Journal of Cardiology

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Review

Swimming and the heart

Jason M. Lazar a,⁎, Neel Khanna b, Roseann Chesler a, Louis Salciccioli a
a
Division of Cardiovascular Medicine, State University of New York Downstate Medical Center, Brooklyn, New York, United States
b
Department of Medicine, State University of New York Downstate Medical Center, Brooklyn, New York, United States

a r t i c l e i n f o a b s t r a c t

Article history: Exercise training is accepted to be beneficial in lowering morbidity and mortality in patients with cardiac dis-
Received 6 September 2012 ease. Swimming is a popular recreational activity, gaining recognition as an effective option in maintaining
Received in revised form 4 February 2013 and improving cardiovascular fitness. Swimming is a unique form of exercise, differing from land-based
Accepted 17 March 2013
exercises such as running in many aspects including medium, position, breathing pattern, and the muscle
Available online 18 April 2013
groups used. Water immersion places compressive forces on the body with resulting physiologic effects.
Keywords:
We reviewed the physiologic effects and cardiovascular responses to swimming, the cardiac adaptations to
Swimming swim training, swimming as a cardiac disease risk factor modifier, and the effects of swimming in those
Exercise with cardiac disease conditions such as coronary artery disease, congestive heart failure and the long-QT
Training syndrome.
Cardiovascular disease Published by Elsevier Ireland Ltd.

1. Introduction
Swimming has long been a popular recreational activity, but is re-
cently gaining widespread acclaim as an effective option in maintaining
and improving cardiovascular fitness. In the United States, swimming is
second behind walking as the most popular sports activity [1]. Interna-
tionally, there are a reported 18,784 facilities with 20,108 full size year
round swimming pools in 168 countries. Its appeal for elderly patients
and those with cardiovascular disease primarily lies in its low impact
nature. In patients with arthritis, swimming and other water-based
activities were shown to improve joint function, without worsening
symptoms, thereby making it particularly attractive to those who strug-
gle with these issues [2].
Exercise training is presently accepted to be beneficial in lowering
morbidity and mortality in patients with cardiac disease [3]. However,
in past studies, swimming has been attributed with sudden cardiac
death. One study found that 11% of recreational deaths in Rhode Island
were related to swimming [4]. However, cardiovascular deaths that
result from swimming must be differentiated from drowning deaths,
which are more likely to occur in unsupervised locations than those
due to a primary cardiac cause. While some studies have shown that
swimming can be an arrhythmogenic trigger for long QT-syndrome
[5], data shows that swimming comprises only 2% of all deaths in
young athletes, the majority of whom had an underlying cardiac condi-
tion [6]. In addition, recent evidence shows that swimmers may have
lower all-cause mortality risk as compared to sedentary, walking and
⁎ Corresponding author at: SUNY Downstate Medical Center, Cardiology Division,
450 Clarkson Avenue, Box 1199, Brooklyn, New York 11203, United States. Tel.: +1 718
221 5222; fax: +1 718 221 5220.
E-mail address: Jason.lazar@downstate.edu (J.M. Lazar).
running counterparts [7]. Of course, results are dependent on the dura-
tion and intensity of the exercise. Accordingly, the risks and benefits of
swimming as a cardiovascular exercise merits review, particularly in
those with cardiac disease. Additional objectives of this article are to
outline the physiologic effects of swimming, and to describe the cardio-
vascular responses of swimming and the cardiac adaptations to swim
training.
2. Physiologic effects
Swimming differs from most other exercises such as running in
many aspects including medium, position, breathing pattern, and the
muscle groups used. Body position and medium make swimming an es-
pecially unique form of exercise. Water immersion places compressive
forces on the body, which serve to increase pressure in the capacitance
vessels, thereby causing a shift of volume into the thoracic cavity. This
shift of volume into the thoracic cavity thereby augments venous return
[8,9]. Greater venous return provides higher preload to the right and left
ventricles. Left and right heart filling pressures including central
venous, right ventricular end-diastolic, left atrial, and left ventricular
end-diastolic pressures increase. Left and right ventricular stroke
volume increase according to the Starling mechanism by as much as
75–120 cc, with a resulting increase in cardiac output by 30–60%.
Blood pressure elevation then activates baroreceptors, which reduce
heart rate [10]. The interplay between the nervous and cardiovascular
systems in water is also exemplified by water induced skin wrinkling
(WISW). Several studies have shown a relation between the degree of
WISW and central autonomic function, which may have prognostic
value in cardiovascular health [11–13].
Muscle tissue is thought to be hyperperfused in water since oxy-
gen consumption is identical to land, yet cardiac output is increased

0167-5273/$ – see front matter. Published by Elsevier Ireland Ltd.

http://dx.doi.org/10.1016/j.ijcard.2013.03.063
20 J.M. Lazar et al. / International Journal of Cardiology 168 (2013) 19–26
[14]. In addition, the redistribution of volume that occurs with swim-
ming leads to an elevation of left and right atrial pressure. This stim-
ulates the release of atrial natriuretic peptide, which acts to increase
urine output and sodium excretion and leads to antidiuretic hormone
(ADH) inhibition, thereby reducing intravascular volume [15]. Differ-
ent forms of exercise have also been shown to affect the autonomic
nervous system differently. The lower levels of epinephrine, norepi-
nephrine and renin levels seen in swimmers is indicative of a blunted
sympathoadrenal response with high-intensity exercise [16,17]. A
comparison of resting plasma catecholamine levels and adrenergic
receptor density and responsiveness in swimmers, runners, weight
lifters, wrestlers, and untrained men demonstrated a lower resting
sympathetic activity in swimmers and runners [18]. Swimmers and
runners had lower baseline plasma norepinephrine levels, lower
norepinephrine/epinephrine ratios as well as lower beta receptor
density and increased alpha II receptor sensitivity (primarily in vas-
cular and skeletal tissue) as compared to the other groups when mea-
sured at rest. Swimmers were unique in that they had labile blood
pressure readings, due to reduced baroreceptor sensitivity. While
swimmers have demonstrated lower sympathetic activity and lower
catecholamine levels at rest, they have a different response with
activity. Guezennec et al showed that the volume shift induced by
the supine position and water pressure during swimming attenuated
the plasma renin activity response, although plasma catecholamine
levels were higher than in runners when measured with maximal
activity. Both runners and swimmers still demonstrated a lower cate-
cholamine surge when compared to untrained athletes [19]. These fac-
tors, coupled with nitric oxide release induced by external compression
from hydrostatic pressure, leads to a decrease in systemic vascular
resistance [20,21]. Evidence shows, however, that previous physical fit-
ness and skill level determines the extent of sympathoadrenal response,
with a reduced response seen in those who were more physically fit
[21]. Water immersion has also been shown to increase the amplitude
and duration of reflected aortic pressure waves using applanation
tonometry, indicating an increased left ventricular workload and oxy-
gen demand. These findings are likely due to increased venous return
and LV preload [22].
The energy requirements of swimming are related to translational
motion (drag forces) and horizontal motion (lift forces) [23–25]. Drag
forces increase exponentially and lift forces decrease as the speed of
swimming increases by the following relationship: Vmax = (Emax)
(e/D), where Vmax is the maximal attainable velocity and Emax is
maximal total energy production rate of the swimmer, e is mechanical
efficiency and D is the water resistance to overcome. These factors col-
lectively reduce the mechanical efficiency of front-crawl swimming,
which ranges between 5% and 9.5% [26]. Accordingly, the energy cost
of swimming a given distance is about four times greater than the cost
of running the same distance. Energy expenditure is also related to
other variables including individual skill, gender, and stroke. At any
given velocity, the energy requirement of an unskilled swimmer is
nearly twice as high as that of an elite swimmer [27]. Women swim a
given distance at 30% lower energy cost than men due to their higher
percentage and more peripheral distribution of body fat, which serve
to decrease lift forces required to stay afloat [26]. Therefore, women
swim faster at any given energy expenditure. The energy cost at any
given swimming speed is lowest for the front-crawl, followed by
back-stroke, butterfly and breast stroke [27].
Water poses thermal stress on the body, which has physiologic
effects and consequences on performance. In well-trained swimmers,
swimming speed, peak heart rate, and lactate production are directly
related to water temperature, with faster times, greater heart rates,
and higher lactate levels observed at warmer water temperatures
[28]. In addition, greater sympathetic tone leading to higher norepi-
nephrine levels and blood pressures were seen in healthy subjects
immersed in 20 °C water as compared to 32 °C [29,30]. The increase
in parasympathetic tone that is experienced with water immersion
is counteracted by increased sympathetic tone on entering cold water
[30]. Further, colder water temperatures are associated with greater
left ventricular end diastolic volumes, indicating increased preload in
lower temperatures, while higher temperatures are associated with
vasodilatation and decreased afterload [14]. This increased preload is
the likely result of increased peripheral vasoconstriction. Additionally,
the horizontal position of the swimmer provides for greater venous
return and is augmented by kicking of the legs. The aquatic environ-
ment also necessitates controlled breathing frequency, which varies
with stroke mechanics. Breathing frequency has been shown to affect
oxygen uptake and minute ventilation but not heart rate or lactate pro-
duction [31]. As compared to air, water poses greater resistive forces
and less gravitational forces to the moving athlete.
3. Cardiovascular responses and adaptations during swimming
Many studies have shown an 8–10% lower VO2max during swimming
as compared to other exercises [32,33]. This is likely caused by the
smaller size of the active muscle mass, which limits oxygen extraction,
and possibly related to previous findings that the supine position results
in a 15% decrease in VO2 relative to being erect [34]. O'Toole reported
VO2max in triathletes to be 13–18% less in tethered swimming, com-
pared to treadmill running values [35]. However, this has not been a
universal finding in other groups of subjects. While one study showed
recreational swimmers to average 19% lower VO2max during swimming
than treadmill exercise [36], another found trained swimmers to attain
higher VO2max during swimming than during running and cycling [37],
and a third study found sedentary subjects to attain similar VO2max dur-
ing swimming and cycling [38]. The results of these studies likely vary
because of differences in the following factors known to influence either
oxygen consumption or energy consumption, which are interrelated:
individual skill, speed, cardiac status, water temperature, and attire.
Previous studies have shown that at any given velocity, the oxygen
uptake of an unskilled swimmer is higher than for a trained swimmer
[27], and that there is a linear relationship between oxygen uptake
and swimming speed. The additional oxygen consumption of swimming
in cold water results primarily from the energy expended in shivering as
the body attempts to regulate core temperature. A swimmer's attire can
also affect oxygen consumption. In one study, oxygen uptake and minute
ventilation were lower during swimming with a wet suit as compared to
without [39]. Swim training has also been shown to improve perfor-
mance and physiologic adaptation to future exercise. Lieber et al showed
that both run and swim training increases subsequent treadmill VO2max
significantly and to the same extent [40]. This finding was in contrast to
previous studies, which showed smaller improvements in VO2max after
swim training. It was postulated that the differences in the results
[41,42]. Lieber et al exercised participants in the swim arm of the study
at 75% of the VO2max achieved on the treadmill, which is the may have
been due to a difference in the specificity of skeletal muscles trained,
and a lower cardiovascular training intensity among the swimmers
same as they did for participants in the running arm of the study. In
previous studies, swimmers were not exercised at the same maximal in-
tensity. Swimming was also found to improve bicycle exercise perfor-
mance with VO2max increasing by 16% in 12 sedentary middle-aged
persons [43]. Although there were no changes in ejection fraction or
end-systolic volume, there was an 18% increase in peak left ventricular
end-diastolic volume and an 8% rise in peak systolic blood pressure.
At any given oxygen consumption, cardiac output is about the same
in swimming as it is in running; however the maximum value is signif-
icantly lower for swimming. Cardiac output is probably not limiting for
performance since swimmers easily achieve higher values during run-
ning [27]. Despite similar cardiac output, stroke volume is greater and
heart rate is lower during swimming as compared to other aerobic
sports. Higher stroke volume is related to water immersion and supine
body position augmenting venous return and enhancing diastolic filling.
The peak heart rate achieved is approximately 10–15 beats/min lower
 J.M. Lazar et al. / International Journal of Cardiology 168 (2013) 19–26
in swimming than in running. DiCarlo has suggested a correction factor
for reducing the maximal heart rate obtained from treadmill exercise by
12 beats/min in order to obtain the predicted maximal heart rate of
swimming [44]. Mean arterial pressure tends to be higher during max-
imal swimming compared to running, possibly related to higher stroke
volume or as previously noted a greater catecholamine surge in swim-
mers [45]. The combination of higher mean arterial pressure with
higher stroke volume suggests the work of the heart is greater for swim-
ming than for other forms of exercise.
The changes in cardiac structure and function resultant from swim
training have been characterized by echocardiography. Colan com-
pared echocardiographic measurements of 11 swimmers to 22 con-
trols and found significantly higher values for Left Ventricular (LV)
end diastolic dimension (5.4 ± 0.5 cm vs. 4.8 ± 0.4 cm) and LV
mass (136 ± 35 g/m2 vs. 98 ± 26 g/m2) in swimmers [46]. Mea-
sures of LV systolic function including fractional shortening and frac-
tional wall thickening were also higher in swimmers. Increases in
echocardiographic parameters of LV diastolic filling, including peak
chamber enlargement and peak rate of dimension, were greater in
swimmers before, but not after, adjustment for increased ventricular
size and performance. Swan studied 31 master swimmers, age 30–
78 years, and also found a trend towards eccentric hypertrophy
[47]. Left ventricular dilatation was related to body size but not to
age. Similar results have been observed in children. Medved studied
72 children who swim trained for a mean 29 months and found sig-
nificant increases in left ventricular systolic and diastolic dimensions
and in left atrial diameter [48]. Therefore, it would appear that struc-
tural changes of the heart as a result of swimming are similar to run-
ning in which LV volume is increased without a significant change in
LV wall thickness. Swimming related eccentric hypertrophy likely
results from volume overload of the heart due to water immersion
and horizontal body position.
4. Swimming and risk factor modification
Risk factor modification is an essential part of the primary preven-
tion of Coronary Heart Disease (CHD), and for the treatment of those
patients with established disease. Aerobic exercise is recommended
by the World Health Organization and the Joint National Committee
for the Treatment of Hypertension [49,50]. However, the role of
swimming in blood pressure lowering has had inconsistent results
in studies to date. Tanaka et al found systolic blood pressure to
decrease from 150 mmHg to 144 mmHg in 18 sedentary men and
women after a 10-week swimming training program. However,
there were no changes in diastolic blood pressure [51]. Subsequent
studies demonstrated that swimming lowers blood pressure in
patients with moderate essential hypertension [52], and these results
were repeated recently in pre-hypertensive and stage 1 hypertensive
patients [53]. Other studies, however, did not demonstrate similar
improvements in BP. Cox et al showed in the Sedentary Women
Exercise Adherence Trial 2 (SWEAT 2) that there was an increase in
systolic and diastolic Blood Pressure (BP) in swimmers, relative to
walkers after a 6 month program, although there were improvements
in physical fitness as evidenced by improved swim distance and
walk time [54]. Of note, the women involved in this study were pre-
dominantly normotensive at baseline. These results were recently
repeated by Chen et al who showed that there was no significant
reduction in BP after a 1 year swim program. However, on further
breakdown of data, it was evident that there was ~17 mmHg reduction
of BP in hypertensive subjects, while normotensive subjects had
~6 mmHg increase in BP after training, resulting in no significant
change in BP once data was pooled [55]. The etiology for the rise in BP
in normotensive subjects is not clear, and may be related to low circu-
lating blood volume accentuated with swimming associated diuresis,
and subsequent stimulation of the Plasma Renin Activity (PRA) axis. Al-
ternatively, lower baroreceptor sensitivity has also been demonstrated
21
in swimmers, which can help to explain labile blood pressure readings
at rest [18]. Additionally, this rise in BP in normotensive subjects did
not bring them into the hypertensive category. The effect of swimming
on hypertensive patients, however, has consistently demonstrated a
benefit. Of note, as compared to subjects with normal blood pressure,
hypertensive subjects show lower cardiac output and stroke volume
but no difference in heart rate and oxygen consumption. This has
been demonstrated in other forms of exercise, but it is not known if
this is the case with swimming (Tables 1) [56].
All modalities of aerobic exercise, if performed regularly, possess the
potential to provide a negative energy balance making it a favorable
choice for successful weight reduction and management. Swimming,
with its greater energy cost and reduced musculoskeletal and thermoreg-
ulatory stresses provide a more appealing training modality particularly
among obese individuals. Despite this contention, the effectiveness of
swim training, compared with land based exercise; in promoting weight
loss remains contentious (Table 3). Prior training studies performed on
obese individuals have provided evidence to suggest that swimming
was a less effective training modality compared with land-based exercise
for weight loss and management [57–59]. Gwinup compared swimming
with walking and stationary cycling for 60 min per day over a 6 month
period of time. The data supported reductions in weight loss among the
walkers and cyclist (10–12% of their initial body weight) and a near
40 % reduction in subcutaneous fat over the upper arm. On the other
hand, the lap swimmers had a 5 lb weight gain and no change in
% body fat. It is interesting to note that there was a dose responsive rela-
tionship between weight change and time spent in exercise. There was
very little weight loss in any group (walkers or cyclists) until the duration
of exercise reached at least 30 min daily. Gappmaier and co-workers
reported similar reductions in body weight, percent fat loss and distribu-
tion among 3 groups of obese women performing a 13 week training pro-
gram on land (walking) and in water (swimming), at similar intensities,
durations and frequencies of training. Tanaka et al studied the effects of
a 10 week swim training program on body composition, lipid and lipo-
protein profile and carbohydrate metabolism and cardiovascular fitness
in Stage I and II hypertensive patients compared with controls. Their
data showed no significant changes in body weight, percent fat (36% vs.
35%), body mass index and regional fat distribution comparing the swim-
mers with controls. Neither group (training or control) showed signifi-
cant improvements in metabolic or lipoprotein profiles. The findings did
however demonstrate significant improvements in submaximal heart
rates, blood lactates and ratings of perceived exertion indicating an overall
improvement in cardiovascular fitness.
Contrary to the above studies, some have noted improvements in
weight control and management following swim training. Sideraviciute
et al reported a reduction in body mass following a 14-wk swimming
program in both healthy and Type I diabetic women [60]. Cox et al
noted a greater improvement in body weight, and fat distribution
(waist and hip circumference) following a 12 month moderate intensity
swimming program compared with walking, in sedentary older women
[61]. To date, studies have provided novel but contradictory information
regarding the efficacy of swimming as a training modality for successful
weight loss and management.
Modification of other risk factors important in the evolution of CHD
in relation to swimming continues to be studied. In patients with Coro-
nary Artery Disease, without depressed left ventricular systolic function
or active angina, water training exercises were shown to significantly
reduce cholesterol, triglycerides, and to increase exercise tolerance as
compared to controls. In addition, it was comparable to land exercises
such as running in risk factor modification [62]. Swimming results in a
significant increase in high density lipoprotein levels in swimmers par-
taking in intense activity, while the benefit was not seen to the same
extent in more moderate exercise (Table 2) [63]. More recent studies
have shown that swimming has a role in preventing loss in central artery
compliance, which is comparable to running in this regard [64]. Improve-
ments were seen in flow mediated dilation and cardiovagal baroreflex,
22 J.M. Lazar et al. / International Journal of Cardiology 168 (2013) 19–26
Table 1
Blood pressure change with swimming.
Study No. participants Length of intervention
Tanaka et al. 18 10 weeks
Nualnim et al. 43 12 weeks
Cox et al. (SWEAT-2) 116 6 months
Chen et al. 23 1 year
indicating improvement in vascular health in previously sedentary, older
adults. This indicates that swimming can be a useful adjunct for people
looking to prevent stiffening of arteries and hence adverse cardiac
outcomes. The SWEAT-2 trial further showed that swim training at
6 months reduced area under the curve (AUC) insulin levels, in older
sedentary women as compared to walking. Additionally, at 12 months
there was a reduction in low density lipoprotein (LDL) relative to walk-
ing [61]. As previously discussed, much of the benefit of swim training is
dependent on duration and intensity of exercise. Swimming resulted in a
significant increase in HDL levels in swimmers partaking in intense activ-
ity, while the benefit was not seen to the same extent in more moderate
exercise [63]. With more moderate exercise, duration of the activity
became more important [61]. Many of these studies work with small
sample sizes, and studies involving more subjects may help to further
elucidate the link between swimming and modifiable risk factors.
5. Swimming and heart disease
Few studies have specifically evaluated the risks and benefits of
swimming in patients with cardiovascular disease. While it has been
touted as an aerobic exercise that can be useful in the prevention of car-
diovascular risk factors, its use in patients with established cardiovascu-
lar disease has long been debated. Specifically, its growing use in cardiac
rehab programs in patients with coronary artery disease (CAD) and/or
congestive heart failure (CHF) is especially important to evaluate.
As previously described, the increase in parasympathetic tone and
decrease heart rate that occurs with water immersion, in theory, may
allow symptomatic patients to exercise longer. In addition, benefits to
swimming have been shown in patients with intermittent claudication,
limb amputation, and paralysis [65,66]. There have not been many stud-
ies comparing swimming to other forms of physical activity in relation
to Coronary Heart Disease (CHD). One of the first studies to make the
comparison, and to relate it to CHD mortality and non-fatal heart
attacks, showed that swimming did not result in decreased risk of CHD
(defined as fatal and non-fatal myocardial infarction (MI)). Running,
walking and weight training all did, however, result in a decreased
CHD risk. However, on closer examination, exposure to the activity was
a limiting factor as only 2% of the cohort examined spent more than
1 h/week swimming [67]. Other studies have demonstrated that swim-
ming may be a justifiable exercise in slight left heart damage, but may
lead to overexertion with increasing levels of left heart impairment [9].
As in other forms of aerobic exercise, the benefits are related to intensity
and frequency of work-outs. With the varied results, and unclear guide-
lines, a more in-depth analysis is needed.
Table 2
Cholesterol change with swimming.
Study Study length Cholesterol type Change in cholesterol
Tanaka et al 10 weeks Total, HDL, LDL NS
Volaklis et al 4 months Total, HDL, LDL −8.2, +2.8(NS), -6.8
Cox et al. 12 months Total, HDL, LDL +3.9, NS, +3.9
NS = Not significant.
Predominant type of HTN Systolic BP change (mm Hg) Significance (p value)
Stage I −6 b.05
Stage II
Pre-hypertensive −9 b.05
Stage I
Normotensive +4.4 b.008
Stage I (7) −17 b.05
Normotensive (16) +6
6. Swimming and coronary artery disease
There is evidence that water immersion may have different effects
in those with prior MI. In fact, cardiac responses to increased preload
resulting from hydrostatic pressures may be blunted in patients with
coronary artery disease. In 15 men with prior MI, water immersion
resulted in increased cardiac output and stroke volume as compared
to land. This is similar to responses seen in healthy swimmers. How-
ever, with exercise in water, no differences were found in heart rate,
cardiac output, and stroke volume between cycle ergometry on land
and the same exercise in water [68]. In addition, Heigenhauser et al
showed lower cardiac outputs and higher heart rates in post MI
patients with swimming as compared to cycling [38]. Subnormal
increases in cardiac output likely resulted from failure of stroke
volume to increase with an appropriate increase in heart rate. These
results support the earlier findings, which reported similar values
for VO2max and heart rate during swimming and cycling in 8 males
with prior MI [65]. These results may be due to a general loss of com-
pliance in myocardial tissue or full use of Frank-Starling reserve in
patients with prior MI.
Exercise has proven beneficial to the rehabilitation of cardiac
patients [69]. The specific use of swimming in cardiac rehabilitation in
patients with CAD is gaining increasing attention, though there have
been mixed results. Niebauer studied 23 patients with coronary disease
by bipolar Holter monitoring during swimming, jogging, and treadmill
testing [70]. Although there was no difference in heart rate at the
onset of angina in symptomatic patients during swimming and tread-
mill testing, the mean heart rate at the onset of ST segment depression
was significantly lower during swimming (110 ± 11 beats/min vs.
133 ± 23 beats/min, p b 0.002) than for treadmill exercise. These
results suggest a lower ischemic threshold for swimming as compared
to walking or running, with a similar pain threshold for angina. This
delayed sensation of ischemic symptoms is analogous to the lower per-
ception of exertion previously observed in subjects who swim. Other
studies have also shown a delayed sensation of angina during swim-
ming as compared to land exercise [65]. Further, it has been demon-
strated that swimming with holter monitoring can be useful in
detecting arrhythmias and ischemia in patients who had previous
normal stress testing [71]. Premature Ventricular Contractions (PVC’s)
as well as an acute rise in blood pressure were also observed in elderly
patients undergoing swim training [72]. These results have not been
universal. In comparing patients with CAD to those without, Hoffman
et al showed that the rate of ischemia and arrhythmias, including
PVCs, were higher during exercise training in CAD patients. The two
modes of exercise compared were swimming and sauna versus station-
ary leg cycle ergometry on land. While there was a 10% lower maximal
heart rate achieved during swimming as compared to leg cycle
ergometry, the rates of ischemia and/or PVCs tended to be lower during
the water exercises [73]. Swimming and other water exercises were
also well tolerated in warm and cold water (32 °C, 22 °C) in patients
with stable coronary artery disease. This study showed that the energy
consumption of the heart increased during swimming in warm and cold
water, as evidenced by significantly increased rate pressure product.
However, this energy demand was not accompanied by an increased
rate of arrhythmias [74]. While studies evaluating the use of swimming
 J.M. Lazar et al. / International Journal of Cardiology 168 (2013) 19–26 23

Table 3
Body Weight and body composition changes with swimming.

Study Exercise program Length of intervention Population studied sample size Body weight (lb) Body composition (%)

Gwinup Swimming 6 monts 3 groups moderately obese females N = 29 randomized Walk ↓12% IBW Upper arm circumference
temp: (23–25 °C) Exercise only Cycling ↓10%IBW Walk ↓ 13 mm
cycling or P b 0.001 Cycle ↓13 mm
walking Swim NC p b 0.001
Swim NC
Tanaka et al. Swimming 10 weeks Stage I and II hypertensive males and females N = 18 Training p NC Training NC
temp 27–28 °C Exercise only Control NC Control NC
P b 0.05 P b 0.05
Gappmaier et al. (SW) Temp27 °C 13 weeks 3 groups obese females N = 38 randomized All groups All groups
(WL) Dietary monitoring ↓ 5.9 kg ↓ 3.7%
(WW) Temp 29 °C p b 0.001 p b 0.001
Sideraviciute et al. Swimming 14 weeks 28 healthy Vs. 19 Type I diabetic females Healthy NC Healthy ↓ 1.7%
temp not reported Exercise only Type I Diabetic NC Diabetic ↓2.7%
p b 0.001
Cox et al. (SWEAT-2) Swimming 12 months Sedentary females N = 116 randomized Swim ↓2.3 Swim WC ↓2.3 cm
temp 26.5 °C Exercise only p = 0.039 P = 0.023
walking Walk NC HC ↓ 0.6 cm
P = 0.042
Walk NC

IBW = Initial Body Weight, NC = no change, WC Waist Circumference (cm), HC Hip Circumference (cm), SW (swimming), WL (walking on land), WW (Walking in Water).

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 significant-
ly 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 an MI in rats. Data did not show a mortality
or remodeling benefit or harm after a small infarction. However, swim-
ming was actually shown to cause harm in rats that had a large infarc-
tion area. The harm was caused whether the swimming was initiated
early or late after an MI, but more profound in exercise regimens initiat-
ed early after an MI. Death was 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 differ-
ences in species, and due to difficulty in standardizing the extent of
infarct and intensity of exercise. However, results indicate that swim-
ming 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 decompensa-
tion. 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 dys-
kinesia and overload with water immersion. Of note, patients did not ex-
hibit 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 com-
pared 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 exer-
cises; 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 CAD with pre-
served 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 [81].
Water temperature may also play a role in how well water exercises
are tolerated [82]. Warm water immersion resulted in an increase in car-
diac output, decrease in heart rate and a general improvement in systolic
and diastolic dysfunction in patients with heart failure (average LVEF
of 31%) [83]. While cardiac index was shown to increase appropriately
in moderately cold water (22 °C), there was a significant increase in
the number of PVC’s as compared to warm water (32 °C) in patients
with heart failure [74]. The benefit of warm water exercises may be
due in part to afterload reduction resulting from the peripheral vasodila-
tation caused by the higher temperatures.
24 J.M. Lazar et al. / International Journal of Cardiology 168 (2013) 19–26
Aside from increases in cardiac index, there is evidence that there
may be an enhancement in endothelial function in patients with
heart failure. Water based exercising was shown to cause a significant
increase in plasma levels of nitrates in patients with stable heart fail-
ure or coronary artery disease [84]. Still some rehabilitation programs
are hesitant to prescribe water-based exercises such as swimming for
patients with stable heart failure. Nevertheless, cardiac rehabilitation
has been proven to be beneficial in patients with heart failure and
specific exercise prescriptions may be needed to monitor heart rate
and symptoms as in other forms of exercise [85].
8. Swimming and long QT syndrome (LQTS)
As mentioned earlier, long-QT syndrome (LQTS) is a well docu-
mented, rare cause of death in any age group characterized by prolonged
ventricular repolarization. However, swimming has been particularly
implicated as a trigger for syncopal episodes and near-drowning, mostly
in children [86,87]. Cases of drowning victims with a personal or family
history of LQTS were reviewed and revealed that there may be a gene
specific arrhythmogenic trigger for LQTS. The gene KVLQT1, was particu-
larly implicated as the genetic source of unexplained drowning deaths
[88]. Subsequent studies confirmed KVLQT1 as the gene responsible for
more than two-thirds of unexplained drowning deaths, particularly if
the clinical suspicion for LQTS is high. However, in cases where there
was no evidence of LQTS, other genes have been found, most notably
CPVT1 [89]. Both genes are characterized by greater catecholamine
release with specific triggers. Prevailing thought is that the exertion,
voluntary apnea, face immersion and possibly cold water temperature
cause activation of the sympathetic and parasympathetic nervous sys-
tems through the activation of the ‘dive reflex’. This coupled with fear
can cause increased amounts of PVCs [90]. Further, face immersion in
cold water has been shown to lengthen the QT interval, and to trigger
bradycardic responses, which have been associated with cardiac events
in LQTS [91]. With this known relationship between swimming and
LQTS, it is important to identify those patients most at risk. For one, it
has been shown that non-compliance with medications, most notably
beta-blockers, which have proven benefit in this group, leads to an
increase chance of a repeat cardiac event in a patient with a history of
a cardiac event. In addition, younger age at diagnosis of LQTS placed a
patient at increased risk of a subsequent cardiac event [92]. Other coun-
tries such as Japan have experimented with screening programs to iden-
tify children in grade school with prolonged QT intervals. However, this
remains controversial because most children with no past medical histo-
ry and with isolated prolonged QT time will not have a cardiac event.
Further, the LQTS score [93], which factors in EKG findings, along with
clinical and family history, has predictive value in determining those
patients who have a low-likelihood of a cardiac event if they have not
had one in the past. Even with the predictive value of the LQTS score,
and the benefit of medication compliance, most physicians would rec-
ommend that swimming be avoided in patients with documented
LQTS [94].
9. Swimming on the cellular level
The effect of swim training on modifiable risk factors and cardiac func-
tion has been studied on a cellular level. Most molecular studies have
been done in mice and rat models to date. Studies have evaluated the
effect of swim training on the expression of peroxisome proliferator-
activated receptor (PPAR-γ) and carnitine palmitoy1 transferase-1
(CPT-I) [95]. The expression of these molecules has been found to
be increased in all muscles including cardiac muscle, after swim
training in mice. Specifically, PPAR-γ and PPAR-α in cardiac muscle
has been shown to have anti-inflammatory and anti-atherosclerotic
properties [96]. Obesity and lipid disorders in mice have also been
shown to be ameliorated with swim training through increased levels
of mRNAs and proteins encoding uncoupling protein 1 (UCP1), UCP2
and UCP3 in brown adipose tissue, white adipose tissue and skeletal
muscle. These uncoupling proteins may have a role in preventing build-
up of adipose tissue and production of lipids [97]. Zhang et al showed
that swim training in mice had beneficial effects on the heart's contrac-
tile function and response to insulin. This was accomplished primarily
by facilitation of insulin stimulated glucose uptake in cardiac muscle.
The molecular basis of this relied on the increased translocation of
Glucose transporter type 4 (GLUT4). They also noted an upregulation
in protein kinase (akt) and endothelial nitric oxide synthase (eNOS)
phosphorylation in the exercised group. This significantly increased
insulin induced cardiac nitric oxide production [98]. Other rat studies
have shown that swim training may have a role in preventing acute
cardiac events by promoting plaque stability as demonstrated by de-
creased macrophage and increased smooth muscle content [99]. Under-
standing the molecular basis of swim training's beneficial effect on
protein regulation, glucose metabolism and cardiac muscle function
may help to target specific training to patients with heart disease.
10. Summary
In summary, swimming is a popular sport worldwide amongst peo-
ple of all ages. Its popularity primarily rests in its low impact nature,
which makes it an attractive option for patients with joint diseases,
who cannot tolerate land exercises. As compared to other forms of aer-
obic exercise, swimmers attain lower VO2max, associated with lower
arterio-venous oxygen differences, and similar cardiac output charac-
terized by lower heart rate, and greater stroke volume. Left ventricular
dilatation, normal wall thickness to dimension ratio, and increased
stroke volume with normal diastolic filling characterize the cardiac
adaptations to swim training. The evidence is emerging to suggest
that swimming is comparable to land exercises in its effect on cardio-
vascular risk factors, most notably blood pressure reduction. In addition,
its use in cardiac rehabilitation programs, particularly in patients with
stable CAD and CHF, appears to be well tolerated. Controlled pool con-
ditions, particularly with warmer temperatures appear to be important.
As in all forms of exercise, activity in moderation and under the super-
vision of healthcare providers is advised in this population. In addition,
exercise prescriptions with specific attention to heart rate monitoring
may be needed given the evidence of a possible asymptomatic, lower
ischemic threshold for these patients. Lastly, in patients with a history
of LQTS, particularly if there is genetic verification, swimming should
be avoided because of the increased risk of a cardiac event.
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