Sports Med 2009; 39 (5): 377-387

REVIEW ARTICLE 0112-1642/09/0005-0377/$49.95/0

ª 2009 Adis Data Information BV. All rights reserved.

Swimming Exercise
Impact of Aquatic Exercise on Cardiovascular Health
Hirofumi Tanaka
Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, Texas, USA

Contents
Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 377
1. Benefits and Popularity of Swimming. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 378
2. Lack of Swimming Research . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 379
3. Swimming and Coronary Heart Disease Risk Factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 379
3.1 Maximal Aerobic Capacity. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 379
3.2 Arterial Blood Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 380
3.3 Blood Lipids and Lipoproteins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 381
3.4 Carbohydrate Metabolism and Insulin Sensitivity. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 382
3.5 Bodyweight and Body Composition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 383
4. Swimming and Mortality . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 384
5. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 384

Abstract Swimming is an exercise modality that is highly suitable for health

promotion and disease prevention, and is one of the most popular, most
practiced and most recommended forms of physical activity. Yet little in-
formation is available concerning the influence of regular swimming on cor-
onary heart disease (CHD). Exercise recommendations involving swimming
have been generated primarily from unjustified extrapolation of the data
from other modes of exercise (e.g. walking and cycling). Available evidence
indicates that, similarly to other physically active adults, the CHD risk profile
is more favourable in swimmers than in sedentary counterparts and that swim
training results in the lowering of some CHD risk factors. However, the
beneficial impact of regular swimming may be smaller than land-based ex-
ercises. In some cases, regular swimming does not appear to confer beneficial
effects on some CHD risk factors. Moreover, swimming has not been asso-
ciated with the reduced risks of developing CHD. Thus, extrapolation of
research findings using land-based exercises into swimming cannot be justi-
fied, based on the available research. Clearly, more research is required to
properly assess the effects of regular swimming on CHD risks in humans.

A number of epidemiological studies have of proper exercise programmes, a variety of na-

demonstrated the benefits of regular physical tional and international health and exercise orga-
activity for the prevention of cardiovascular dis- nizations have published a number of exercise
ease.[1-3] In order to facilitate the implementation guidelines.[3-7] According to these guidelines,
378
any activity that uses large muscle groups,
can be maintained continuously, and is rhythmi-
cal and aerobic in nature is recommended as
the modality of physical activity. Swimming
fits perfectly with the recommended exercise
modality description. Indeed, swimming is al-
ways included as a form of regular aerobic
exercise that is recommended for health promo-
tion as well as prevention and treatment of risk
factors for cardiovascular disease in men and
women.[4-8] However, there is little scientific
evidence to date indicating that swimming is
equally efficacious to land-based exercise modes
(e.g. walking and cycling) in reducing cardiovas-
cular risks. Regular swimming has been widely
promoted and prescribed without the under-
pinning of firm scientific support from clinical
studies. These recommendations have been gen-
erated primarily from unjustified extrapolation
of the data from other modes of exercise. This is
unfortunate, because the public expects that the
authoritative advice from medical and scientific
bodies is supported and justified by scientific
studies.
In this review, using the limited research stu-
dies conducted in swimming or swimmers, we
address general questions such as whether swim-
mers who train just as hard, as long and as fre-
quently as other athletes in land-based exercise
modes demonstrate the same favourable risk
profiles for coronary heart disease (CHD), and
whether swimming training interventions re-
duce risk factors for CHD. It should be noted
that swimming is a popular mode of physical
activity to determine the effects of exercise in
rodents, and a number of research studies have
been conducted using rodents.[9-11] However,
swimming in rodents may not be directly applic-
able to humans, because swimming rats spend
more than 50% of the time being submerged and
exhibit signs of hypoxia, hypercapnia, acidosis
and an exaggerated diving reflex.[12] For this
reason, the primary focus is placed on human
studies, and only a few animal studies are in-
cluded in this review. Additionally, because
human studies focusing on swimming and cardio-
vascular health are very limited, studies using
a wide variety of participants of different ages,
ª 2009 Adis Data Information BV. All rights reserved.
Tanaka
sex and health states are compiled and presented
together in this review.
1. Benefits and Popularity of Swimming
Swimming is an attractive form of exercise, as
it is easily accessible, inexpensive and isotonic.
Because it does not involve bearing of body-
weight, due to the buoyancy of water, compres-
sive joint forces are lower and, as a consequence,
adverse impact on the musculoskeletal system as
well as injuries are rare.[13,14] Indeed, the in-
cidence of orthopaedic injury among swimmers is
substantially lower than in runners or cyclists.[14]
Moreover, because of colder temperature as well
as increased thermoconductivity of water, the
incidence of heat-related illness is small.[15] As
such, it is an ideal form of exercise for obese pa-
tients, the elderly and patients with arthritis.
However, surprisingly little is known about the
effects of regular swimming for health promotion
and disease prevention.
In contrast to the public perception that
swimming is a ‘minor’ form of exercise, it is one
of the most popular and most practiced forms
of physical activity.[16-21] In the US and most
industrialized countries, swimming is the second
most popular dynamic exercise modality, second
only to walking.[16-21] According to the US cen-
sus, approximately 20% of the US population
performed swimming in a year, whereas about
33% did walking.[21] Among overweight and
pregnant women, swimming is the most preferred
type of physical activity.[22] Swimming is parti-
cularly popular in the Southern states, where the
climate is more suitable for swimming. As one of
the moderate-sized metropolitan cities in the
South of the US, the city of Austin, Texas, has
27 neighbourhood pools, 12 wading pools and six
municipal pools. Additionally, many residents
have swimming pools at their homes. Indeed, an
estimated 8.6 million swimming pools are in
public or residential use in the US.[23] Use of
swimming as an exercise therapy will have en-
ormous public health implications as more older
adults, who exhibit elevated risks of developing
CHD, migrate to warmer climates, where the
prevalence of obesity is highest.
Sports Med 2009; 39 (5)
Swimming Exercise and Cardiovascular Risk Factors
2. Lack of Swimming Research
In spite of the widespread popularity of
swimming,[16-21] research focusing on swimming
and cardiovascular disease is heavily under-
pursued. The relative lack of swimming research
can be attributed to a number of factors. Firstly,
it is difficult to make physiological measurements
in the water. This makes the constant monitoring
of subjects/patients difficult during swimming
exercises. Secondly, unlike walking or cycling,
swimming requires skills and techniques in order
to achieve a proper exercise intensity, and many
at-risk populations may not be able to exercise
at such a prescribed exercise intensity. From an
experimental standpoint, this would necessitate
an initial training or skill acquisition phase to
introduce naive sedentary subjects into a swim-
ming training programme, resulting in a longer
study period and greater study expense. Thirdly,
swimming had been discouraged or cautiously
prescribed to patient populations in the past
because of potential concerns associated with
excess demands placed on the cardiovascular
system.[24-26] For example, because immersion in
cold water produces central volume expansion[27]
as well as pressor responses,[24,25] it was thought
that these haemodynamic changes would place
extra stress on the limited cardiovascular re-
serves of cardiac patients. However, a number
of studies have demonstrated that swimming can
be performed as safely as other exercise modes,
including walking and cycling, as there are
no differences in exercise-induced angina, ST-
segment changes or arrhythmias between land-
based exercise (e.g. walking and cycling) and
water-based exercise (e.g. swimming), even in
patients with cardiovascular disease.[28-31]
3. Swimming and Coronary Heart Disease
Risk Factors
The concept of risk factors for cardiovascular
disease was originally introduced by the Fra-
mingham Heart Study and now serves as the
cornerstone of the prevention of CHD.[32] Reg-
ular land-based physical activity (e.g. walking
and running) has well established benefits for
ª 2009 Adis Data Information BV. All rights reserved.
379
reducing the risk of CHD and stroke, and is the
first-line approach for preventing and treating
various CHD risk factors.[3-5] Does water-based
exercise (i.e. swimming) confer similar cardio-
vascular benefits as land-based physical activity?
In this section, we review and evaluate the past
research, including our own,[33-40] conducted in
the area of regular swimming and key risk factors
for CHD. The established CHD risk factors we
address are maximal aerobic capacity, arterial
blood pressure, blood lipids and lipoproteins,
carbohydrate metabolism and insulin sensitivity,
and bodyweight and fatness. Information derived
from both cross-sectional and interventional
studies is presented to provide more comprehen-
sive views on this topic.
3.1 Maximal Aerobic Capacity
Maximal aerobic capacity is widely known as
a primary factor in predicting endurance exercise
performance and is an important indicator of
physiological functional capacity.[41,42] It is also
established that reduced maximal aerobic capa-
city, as estimated by either maximal oxygen con-
.
sumption (VO2max) or the time to exhaustion in
graded treadmill exercise tests, is an independent
risk factor for cardiovascular and all-cause mor-
tality.[43,44] Moreover, lower maximal values are
associated with increased risks for disability[45]
and reductions in cognitive function[46] and
quality of life.[45] A greater maximal aerobic ca-
pacity is the hallmark of endurance-trained ath-
letes, including runners and cyclists.[42,47] Even
though most swimming events last <2 minutes,
the routine training regimen that most swimmers
engage in is considered aerobic endurance train-
ing in nature. Indeed, similar to runners and
cyclists,
. trained swimmers possess greater swim-
ming VO2max values and high activities of oxida-
tive enzymes in their skeletal muscles.[48-50]
An important question is whether swimmers
exhibit greater maximal aerobic capacity as as-
sessed by conventional measures of maximal
oxygen consumption. When evaluated on a tread-
mill, swimmers exhibit either similar or slightly
higher maximal oxygen consumption compared
with sedentary controls.[38,50,51] For example, in a
Sports Med 2009; 39 (5)
380
study of monozygotic female twins, the. swim-
trained twin attained a 49% higher swim VO2max
than her sedentary twin sister, whereas there
. was
no difference between the twins when VO2max
was measured during treadmill running.[52] Inter-
ventional studies are consistent with these cross-
sectional comparisons. A 9-month programme
of intense swim training. produced a significant
increase
. in swimming VO2max, while running
VO2max was unchanged.[53] Similarly, interval
swim training
. has failed to elicit improvements in
treadmill VO2max and time to exhaustion on a
treadmill.[54] Even in postmenopausal women in
which the .effect of aging is superimposed, the
treadmill VO2max of swimmers is >20% lower
than that of runners, although its value was
significantly greater than their sedentary peers
(figure 1).[38,55] Obviously,
. a lack of transfer in
the training effects on VO2max between swimming
(performed in prone or supine posture in the
water) and running (performed in upright pos-
ture on land) is attributed to the principles
of specificity of training and has been reviewed in
detail elsewhere.[40] Thus, the available evidence
indicates that the effects of regular swimming
do not appear to manifest in the conventional
measures of maximal aerobic capacity that have
been associated with reduced risk of CHD.[43,44]
Currently, it is not known whether having a
p < 0.0001
50
p < 0.001
40
VO2max (mL/kg/min)
30
30.7
20
23.2
.
10
0
Controls Swimmers
. changes in blood pressure were observed in the
Fig. 1. Maximal oxygen consumption (VO2max) of postmenopausal
runners, swimmers and sedentary controls (reproduced from Parker
Jones et al.,[38] with permission from Wiley-Blackwell).
ª 2009 Adis Data Information BV. All rights reserved.
Tanaka
.
high VO2max in swimming is cardioprotective.
However, as described below, an epidemiological
study suggests otherwise.[56]
3.2 Arterial Blood Pressure
Hypertension poses a major public health pro-
blem as the most prevalent vascular disease. Be-
cause of the side effects and cost of hypertensive
drugs, non-pharmacological treatment, including
regular exercise, is the first-line approach uni-
versally recommended for hypertension.[4,6,57]
Land-based exercise training in patients with essen-
tial hypertension decreases blood pressure signifi-
cantly, with systolic and diastolic blood pressure
reductions averaging 11 and 8 mmHg, respec-
tively.[4,58-60] Exercise training performed with cy-
cling and walking appears to produce a similar
magnitude of hypotensive effects.[61] To the best of
our knowledge, there has been no direct compar-
ison of swim training and other exercise modes on
the efficacy for lowering blood pressure in patients
with hypertension. Moreover, very few studies
have been conducted to evaluate the potential hypo-
tensive effects of regular swimming.
Arterial blood pressure is known to increase
during exercise. Compared with that during
walking/jogging, average arterial blood pressure
tends to be greater during swimming at the same
heart rate values.[62] Cross-sectional comparisons
indicate that swimmers tend to have chronically
higher blood pressure at rest than other en-
durance athletes.[63-65] Moreover, a recent inter-
vention study, in which previously sedentary
p < 0.001
normotensive older women were randomized
into either a 6-month walking or swimming
training programme, suggests that swimming
may bring unfavourable, rather than beneficial,
39.5 effects on blood pressure.[66] In the first study to
date to evaluate the relative efficacy of swimming
and walking exercise on blood pressure, these
investigators found small but significant in-
creases (rather than decreases) in both systolic
and diastolic blood pressure (»D4 and D2 mmHg)
Runners after 6 months of swim training, whereas no
walking training group. These observations are
certainly surprising, but the interpretation of
Sports Med 2009; 39 (5)
Swimming Exercise and Cardiovascular Risk Factors
their data is difficult because of several metho-
dological issues. In this study, average blood
pressure values at the start of the interventions
were 116/67 mmHg (completely ‘normal’ blood
pressure). The beneficial effects of regular ex-
ercise on blood pressure are more likely to be
manifested in human populations with elevated
blood pressure. These low baseline blood pres-
sure values may also explain why the researchers
did not observe any hypotensive effects of walk-
ing training that have been previously reported in
the literature.[4,58,67-70] It is understandable that a
non-exercising sedentary control group (i.e. time
control) was not included, because the stated aim
was to compare the effects of swimming and
walking on blood pressure. However, a lack of a
time control group makes it difficult to determine
whether the increase in blood pressure observed
in the swimming training group was due to
spontaneous changes in blood pressure. Taken
together, these previous studies cast some doubts
on the exercise recommendations/guidelines pro-
moting regular swimming as an exercise modality
of choice.
Current exercise recommendations to include
swimming for lowering blood pressure are based
primarily on the results of a small-scale study in
which 12 adults with essential hypertension un-
derwent a 10-week swim training programme.[34]
We found that swim training produced a sig-
nificant reduction in systolic blood pressure
whereas no significant changes in blood pressure
were observed in the sedentary control group
(figure 2).[34] However, the relative magnitude of
the blood pressure reduction observed after swim
training was slightly smaller than that typically
reported for land-based physical activity. Studies
using equivalent training programmes (of similar
intensity, frequency and duration) but employing
walking/jogging and cycling, reported 11 and
8 mmHg reductions in resting systolic and dia-
stolic blood pressures, respectively.[4,58-60] The
reductions in systolic and diastolic blood pres-
sures observed in the swim training study aver-
aged 7 and 3 mmHg, respectively.[34] Clearly,
more studies are needed to answer the questions
regarding the hypotensive effects of swimming
exercise in patients with hypertension.
ª 2009 Adis Data Information BV. All rights reserved.
381
160
150 *
Systolic BP (mmHg)
140
130
120
Before After
Swim training
Fig. 2. Reductions in arterial blood pressure (BP) after swim train-
ing intervention in patients with essential hypertension.[34] * p < 0.05
vs before swim training (reproduced with permission from
Lippincott Williams & Wilkins).
3.3 Blood Lipids and Lipoproteins
Dyslipidaemia has long been acknowledged as
a major risk factor in the development of athero-
sclerosis and CHD.[32] The effects of regular exer-
cise on lipoprotein metabolism have been widely
studied, and a number of indepth narrative re-
views and meta-analyses have been published.[71]
These studies conclude that the most consistent
findings associated with exercise training are an
increase in high-density lipoprotein cholesterol
(HDL-C) and a decrease in triglyceride con-
centrations.[71] Unfortunately, swim training stu-
dies have not been included in these analyses, due
primarily to a lack of well controlled studies in
this area. Yet swimming is specifically mentioned
as a recommended form of physical activity when
the exercise guidelines for dyslipidaemia are pro-
mulgated. In most cases, similar to other CHD
risk factors, findings of land-based exercise stu-
dies are unjustifiably extrapolated to swimming.
Does the available evidence conducted in this area
support such a notion?
Considering that an acute (single) bout of
swimming exercise elevates HDL-C levels follow-
ing exercise,[72] it is reasonable to hypothesize
that regular (repeated bouts of) swimming would
chronically increase HDL-C concentrations si-
milar to other land-based exercise modes.[71]
Sports Med 2009; 39 (5)
382
Most of the information available in this area
comes from cross-sectional comparisons of swim-
mers with sedentary controls and other athletic
populations. In studies involving age-group
swimmers and collegiate swimmers, HDL-C
levels were similar or somewhat lower than their
age-matched sedentary counterparts.[73-75] In
healthy postmenopausal women, we also de-
monstrated that HDL-C of swimmers was not
different from their sedentary counterparts.[35]
Longitudinal or interventional studies are
consistent with these cross-sectional findings. In a
season-long follow-up study, in which male col-
legiate swimmers were followed for 25 weeks,
mean levels of HDL-C remained stable through-
out the season in spite of significant changes in
swim training volume.[73] We have also reported
that a short-term supervised swim training did
not result in significant increases in HDL-C
concentrations in previously sedentary, obese
middle-aged adults.[33] Thus, the available evi-
dence is not consistent with the idea that regular
swimming is associated with favourable levels
of HDL-C.
An interesting collective observation from the
cross-sectional studies is that middle-aged and
older swimmers demonstrate lower total choles-
terol as well as low-density lipoprotein cholesterol
(LDL-C) values than their sedentary counter-
parts, and in some cases the values are even lower
than the age-matched runners.[35,76,77] The lower
total cholesterol and LDL-C concentrations are
not typically observed in land-based exercise-
trained athletes and appear to be unique to
swimmers. These cross-sectional studies need to
be confirmed with a randomized, controlled, in-
terventional study, but our short-term swim
training study exhibited a trend for total choles-
terol and LDL-C to decrease by »10% following
the training in obese hypertensive subjects.[33]
3.4 Carbohydrate Metabolism and Insulin
Sensitivity
Patients with diabetes mellitus exhibit mark-
edly increased risks of developing all forms of
cardiovascular disorders affecting the heart,
brain and peripheral tissues. The underlying
ª 2009 Adis Data Information BV. All rights reserved.
Tanaka
metabolic impairments in type 2 diabetes are at-
tributed to defects in insulin-mediated glucose
disposal (insulin resistance) and impaired secre-
tion of insulin by pancreatic b cells. Insulin
resistance typically precedes the onset of type 2
diabetes and is also a hallmark in the metabolic
syndrome, which involves abdominal obesity,
dyslipidaemia and hypertension. It has become
increasingly recognized that the increasing pre-
valence of obesity and a sedentary lifestyle
(or inactivity) are two key contributors to the
rising epidemic of type 2 diabetes.[78]
In epidemiological studies, the amount of
daily aerobic exercise (primarily walking) is sig-
nificantly and inversely associated with the
risk/incidence of type 2 diabetes.[78,79] Likewise,
intervention studies have demonstrated that ex-
ercise training, incorporating walking and jog-
ging can normalize glucose tolerance by reducing
insulin resistance in patients with type 2 dia-
betes.[80] As many diabetic patients are obese,
swimming may be an ideal form of exercise for
these patients. However, surprisingly few studies
are available to evaluate the impact of regular
swimming on glycaemic control in humans.
We have previously demonstrated that the
fasting plasma concentration of insulin was lower
and insulin sensitivity, as determined from a fre-
quently sampled intravenous glucose tolerance
test and Bergman’s minimal model, was greater
in postmenopausal swimmers compared with
their age-matched sedentary controls (figure 3).[35]
The level of insulin sensitivity achieved by the
swimmers was not different from the runners, who
were matched for age, training volume and exercise
performance levels.[35] Interestingly, the high level
of insulin sensitivity was achieved in swimmers
even though swimmers had significantly higher
bodyweight and body fatness than runners.
In an exercise training intervention study in-
volving young girls with type 1 diabetes, 14 weeks
of swimming twice a week produced a significant
reduction in the concentration of haemoglobin
A1c, an indicator of average glucose load over
the past several months.[81] Similarly, a long-term
(2 years) exercise programme incorporating
swimming resulted in a significant reduction in
glycosylated haemoglobin in middle-aged women
Sports Med 2009; 39 (5)
Swimming Exercise and Cardiovascular Risk Factors
10
Insulin sensitivity (×10−4 min/μU/mL)
8 mass index values (27–30 kg/m2).[88,89] Although a
* higher body fat percentage may be a requisite
6
4 endurance athletes, who spend a considerable
2 ities, is certainly surprising. Higher body fat in
0
Sedentary Swimmers
Fig. 3. Insulin sensitivity of postmenopausal runners, swimmers
and sedentary controls.[35] * p < 0.05 vs sedentary controls (repro-
duced with permission from Elsevier).
with type 2 diabetes, although the number of
subjects was very small (n = 5).[82] Unfortunately,
in both of these studies a time-control group was
not included and their measurement stability over
the training intervention period was not estab-
lished. Nevertheless, the available evidence is
consistent with the notion that regular swimming
is associated with better glycaemic control.
3.5 Bodyweight and Body Composition
Until recently, the association between obesity
and CHD was viewed as indirect through common
covariates such as diabetes. Longitudinal studies,
however, demonstrated that obesity is an indepen-
dent predictor of CHD.[83] In general, increased
physical activity, more specifically aerobic (end-
urance) exercises, is associated with maintenance
of healthy levels of bodyweight and adiposity.[84]
As described above, the daily training routine
that swimmers perform is considered to be aerobic
endurance training in nature. Given this, trained
swimmers should exhibit low body fat levels simi-
lar to runners and cyclists. However, competitive
swimmers tend to have higher body fat values
compared with other endurance athletes[35,85,86]
(although their values are lower than their seden-
tary peers[87]). This trend is more pronounced when
ultra-endurance athletes in both running and
swimming are compared.[88] In marked contrast to
very low adiposity values frequently reported in
ª 2009 Adis Data Information BV. All rights reserved.
383
ultra-endurance runners, ultra-endurance (chan-
*
nel) swimmers exhibit substantially higher body
phenotype for success in swimming the English
channel in cold water, as fat storage serves as in-
sulation,[89] observing such high adiposity in ultra-
amount of time in high energy-expending activ-
swimmers may be an adaptive response to daily
swimming routine, as a greater amount of body fat
Runners acts to enhance buoyancy and economy during
distance swimming.
At present, few studies have addressed the
effects of swimming exercise intervention on
bodyweight and body fat. A randomized, con-
trolled study has reported that with 6 months of
exercise intervention, young and middle-aged
obese women who were assigned to walking or
cycling lost »10% of initial bodyweight whereas
those assigned to swimming experienced no
change in bodyweight.[90] Although this is the
only randomized, controlled study to address the
relative efficacy of swimming to reduce body fat
in obese subjects, exercise stimuli were not mon-
itored and it is not clear how much swimming was
performed by the subjects. However, the results
of this study are consistent with a short-term
swim intervention study showing that a closely
supervised swimming programme did not result
in a loss of bodyweight or body fat.[33] Ad-
ditionally, a long-term study of swimming for
40 minutes a day three times a week for 2 years in
middle-aged men also failed to demonstrate
changes in bodyweight.[91] A recent epidemiolo-
gical study has assessed how type/mode of regular
physical activity, including swimming, is asso-
ciated with weight gain attenuation over a
10-year period.[92] Although jogging, aerobic
dancing and cycling were associated with the at-
tenuation of age-related weight gain, swimming
did not exert such effects.[92] Taken together, the
available evidence indicates that long-term
swimming may not be effective in reducing or
maintaining bodyweight and body fatness.
It is not clear why regular swimming is not as-
sociated with bodyweight or body fat reduction.
Sports Med 2009; 39 (5)
384
65 p = 0.001
Resting metabolic rate (cal /h)
60
55
50
45
40
35
30
Premenopausal Postmenopausal
sedentary sedentary
Fig. 4. Resting metabolic rates of premenopausal and postmenopausal female runners and swimmers and sedentary women[39] (reproduced
with permission from the Endocrine Society). NS = not significant.
Theoretically, an increase in physical activity will
increase total energy expenditure, thereby creat-
ing an overall negative energy balance if there is
no compensation from increased caloric intake.
Bodyweight and fat mass should, in turn, de-
crease in the long term. A study using doubly
labelled water confirmed that the energy ex-
penditure of swimmers is similar or even greater
than other endurance athletes.[93] Additionally,
swimmers demonstrate a similar level of baseline
metabolic rate as runners (figure 4).[39] A current
hypothesis is that exercise in cold water somehow
stimulates appetite, thereby increasing energy
intake in swimmers. In a randomized, crossover
study design, young men exercised on a sub-
merged cycle ergometer in 33C (neutral) and
20C (cold) water.[94] Although the energy ex-
penditure between the two exercise conditions
was kept at the same level, energy intake after
exercise in cold water was 44% greater than that
in neutral water.[94] In this context, it is interest-
ing to note that swim-trained rats consume a
greater amount of calories compared with run-
trained rats,[10,11] and that energy intake of swim-
trained rats increases as a function of decreasing
water temperature in which rats exercised.[10]
4. Swimming and Mortality
A number of epidemiological studies have re-
ported that regular physical activity is associated
with reduced risks of cardiovascular and all-
ª 2009 Adis Data Information BV. All rights reserved.
Tanaka
NS NS
65 65
60 60
55 55
50 50
45 45
40 40
35 35
30 30
Premenopausal Postmenopausal Postmenopausal Postmenopausal
runners runners runners swimmers
cause mortality.[1,2,7] The primary modes of
physical activity that have been addressed in
these epidemiological studies are walking, jog-
ging and running. To the best of our knowledge,
only one epidemiological study has specifically
addressed the association between regular swim-
ming and risks of CHD.[56] As expected, both
walking and running were significantly and in-
versely associated with CHD risk. However, such
an association was not observed in regular
swimmers.[56] Thus, at present, unlike land-based
exercise activities, regular swimming is not asso-
ciated with reduced risks of developing CHD.
5. Conclusions
Since swimming is a rhythmic, dynamic form
of endurance exercise involving a large muscle
mass, it is a potentially useful alternative to land-
based exercises insofar as the efficacy and safety
of swimming can be assured. Swimming, how-
ever, is inherently different from land-based
exercise in many respects due to water immersion
and the prone body position. Physiological
responses to swimming are affected by many
factors, including hydrostatic pressure, facial
immersion and high thermal conductivity of
water. As a result, research findings obtained in
land-based exercise training studies cannot be
extrapolated simply to swimming. Available evi-
dence indicates that regular swimming appears to
exert beneficial effects on arterial blood pressure
Sports Med 2009; 39 (5)
Swimming Exercise and Cardiovascular Risk Factors
and insulin sensitivity, while elevating the level of
mood state.[36] However, the impacts of swimming
on blood lipid profile, bodyweight and fatness,
bone mineral density[95] and relative risk of
developing CHD seem to be small or none. The
available research studies using swimming ex-
ercise intervention are very limited. Clearly, fur-
ther studies are warranted to establish the effects
of regular swimming on CHD risks in humans.
Acknowledgements
No sources of funding were used to assist in the prepara-
tion of this review. The author has no conflicts of interest that
are directly relevant to the content of this review.
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Correspondence: Dr Hirofumi Tanaka, Department of Kine-
siology and Health Education, The University of Texas at
Austin, 1 University Station (D3700), Austin, TX 78712, USA.
E-mail: htanaka@mail.utexas.edu
Sports Med 2009; 39 (5)