R E V I E W P A P E R

Individual and Joint Associations of Obesity and Physical Activity onthe Risk of Heart Failure

H eart failure (HF) has emerged asa major public health issue

throughout the developed and develop-ing regions of the world. In the UnitedStates alone, HF costs were more than$33 billion in 2007 according to the esti-mation of the American Heart Associa-tion.1 Although medical and surgicalmanagement has been improved, mor-bidity and mortality after onset ofHF remain substantial.1 Consequently,increasing attention has been drawn topreventing HF with management oflifestyle factors.

The data from a community-basedstudy conducted among persons 65 yearsand older living in New Haven, CT, hasshown that obesity, as assessed by bodymass index (BMI; calculated as weight[kg] divided by height squared [m2])�28, is a predictor of HF risk.2 Thisfinding has been confirmed by manyother studies.3–12 It was not until recentyears that scientists began to include theindexes of abdominal obesity: waist cir-cumference (WC), waist-hip ratio(WHR; WC [cm] divided by hip cir-cumference [cm]), waist-height ratio(WHtR; WC [cm] divided by height[am]) and waist-thigh ratio (WTR; WC[cm] divided by thigh circumference[cm]) into their studies.4,5,7,9,10,12 Thesestudies reveal that these indexes are alsopredictors of HF risk.

The increase in computerization andmechanization during the past decadeshas resulted in ever-increasing numbersof people being sedentary for most oftheir time. In the United States, morethan one half of adults do not engage inphysical activity at the level currentlyrecommended for health promotion.13,14

In response to this severe situation, 3studies have looked into the associationbetween regular physical activity and

HF risk.6,8,10 Two of them dug evendeeper: their research related to the jointassociation of obesity and physical activ-ity on HF risk showed that lean andactive individuals had the lowest risk ofHF.8,10 In this review, we summarizecurrent findings of prospective epidemi-ologic studies on the role of physicalactivity and body weight in the develop-ment of HF risk.

Obesity and HF: Data FromProspective EpidemiologicStudiesGeneral Obesity. The first prospectivestudy on the relation between obesityand the risk of HF was conducted among1749 people living in New Haven, CT,and BMI was classified into approximatetertiles of the distribution: <24, 24 to27.9, and�28 kg ⁄m2.2 The result of thisstudy indicated that BMI �28 kg ⁄m2

(relative risk, 1.6; 95% confidence inter-

val [CI], 1.0–2.4, compared with<24 kg ⁄m2) was an independent predic-tor of HF.2 The positive associationbetween BMI and HF risk only slightlychanged after adjusting for the occur-rence of myocardial infarction during fol-low-up.2 This finding was subsequentlyconfirmed by several large studies (TableI). The First National Health and Nutri-tion Examination Survey (NHANES I)epidemiologic follow-up study followed atotal of 13,643 men and women for19 years.6 Overweight, defined asBMI �27.8 kg ⁄m2 for men and �27.3kg ⁄m2 for women, was associated with a23% increment of HF risk in men and a34% increment of HF risk in women.6

The Multi-Ethnic Study of Atheroscle-rosis (MESA) among 6814 participantsof 4 ethnicities—Caucasian, AfricanAmerican, Hispanic, and ChineseAmerican—assessed the role of obesity(defined as BMI �30 kg ⁄m2) in the

Heart failure (HF) has become a major public health problem in both developed anddeveloping countries of the world. The individual and joint associations of physical activ-ity and obesity on the risk of HF have been extensively studied in recent years. The resultsfrom prospective studies consistently indicate that regular physical activity reduces the riskof HF, while both general obesity and abdominal obesity increase the risk of HF. Further-more, research related to the joint association of obesity and physical activity on HF riskindicates that lean and active individuals had the lowest risk of HF. Therefore, preventingHF by maintaining optimal weight and engaging in regular physical activity may reducethe public health burden of HF worldwide. Congest Heart Fail. 2010;16:292–299.�2010 Wiley Periodicals, Inc.

Yujie Wang, MSc;1,2 Gang Hu, MD, PhD1

From the Pennington Biomedical Research Center;1 and the School of HumanEcology, Louisiana State University Agricultural Center, Baton Rouge, LA2

Address for correspondence:Gang Hu, MD, PhD, Chronic Disease Epidemiology Laboratory,Pennington Biomedical Research Center, 6400 Perkins Road,Baton Rouge, LA 70808E-mail: gang.hu@pbrc.eduManuscript received March 24, 2010; revised May 30, 2010;accepted July 11, 2010

doi: 10.1111/j.1751-7133.2010.00189.x

obesity, physical activity, and risk of HF november • december 2010292

Table

I.Se

lect

Find

ings

onth

eA

ssoc

iatio

nBe

twee

nO

besi

tyan

dth

eRi

skof

Hea

rtFa

ilure

AU

TH

OR

,Y

UTH

OR

,Y

NO

.O

FO

.O

FH

EA

RT

EA

RT

FAIL

UR

EA

ILU

RE

CA

SE

SA

SE

S⁄⁄N

O.

OF

O.

OF

PAR

TIC

IPA

NTS

AR

TIC

IPA

NTS

aA

GE

GE

RAN

GE

,Y

AN

GE

,Y

FOLL

OW

-O

LLO

W-U

PP

MA

JOR

AJO

RFI

ND

ING

S:

IND

ING

S:

BMI,

kg⁄m

2;

HR

(95

%(9

5%

CI))

AD

JUS

TM

EN

TD

JUS

TM

EN

TFA

CTO

RS

AC

TO

RS

Gen

eral

Obe

sity

Che

net

al,

1999

2173

(85

M⁄8

8F)

⁄1749

(718

M⁄1

031

F)�

65

10

yBM

I<24;

HR,

1.0

0(ref

eren

ce);

BMI,

24–2

7.9

;H

R,1.1

(0.7

–1.7

);BM

I�28;

HR,

1.8

(1.1

–2.7

)

Sex,

age,

DM

,pu

lse

pres

sure

,M

Idur

ing

follo

w-u

p,an

dty

peof

hous

ing

He

etal

,2001

61382

(741

M⁄6

41

F)⁄

13,6

43

(5545

M⁄8

098

F)25–7

419

yM

ale:

BMI<

27.8

,H

R,1.0

0(ref

eren

ce);

BMI�

27.8

;H

R,1.2

3(1

.00–1

.52);

fem

ale:

BMI<

27.3

;H

R,1.0

0(ref

eren

ce);

BMI�

27.3

;H

R,1.3

4(1

.10–1

.64)

Age

,ra

ce,

educ

atio

nle

vel,

smok

ing,

regul

aral

coho

lco

nsum

ptio

n,SB

P,lo

wph

ysic

alac

tivity

,hy

perte

nsio

n,hi

stor

yof

DM

,hi

stor

yof

valv

ular

hear

tdis

ease

,an

dhi

stor

yof

CH

DKen

chai

ahet

al,

2002

11

496

(238

M⁄2

58

F)⁄

5881(2

704

M⁄3

177

F)55

(mea

n)14

yEa

ch1-u

niti

ncre

ase

inBM

I:m

ale:

HR,

1.0

5(1

.02–1

.09);

fem

ale:

HR,

1.0

7(1

.04–1

.10)

Alc

ohol

cons

umpt

ion,

seru

mto

tal

chol

este

rol,

pres

ence

orab

senc

eof

curr

ents

mok

ing,

valv

edi

seas

e,hy

perte

nsio

n,D

M,

ECG

-LV

H,

and

MI

Ingel

sson

etal

,2005

4104

M⁄1

187

M�

70

8.9

y(m

edia

n)Ea

ch1-S

Din

crea

sein

BMI:

HR,

1.3

5(1

.11–1

.65)

DM

,pr

ior

MI,

hype

rtens

ion,

ECG

-LVH

,sm

okin

g,

and

seru

mch

oles

tero

lIn

gel

sson

etal

,2005

3259M

⁄2321M

�50

28.8

y(m

edia

n)Ea

ch1-S

Din

crea

sein

BMI:

HR,

1.4

7(1

.31–1

.65)

Prio

rac

ute

MI,

hype

rtens

ion,

DM

,EC

G-LV

H,

smok

ing,

and

seru

mch

oles

tero

lN

ickl

aset

al,

2006

12

166

(73M

⁄93F)

⁄2435

(1081M

⁄1354F)

6.1

y(m

edia

n)Ea

ch1-S

Din

crea

sein

BMI:

HR,

1.2

5(1

.02–1

.53)

Age

,se

x,ra

ce,

site

,ed

ucat

ion,

smok

ing,

chro

nic

obst

ruct

ive

pulm

onar

ydi

seas

e,in

flam

mat

ion,

inci

dent

MI,

hom

eost

asis

mod

elas

sess

men

tof

insu

linse

nsiti

vity

inde

x,D

M,

and

hype

rtens

ion

Bahr

amiet

al,

2008

579

⁄6814

(3204

M⁄3

610

F)45–8

44

y(m

edia

n)BM

I<30,

HR,

1.0

0(ref

eren

ce);

BMI�

30;

HR,

1.8

3(1

.14–2

.92)

Age

,se

x,hy

perte

nsio

n,D

M,

LVH

,se

rum

tota

lcho

lest

erol

,an

dcu

rren

tsm

okin

gLo

ehr

etal

,2009

71528

(825

M⁄7

03

F)⁄

14,6

41

(6632

M⁄8

009

F)45–6

516

y(m

edia

n)Ea

ch1-S

Din

crea

sein

BMI:

mal

e:H

R,1.4

7(1

.39–1

.57);

fem

ale:

HR,

1.4

9(1

.39–1

.59)

Age

,al

coho

luse

,ed

ucat

iona

llev

el,

smok

ing

stat

us,

and

cent

er

Ken

chai

ahet

al,

2009

81109

M⁄2

1,0

94

M40–8

420.5

yBM

I<25;

HR,

1.0

0(ref

eren

ce);

BMI,

25–2

9.9

;H

R,1.4

9(1

.32–1

.69);

BMI�

30;

HR,

2.8

0(2

.24–3

.50)

Age

,sm

okin

g,

alco

holc

onsu

mpt

ion,

pare

ntal

hist

ory

ofM

I,ra

ndom

assi

gnm

entt

oas

pirin

orb-

caro

tene

,vi

gor

ous

phys

ical

activ

ity,

hist

ory

ofhy

perte

nsio

n,D

M,

and

hype

rcho

lest

erol

emia

Levi

tan

etal

,2009

91100

(718

M⁄3

82

F)⁄

80,3

60

(43,4

87

M⁄3

6,8

73

F)45–7

9M

⁄48–8

3F

7y

(med

ian)

An

inte

rqua

rtile

rang

ein

crea

sein

BMI:

mal

e:H

R,1.2

7(1

.19–1

.36);

fem

ale:

HR,

1.1

2(1

.00–1

.24)

Age

,ed

ucat

ion,

smok

ing,

alco

holc

onsu

mpt

ion,

tota

lphy

sica

lac

tivity

,po

stm

enop

ausa

lhor

mon

eth

erap

y,liv

ing

alon

e,m

arita

lsta

tus,

and

fam

ilyhi

stor

yof

MI,

hype

rtens

ion,

high

chol

este

rol,

and

DM

Hu

etal

,2010

10

3614

(1921

M⁄1

693

F)⁄

59,1

78

(28,8

42

M⁄3

0,3

36

F)25–7

418.4

yM

ale:

BMI<

25;

HR,

1.0

0(ref

eren

ce);

BMI2

5–2

9.9

;H

R,1.2

5(1

.12–1

.39);

BMI�

30;

HR,

1.9

9(1

.74–2

.27);

fem

ale:

BMI<

25;

HR,

1.0

0(ref

eren

ce);

BMI2

5–2

9.9

;H

R,1.3

3(1

.16–1

.51);

BMI�

30;

HR,

2.0

6(1

.80–2

.37)

Age

,st

udy

year

,ed

ucat

ion,

smok

ing,

alco

holc

onsu

mpt

ion,

hist

ory

ofM

I,va

lvul

arhe

artd

isea

se,

DM

,SB

P,to

talc

hole

ster

ol,

and

phys

ical

activ

ity

obesity, physical activity, and risk of HF november • december 2010 293

Table

I.Se

lect

Find

ings

onth

eA

ssoc

iatio

nBe

twee

nO

besi

tyan

dth

eRi

skof

Hea

rtFa

ilure

(Con

tinue

d)

AU

TH

OR

,Y

UTH

OR

,Y

NO

.O

FO

.O

FH

EA

RT

EA

RT

FAIL

UR

EA

ILU

RE

CA

SE

SA

SE

S⁄⁄N

O.

OF

O.

OF

PAR

TIC

IPA

NTS

AR

TIC

IPA

NTS

aA

GE

GE

RAN

GE

,Y

AN

GE

,Y

FOLL

OW

-O

LLO

W-U

PP

MA

JOR

AJO

RFI

ND

ING

S:

IND

ING

S:

BMI,

kg⁄m

2;

HR

(95

%(9

5%

CI))

AD

JUS

TM

EN

TD

JUS

TM

EN

TFA

CTO

RS

AC

TO

RS

Abd

omin

alO

besi

tyIn

gel

sson

etal

,2005

4104

M⁄1

187

M�

70

8.9

y(m

edia

n)Ea

ch1-S

Din

crea

sein

WC

:H

R,1.3

6(1

.10–1

.69)

DM

,pr

ior

MI,

hype

rtens

ion,

smok

ing,

ECG

-LVH

,an

dse

rum

tota

lcho

lest

erol

Nic

klas

etal

,2006

12

166

(73

M⁄9

3F)

⁄2435

(1081

M⁄1

354

F)6.1

y(m

edia

n)Ea

ch1-S

Din

crea

sein

WC

:H

R,1.3

2(1

.12–1

.55);

each

1-S

Din

crea

sein

WTR

:H

R,1.1

5(0

.96–1

.36)

Age,

sex,

race

,si

te,

educ

atio

n,sm

okin

g,

chro

nic

obst

ruct

ive

pulm

onar

ydi

seas

e,in

flam

mat

ion,

inci

dent

MI,

hom

eost

asis

mod

elas

sess

men

tofin

sulin

sens

itivi

tyin

dex,

DM

,an

dhy

perte

nsio

nBa

hram

iet

al,

2008

579

⁄6814

(3204

M⁄3

610

F)45–8

44

y(m

edia

n)W

C>

102

cmin

men

;W

C>

88

cmin

wom

en;

HR,

2.0

6(1

.25–3

.41)

Age,

sex,

hype

rtens

ion,

DM

,LV

H,

seru

mch

oles

tero

l,an

dcu

rren

tsm

okin

g

Loeh

ret

al,

2009

71528

(825

M⁄7

03

F)⁄

14,6

41

(6632

M⁄8

009

F)45–6

516

y(m

edia

n)Ea

ch1-S

Din

crea

sein

WC

:m

ale:

HR,

1.5

2(1

.43–1

.62);

fem

ale:

HR,

1.5

4(1

.44–1

.66);

each

1-S

Din

crea

sein

WH

R:m

ale:

HR,

1.5

0(1

.41–1

.60);

fem

ale,

HR,

1.5

9(1

.46–1

.72)

Age,

alco

holu

se,

educ

atio

nall

evel

,sm

okin

gst

atus

,an

dce

nter

Levi

tan

etal

,2009

91100

(718

M⁄3

82

F)⁄

80,3

60

(43,4

87

M⁄3

6,8

73

F)45–7

9M

⁄48–8

3F

7y

(med

ian)

An

inte

rqua

rtile

rang

ein

crea

sein

WC

:m

ale:

HR,

1.3

1(1

.21–1

.42);

fem

ale:

HR,

1.2

0(1

.05–1

.36);

anin

terq

uarti

lera

nge

incr

ease

inW

HR:

mal

e:H

R,1.0

8(1

.00–1

.17);

fem

ale:

HR,

1.0

2(0

.93–1

.12);

anin

terq

uarti

lera

nge

incr

ease

inW

HtR

:m

ale:

HR,

1.2

8(1

.18–1

.39);

fem

ale:

HR,

1.1

4(1

.00–1

.31)

Age,

educ

atio

n,sm

okin

g,

alco

holc

onsu

mpt

ion,

tota

lphy

sica

lact

ivity

,po

stm

enop

ausa

lhor

mon

eth

erap

y,liv

ing

alon

e,m

arita

lsta

tus,

and

fam

ilyhi

stor

yof

MI,

hype

rtens

ion,

high

chol

este

rol,

and

DM

Hu

etal

,2010

10

3614

(1921

M⁄1

693

F)⁄

59,1

78

(28,8

42

M⁄3

0,3

36

F)25–7

418.4

yEa

ch1-c

min

crea

sein

WC

:m

ale:

HR,

1.0

3(1

.02–1

.04);

fem

ale:

HR,

1.0

4(1

.03–1

.05);

each

0.1

-uni

tinc

reas

ein

WH

R:m

ale:

HR,

1.4

8(1

.25–1

.75);

fem

ale:

HR,

1.6

4(1

.31–2

.04)

Age,

stud

yye

ar,

educ

atio

n,sm

okin

g,

alco

holc

onsu

mpt

ion,

hist

ory

ofM

I,va

lvul

arhe

artd

isea

se,

DM

,SB

P,to

talc

hole

ster

ol,

and

phys

ical

activ

ity

Abb

revi

atio

ns:

BMI,

body

mas

sin

dex;

CH

D,

coro

nary

hear

tdis

ease

;C

I,co

nfide

nce

inte

rval

;D

M,

diab

etes

mel

litus

;EC

G,

elec

troca

rdio

gra

phy;

HR,

haza

rdra

tio;

LVH

,le

ftve

ntricu

lar

hype

rtrop

hy;

MI,

myo

card

iali

nfar

ctio

n;SB

P,sy

stol

icbl

ood

pres

sure

;W

C,

wai

stci

rcum

fere

nce;

WH

R,w

aist

-hip

ratio

;W

HtR

,w

aist

-hei

ght

ratio

;W

TR,

wai

st-th

igh

ratio

.aN

umbe

rsre

pres

ent

pers

ons

who

wer

ein

clud

edin

the

final

anal

yses

.

obesity, physical activity, and risk of HF november • december 2010294

development of congestive heart failure(CHF).5 After adjustment of the estab-lished risk factors of HF, obesity was asso-ciated with a significant increase in therisk of HF (hazard ratio [HR], 1.83; 95%CI, 1.14–2.92) compared with BMI<30 kg ⁄m2.5 Levitan and associates9

indicated that the multivariate-adjustedHRs of HF were 1.27 (95% CI, 1.19–1.36) in men and 1.12 (95% CI, 1.00–1.24) in women for an interquartile rangedifference in BMI.9

Results from the Uppsala LongitudinalStudy of Adult Men (ULSAM) of 2321persons aged 50 years (median follow-up, 28.8 years) indicated that there was a47% increase in the risk of HF for each1–standard deviation (SD) increment inBMI.3 In another cohort (1187 elderlymen; median follow-up, 8.9 years) of theULSAM study, the positive associationbetween BMI as a continuous variableand the risk of CHF was also observed.4

The authors proposed that the associa-tion between obesity and subsequentCHF may be mediated partly by insulinresistance.4 The Health, Aging, andBody Composition (Health ABC) studyconducted among 2435 participants in 2metropolitan areas—Memphis and Pitts-burgh—found that a 4.88-kg ⁄m2 (1-SD)increase in BMI was associated with a25% increase in HF risk after adjustmentof potential confounding variables andpotential explanatory variables.12

In a recent analysis of the FraminghamHeart Study with a follow-up of 14 years,each 1-unit increase in BMI was found tobe associated with a 5% increased risk ofHF for men and a 7% increased risk ofHF for women after adjustment forknown risk factors.11 When BMI andother covariates were analyzed as time-dependent variables, the positive associa-tion between BMI and HF risk remainedrobust. When BMI was considered as acategorical variable (normal weight,18.5–24.9 [reference]; overweight, 25.0–29.9; and obese �30 kg ⁄m2), increasingcategories of BMI were associated with astepwise increase in the risk of HF.11

Likewise, in the Physicians’ Health Study(PHS), conducted among 22,071 USmale physicians aged 40 to 84 years witha mean follow-up of 20.5 years, BMI wasevaluated as both a continuous variable

and as World Health Organization(WHO) body weight categories(lean, <25.0 [reference]; overweight,25.0–29.9; and obese, �30 kg ⁄m2).8

After adjustment of baseline covariablesnot likely in the causal pathway andlikely in the causal pathway, each 1-kg ⁄m2 increase in BMI was associatedwith an 11% increase in the risk of HF.Increasing categories of BMI were associ-ated with a stepwise increase in the riskof HF.8 A graded increase in the risk ofHF was observed across categories ofBMI.8 In the FINRISK study among28,842 Finnish men and 30,336 Finnishwomen who were 25 to 64 years of age,Hu and colleagues10 also took BMI asboth a continuous variable and WHOweight categories. Compared withnormal-weight men, overweight menshowed a 25% increased risk of HF andobese men a 99% increased risk afteradjustment for all confounders. Amongwomen, a similar trend was observed.10

Similarly, the WHO weight categorieswere used in the Atherosclerosis Risk inCommunities (ARIC) study for measur-ing HF incident rates.7 This study com-prised 2 races in 4 US communities.When BMI is taken as a continuous vari-able, each 1-SD increment in BMI wasfound to be associated with a 47%increased risk of HF for men and a 49%increased risk of HF for women.7 ThePHS,8 the FINRISK study,10 and theARIC study7 consistently proved thatbesides obesity, overweight was also asso-ciated with an increased risk of HF. Adose-effect relationship between BMIand HF risk was found in the study con-ducted by Chen and colleagues,2 theARIC study,7 the PHS,8 the FINRISKstudy,10 and the Framingham Heartstudy,11 where BMI was evaluated as a 3-category variable.

Abdominal Obesity. Prediction of HFby different types of abdominal obesityindexes was recently documented. TheULSAM study4 and the MESA study5

only included WC in their studies. Thefirst study assessed WC as a continuousvariable and indicated that each 1-SDincrease was associated with a 36%increase in HF risk,4 while the secondstudy investigated WC as a 2-category

variable (abdominal obesity is defined asWC >102 cm in men and >88 inwomen) and found that abdominal obes-ity predicted 106% increase in the risk ofHF.5 Two more recent studies, the ARICstudy7 and the FINRISK study,10 assessedthe association between WHR and therisk of HF, which found similar resultsthat WHR was an independent predictorof HF risk. A population-based prospec-tive study with 43,487 men and 36,873women9 provided evidence that, in themultivariable-adjusted model, abdominaladiposity, measured by WC, was signifi-cantly and independently associated withan increased risk of HF among both menand women, while the positive associa-tion between WHR and HF risk wasfound only in men. For the first time,WHtR was included as one of theindexes of abdominal adiposity for assess-ing its association with HF risk, and apositive association was found both inmen and women.9 The Health ABCstudy12 also evaluated the associationbetween HF risk and abdominal adipos-ity assessed by WC and, for the first time,WTR. Results from this study indicatedthat a 13.38-cm (1-SD) increase in WCwas associated with a 32% increase inHF risk in the multivariable-adjustedmodel, while no significant associationwas found between HF risk and WTR inthe same model.12

General Obesity and AbdominalObesity. So far, only the Health ABCStudy12 and the study conducted by Lev-itan and associates9 compared the predic-tive power of general obesity, as assessedby BMI, with that of abdominal obesity,as assessed by WC, on HF.9,12 When WCand BMI were included together, the for-mer found that WC was associated withincreased risk of CHF (HR, 1.27; 95%CI, 1.04–1.54 per 1-SD increase), butBMI was not (HR, 1.08; 95% CI, 0.86–1.35), and the latter found that WC pre-dicted HF events regardless of BMI, butthe association between BMI and HFonly existed at high WCs among women.Results from both studies indicated thatabdominal obesity was a stronger risk fac-tor for HF than general obesity.9,12

Results from the above studies indi-cated that all the obesity indexes were

obesity, physical activity, and risk of HF november • december 2010 295

associated with an increased risk of HF;however, only BMI or WC was con-stantly found to be significantly associ-ated with an increased risk of HF in allthe multivariable-adjusted models. Theevidence indicated that maintainingoptimal body weight should be animportant strategy to prevent HF in thegeneral population.

Physical Activity and HF:Data From ProspectiveEpidemiologic StudiesRecently, protection against HF byphysical activity was documented by 3cohort studies (Table II). In all 3 studies,physical activity was assessed with self-administered questionnaires. In thePHS, physical activity was assessedboth as a categorical variable (inactive[rarely ⁄never exercise vigorously enoughto work up a sweat], low active [1–3 times ⁄month], medium active [1–4 times ⁄week], and highly active [5–7times ⁄week]) and a dichotomous vari-able (inactive versus active [�1–3 time-

s ⁄month]).8 Compared with participantswho rarely or never vigorously exercised,a 18% reduction in the risk of HF wasfound among participants who exercised�1–3 times a month.8 The FINRISKstudy,10 assessing the association betweenphysical activity and HF risk, classifiedoccupational, commuting, and leisure-time physical activity into 3 categories:(1) low was defined as persons whoreported light levels of occupational,commuting (<1 minute), and leisure-time physical activity; (2) moderate wasdefined as those who reported only 1 ofthe 3 types of moderate to high physicalactivity; and (3) high was defined asthose who reported 2 or 3 types of moder-ate to high physical activity. In this Finn-ish study, a graded decrease in the risk ofHF was observed across categories ofphysical activity both in men andwomen.10 The NHANES I epidemiolog-ic follow-up study identified a significantinverse association between recreationalphysical activity and HF risk in womenbut not in men.6 Overall, a dose-effect

relationship between physical activityand HF risk was found only in theFINRISK study.10

The Joint Association ofObesity and PhysicalActivity in HF: Data FromProspective EpidemiologicStudiesIn order to understand the interactionbetween physical activity and obesity onthe risk of HF, 2 prospective epidemio-logic studies have assessed the joint asso-ciation of physical activity with the riskof HF.8,10 In the PHS conducted amongUS male physicians, compared with par-ticipants who were lean and active, therisk of HF increased by 293% in theobese and inactive group after adjust-ment for all baseline covariates (TableIII).8 In the FINRISK study,10 theauthors investigated the joint associa-tion of physical activity and obesity onHF risk, as assessed by not only BMI(Figure) but also WC and WHR(Table III). This study showed that the

Table II. Select Findings on the Association Between Physical Activity and the Risk of Heart Failure

AUTHOR, YUTHOR, Y

NO. OFO. OF HEARTEART

FAILUREAILURE CASESASES ⁄⁄ NO.O.

of PARTICIPANTSARTICIPANTSa

AgeRange, y FOLLOW-OLLOW-UPP

MAJORAJOR FINDINGS:INDINGS:

HR (95%(95% CI)) ADJUSTMENTDJUSTMENT FACTORSACTORS

He et al, 20016 1382 (741 M ⁄ 641 F) ⁄13,643 (5545 M ⁄8098 F)

25–74 19 y Regular exercise: HR,1.00 (reference);low exercise:

male: HR, 1.14(0.94–1.38);

female:, HR, 1.31(1.11–1.54)

Age, race, education level,smoking, regular alcoholconsumption, SBP,overweight, hypertension,history of DM, history ofvalvular heart disease,and history of CHD

Kenchaiah et al, 20098 1109 M ⁄ 21,094 M 40–84 20.5 y Vigorous physical activity:low: HR, 1.00 (reference);active (�1–3 times ⁄ mo):HR, 0.82 (0.70–0.96)

Age, cigarette smoking,alcohol consumption,parental history of MI,random assignment toaspirin or b-carotene, BMI,the presence or absenceof history of hypertension,DM, and hypercholesterolemia

Hu et al, 201010 3614 (1921 M ⁄ 1693 F) ⁄59,178 (28,842 M ⁄30,336 F)

25–74 18.4 y Low exercise: HR,1.00 (reference);moderate exercise:

male: HR, 0.79(0.68–0.92);

female: HR, 0.86(0.75–0.99);high exercise:

male: HR, 0.69(0.60–0.80);

female: HR, 0.68(0.59–0.78)

Age, study year, education,smoking, alcohol consumption,history of MI, valvularheart disease, DM, SBP,total cholesterol, and BMI

Abbreviations: BMI, body mass index; CHD, coronary heart disease; CI, confidence interval; DM, diabetes mellitus; HR, hazard ratio; MI,myocardial infarction; SBP, systolic blood pressure. aNumbers represent persons who were included in the final analyses.

obesity, physical activity, and risk of HF november • december 2010296

inverse association between physicalactivity and HF risk was observed at alllevels of BMI, WC, and WHR.10

MechanismDuring past decades, previous studieshave made great strides in exploring thepathways linking obesity and physicalactivity to HF. Obesity has been foundto be a risk factor for hypertension,15

coronary heart disease (CHD),16 insulinresistance,3,4,17 type 2 diabetes,18 dyslipi-demia,3,19 and inflammation5 and is animportant component of the metabolicsyndrome20; all of these disorders areknown risk factors of HF.11,21–27 Further-more, obesity is related to increasedblood volume, increased cardiac work-load, diastolic dysfunction, hypertrophyand dilation of the left ventricle, and fatdeposits in the heart, which may lead toHF.28 Obesity’s role in the developmentof HF may be partly explained by theabove direct or indirect mechanisms.

The protective effect of physicalactivity on HF may be partly mediatedby its effect on other risk factors for HF.Physical activity has a favorable effecton blood pressure, lipid profile, insulinsensitivity, body weight, blood coagula-tion, and fibrinolysis,29–34 and it alsocontributes to a decreased risk of hyper-tension, type 2 diabetes, the metabolicsyndrome, and CHD.29,30,35–37

ConclusionsHF has become a major economic,social, and personal burden worldwide.Our review based on the scientific evi-dence concludes that general over-weight, general obesity, and abdominalobesity were associated with anincreased risk of HF, while a moderateor high level of physical activity wasassociated with a decreased risk of HF,which indicated that moderate or highlevel of physical activity and avoidingexcessive weight gain may be effectiveways to prevent HF in all populations.This is consistent with the recommen-dations of a variety of organizations,including the American Heart Associa-tion,38 the American College of SportsMedicine, the National Institutes ofHealth, and the WHO.Ta

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obesity, physical activity, and risk of HF november • december 2010 297

Until now, to the best of our knowl-edge, only 2 studies have evaluated therelatively predictive power of general

obesity and abdominal obesity in therisk of HF. Future research is neededto generate enough information to

make clear which one is a more usefulpredictor of HF. In addition, moststudies on obesity, physical activity,and HF were conducted in populationswith European (especially NorthernEuropean) and American (especiallyNorthern American) ancestry, and lit-tle is known about whether obesityand physical activity affect other eth-nicities. To close this gap, continuousresearch on the causality between obes-ity and HF risk as well as physicalactivity and HF risk is needed. Thedevelopment in this field presents anexciting opportunity to address whetherlifestyle interventions can reduce ordelay the incidence of HF. In addition,it will provide the basis for decisionsthat physicians and policy makers mustmake in their everyday work. How-ever, in order to determine interven-tions that would prevent or delay theonset of HF, more modifiable risk fac-tors for the disease have to be identi-fied. These risk factors could then beused as targets for intervention, andpopulation-based health educationand intervention programs could bedeveloped.

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