(Stroke. 2000;31:14.)
© 2000 American Heart Association, Inc.
Original Contributions |
From the National Institute of Public Health, Community Medicine Research Unit, Verdal (H.E., J.H.); Department of Medicine, Innherred Hospital, Levanger (E.E.); and Department of Community Medicine and General Practice, Norwegian University of Science and Technology, Trondheim (L.V.), Norway.
Correspondence to Hanne Ellekjær, MD, National Institute of Public Health, Community Medicine Research Unit, N-7650 Verdal, Norway. E-mail verdalfh{at}online.no
| Abstract |
|---|
|
|
|---|
MethodsWe conducted a 10-year mortality follow-up of women aged
50 years, free from stroke at baseline (n=14 101), who participated
in the Nord-Trøndelag Health Survey in Norway during 19841986. Main
outcome measures were relative risk of stroke mortality according to
increasing levels of physical activity, with the least active group
used as reference.
ResultsIn groups aged 50 to 69, 70 to 79, and 80 to 101 years, the relative risk of dying decreased with increasing physical activity, after adjustment for potentially confounding factors. In groups aged 50 to 69 and 70 to 79 years, the most active women had an adjusted relative risk of 0.42 (95% CI, 0.24 to 0.75) and 0.56 (95% CI, 0.36 to 0.88), respectively. In the group aged 80 to 101 years, there was a consistent negative association with physical activity; the adjusted relative risk for the most active was 0.57 (95% CI, 0.30 to 1.09).
ConclusionsPhysical activity was associated with reduced risk of death from stroke in middle-aged and elderly women. This association persisted after we excluded individuals with prevalent cardiovascular and cerebrovascular disease at baseline and women who died during the first 2 years of follow-up. These observations strengthen the evidence that physical activity should be part of a primary prevention strategy against stroke in women.
Key Words: epidemiology exercise risk factors stroke prevention
| Introduction |
|---|
|
|
|---|
Results of prospective studies among women have been divergent, showing no association,1 14 16 increased risk only in the low-activity group,2 3 4 12 and a negative dose-risk association between levels of physical activity and stroke morbidity and mortality.8 9 15
Physical activity may have beneficial effects on biochemical (glucose intolerance, HDL cholesterol, fibrinolytic activity) and physiological (body mass index [BMI], blood pressure, pulse rate, vital capacity, O2 uptake) factors. A recent study6 suggested that physical activity may mediate its effect by lowering body weight, blood pressure, and serum cholesterol, whereas others claim that physical activity may exert effects independent of these factors.1 5 9
The extent of physical activity is likely to vary between populations. Few studies have been conducted in Scandinavia, where leisure-time activities may differ from those in urban populations studied in the United States. The aim of this study was to examine the association between levels of leisure-time physical activity and stroke mortality in a large prospective study of middle-aged and elderly women.
| Subjects and Methods |
|---|
|
|
|---|
20 years in Nord-Trøndelag county in Norway.
Among 85 100 eligible persons, 77 310 (90.8%) returned the
questionnaire that was mailed with the invitation (questionnaire 1),
and 74 977 (88.1%) participated in the health examination. At the
examination, a second questionnaire (questionnaire 2) was distributed,
which the participants were asked to complete and return by mail. In
all, 18 627 women aged
50 years attended and received the second
questionnaire, which included questions on physical activity. Among
those, 14 101 women (75.7%) who were free from stroke at baseline
completed questions about leisure-time physical activity and were
eligible for the follow-up. A detailed description of participants,
questionnaires, and screening procedures in the Nord-Trøndelag Health
Survey is given elsewhere.17
Assessment of Physical Activity and Other Characteristics
Information on physical activity and risk factors for stroke was
provided by the 2 self-administered questionnaires (questionnaires 1
and 2) and clinical measurements included in the screening program.
From questionnaire 2, detailed information about leisure-time physical
activity was obtained and used to classify activity into 3 separate
levels: low, medium, and high (Appendix). Activity among women who
exercised less than once per week was classified as low. For those who
engaged in physical activity once or several times per week, we also
queried about intensity and duration, and we constructed a summary
measure (index) that was dichotomized at the median value and labeled
medium and high activity.
Information on prevalent and current diseases (questionnaire 1) was provided, including diabetes, stroke, coronary heart disease, and long-term illness, in addition to use of antihypertensive medication. Information on current smoking and years of education was also available (questionnaire 2). Measurements of height, weight, systolic blood pressure (mm Hg), and pulse rate (bpm) were made at the health examination.
Follow-Up and End Points
The unique 11-digit identification number of every Norwegian
citizen enabled individual linkage between the collected information
and the register of deaths at Statistics Norway to determine vital
status (alive, emigrated, dead) and cause-specific deaths. Each
participant contributed person-years from the date of study entry until
the date of death from stroke (n=457), death from other causes
(n=3314), emigration (n=18), or the end of follow-up of December 31,
1994 (n=10 312). Median follow-up time was 9.8 years (mean, 9.0
years). Stroke-specific deaths were identified by death certificates
using underlying cause of death from stroke according to the
International Classification of Diseases (ICD) codes of
cerebrovascular disease: ICD-8 codes 430 to 438 until December 31,
1985, and ICD-9 codes 430 to 438 from 1986.
Ethics
The Stroke in Nord-Trøndelag Study was approved by the Regional
Committee for Ethics in Medical Research and the Norwegian Data
Inspectorate. The Ministry of Health and Social Affairs accepted
linkage to mortality statistics.
Statistical Analyses
We used Cox regression analysis18 to
calculate age- and multivariate-adjusted risk ratios
(with 95% CIs) for death of stroke associated with different levels of
physical activity, using the least active group as reference. We
evaluated potentially confounding factors in a
multivariate analysis including history of
diabetes (yes/no), history of myocardial infarction or angina pectoris
(yes/no), use of antihypertensive medication (yes/no), diabetes
(yes/no), years of education (3 categories: primary and lower secondary
school [<10 years], upper secondary school [10 to 12 years], and
college or university [>12 years]), long-term illness that impairs
function in daily life (yes/no), current smoking (yes/no), BMI
(kg/m2), systolic blood pressure
(mm Hg), and age (years). Tests of significance of trend in relative
risks (RRs) across categories of physical activity were conducted by
treating the levels of physical activity as a single ordinal
variable in the proportional hazards model. Trend was
considered statistically significant at P<0.05. To
reduce any further confounding with underlying disease, we performed
secondary analyses by (1) excluding subjects with prevalent
coronary heart disease (angina pectoris and myocardial
infarction), subjects with diabetes, and users of antihypertensive
medication at baseline, and (2) excluding individuals who died during
the first 2 years of follow-up.
We used the SPSS statistical package, version 8.0, for the analyses.
| Results |
|---|
|
|
|---|
The health characteristics at baseline are shown in Table 1
. Women with a high level of physical
activity tended to be younger, leaner, and had lower systolic
blood pressure than less active women. There was a decline in resting
pulse across categories of physical activity, and the prevalence of
coronary heart disease, diabetes, and use of antihypertensive
medication decreased with increasing physical activity. Smoking tended
to be more prevalent among the least physically active, and there was
an increasing level of education with increasing physical activity.
|
In Table 2
, we show age-adjusted and
multivariate-adjusted analyses for women aged
50 to 69 years, 70 to 79 years, and 80 to 101 years. In all age groups,
the age-adjusted RRs decreased with increasing physical activity. The
negative association was slightly weaker in the
multivariate analyses, but tests for trend were
significant in groups aged 50 to 69 and 70 to 79 years
(P=0.0021 and P=0.0093 for trend, respectively).
In groups aged 50 to 69 and 70 to 79 years, the most active women had a
multivariate adjusted RR of 0.39 (95% CI, 0.24 to
0.75) and 0.48 (95% CI, 0.36 to 0.88), respectively. In the group aged
80 to 101 years, there was a consistent negative association of
similar magnitude in both age-adjusted and multivariate
analyses, but the estimates of effect were not statistically
significant.
|
Women in the least active category were more likely to report ill
health and prevalent diseases. In separate analyses, we
therefore restricted the participants to women who were free from
cerebrovascular and cardiovascular diseases, and we
excluded individuals who died during the first 2 years of follow-up
(Tables 3
and 4
). Among the former, the overall
multivariate-adjusted RR in the high-physical-activity
group was 0.47 (95% CI, 0.29 to 0.75) and in the latter, the adjusted
RR was 0.54 (95% CI, 0.39 to 0.75). In both groups, the test for trend
across levels of physical activity was statistically significant.
|
|
| Discussion |
|---|
|
|
|---|
Our findings are consistent with those of previous studies,3 4 8 9 12 13 15 but only 3 studies8 9 15 have shown a graded negative effect. In 2 of these studies,13 15 the combined effects on fatal myocardial infarction and stroke were assessed.
Comparison of results between studies is complicated by differences in
design, assessment of physical activity, and different outcomes. For
example, discrepancies in results may be due to inadequate assessment
of physical activity in women, as suggested by Blair et
al.19 Most physical activity questionnaires have been
developed for and validated in male populations, and activities
traditionally related to women, such as child care and housework, are
usually not recorded.20 21 Therefore, Weller and
Corey13 have argued that failing to take into account
nonleisure physical activity among women would lead to
misclassification that may result in an underestimate of the RR. In
this study, the validity of the reported physical activity could be
indirectly validated by surrogate measures of physical fitness, as
reflected by decreasing resting pulse and BMI with increasing physical
activity (Table 1
).21 22 23 The potential bias of
misclassification due to inaccuracy of diagnosis coded on death
certificates is unlikely to be related to different levels of physical
activity and to explain the negative association observed.
The prospective design of the study makes it unlikely that the results may be biased because of selection of participants or misclassification of information. After the exclusion of women with a previous stroke, 75.7% of all women who received the physical activity questionnaire (questionnaire 2) were included in the analyses. Reasons for not completing the physical activity questions are not known. However, individuals not performing regular exercise because of illness are more likely to omit these questions. Among women who did not answer the questions, it is therefore conceivable that mortality, including stroke mortality, may be highest among the least active. As a consequence, our results would be an underestimate of the true negative association between physical activity and stroke mortality.
The possible biological mechanisms of a negative association between physical activity and stroke mortality may be mediated by decelerating the atherosclerotic process, modifying the structure of the arteries, reducing vasospasm, enhancing myocardial electric stability, or increasing fibrinolysis.24 Physical activity is also associated with improved diabetes control,25 increased HDL levels,26 and lower body weight.27 Nonsmokers and people of higher education are more likely to participate in physical activities.28 BMI, blood pressure, history of hypertension, history of high cholesterol, and diabetes mellitus may be considered intermediate factors, and one may argue not to adjust for such baseline factors in the analysis. However, adjustment had only a minor influence on the estimates of RR, suggesting no material confounding with physical activity. Whether other, unmeasured factors could explain the strong negative association between physical activity and stroke mortality, however, cannot be excluded.
| Acknowledgments |
|---|
| Appendix 1 |
|---|
|
|
|---|
By exercise we mean walking, skiing, swimming, or working out with sports.
How often do you exercise?
Never
Less than once a week
Once a week
2 to 3 times a week
Nearly every day
If you exercise as often as once or several times a week:
How hard do you exercise?
I take it easy without losing my breath or breaking into sweat
I push until I lose my breath and break into sweat
I practically exhaust myself
How long do you exercise each time?
Less than 15 minutes
16 to 30 minutes
30 minutes to 1 hour
More than 1 hour
Received August 8, 1999; revision received October 4, 1999; accepted October 4, 1999.
| References |
|---|
|
|
|---|
2.
Lapidus L, Bengtsson C. Socioeconomic factors and
physical activity in relation to cardiovascular disease
and death: a 12 year follow up of participants in a population study of
women in Gothenburg, Sweden. Br Heart J. 1986;55:295301.
3.
Gillum RF, Mussolino ME, Ingram DD. Physical activity
and stroke incidence in women and men: the NHANES I Epidemiologic
Follow-up Study. Am J Epidemiol. 1996;143:860869.
4.
Salonen J, Puska P, Tuomilehto J. Physical
activity and risk of myocardial infarction, cerebral stroke and death.
Am J Epidemiol. 1982;115:526537.
5.
Abbot RD, Rodriguez BL, Burchfiel CM, Curb JD.
Physical activity in older middle-aged men and reduced risk of stroke:
the Honolulu Heart Program. Am J Epidemiol. 1994;139:881893.
6.
Lee I-M, Hennekens CH, Berger K, Buring JE, Manson JE.
Exercise and risk of stroke in male physicians. Stroke. 1999;30:16.
7.
Lee I-M, Paffenbarger RS. Physical activity and stroke
incidence: the Harvard Alumni Health Study. Stroke. 1998;29:20492054.
8. Shinton R, Sagar G. Lifelong exercise and stroke. BMJ. 1993;307:231234.
9.
Sacco RL, Gan R, Boden-Albala B, Lin I-F, Kargman DE,
Hauser WA, Shea S, Paik MC. Leisure-time physical activity and
ischemic stroke risk: the Northern Manhattan Stroke Study.
Stroke. 1998;29:380387.
10. Wannamethee SG, Shaper AG, Walker M. Changes in physical activity, mortality, and incidence of coronary heart disease in older men. Lancet. 1998;351:16031608.[Medline] [Order article via Infotrieve]
11.
Haaheim LL, Holme I, Hjermann I, Leren P. Risk factors
of stroke incidence and mortality: a 12-year follow-up of the Oslo
Study. Stroke. 1993;24:14841489.
12. Lindenstrom E, Boysen G, Nyboe J. Risk factors for stroke in Copenhagen, Denmark, II: life-style factors. Neuroepidemiology. 1993;12:4350.[Medline] [Order article via Infotrieve]
13. Weller I, Corey P. The impact of excluding non-leisure energy expenditure on the relation between physical activity and mortality in women. Epidemiology. 1998;9:632635.[Medline] [Order article via Infotrieve]
14. Mensink G, Deketh M, Mul M, Schuit A, Hoffmeister H. Physical activity and its association with cardiovascular risk factors and mortality. Epidemiology. 1996;7:391397.[Medline] [Order article via Infotrieve]
15.
Kushi L, Fee R, Folsom AR, Mink P, Anderson K, Sellers
T. Physical activity and mortality in postmenopausal women.
JAMA. 1997;277:12871292.
16.
Ellekjær EF, Wyller TB, Sverre JM, Holmen J. Lifestyle
factors and risk of cerebral infarction. Stroke. 1992;23:829834.
17. Holmen J, Midthjell K, Bjartveit K, Hjort PF, Lund-Larsen PG, Moum T, Naess S, Waaler T. The Nord-Trøndelag Health Survey 198486: Purpose, Background and Methods: Participation, Non-Participation and Frequency Distributions. Verdal, Norway: Statens Institutt for folkehelse, Senter for samfunnsmedisinsk forskning; 1984. Report No. 4/1990.
18. Altman D. Practical Statistics for Medical Research. London, UK: Chapman & Hall; 1991.
19. Blair S, Kohl H, Barlow C. Physical activity, physical fitness, and all-cause mortality in women: do women need to be active? J Am Coll Nutr. 1993;12:368371.[Abstract]
20.
Kohl H, Blair S, Paffenbarger RS, Macera C, Kronenfeld
J. A mail survey of physical activity habits as related to measured
physical activity. Am J Epidemiol. 1988;127:12281239.
21.
Taylor C, Coffey T, Berra K, Iaffaldano R, Casey K,
Haskell W. Seven-day activity and self-report compared to a direct
measure of physical activity. Am J Epidemiol. 1984;120:818824.
22.
Blair S, Kannel WB, Kohl H, Goodyear N, Wilson P.
Surrogate measures of physical activity and physical fitness.
Am J Epidemiol. 1989;129:11451156.
23. Wilson P, Paffenbarger RS, Morris J, Havlik R. Assessment methods for physical activity and physical fitness in population studies: report of NHLBI workshop. Am Heart J. 1986;111:11771187.[Medline] [Order article via Infotrieve]
24. Powell K, Thompsen P, Caspersen C, Kendrick J. Physical activity and the incidence of coronary heart disease. Ann Rev Public Health. 1987;8:253287.[Medline] [Order article via Infotrieve]
25. Manson J, Rimm EB, Stampfer MJ, Colditz GA, Willett WC, Krolewski AS, Rosner B, Hennekens CH, Speizer FE. Physical activity and incidence of non-insulin-dependent diabetes mellitus in women. Lancet. 1991;338:774778.[Medline] [Order article via Infotrieve]
26. Thompsen P, Lazarus B, Cullinane E, Henderson L, Musliner T, Eshleman R, Herbert P. Exercise, diet, or physical characteristics as determinants of HDL-levels in endurance athletics. Atherosclerosis. 1983;46:333339.[Medline] [Order article via Infotrieve]
27. Garrow J. Effect of exercise on obesity. Acta Med Scand Suppl. 1985;711:6773.
28. Caspersen C, Christenson G, Pollard R. Status of the 1990 physical fitness and exercise objectives: evidence from NHIS. Public Health Rep. 1986;101:587592.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
![]() |
J. Z. Willey, Y. P. Moon, M. C. Paik, B. Boden-Albala, R. L. Sacco, and M.S.V. Elkind Physical activity and risk of ischemic stroke in the Northern Manhattan Study Neurology, November 24, 2009; 73(21): 1774 - 1779. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. Boysen, L.-H. Krarup, X. Zeng, A. Oskedra, J. Korv, G. Andersen, C. Gluud, A. Pedersen, M. Lindahl, L. Hansen, et al. ExStroke Pilot Trial of the effect of repeated instructions to improve physical activity after ischaemic stroke: a multinational randomised controlled clinical trial BMJ, July 22, 2009; 339(jul20_3): b2810 - b2810. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. J. Grau, C. Barth, B. Geletneky, P. Ling, F. Palm, C. Lichy, H. Becher, and F. Buggle Association Between Recent Sports Activity, Sports Activity in Young Adulthood, and Stroke Stroke, February 1, 2009; 40(2): 426 - 431. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. P. Hooker, X. Sui, N. Colabianchi, J. Vena, J. Laditka, M. J. LaMonte, and S. N. Blair Cardiorespiratory Fitness as a Predictor of Fatal and Nonfatal Stroke in Asymptomatic Women and Men Stroke, November 1, 2008; 39(11): 2950 - 2957. [Abstract] [Full Text] [PDF] |
||||
![]() |
A.-C. Jonsson, I. Lindgren, B. Norrving, and A. Lindgren Weight Loss After Stroke: A Population-Based Study From the Lund Stroke Register Stroke, March 1, 2008; 39(3): 918 - 923. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Kurtze, V. Rangul, B.-E. Hustvedt, and W D. Flanders Reliability and validity of self-reported physical activity in the Nord-Trondelag Health Study -- HUNT 1 Scand J Public Health, January 1, 2008; 36(1): 52 - 61. [Abstract] [PDF] |
||||
![]() |
A-C Jonsson, I Lindgren, B Hallstrom, B Norrving, and A Lindgren Prevalence and intensity of pain after stroke: a population based study focusing on patients' perspectives J. Neurol. Neurosurg. Psychiatry, May 1, 2006; 77(5): 590 - 595. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. I. Paraskevas, S. S. Daskalopoulou, M. E. Daskalopoulos, and C. D. Liapis Secondary Prevention of Ischemic Cerebrovascular Disease. What Is the Evidence? Angiology, September 1, 2005; 56(5): 539 - 552. [Abstract] [PDF] |
||||
![]() |
G. Hu, C. Sarti, P. Jousilahti, K. Silventoinen, N. C. Barengo, and J. Tuomilehto Leisure Time, Occupational, and Commuting Physical Activity and the Risk of Stroke Stroke, September 1, 2005; 36(9): 1994 - 1999. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Ferris, R. M. Robertson, R. Fabunmi, and L. Mosca American Heart Association and American Stroke Association National Survey of Stroke Risk Awareness Among Women Circulation, March 15, 2005; 111(10): 1321 - 1326. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. Wendel-Vos, A. Schuit, E. Feskens, H. Boshuizen, W. Verschuren, W. Saris, and D Kromhout Physical activity and stroke. A meta-analysis of observational data Int. J. Epidemiol., August 1, 2004; 33(4): 787 - 798. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. D. Lee, A. R. Folsom, and S. N. Blair Physical Activity and Stroke Risk: A Meta-Analysis Stroke, October 1, 2003; 34(10): 2475 - 2481. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Brainin Editorial Commen: Physical Exercise and Stroke: The Sitting Majority Has a Lesson to Learn Stroke, October 1, 2003; 34(10): 2481 - 2482. [Full Text] [PDF] |
||||
![]() |
K. J. Greenlund, W. H. Giles, N. L. Keenan, J. B. Croft, G. A. Mensah, and S. L. Huston Physician Advice, Patient Actions, and Health-Related Quality of Life in Secondary Prevention of Stroke Through Diet and Exercise * The Physician's Role in Helping Patients to Increase Physical Activity and Improve Eating Habits Stroke, February 1, 2002; 33(2): 565 - 571. [Abstract] [Full Text] [PDF] |
||||
![]() |
T.L. Holmen, E. Barrett-Connor, J. Clausen, J. Holmen, and L. Bjermer Physical exercise, sports, and lung function in smoking versus nonsmoking adolescents Eur. Respir. J., January 1, 2002; 19(1): 8 - 15. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2000 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |