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1 Human Cardiovascular Research Laboratory, Department of Kinesiology and Applied Physiology, University of Colorado at Boulder, Boulder 80309; and 2 Divisions of Cardiology and Geriatric Medicine, Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Carotid artery intima-media thickness (IMT), an independent risk factor for stroke, increases with age. Habitual exercise is associated with a lower prevalence of stroke, but it is unclear whether this protective effect could be mediated through a favorable influence on carotid IMT. We examined this possibility using both cross-sectional and intervention approaches. First, 137 healthy men (age 18-77 yr) who were either sedentary or endurance trained were studied. In both groups, carotid IMT and IMT-to-lumen ratio were progressively higher with age (P < 0.05). There were no significant differences in measures of carotid IMT between sedentary and endurance-trained men at any age. Carotid systolic blood pressure increased progressively with age and was related to carotid IMT (r = 0.63, P < 0.01). Second, 18 healthy sedentary subjects (54 ± 2 yr) were studied before and after 3 mo of endurance training. Carotid IMT, IMT/lumen ratio, and carotid systolic blood pressure did not change with exercise intervention. Our results do not support the hypothesis that regular aerobic exercise exerts its protective effect against stroke by attenuating the age-related increase in carotid IMT. This lack of effect on carotid IMT may be due to the apparent inability of habitual exercise to prevent or reduce the age-associated elevation in carotid distending pressure.
atherosclerosis; lifestyle; ultrasound
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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STROKE IS THE THIRD LEADING cause of death in the United States behind coronary heart disease and cancer (1). The incidence of stroke increases exponentially with advancing age, doubling in each successive decade after age 55 yr (1). Our laboratory and others have demonstrated that carotid artery intima-media thickness (IMT), an independent risk factor for stroke (11, 28), increases with advancing age in sedentary humans (12, 28, 37) and, therefore, presumably contributes to the age-associated increase in the incidence of this disorder.
Regular aerobic exercise generally is associated with a lower incidence of stroke, particularly in middle-aged and older adults (16, 25). Although the mechanisms underlying this apparent protective effect are not fully understood, one possibility is that regular aerobic exercise acts to attenuate the age-related increase in carotid IMT. Currently, there is limited information on this potential influence of habitual exercise in general and no information at all from intervention studies.
Accordingly, the aim of the present investigation was to determine the possible influence of regular aerobic exercise on the age-related increase in carotid artery IMT. To systematically address this aim, we used two different approaches. First, we used a cross-sectional study to determine the influence of habitual exercise on the age-related increase in carotid IMT. Second, we performed an intervention study to determine whether regular aerobic exercise could reverse the age-associated increase in carotid IMT.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
For the cross-sectional study, a total of 137 healthy men were studied. Subjects were grouped in consecutive 20-yr age ranges starting from age 18: "young" (18-37 yr), "middle aged" (38-57), and "older" (58-77). For at least the previous 2 yr, subjects were either sedentary (no regular physical activity) or endurance trained (vigorous endurance exercise >5 times/week and active in local road running races). Young, middle-aged, and older endurance-trained subjects had been training for 9 ± 1, 19 ± 3, and 24 ± 4 yr, respectively. The endurance-trained subjects were recruited from various running clubs throughout the proximal regions. The sedentary subjects were recruited through various forms of advertisements. For the intervention study, 18 healthy middle-aged and older sedentary subjects were studied before and after 3 mo of aerobic exercise training.All subjects were normotensive, nonobese, and free of overt chronic diseases as assessed by medical history, physical examination, and blood chemistries and hematologic evaluation. Men over 40 yr of age were further evaluated by electrocardiograph and blood pressure responses to treadmill exercise to exhaustion (10). Candidates who had smoked in the past 4 yr, were taking medications, or demonstrated significant plaque formation (12) [defined as a localized focal (echo) region encroaching into the lumen at least 1.5 mm thick in the common carotid artery, carotid bifurcation, and internal carotid artery] were excluded. None of the subjects had ankle-brachial blood pressure index of <0.9. All subjects gave their written informed consent to participate. All procedures were reviewed and approved by the Human Research Committee of the University of Colorado at Boulder.
Measurements
All measurements were performed after an abstinence of caffeine and a fast of 4 h (a 12-h overnight fast was used for determination of metabolic risk factors and blood viscosity). During the experimental sessions, each subject rested supine for 15 min in a quiet, temperature-controlled room.Carotid artery IMT. Carotid artery IMT was measured from the images derived from an ultrasound machine (model SSH-140, Toshiba) equipped with a high-resolution linear array transducer as described originally by Pignoli et al. (21). The longitudinal two-dimensional ultrasound images were obtained at the proximal 1- to 2-cm straight portion of the common carotid artery. These images were recorded on a super VHS recorder (model AG7350, Panasonic) for later off-line analysis and were digitized with a video-frame grabber (model DT-3152, Data Translation) and stored in a personal computer. All scans were performed by the same sonographer.
Ultrasound carotid images were analyzed by using a computerized image-analysis software as previously described (6). The spatial resolution using the ultrasound machine used in the present study is 0.3 mm. However, the minimum difference detectable when our ultrasound images were interfaced with our image analysis software is 0.1 mm (7). Carotid IMT was defined as the distance from the leading edge of the lumen-intima interface to the leading edge of the media-adventitia interface (21). Lumen diameter was defined as the distance between the vessel far-wall boundary, corresponding to the interface between the lumen and intima, and a near-wall boundary, corresponding to the interface of the adventitia and media. These measurements were made at end diastole as previously described (21). At least 10 measurements of IMT and lumen diameter were taken at each segment. The mean values of these 10 measurements were used for analysis. Carotid IMT/lumen diameter ratio was used as a measure of wall thickness normalized for lumen size (8, 13). All image analyses were performed by the same investigator, who was blinded to the group assignment of subjects. In our laboratory, this technique has excellent day-to-day reproducibility (coefficient of variation 3 ± 1%) for the carotid IMT.Carotid arterial blood pressure. The pressure waveform and amplitude were obtained from the common carotid artery with a pencil-type probe incorporating a high-fidelity strain gauge transducer (model TCB-500, Millar Instruments) as previously described in detail by our laboratory (34, 35). This tonometer has been shown to register a pressure wave with harmonic content that does not differ from that of an intra-arterially recorded wave, and the use of the tonometer on an exposed artery records a waveform identical to that recorded intra-arterially (14). Because the baseline levels of carotid blood pressure are subjected to hold-down force, the pressure signal obtained by tonometry was calibrated by equating the carotid mean arterial pressure to the brachial artery measurement as previously described (2). Mean arterial blood pressure in the resting supine position does not vary significantly within the large conduit arteries (2).
Brachial arterial blood pressure. Peripheral arterial blood pressure was measured with a semiautomated device (Dinamap, Johnson & Johnson) over the brachial artery with subjects in the supine positions. All measurements conformed strictly to American Heart Association guidelines (20). We also measured brachial blood pressure with a random-zero sphygmomanometer (Hawksley & Sons, Sussex, UK) in the same subjects and obtained similar results (data not shown).
Ankle-brachial pressure index. To exclude the possibility of overt peripheral artery disease, systolic blood pressure of the posterior tibial artery was measured by using a Doppler flowmeter (Parks Medical) and a sphygmomanometer (W. A. Baum). The ratio of the ankle systolic blood pressure to the brachial systolic blood pressure (Dinamap) was taken as the ankle-arm pressure index. Peripheral artery disease was considered present when the index was <0.90.
Whole blood and plasma viscosity. An increase in blood viscosity has been associated with elevated carotid IMT (15). Whole blood and plasma viscosities were measured at 37°C by using a Brookfield cone and plate viscometer as previously described (15, 23). All measurements were performed within 2 h after blood withdrawal. Viscosity values obtained at the highest shear rate (i.e., 60 rpm) are reported.
Body composition. Total fat mass and fat-free mass were determined by using dual-energy X-ray absorptiometry (Lunar) as previously described (5, 36). Waist circumference was measured at the narrowest part of the torso (32).
Daily physical activity. Estimated daily energy expenditure was assessed by the Stanford Physical Activity Questionnaire (26) and was used to document the absence of regular aerobic and other types of exercise in the sedentary subjects.
Maximal oxygen consumption. Maximal oxygen consumption was assessed with on-line computer-assisted open-circuit spirometry during incremental treadmill exercise as described in detail previously (33). Heart rate (electrocardiograph) and rating of perceived exertion (Borg scale) were also measured throughout the protocol.
Metabolic risk factors for atherosclerosis. Fasting plasma concentrations of cholesterol, glucose, insulin, and fibrinogen were performed in the clinical laboratory affiliated with the General Clinical Research Center as previously described (32).
Exercise Intervention
Subjects underwent a supervised orientation and thereafter performed exercise on their own. Initially, subjects walked 25-30 min/day, 3-4 days/wk, at a relatively low intensity of exercise (~60% of their individually determined maximal heart rate obtained during the measurement of maximal oxygen consumption). As their exercise tolerance improved, the intensity and duration of walking were increased to 40-45 min/day, 4-6 days/wk, at an intensity of 70-75% of maximal heart rate (30-40% of subjects were advised to walk/jog or jog continuously to reach their target heart rate range). Subjects recorded their actual exercise and any additional physical activity on a daily basis. Adherence to the exercise prescription was documented through the use of heart rate monitors (Polar heart rate monitor) and physical activity logs as described previously (30).Statistical Analyses
Two-way (age group × exercise status) ANOVA was used to assess the results for the cross-sectional study. Repeated-measures ANOVA was used to examine the results for the intervention study. In the case of a significant F value, a post hoc test using Newman-Keuls method was used to identify significant differences among mean values. Univariate regression and correlation analyses were used to analyze the relations between variables of interest. Forward stepwise multiple-regression analyses were used to identify significant independent determinants for carotid IMT. To do so, only variables that had significant univariate correlations with carotid IMT were included in the model. Because plasma and blood viscosity values were obtained in only ~50% of the subjects, analyses of these variables were performed on this sample of the overall study population. All data are reported as means ± SE.| |
RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Cross-sectional Study
Table 1 shows the subject characteristics for the cross-sectional study. There were no significant group differences in height or brachial systolic blood pressure. Body mass and body mass index were lower in endurance-trained than in sedentary men (P < 0.05). In general, percent body fat values increased with age and were lower in endurance-trained than in sedentary men. Maximal oxygen consumption values decreased with age and were higher in endurance-trained men at any age than in sedentary men (P < 0.01). Total and low-density lipoprotein cholesterol concentrations generally increased with age (Table 2). Fasting plasma insulin concentrations were lower in endurance-trained than in sedentary men (P < 0.05). There were no significant group differences in fasting plasma glucose, blood viscosity, or plasma viscosity.
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In both groups, carotid IMT and IMT/lumen ratio were progressively
higher in the young, middle-aged, and older men (Fig.
1). The magnitude of increase in carotid
IMT from young to older adulthood was ~50% in both groups. There
were no statistically significant differences between sedentary and
endurance-trained men at any age. Carotid artery diameter modestly
increased with age in both groups (P < 0.05) but was not
different between sedentary and endurance-trained men at any age (data
not shown).
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Carotid systolic blood pressure increased progressively with age in
both groups (Fig. 2). However, there were
no significant differences between sedentary and endurance-trained men
at any age.
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In the overall population, carotid IMT was significantly related to
body fat percent (r = 0.34), waist circumference (0.29), maximal oxygen consumption (
0.47), brachial systolic blood pressure (0.21), total cholesterol (0.28), low-density-lipoprotein cholesterol (0.27), carotid systolic blood pressure (0.63), and carotid pulse pressure (0.45). No other variables were significantly related to
carotid IMT. When we performed a stepwise regression analysis to
establish which of these correlates were independent predictors of
carotid IMT, carotid systolic blood pressure appeared first in the
analysis and accounted for 33% of the variability (P < 0.001). An additional 5% of the variability was explained by maximal oxygen consumption (P < 0.05).
Intervention Study
All 18 subjects completed the exercise intervention study. Subjects exercised for an average of 5.3 ± 0.3 days/wk, 42.3 ± 1.4 min/session, and at 73 ± 1% of maximal heart rate. Maximal oxygen consumption increased significantly in response to exercise training (Table 3). There were no significant changes in any other variables.
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Carotid IMT, carotid IMT/lumen ratio, and carotid systolic blood
pressure did not change in response to aerobic exercise intervention (Fig. 3). Carotid artery IMT values
before and after exercise intervention were identical. Carotid lumen
diameter did not change with exercise training (6.9 ± 0.2 mm
before vs. 7.0 ± 0.2 after). When a subgroup of subjects in the
older age group was selected (n = 7), the results were
essentially the same; carotid IMT did not change with exercise
intervention.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The salient findings of the present study were as follows. First, carotid artery IMT increases with advancing age even in healthy endurance exercise-trained men, indicating a primary effect that is independent of sedentary lifestyle. Second, regular vigorous endurance exercise does not obviously attenuate the age-associated increase in IMT. Third, a 3-mo aerobic exercise intervention does not affect carotid IMT in previously sedentary middle-aged and older men. Fourth, the apparent inability of regular aerobic exercise to favorably modulate the increase in carotid IMT with age appears to be due, at least in part, to a lack of effect on the age-associated elevation in carotid distending pressure. Thus our results do not support the hypothesis that an attenuation of the increase in carotid IMT with age may be a mechanism contributing to the reduced incidence of stroke in middle-aged and older physically active adults.
Our laboratory (37) and others (12, 28) have reported that carotid artery IMT increases with advancing age in sedentary men and women. However, because a sedentary lifestyle is independently associated with increased incidence of cardiovascular diseases (1), it was possible that the age-related increase in carotid IMT may have been due to the effect of prolonged physical inactivity rather than some event(s) linked more directly to aging per se. The results of the present study indicate that age-related increases in carotid artery IMT can occur in the absence of a sedentary lifestyle.
Previous cross-sectional studies comparing sedentary and physically active adults have produced inconsistent findings regarding the influence of regular exercise on carotid artery IMT. Specifically, habitual exercise has been associated with lower (9, 31), not different (9, 24, 27), or even greater (3, 19) carotid artery IMT. In the Atherosclerosis Risk in Communities study (9), carotid IMT was associated with work-related, but not sports-related, physical activity.
We believe that the results of the present study provide more definitive insight regarding the potential influence of regular exercise on carotid IMT than previous investigations for several reasons. First, unlike earlier studies that used estimation of physical activity levels via questionnaires as the sole basis for subject group classification, we also employed the objective criterion of aerobic fitness (i.e., maximal oxygen consumption) (22). Results obtained from activity questionnaires can be associated with substantial error, and, thus, a misclassification of subjects to the appropriate physical activity group may have contributed to the marked variability in prior findings. Second and relatedly, it is possible that the lack of association between habitual exercise and carotid IMT in some previous investigations may have been due in part to relatively modest physical activity levels in the so-called "active" groups. To avoid this potential confound, in the present study we maximized our ability to show group differences (if present) by comparing sedentary adults with endurance-trained men who had performed vigorous endurance exercise greater than five times per week and were active in local road running races. Third, in the present study we used complimentary cross-sectional and intervention study designs. The latter approach allowed us to isolate the direct effects of exercise by excluding the influence of constitutional factors that can confound the interpretation of results based only on cross-sectional group comparisons.
In our intervention study, subjects exercised for an average of 5.3 ± 0.3 days/week, 42.3 ± 1.4 min/session, and at 73 ± 1% of maximal heart rate for 3 mo. Maximal oxygen consumption increased modestly but significantly in response to exercise training in previously sedentary middle-aged and older men. However, we observed no changes in carotid IMT or carotid IMT/lumen ratio. It may be argued that a 3-mo period simply is insufficient for any intervention to reduce carotid IMT. However, reductions in carotid IMT, combined with the reduction in arterial blood pressure, have been demonstrated after only 2 mo of pharmacological intervention in hypertensive humans (17). Moreover, the results of the intervention study were consistent with those in the cross-sectional study. In the latter, middle-aged and older distance runners who had been performing strenuous endurance exercise essentially on a daily basis for ~20-25 yr demonstrated similar levels of carotid IMT as their sedentary peers. Thus we do not believe that the duration of our intervention limits our conclusions regarding the effects of habitual exercise on carotid IMT.
The present study was not designed specifically to determine the mechanism underlying the effect (or, in this case, lack of effect) of regular exercise on carotid IMT with age. However, we believe that our data may provide insight into this question. We recently showed that the age-related increase in local (carotid) distending pressure may be mechanistically linked to the increase in carotid IMT (37). This process is thought to constitute a functional adaptation intended to maintain normal wall stress. As such, we believe that the inability of regular aerobic exercise to prevent or even attenuate age-related increases in carotid IMT may be due, at least in part, to a lack of effect on local distending pressure. At least four observations support this view. First, carotid systolic blood pressure was strongly and positively associated with carotid IMT in the overall study population (r = 0.63). Second, when we performed stepwise regression analyses to establish independent predictors of carotid IMT, carotid systolic blood pressure appeared first in the analysis and accounted for 33% of the interindividual variability. Third, the temporal patterns of the age-related elevations in carotid artery IMT and carotid systolic blood pressure were similar (Figs. 1 and 2). Fourth, the absence of reductions in carotid IMT with exercise intervention was accompanied by a corresponding absence of reduction in carotid systolic blood pressure.
A lack of a modulatory effect of regular exercise on carotid systolic blood pressure appears to contradict with our previous observation that regular aerobic exercise can attenuate reductions in and partially restore the loss of central arterial compliance with age. We wish to emphasize that the increase in central systolic blood pressure with age is thought to be due to not only the reduction in arterial compliance but also an increase in pulse waves reflected back from the periphery as well (18). Our present results may suggest that the earlier return and higher magnitude of wave reflection coming back from the periphery may be a more important factor determining the increase in central systolic blood pressure with age in healthy adults. The wave reflection represents a summation of reflected waves coming back from the peripheral vasculature, especially in the lower body (18). In this context, recent data from our laboratory indicated that femoral vascular resistance increases with age in healthy humans (5) and that regular aerobic exercise does not appear to influence this age-related change (4).
We should emphasize at least two important limitations of the present study. First, we studied only healthy men without evidence of overt chronic diseases. It is possible that regular aerobic exercise could have a beneficial effect on carotid IMT in middle-aged and older adults with clinically elevated levels of carotid IMT due to atherosclerosis. Thus our results relate more to the potential for regular exercise to prevent elevations in carotid IMT with advancing age in the absence of clinically documented disease, rather than as a therapeutic approach for patients with occlusive arterial disease. Second, high-resolution ultrasonography of the carotid artery cannot distinguish between the intimal and medial layers (29). As such, it is not possible to determine the nature of the specific changes in the arterial wall contributing to the increases in carotid IMT with age (i.e., diffusive intimal atherosclerosis, medial smooth muscle cell hypertrophy or hyperplasia, increased medial collagen deposition, etc.). Similarly, we cannot assess the possibility that regular exercise might have beneficial influences on the composition within the intima-media layer (e.g., changes in matrix metalloprotease activity and endothelial cell permeability). The development of new technology and the improvement of existing equipment would be expected to increase the precision and resolution of the IMT measurements (38).
In conclusion, our results do not support the hypothesis that regular aerobic exercise exerts its protective effect against stroke in part by attenuating the age-related increase in carotid IMT. This lack of modulatory effect on carotid IMT may be due to the apparent inability of habitual exercise to prevent or reduce the age-associated elevation in carotid distending pressure.
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ACKNOWLEDGEMENTS |
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We thank Yoli Casas, Linda Shapiro, Jayne Semmler, and Teresa Wilson for technical assistance for the present study.
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FOOTNOTES |
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This study was supported by American Heart Association Award 9960234Z (to H. Tanaka); by National Institutes of Health Awards AG-00847 (to H. Tanaka), AG-06537, AG-13038, and AG-16071 (to D. R. Seals) and HL-03840 (to C. A. DeSouza); and by General Clinical Research Center Grant 5-01-RR00051.
Address for reprint requests and other correspondence: H. Tanaka, Dept. of Kinesiology and Health Education, Univ. of Texas at Austin, Austin, TX 78712 (E-mail: htanaka{at}mail.utexas.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
10.1152/japplphysiol.00824.2001
Received 3 August 2001; accepted in final form 10 December 2001.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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P < 0.05 vs.
middle.
