Journal Logo

Basic Sciences: Original Investigations

A Longitudinal Study of Physical Activity and Heart Rate Recovery: CARDIA, 1987–1993

CARNETHON, MERCEDES R.1; JACOBS, DAVID R. JR2,3; SIDNEY, STEPHEN4; STERNFELD, BARBARA4; GIDDING, SAMUEL S.5; SHOUSHTARI, CHRISTIANA1; LIU, KIANG1

Author Information
Medicine & Science in Sports & Exercise: April 2005 - Volume 37 - Issue 4 - p 606-612
doi: 10.1249/01.MSS.0000158190.56061.32
  • Free

Abstract

The favorable effect of physical activity and improved fitness on cardiovascular disease morbidity (5,24,27) and mortality (15,26,36) and total mortality (26) is well established. Numerous physiologic mechanisms could account for this association. The autonomic nervous system is a compelling system to investigate because it exerts a fine degree of control over the cardiovascular system—from arterial and venous constriction to heart rate (19). In healthy individuals, dual innervation from sympathetic and parasympathetic (vagal) components permits simultaneous antagonistic contributions. Most commonly, the sympathetic system facilitates stroke volume, heart rate and rhythm, arterial and venous constriction, and cardiac contractility, whereas the parasympathetic system inhibits those same functions (30). Autonomic dysfunction has been implicated in the development of cardiovascular disease risk factors such as hypertension (32) and diabetes (6,7), and has been directly related to coronary heart disease (CHD) morbidity (33) and mortality (47), including sudden cardiac death (37) and total mortality (9,13,14).

With one exception (35), the majority of research on the association between physical activity or fitness and autonomic function has been conducted in small (N < 100) highly selected population segments, thus limiting the generalizability of results. Although most studies report a positive association between physical activity and autonomic function, the strength of this association varies with the type and intensity of physical activity studied. This question has not been tested longitudinally in a large population-based sample of men and women with a range of physical activity patterns.

Heart rate recovery (HRR) is the return of heart rate from maximal intensity to preexercise levels after cessation of a graded exercise test. Recovery is thought to result primarily from parasympathetic reactivation, thus making HRR a useful estimate of autonomic nervous system function (2,21). HRR has been shown to predict mortality independently of other fitness parameters and markers atherosclerosis severity (11). In a large population sample of young adult men and women, we tested the hypothesis that higher levels of physical activity were associated with better parasympathetic function, as estimated by faster HRR from exercise treadmill testing. Additionally, we investigated whether this pattern was consistent across demographic characteristics and measured covariates. Using multiple measurements of physical activity and HRR over 7 yr, we tested the hypothesis that increasing or maintaining physical activity was associated with more favorable changes in parasympathetic function over time.

METHODS

Study Population and Design

The Coronary Artery Risk Development in Young Adults (CARDIA) Study is a longitudinal cohort study of the evolution of CHD risk factors in a population sample of 5115 adults aged 18–30 yr at baseline (1985–1986). Roughly equal numbers of black and white men and women were sampled from three U.S. geographic areas—Birmingham, AL, Chicago, IL, Minneapolis, MN—and from the membership of a large, integrated health care delivery system in Oakland, CA. Participants were reexamined 2, 5, 7, 10, and 15 yr after baseline; examinations through year 7 (when follow-up exercise testing was performed) are used for this report. A detailed description of study design, sampling, and response rates has been published (17).

For this report, we excluded 154 participants who did not complete an exercise treadmill test at baseline, an additional 18 in whom HRR could not be calculated, one who did not complete the physical activity interview, three pregnant women, and 127 who reported using β-blockers, angiotensin-converting enzyme inhibitors, calcium channel blockers, medications to treat congestive heart failure, antiarrhythmics, and antianginals. After excluding 51 participants without a preexercise heart rate value, we excluded 1315 participants who did not exercise to at least 80% of their heart rate reserve during the exercise test, calculated as follows: [(maximum heart rate − resting heart rate)/(220 − age − resting heart rate] × 100 (49). Baseline cross-sectional analyses included 3446 participants. For longitudinal analyses, we additionally excluded 634 participants who did not attend the 7-yr examination, 1 person who reported a history of myocardial infarction, 958 who did not complete the exercise test, 2 persons missing a 2-min recovery heart rate, 27 on the medications listed above, 6 without a preexercise heart rate, and 191 who did not exercise to 80% of their heart rate reserve; 1627 participants were included in longitudinal analyses. The institutional review boards for the protection of human subjects for the participating study sites provided approval for the study, and written informed consent was obtained from all participants.

Data Collection

Physical activity.

At each examination, self-reported physical activity was ascertained by an interviewer-administered questionnaire designed for CARDIA. Participants were asked about the frequency of participation in 13 different activity categories (eight vigorous and five moderate) of recreational sports, exercise, leisure, and occupational activities over the previous 12 months. Vigorous activities included running, racquet sports, bicycling faster than 10 miles·h−1, swimming, vigorous exercise classes, sports (e.g., basketball, football), heavy lifting, carrying or digging on the job, and home activities such as snow shoveling or lifting heavy objects. Moderate activities included nonstrenuous sports (e.g., softball), walking, bowling/golf, home maintenance (e.g., gardening, raking), and calisthenics. Because participants were not asked explicitly about duration of activity, physical activity scores are expressed in exercise units (EU). Scores were computed by multiplying the frequency of participation by the intensity of the activity separately for heavy (i.e., vigorous) and moderate activities. A score of 100 EU is roughly equivalent to participation in a vigorous activity, 2 or 3 h·wk−1 for 6 months of the year. The reliability and validity of the instrument is comparable to other activity questionnaires (22,23).

Graded exercise testing.

At baseline and year 7, all medically eligible participants underwent a graded symptom-limited maximal exercise test according to the modified Balke protocol (42). Participants were excluded from participating in the treadmill test for the following reasons: acute illness with fever, history of CHD or exercise-induced asthma, abnormal resting ECG, cardiovascular medications except antihypertensives, or resting blood pressure > 160 mm Hg (systolic) or 100 mm Hg (diastolic) (42). In brief, the test included up to nine 2-min stages of progressively increasing difficulty; participants were asked to exercise to maximal exertion. At the end of each stage, and at 1 (standing), 2 (seated), and 3 (seated) min after cessation of the test, heart rate and blood pressure were measured. All participants included in this analysis achieved at least 95% of their age-predicted maximum heart rate.

HRR was calculated as the difference between maximum heart rate and seated heart rate 2 min after test cessation. HRR of ≤22 beats·min−1 was defined as “abnormal.” In prospective analyses, the change in HRR was calculated as the difference between HRR at year 7 and baseline. Greater declines in HRR represent worsening parasympathetic reactivation over time. Incident abnormal HRR was defined as HRR ≤ 22 beats·min−1 (38) at year 7 in participants who had normal HRR at baseline.

Other measurements.

Age, race, gender, cigarette smoking, family history of disease, and medication use were ascertained by interview. Height and weight were measured from participants in light examination clothes and no shoes. Body mass index (BMI) was calculated as the ratio of weight (kg) to standing height (m) squared (kg·m−2). Normal, overweight, and obese were categorized as BMI 18.5–25, 25–30, and ≥30 kg·m−2. Laboratory measurements of glucose were collected fasting (8 h minimum) according to standardized CARDIA procedures, and processed at central laboratories (16,48). Classification of impaired fasting glucose (fasting glucose 5.55–7 mmol·L−1) and diabetes (≥7 mmol·L−1) was made according to American Diabetes Association 2004 criteria (1). Before the exercise test and after 5 min of rest, blood pressure was measured from participants in the seated position three times at 1-min intervals; the average of the last two measurements was used. Blood pressure was classified according to JNC-7 criteria (10).

Statistical Analysis

We compared baseline characteristics of the study population across tertiles of total physical activity (labeled “low,” “moderate,” and “high”), and calculated tests of linear trend between physical activity score (continuously measured) and each covariate. Next, we tested whether the observed association between physical activity and HRR was consistent across strata of covariates using multiplicative interaction terms in multivariable linear and logistic regression models. In lieu of evidence of strong (P < 0.05) effect modification by any covariates except race–gender group (primarily differences in magnitude), we calculated the association between baseline physical activity (total, heavy, and moderate) and HRR in the total sample. Crude, demographic- (age, race, and gender), and multivariable-adjusted (smoking status, BMI, triglyceride/high density lipoprotein (HDL) cholesterol ratio, resting heart rate, and diastolic blood pressure) means and 95% confidence intervals (CI) of HRR were calculated from linear regression models. Variables were selected for multivariable analysis based on observed associations between those variables and physical activity or HRR in this data set, or based on previously reported relationships in the literature (41). The odds of having abnormal HRR (HRR ≤ 22 beats·min−1) was calculated from logistic regression models (odds ratios (OR)).

We investigated the association between physical activity change over 7 yr and HRR change using crude and multivariable-adjusted linear (mean changes) and logistic (incident abnormal HRR) regression models. Activity change was investigated per standard deviation, and categorized as an increase (change of >100 EU), stable (−100 to 100 EU), or a decrease (−100 or less EU) (45). Participants whose activity declined or remained stable were compared with those whose activity increased. Participants from Minnesota were determined to have violated the exercise test protocol at year 7 by holding onto the handrails, leading to artificially elevated treadmill test times (43); in a secondary analysis we excluded those participants. Because the effect estimates did not change, we report analyses of HRR change with Minnesota participants included. Statistical significance was defined at P < 0.05. All analyses were conducted using SAS software version 8.1 (SAS, Cary, NC).

RESULTS

Demographic characteristics of the study sample (N = 3446) are consistent with published reports of the full cohort (17). Half the participants were women, and 45% were black. Because black participants and women (54 and 68%, respectively) are more likely to be in the lowest tertile of physical activity participation, baseline characteristics were statistically adjusted for race and gender for comparison across activity tertiles (Table 1). Participants in the lowest tertile of activity were slightly older, heavier, and more likely to have had nonoptimal blood pressure and lipids. Compared with the most active participants, the least active spent less time on the treadmill, and supine and standing (preexercise) heart rates were higher.

TABLE 1
TABLE 1:
Baseline characteristics of the study population (N = 3446) by tertiles of total physical activity score.

Cross-sectional analyses.

At baseline, tertiles of total, heavy-, and moderate-intensity physical activity were directly associated with HRR recovery. Because total and heavy-intensity activity were so highly correlated (r = 0.95), and because moderate activity was not significantly associated with HRR in multivariable models, we report results only from total activity (Table 2). Participants who engaged in low and moderate levels of activity had slower HRR than participants who were the most physically active, even with adjustment for demographic characteristics, BMI, smoking status, resting heart rate, triglyceride/HDL cholesterol ratio, and blood pressure (model 3). Treadmill test duration was associated with physical activity (Table 1) and moderately with HRR (r = 0.15; P < 0.0001), so in secondary analyses we investigated whether the association between activity and HRR remained when adjusted for treadmill test duration. After adjustment for test duration, the association between total activity and HRR decreased by 31% to 0.6 beats·min−1 (SE = 0.2) per standard deviation increase in activity, but remained statistically significant (P < 0.01).

TABLE 2
TABLE 2:
Cross-sectional association of physical activity score and mean heart rate recovery (beats·min−1).

At baseline, 90 participants (2.6%) had abnormal HRR (≤22 beats·min−1). The odds of having abnormal HRR were twofold higher among participants who engaged in low physical activity compared with those who were the most active (Table 3). In secondary analyses, we adjusted for peak heart rate, and the effect estimates did not change. When we instead adjusted for treadmill test duration, the association between total activity and HRR attenuated 3% but remained statistically significant (OR = 1.4, 95% CI: 1.03, 1.9, per SD).

TABLE 3
TABLE 3:
Cross-sectional association of physical activity score and abnormal (≤22 beats·min−1) heart rate recovery.

Mean HRR was faster among younger, black, and male participants, as well as those with normal body weight, normal fasting glucose, and optimal blood pressure. Current smokers and participants without a family history of diabetes or premature CHD had faster HRR. Physical activity was positively associated with mean HRR across categories of all covariates with no evidence of effect modification except for race and gender (P interaction = 0.01). Although the pattern of association between physical activity and HRR is qualitatively similar across race and gender, HRR was notably higher at every level of physical activity among black men (low: 45.2, moderate: 45.7, high: 47.3 beats·min−1) compared with black women (low: 41.9; moderate: 41.6; high 44.0 beats·min−1), white men (low: 41.3; moderate: 43.5; high: 44.8 beats·min−1), and white women (low: 38.7; moderate: 42.6; high: 44.9 beats·min−1). There were no meaningful differences by covariates for the odds of having abnormal HRR by race–gender or any other covariates (data not shown), with the exception of blood pressure. The magnitude of the association between low and high physical activity was slightly higher among persons with nonoptimal (≥130/85 mm Hg; OR = 3.8, 95% CI: 1.5, 9.6) versus optimal (OR = 2.2, 95% CI: 1.2, 4.1) blood pressure (P interaction = 0.047).

Longitudinal analyses.

Between baseline and year 7, physical activity decreased an average of 90 EU (range: −1491 to 1055 EU; SD: 295). The largest proportion of participants decreased their activity (N = 742, 46%), whereas 503 (31%) remained stable, and 380 (23%) increased activity. Participants who were the most physically active at baseline had the smallest activity decline (r = −0.57, P < 0.0001). Over 7 yr, HRR declined an average of 2.5 beats·min−1 (range: −85 to 58 beats·min−1; SD: 10.8). Among participants with normal HRR at baseline, 43 (2.7%) developed abnormal HRR at year 7. HRR at baseline was inversely (r = −0.57, P < 0.0001) associated with HRR change between examinations.

Because the association between physical activity change and HRR change did not differ by baseline covariates, only pooled analyses are presented. Although participants in each category of physical activity change experienced a decline in HRR, participants whose activity increased (−1.5 beats·min−1, 95% CI: −0.4, −2.6) or remained stable (−1.8 beats·min−1, 95% CI: −0.8, −2.7) had smaller HRR declines with time than those participants whose activity decreased (−3.5 beats·min−1, 95% CI: −2.8, −4.3; P < 0.01 compared with increased activity) in models adjusted for age, race, and gender. HRR change was 0.85 beats·min−1 (SE = 0.27) higher (P < 0.01) per standard deviation increase in physical activity change. In a multivariable model (Fig. 1), we adjusted for both baseline physical activity level and HRR in addition to demographic characteristics, baseline BMI, triglyceride/HDL ratio, resting heart rate, smoking status, incident diabetes, and diastolic blood pressure; results remained highly statistically significant (P < 0.0001). HRR change was 1.06 beats·min−1 (SE = 0.28) higher per standard deviation increase in physical activity change (P = 0.0002). Participants whose physical activity decreased were three times more likely to develop abnormal HRR over time than participants whose activity increased (Fig. 2), but increasing activity per standard deviation was moderately (OR = 0.7), but nonsignificantly (95% CI: 0.5, 1.1), associated with a lower probability of developing abnormal HRR.

FIGURE 1— Adjusted (for age, race, gender, smoking status, baseline BMI, diastolic blood pressure, baseline HRR, and baseline physical activity score) mean change (95% confidence interval) in heart rate recovery (HRR) from baseline to examination year 7 by physical activity score change category. Physical activity change categories: Decrease = physical activity score change < −100, Stable = −100 to 100, Increase ≥ 100. **
FIGURE 1— Adjusted (for age, race, gender, smoking status, baseline BMI, diastolic blood pressure, baseline HRR, and baseline physical activity score) mean change (95% confidence interval) in heart rate recovery (HRR) from baseline to examination year 7 by physical activity score change category. Physical activity change categories: Decrease = physical activity score change < −100, Stable = −100 to 100, Increase ≥ 100. **:
P< 0.0001 decrease vs increase in physical activity and decrease vs stable physical activity change.
FIGURE 2— Adjusted (for age, race, gender, smoking status, baseline BMI, diastolic blood pressure, baseline HRR, and baseline physical activity score) odds ratios (95% confidence intervals) of incident abnormal heart rate recovery (HRR ≥ 22 beats·min−1) by physical activity change category. Physical activity change categories: Decrease = physical activity score change < −100, Stable = −100 to 100, Increase ≥ 100.
FIGURE 2— Adjusted (for age, race, gender, smoking status, baseline BMI, diastolic blood pressure, baseline HRR, and baseline physical activity score) odds ratios (95% confidence intervals) of incident abnormal heart rate recovery (HRR ≥ 22 beats·min−1) by physical activity change category. Physical activity change categories: Decrease = physical activity score change < −100, Stable = −100 to 100, Increase ≥ 100.

DISCUSSION

In this population-based cohort study of young adults, we observed that regular physical activity is associated with better autonomic function, as estimated by faster HRR from an exercise treadmill test. Furthermore, we observed that participants whose physical activity decreased over 7 yr had significantly greater declines in parasympathetic function with time than did participants who maintained or increased their physical activity during this period. These findings were consistent across strata of known correlates of poor autonomic function and persisted with secondary adjustment for total treadmill test duration and peak heart rate. While activity is positively associated with autonomic function across race and gender groups, black participants in this study sample, particularly black men, had faster HRR at each level of activity.

The activities related to better autonomic function in this study are a broad representation of physical activities that adults typically (at least 1 h in the past year) engage in, including leisure-time sports, household, and work activities. In addition to threshold effects relating the most activity to better autonomic functioning, we observed a positive dose–response association between activity and autonomic functioning across the range of scores. Our findings suggest that engaging in at least some vigorous activities that lead to sweating, increased body temperature, or shortness of breath (requirements for an activity to qualify as “vigorous” by our interviewers) is associated with better autonomic nervous system function, as moderate-intensity activity alone was not associated with improved autonomic function.

Prior studies have focused on differences in autonomic function between highly trained athletes and sedentary adults, and provide evidence that more activity and better fitness improve autonomic function (3,4,11,12,20,39,40,50). In a large population of consecutive patients undergoing diagnostic stress testing (N = 2428), Cole and colleagues (11) reported that the proportion of adults with abnormal 1-min HRR (<12 beats·min−1) was higher among adults with low exercise capacity. Our report extends upon these findings to demonstrate that slower HRR can also be observed in healthy young adults who self-report less physical activity.

Previous short duration (<1 yr) trials in small populations (N < 100) report that autonomic function can be modified with regular activity, but they do not describe how regular physical activity that a person engages in over years influences autonomic function. The established age-related declines in parasympathetic functioning (31,46) were blunted in adults who maintained or increased their physical activity over 7 yr in this study.

In our diverse population-based sample, we confirmed that physical activity is positively associated with autonomic function in healthy young adults, as well as adults who smoke cigarettes, are overweight or obese, or have elevated fasting glucose, nonoptimal blood pressure, or a family history of diabetes or premature myocardial infarction. Prior studies have addressed this question in postinfarction patients (34), obese children (18), and healthy participants across age groups (28,29,44), with findings similar to those we report.

Black participants had higher HRR at every level of physical activity as compared with their white counterparts, indicative of more favorable parasympathetic reactivation after exercise. This difference was particularly evident when stratified by race–gender group, as black men had the highest HRR compared with the three other race and gender strata. The effect modification we observed between physical activity and autonomic function by race–gender group appears to be a difference in magnitude (i.e., quantitative), which is typically of less concern than a difference in the direction of effect (i.e., qualitative). Although these findings are surprising in light of poorer health outcomes and a greater prevalence of cardiovascular comorbidity in black adults in this cohort and others, two other studies in the Atherosclerosis Risk in Communities cohort reported more favorable heart rate variability in the supine position (31) and in response to a postural change from supine to standing (8) in black compared with white participants.

One explanation for the observed finding among black participants in this report is that we may have selected black participants with the most favorable cardiorespiratory fitness. When we excluded participants who did not exercise to at least 80% capacity, a marker of chronotropic incompetence (49) that is independently associated with cardiovascular disease and mortality (25), a disproportionate number of black men and women were excluded. If those participants remaining in the sample are the healthiest, then it may be expected that their HRR was more favorable than their white peers; thus, our reports of effect modification should be interpreted with caution.

Our findings must be interpreted in light of some limitations. In this report, we are restricted to only one measure estimating autonomic function. Previous research has validated HRR as an estimate of parasympathetic reactivation after exercise (21), but it would be useful to confirm these findings using other markers of function that might estimate autonomic innervation or resting cardiovascular autonomic control in addition to response to provocation. Additionally, physical activity participation is ascertained by self-report (and thus subject to reporting bias) rather than objectively determined by devices such as an accelerometer or pedometer. However, our reporting of such strong and significant associations using self-reported physical activity is also a strength of this study. Our findings can thus apply to other epidemiological investigations where the objective measurement of cardiorespiratory fitness is unavailable or cumbersome to measure.

In conclusion, we reported for the first time in a large, population-based sample of black and white men and women that physical activity is associated with faster HRR from an exercise treadmill test, a marker of favorable parasympathetic response to exercise. Further, regular physical activity over time can blunt the age-related declines in autonomic nervous system function. This finding persists in subgroups of adults with comorbid disease, and is present among both white and black men and women. Improved autonomic nervous system activity with exercise may be one mechanism by which physical activity is associated with better health outcomes.

REFERENCES

1. Anonymous. Diagnosis and classification of diabetes mellitus. Diabetes Care 27:5S–10S, 2004.
2. Arai, Y., J. P. Saul, P. Albrecht, et al. Modulation of cardiac autonomic activity during and immediately after exercise. Am. J. Physiol. 256:H132–H141, 1989.
3. Aubert, A. E., F. Beckers, and D. Ramaekers. Short-term heart rate variability in young athletes. J. Cardiol. 37(Suppl. 1):85–88, 2001.
4. Bonaduce, D., M. Petretta, V. Cavallaro, et al. Intensive training and cardiac autonomic control in high level athletes. Med. Sci. Sports Exerc. 30:691–696, 1998.
5. Carnethon, M. R., S. S. Gidding, R. Nehgme, S. Sidney, D. R. Jacobs, Jr., and K. Liu. Cardiorespiratory fitness in young adulthood and the development of cardiovascular disease risk factors. JAMA 290:3092–3100, 2003.
6. Carnethon, M. R., S. H. Golden, A. R. Folsom, W. Haskell, and D. Liao. Prospective investigation of autonomic nervous system function and the development of type 2 diabetes: the Atherosclerosis Risk in Communities Study, 1987–1998. Circulation 107:2190–2195, 2003.
7. Carnethon, M. R., D. R. Jacobs, Jr., S. Sidney, and K. Liu. Influence of autonomic nervous system dysfunction on the development of type 2 diabetes: the CARDIA study. Diabetes Care 26:3035–3041, 2003.
8. Carnethon, M. R., D. Liao, G. W. Evans, W. E. Cascio, L. E. Chambless, and G. Heiss. Correlates of the shift in heart rate variability with an active postural change in a healthy population sample: the Atherosclerosis Risk in Communities Study. Am. Heart J. 143:808–813, 2002.
9. Carnethon, M. R., D. Liao, G. W. Evans, et al. Does the cardiac autonomic response to postural change predict incident coronary heart disease and mortality? The Atherosclerosis Risk in Communities Study. Am. J. Epidemiol. 155:48–56, 2002.
10. Chobanian, A. V., G. L. Bakris, H. R. Black, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 Report. JAMA 289:2560–2571, 2003.
11. Cole, C. R., E. H. Blackstone, F. J. Pashkow, C. E. Snader, and M. S. Lauer. Heart-rate recovery immediately after exercise as a predictor of mortality. N. Engl. J. Med. 341:1351–1357, 1999.
12. De Meersman, R. E. Heart rate variability and aerobic fitness. Am. Heart J. 125:726–731, 1993.
13. Dekker, J., E. Schouten, P. Klootwijk, J. Pool, C. Sweene, and D. Kromhout. Heart rate variability from short electrocardiographic recordings predicts mortality from all causes in middle-aged and elderly men: the Zutphen Study. Am. J. Epidemiol. 145:899–908, 1997.
14. Dekker, J. M., R. S. Crow, A. R. Folsom, et al. Low heart rate variability in a 2-minute rhythm strip predicts risk of coronary heart disease and mortality from several causes: the ARIC Study. Circulation 102:1239–1244, 2000.
15. Ekelund, L. G., W. L. Haskell, J. L. Johnson, F. S. Whaley, M. H. Criqui, and D. S. Sheps. Physical fitness as a predictor of cardiovascular mortality in asymptomatic North American men: the Lipid Research Clinics Mortality Follow-up Study. N. Engl. J. Med. 319:1379–1384, 1988.
16. Friedewald, W. T., R. I. Levy, and D. S. Fredrickson. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin. Chem. 18:499–502, 1972.
17. Friedman, G. D., G. R. Cutter, R. P. Donahue, et al. CARDIA: study design, recruitment, and some characteristics of the examined subjects. J. Clin. Epidemiol. 41:1105–1116, 1988.
18. Gutin, B., P. Barbeau, M. S. Litaker, M. Ferguson, and S. Owens. Heart rate variability in obese children: relations to total body and visceral adiposity, and changes with physical training and detraining. Obes. Res. 8:12–19, 2000.
19. Hainsworth, R. The control and physiological importance of heart rate. In: Heart Rate Variability, M. Malik and A. J. Camm (Eds.). Armonk, NY: Futura, 1995, pp. 3–19.
20. Hedelin, R., P. Bjerle, and K. Henriksson-Larsen. Heart rate variability in athletes: relationship with central and peripheral performance. Med. Sci. Sports Exerc. 33:1394–1398, 2001.
21. Imai, K., H. Sato, M. Hori, et al. Vagally mediated heart rate recovery after exercise is accelerated in athletes but blunted in patients with chronic heart failure. J. Am. Coll. Cardiol. 24:1529–1535, 1994.
22. Jacobs, D. R., L. Hahn, W. L. Haskell, P. Pirie, and S. Sidney. Validity and reliability of short physical activity history: CARDIA Study and the Minnesota Heart Health Program. J. Cardiopulm. Rehabil. 9:448–459, 1989.
23. Jacobs, D. R., Jr., B. E. Ainsworth, T. J. Hartman, and A. S. Leon. A simultaneous evaluation of 10 commonly used physical activity questionnaires. Med. Sci. Sports Exerc. 25:81–91, 1993.
24. Laaksonen, D. E., H.-M. Lakka, J. T. Salonen, L. K. Niskanen, R. Rauramaa, and T. A. Lakka. Low levels of leisure-time physical activity and cardiorespiratory fitness predict development of the metabolic syndrome. Diabetes Care 25:1612–1618, 2002.
25. Lauer, M. S., G. S. Francis, P. M. Okin, F. J. Pashkow, C. E. Snader, and T. H. Marwick. Impaired chronotropic response to exercise stress testing as a predictor of mortality. JAMA 281:524–529, 1999.
26. Lee, C. D., S. N. Blair, and A. S. Jackson. Cardiorespiratory fitness, body composition, and all-cause and cardiovascular disease mortality in men. Am. J. Clin. Nutr. 69:373–380, 1999.
27. Lee, I.-M., H. D. Sesso, and R. S. Paffenbarger, Jr. Physical activity and coronary heart disease risk in men: does the duration of exercise episodes predict risk? Circulation 102:981–986, 2000.
28. Lee, M. S., H. J. Huh, B. G. Kim, et al. Effects of Qi-training on heart rate variability. Am. J. Chin. Med. 30:463–470, 2002.
29. Leicht, A. S., G. D. Allen, and A. J. Hoey. Influence of age and moderate-intensity exercise training on heart rate variability in young and mature adults. Can. J. Appl. Physiol. 28:446–461, 2003.
30. Levy, M. N. Autonomic interactions in cardiac control. Ann. N. Y. Acad. Sci. 601:209–221, 1990.
31. Liao, D., R. W. Barnes, L. E. Chambless, R. J. Simpson, Jr., P. Sorlie, and G. Heiss. Age, race, and sex differences in autonomic cardiac function measured by spectral analysis of heart rate variability—the ARIC Study: Atherosclerosis Risk in Communities. Am. J. Cardiol. 76:906–912, 1995.
32. Liao, D., J. Cai, R. W. Barnes, et al. Association of cardiac autonomic function and the development of hypertension: the ARIC Study. Am. J. Hypertens. 9:1147–1156, 1996.
33. Liao, D., M. Carnethon, G. W. Evans, W. E. Cascio, and G. Heiss. Lower heart rate variability is associated with the development of coronary heart disease in individuals with diabetes: the atherosclerosis risk in communities (ARIC) study. Diabetes 51:3524–3531, 2002.
34. Pardo, Y., C. N. Merz, I. Velasquez, M. Paul-Labrador, A. Agarwala, and C. T. Peter. Exercise conditioning and heart rate variability: evidence of a threshold effect. Clin. Cardiol. 23:615–620, 2000.
35. Rennie, K. L., H. Hemingway, M. Kumari, E. Brunner, M. Malik, and M. Marmot. Effects of moderate and vigorous physical activity on heart rate variability in a British study of civil servants. Am. J. Epidemiol. 158:135–143, 2003.
36. Rockhill, B., W. C. Willett, J. E. Manson, et al. Physical activity and mortality: a prospective study among women. Am. J. Public Health 91:578–583, 2001.
37. Schwartz, P. J., M. T. La Rovere, and E. Vanoli. Autonomic nervous system and sudden cardiac death: experimental basis and clinical observations for post-myocardial infarction risk stratification. Circulation 85:I77–I91, 1992.
38. Shetler, K., R. Marcus, V. F. Froelicher, et al. Heart rate recovery: validation and methodologic issues. J. Am. Coll. Cardiol. 38:1980–1987, 2001.
39. Shin, K., H. Minamitani, S. Onishi, H. Yamazaki, and M. Lee. Autonomic differences between athletes and nonathletes: spectral analysis approach. Med. Sci. Sports Exerc. 29:1482–1490, 1997.
40. Shin, K., H. Minamitani, S. Onishi, H. Yamazaki, and M. Lee. The power spectral analysis of heart rate variability in athletes during dynamic exercise: part I. Clin. Cardiol. 18:583–586, 1995.
41. Shishehbor, M. H., B. J. Hoogwerf, and M. S. Lauer. Association of triglyceride-to-HDL cholesterol ratio with heart rate recovery. Diabetes Care 27:936–941, 2004.
42. Sidney, S., W. L. Haskell, R. Crow, et al. Symptom-limited graded treadmill exercise testing in young adults in the CARDIA study. Med. Sci. Sports Exerc. 24:177–183, 1992.
43. Sidney, S., B. Sternfeld, W. L. Haskell, C. P. Quesenberry, Jr., R. S. Crow, and R. J. Thomas. Seven-year change in graded exercise treadmill test performance in young adults in the CARDIA study: Cardiovascular Risk Factors in Young Adults. Med. Sci. Sports Exerc. 30:427–433, 1998.
44. Stein, P. K., A. A. Ehsani, P. P. Domitrovich, R. E. Kleiger, and J. N. Rottman. Effect of exercise training on heart rate variability in healthy older adults. Am. Heart J. 138:567–576, 1999.
45. Sternfeld, B., S. Sidney, D. R. Jacobs, Jr., M. C. Sadler, W. L. Haskell, and P. J. Schreiner. Seven-year changes in physical fitness, physical activity, and lipid profile in the CARDIA study: Coronary Artery Risk Development in Young Adults. Ann. Epidemiol. 9:25–33, 1999.
46. Tsuji, H., J. Ferdinand J Venditti E. S. Manders, et al. Determinants of heart rate variability. J. Am. Coll. Cardiol. 28:1539–1546, 1996.
47. Tsuji, H. F. Venditti, Jr., E. Manders, et al. Reduced heart rate variability and mortality risk in an elderly cohort: the Framingham Heart Study. Circulation 90:878–883, 1994.
48. Warnick, G. R., J. Benderson, and J. J. Albers. Dextran sulfate-Mg2+ precipitation procedure for quantitation of high-density-lipoprotein cholesterol. Clin. Chem. 28:1379–1388, 1982.
49. Wilkoff, B. L., and R. E. Miller. Exercise testing for chronotropic assessment. Cardiol. Clin. 10:705–717, 1992.
50. Yataco, A. R., L. A. Fleisher, and L. I. Katzel. Heart rate variability and cardiovascular fitness in senior athletes. Am. J. Cardiol. 80:1389–1391, 1997.
Keywords:

NERVOUS SYSTEM; AUTONOMIC; EPIDEMIOLOGY; LONGITUDINAL STUDIES

©2005The American College of Sports Medicine