Introduction

Current physical activity guidelines postulate that different activities can be combined to achieve a minimum recommended dose, including activities of different intensities.^1–7 Activities that expend 3- to 6-fold the energy expenditure of sitting at rest (3–6 metabolic equivalents [METs], 1 MET=3.5 mL O₂·kg⁻¹·min⁻¹) are defined as moderate, those that expend more as vigorous, and less as light.¹ Walking is generally performed at moderate intensity⁸ and is specifically recommended by the Centers for Disease Control,¹ the American Heart Association,² the American College of Sports Medicine,^1,2 and others,^6,7 but whether equivalent doses of moderate and vigorous physical activity yield the same long-term health benefits remains unresolved.⁹

The current analyses examined whether equivalent energy expenditure by moderate and vigorous exercise produces similar reductions in coronary heart disease (CHD) risk factors. To this end, we examined the associations of incident hypertension, hypercholesterolemia (high cholesterol), and type 2 diabetes mellitus to reported exercise in the National Runners’ Health Study II and the National Walkers’ Health Study.^10–12 Walking and running provide an ideal test of the health benefits of moderate-intensity versus vigorous-intensity exercise because they involve the same muscle groups. In addition, the National Runners’ and Walkers’ Health Studies assess running and walking energy expenditure from weekly distance run or walk, which seems to be a better metric than the traditional time-based measurements used by other studies.^13–15

Materials and Methods

Materials and Methods are available in the online Supplement.

Results

There were 15 945 walkers (21.0% men), and 33 060 runners (51.4% men) eligible for analysis (Table 1). Baseline hypertension, hypercholesterolemia, and diabetes mellitus excluded 3271 walkers and 1841 runners, 2638 walkers and 2148 runners, 716 walkers and 249 runners from the analyses of incident hypertension, hypercholesterolemia, and diabetes mellitus, respectively. Table 1 presents the baseline characteristics of the cohorts. The combined cohorts were 89.1% white, 5.2% Hispanic, 1.8% Native American, 0.5% black, 2.3% Asian, and 1.2% other racial category. Energy expended by running in the runners was more than twice that reported for walking by walkers. The majority of the other exercise reported by runners and walkers was vigorous.

Runners Versus Walkers

The runners had 38% lower risk for incident hypertension, 36% lower risk for hypercholesterolemia, and 71% lower risk for diabetes mellitus than walkers (Table 2). These differences were independent of the reported exercise but were substantially reduced by adjustment for body mass index (BMI), that is, to 14%, 18%, and 41% lower risk for hypertension, hypercholesterolemia, and diabetes mellitus, respectively (Table 3).

Energy Expended by Running Versus Walking

Equivalent energy spent running and walking was associated with comparable risk reductions for hypertension, hypercholesterolemia, and diabetes mellitus (Figure 1). Moreover, there were incremental reductions in risk at 2-, 3-, and 4-times the dose of exercise recommended by the American Heart Association and the American College of Sports Medicine.²Table 2 shows that greater metabolic equivant hours per day (METh/d) run or walk was associated with significantly lower risks, respectively, for incident hypertension (P<10⁻⁷ and P<10⁻⁶), hypercholesterolemia (P<10⁻¹⁴ and P<10⁻⁸), and diabetes mellitus (P<10⁻⁵ and P<10⁻⁴). The risk reductions per METh/d were not significantly greater for running than walking for hypertension (running versus walking, P=0.06), hypercholesterolemia (P=0.04, significantly greater for walking, and not running), or diabetes mellitus (P=0.94). The equivalent benefits per METh/d run and METh/d walked persisted even after adjustment for BMI for hypertension (running versus walking, P=0.54) and hypercholesterolemia (P=0.56), but not for diabetes mellitus (running > walking, P=0.01; Table 3).

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Other Exercise

Higher levels of nonrunning vigorous exercises were also associated with lower risks of hypertension (P=0.003) and hypercholesterolemia (P=0.0008), but not diabetes mellitus (P=0.16). The METh/d reductions in risk were significantly less for nonrunning vigorous exercise than for running for hypertension: (running–other vigorous exercise, P=0.006), hypercholesterolemia (P<10⁻⁴), and diabetes mellitus (P=0.0006). Other moderate exercise was not significantly related to hypertension (P=0.72), hypercholesterolemia (P=0.79), or diabetes mellitus (P=0.72), and its risk reduction was significantly less than that of walking (walking–other moderate exercise; hypertension: P=0.0002; hypercholesterolemia: P<10⁻⁵; and diabetes mellitus: P=0.03).

Although METh/d for walking and running were calculated from distance and intensity, METh/d for other exercises were calculated from time (duration) and intensity. In part, the weak effects of other exercise may be attributable to its method of estimation rather than the activities themselves. To show that time-based energy estimation underestimates the association of exercise with incident hypertension, hypercholesterolemia, and diabetes mellitus, the analyses of Table 2 were repeated for METh/d run as calculated from reported time and intensity (not displayed), rather than distance (Table 2). This shows that the reductions in risk per METh/d run were much less for the time-based than the distance-based calculations (52% less for hypertension, 29% less for hypercholesterolemia, and 63% less for diabetes mellitus). When the time-based METh/d run and distance-based METh/d run were included together in the same survival analyses so that their coefficients could be compared directly, the distance-based estimates remained significant (hypertension: hazard ratio [HR] 0.961, P=0.0001; hypercholesterolemia: HR 0.963, P=10⁻⁶; and diabetes mellitus: HR 0.876, P=0.0002), whereas the time-based estimates were not (hypertension: HR 0.997, P=0.68; hypercholesterolemia: HR 0.994, P=0.25; and diabetes mellitus: HR 1.003, P=0.88), and in every case the risk reduction for the distance-based estimate was significantly greater than that of the time-based estimate (hypertension: P=0.01; hypercholesterolemia: P=0.007; and diabetes mellitus: P=0.008). Thus, time-based estimates of exercise energy expenditure seem to substantially underestimate the reductions in hypertension, hypercholesterolemia, and diabetes mellitus risk.

Strengthening Exercise

When METh/d of strengthening and nonstrengthening exercises replaced other exercise in the analyses of Table 2, the effects of strengthening exercises and nonstrengthening exercise did not differ significantly from each other for incident hypertension (P=0.08), hypercholesterolemia (P=0.21), or diabetes mellitus (P=0.13). Specifically, the per METh/d effect of strengthening exercise was modestly significant for hypercholesterolemia (HR, 0.973; 95% confidence interval [CI], 0.949–0.998; P=0.03) and diabetes mellitus (HR, 0.902; 95% CI, 0.802–0.999; P=0.05), but not hypertension (HR, 1.011; 95% CI, 0.982–1.040; P=0.49). Nonstrengthening other exercise was significantly associated with hypertension (HR, 0.983; 95% CI, 0.973–0.993; P=0.0007) and hypercholesterolemia risk (HR, 0.990; 95% CI, 0.983–0.998; P=0.01), but not diabetes mellitus risk (HR, 0.984; 95% CI, 0.957–1.009; P=0.21).

Running and Walking Intensity

Within both walkers and runners, faster pace (per m/s) was associated with lower risks of hypertension (runners: HR, 0.609; 95% CI, 0.553–0.671; P<10⁻¹⁵; walkers: HR, 0.758; 95% CI, 0.639–0.899; P=0.002), hypercholesterolemia (runners: HR, 0.667; 95% CI, 0.619–0.720; P<10⁻¹⁵; walkers: HR, 0.823; 95% CI, 0.720–0.942; P=0.005), and diabetes mellitus (runners: HR, 0.433; 95% CI, 0.334–0.574; P<10⁻⁷; walkers: HR, 0.427; 95% CI, 0.331–0.573; P<10⁻⁹), which were, for the most part, independent of exercise dose but largely accounted for by BMI. There were no significant interactions between energy expended (METh/d) and intensity (m/s) to suggest that the same energy expended at a greater intensity produced a greater reduction in the risk of hypertension (significance of interaction, runners: P=0.13; walkers: P=0.33), hypercholesterolemia (runners: P=0.24; walkers: P=0.51), or diabetes mellitus (runners: P=0.98; walkers: P=0.71).

Coronary Heart Disease

The limited number of incident cases (530) provides limited statistical power for testing whether running and walking were associated with equivalent reductions in CHD risk. Nevertheless, the results were at least consistent with their equivalent effects per METh/d. There were 706 walkers (442 men, 264 women) and 370 runners (337 men, 33 women) excluded for preexisting CHD, leaving 189 de novo myocardial infarctions (102 walkers, 87 runners), 122 coronary artery bypass grafts (68 walkers, 54 runners), 185 angioplasties (93 walkers, 92 runners), and 34 angina cases (19 walkers, 15 runners). The runners, as a group, had 52% lower CHD risk than the walkers (P<10⁻⁵; Table 2), which was diminished somewhat by adjustment for BMI (P=0.002; Table 3). Table 2 shows that both METh/d run and METh/d walk were associated with significantly lower CHD risk (P=0.05 and P=0.01, respectively), which did not differ from each other (P=0.26). The hazard ratios of Figure 2 are consistent with equivalent CHD risk reductions for walking and running.

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Adjustment for Recruitment

Different recruitment rates between the runners (51.7%) and walkers (33.2%) did not affect the analyses. Repeating the analyses using only the first 33.2% of the runners recruited (to match the 33.2% recruitment rate in the walkers) produced results entirely consistent with the complete sample, as follows: (1) there were significant declines per METh/d run in risks for hypertension (4.2%; 95% CI, 2.4%–6.0%; P<10⁻⁵), hypercholesterolemia (3.8%; 95% CI, 2.5%–5.2%; P<10⁻⁷), and diabetes mellitus (11.4%; 95% CI, 4.4%–16.1% lower; P=0.001), whose differences from those of the walkers differed little from the complete sample (P=0.08, P=0.02, and P=0.60, respectively); (2) adjustment for BMI did not eliminate the significant declines in risk for hypertension (2.4%; 95% CI, 0.6%–4.3%; P=0.01), hypercholesterolemia (2.8%; 95% CI, 1.4%–4.1% lower; P=0.0001), and diabetes mellitus (6.9%; 95% CI, 0.6%–12.8%; P=0.03) and produced runner-walker differences comparable to the complete sample (P=0.66, P=0.97, and P=0.09, respectively), and (3) declines in CHD risk that were consistent with the complete sample (HR, 0.957; 95% CI, 0.906–1.008 per METh/d run; P=0.10).

Discussion

These results from these very large, prospective, cohorts suggest that equivalent doses of running (a vigorous exercise) and walking (a moderate exercise) are associated with largely equivalent reductions in the risks for new onset hypertension, hypercholesterolemia, and diabetes mellitus. These results also show continued reduction in risk for new onset hypertension, hypercholesterolemia, and diabetes mellitus when the exercise dose exceeds 450 to 750 MET minutes per week (1.1–1.8 METh/d), the amount of exertion currently recommended by the American Heart Association and the American College of Sports Medicine for health (Figure 1). Furthermore, it does not seem to matter whether these exercise doses are achieved by running or by walking. The equivalence of walking, the most commonly performed exercise,¹⁶ and running has not, to our knowledge, been previously demonstrated prospectively in a large sample, nor has the dose–response relationship between walking and these end points been assessed prospectively over such a broad activity range. The additional health benefits of exceeding the currently recommended exercise levels are consistent with cross-sectional data in runners and walkers.^17,18 The runners’ results showing increased benefit with increased running energy expenditure also provide confirmation in a new independent sample of a progressively beneficial dose–response relationship for this activity.¹⁹

Activity in the present study was self-selected both with respect to the intensity, running versus walking, and the total exercise dose. The average exercise dose measured as estimated caloric expenditure was more than twice as great for those who chose running over those who chose walking. Specifically, there were substantially more walkers whose walking was at or below the guideline levels than runners whose running was at or below the guidelines (48.1% versus 12.2%), and substantially fewer walkers than runners whose walking or running exceeded the guideline levels by 2-fold (15.4% versus 61.1%), 3-fold (4.5% versus 40.1%), and 4-fold (1.1% versus 17.9%). This is likely a result of the fact that runners can expend more calories in a given period of time. Our results suggest that this caloric expenditure is the key issue to reducing CHD risk factors and possibly CHD events.

Clinical trials are required to settle the role of exercise intensity on CHD risk, but clinical trials are necessarily restricted by sample size and duration. Available clinical trials on the influence of exercise intensity on new onset blood pressure, cholesterol, and blood glucose control or insulin sensitivity have yielded mixed results. Both moderate and vigorous-intensity training improve blood pressure with approximately equal effects,²⁰ although greater benefits have been ascribed to both moderate²¹ and vigorous intensity.⁹ The ability of exercise to lower total and low-density lipoprotein cholesterol is not widely accepted,^20,22,23 irrespective of intensity, and some maintain that any reduction in low-density lipoprotein is attributable to plasma volume expansion.²⁴ Our results suggest that exercise does affect low-density lipoprotein levels, and that this effect increases with increasing exercise doses, consistent with the suggestion that low-density lipoprotein concentrations are more responsive to the exercise quantity than intensity.²⁵ Both moderate and vigorous exercise have been associated with lower risk of type 2 diabetes mellitus²⁰; however, studies of blood glucose control tend to achieve significant improvement for vigorous and more than moderate physical activity.⁹ The benefits of walking, in particular, in lowering type 2 diabetes mellitus risk are well-documented.²⁶ Prospective epidemiological studies tend to show a greater CHD risk reduction for vigorous than moderate-intensity exercise²⁰; however, vigorous physical activity is more accurately reported than moderate-intensity exercise,²⁷ which could contribute to its stronger relationship to CHD, hypertension, hypercholesterolemia, and diabetes mellitus when studied prospectively in epidemiological cohorts.²⁰ This may be less of an issue for the analyses presented here, which compares 2 specific activities, running and walking, quantified by distance rather than duration. The superiority of vigorous over moderate exercise, in some studies, may simply reflect the fact that more calories can be expended per minute of activity with vigorous exercise. Consequently, when exercise is compared by time spent in activity, vigorous exercise seems more beneficial.

This last point we believe to be of particular significance. In this article, we have shown that the effects of exercise on incident hypertension, hypercholesterolemia, and diabetes mellitus are at least 2-fold greater, when exercise energy expenditure calculated from distance than when exercise is measured by time. Similar results have been shown for using distance to assess energy expenditure cross-sectionally for body weight, hypertension, hypercholesterolemia, and diabetes mellitus.^13–15 Presumably, deficiencies in time-based estimates of exercise energy expenditure apply to nonrunning and nonwalking activities as well, which may contribute to the significant differences between running and other vigorous exercise, and walking versus other moderate exercise (Table 2).

The superiority of the distance-based versus time-based estimation of exercise energy expenditure has other important implications. If runners and walkers substantially overestimate exercise duration for a sustained activity, it is reasonable to assume even greater bias for unsustained activities by more sedentary populations. Most epidemiological studies estimate exercise dose by time and intensity,²⁰ which our analyses would substantially underestimate the true health benefits of physical activity. Moreover, all public health recommendations prescribe physical activity by duration,^1–7,20 and if people overestimate exercise by time, then implementing time-based recommendations may be problematic.

Caveats

The subsample included in this report is a sample of convenience because it was recruited to obtain ≈50 000 subjects to determine their interest in a possible internet-based intervention, and therefore represent only a portion of the original National Runners’ Health Study II and the National Walkers’ Health Study participants. It is unlikely, however, that the biological interaction of between exercise and hypertension, hypercholesterolemia, and diabetes mellitus is different between the current and less-selected populations. We cannot exclude the possibility that subjects who exercise have lower innate risks for hypertension, hypercholesterolemia, diabetes mellitus, or CHD. We have shown that men with higher high-density lipoprotein cholesterol at baseline (a CHD protective factor)²² run longer distances when randomized to exercise training,^28,29 and others have shown that selective breeding for fitness in rats produces substantial inherited differences in CHD risk factors even in the absence of training.³⁰ Diet and other variables that could have affected our results were not collected. We doubt the possibility that lower rates of new onset hypertension, hypercholesterolemia, and diabetes mellitus with greater exercise levels was attributable to less medical care contact in more active men because more vigorously active participants in the Health Professional Study had more frequent medical check-ups than less active men,³¹ and there was no difference in the frequency of routine medical check-ups by activity level in the Nurses Health Study.³² The slightly greater risk reductions for hypertension and hypercholesterolemia for walking than running may relate to residual effects of the walkers’ older age and greater body weight that was not completely removed by statistical adjustment.

Our results probably provide among the best available answers to the important public health question as to what intensity of exercise is required to reduce CHD risk. Our results suggest similar benefit for similar energy expenditures. These results should be used to encourage physical activity in general, regardless of its intensity. However, those who choose running achieved more than twice the exercise doses as those who choose walking, and given the strong dose-response relationship, higher exercise doses and lower risk factors, promoting more vigorous exercise, are likely to produce greater health benefits.

Footnotes