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(Chest. 2005;128:2788-2793.)
© 2005 American College of Chest Physicians

Effects of Exercise Training Amount and Intensity on Peak Oxygen Consumption in Middle-Age Men and Women at Risk for Cardiovascular Disease*

Brian D. Duscha, MS; Cris A. Slentz, PhD; Johanna L. Johnson, MS; Joseph A. Houmard, PhD; Daniel R. Bensimhon, MD; Kenneth J. Knetzger, MS and William E. Kraus, MD

* From the Department of Medicine, Division of Cardiology (Mr. Duscha, Ms. Johnson, Mr. Knetzger, and Drs. Slentz and Bensimhon) and Division of Cell Biology (Dr. Kraus), Duke University Medical Center, Durham; and Department of Exercise and Sports Science and Human Performance Laboratory (Dr. Houmard), East Carolina University, Greenville, NC.

Correspondence to: Brian D. Duscha, MS, Duke University Medical Center, Division of Cardiology, Department of Medicine, Box 3022, Durham, NC 27710; e-mail: dusch001{at}mc.duke.edu


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: Although increasing aerobic fitness by exercise training is advocated as part of a healthy lifestyle, studies examining the different effects of intensity and amount on peak consumption (O2) remain sparse.

Design: This randomized controlled trial compared the effects of three different exercise regimens differing in amount and intensity on fitness improvements.

Participants: Overweight men and women with mild-to-moderate dyslipidemia were recruited.

Interventions: The exercise groups were as follows: (1) low amount/ moderate intensity (LAMI, n = 25), the caloric equivalent of walking 19 kilometers (km)/wk at 40 to 55% of peak O2; (2) low amount/high intensity (LAHI, n = 36), the equivalent of jogging 19 km/wk at 65 to 80% of peak O2; (3) high amount/high intensity (HAHI, n = 35), the equivalent of jogging 32 km/wk at 65 to 80% of peak O2; and (4) a control group (n = 37).

Measurements and results: Peak O2 and time to exhaustion (TTE) were tested before and after 7 to 9 months of training. All exercise groups increased peak O2 and TTE compared to baseline (p ≤ 0.001). Improvements in peak O2 were greater in the LAHI and HAHI groups compared to the control group (p < 0.02); HAHI group improvements were greater than the LAMI group (p < 0.02) and the LAHI group (p < 0.02). Increased TTE for all exercise groups was higher compared to the control group (p < 0.001)

Conclusions: Exercising at a level of 19 km/wk at 40 to 55% of peak O2 is sufficient to increase aerobic fitness levels, and increasing either exercise intensity or the amount beyond these parameters will yield additional separate and combined effects on markers of aerobic fitness. Therefore, it is appropriate to recommend mild exercise to improve fitness and reduce cardiovascular risk yet encourage higher intensities and amounts for additional benefit.

Key Words: cardiovascular risk • dose response • exercise • peak oxygen consumption


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Higher levels of cardiovascular fitness, represented by peak oxygen consumption (O2), are associated with a decreased risk for cardiovascular disease (CVD).1234 This has been substantiated by both randomized and observational studies, such as the Multiple Risk Factor Intervention Trial and the Harvard College Alumni studies,5678 which have established a favorable relationship between physical activity, cardiovascular events, and mortality. Other studies91011 have shown an inverse relationship between physical activity and CVD risk factors. Therefore, the recommendation of regular exercise to prevent CVD is widely accepted throughout the medical community. There are numerous studies in the literature that address the relationship between either intensity or weekly amount on exercise capacity, as outlined in an evidence-based symposium12 on dose-response physical activity and health. However, most of these studies are limited by one or more of the following characteristics: no direct measurement of O2, a small number of subjects, no randomization, no control, exercise amount and intensity not addressed in the same study, or no group at risk for CVD. It is on the basis of this body of literature that the current recommendations are made.

Although regular exercise is recognized as an important part of a healthy lifestyle, studies appear to provide conflicting recommendations regarding the relationship between exercise amount and intensity on increases in cardiovascular fitness and the prevention of CVD. Previous reports14131415 have suggested vigorous physical activity is required to reduce the risk of CVD and all-cause mortality. In contrast, other epidemiologic studies16171819 suggest a relationship between total energy expenditure, CVD, and all-cause mortality independent of exercise intensity. These discrepancies beg the question of how much and at what intensity exercise improves cardiovascular fitness and lowers CVD risk.

These previous studies demonstrate that despite the known clinical benefits gained from exercise training, the specific amount (kilometers [km] or kilocalories [kcal] per week) or intensity (relative percentage of peak O2) of exercise for optimal benefit remains unknown. The purpose of this study was to examine the effects of three different exercise training regimens, differing in amount and intensity, on direct measurement of peak O2 in a subject population at high risk for CVD.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Subject Population
These findings are derived from a cohort of subjects from the Studies of Targeted Risk Reduction Interventions Through Defined Exercise trial.19 Inclusion criteria were: age 40 to 65 years, sedentary, overweight or class-1 obesity (body mass index, 25 to 35 kg/m2), presence of dyslipidemia (either low-density lipoprotein cholesterol of 130 to 190 mg/dL; or high-density lipoprotein cholesterol < 40 mg/dL for men or < 45 mg/dL for women) and nonsmoking status. Subjects were excluded from the study for hypertension (BP > 160/90 mm Hg), diabetes (fasting blood glucose level > 140 mg/dL), or orthopedic limitations to exercise training. Subjects had no cardiopulmonary dysfunction as indicated by history and physical examination, and none exhibited symptoms of ischemic heart disease by exercise ECG tracing. All women were postmenopausal as defined by having had three or fewer periods in the last 12 months or a serum follicle-stimulating hormone concentration of > 40 UI/L. A detailed description of this protocol has previously been described.19

Exercise Testing
All subjects underwent a maximal cardiopulmonary exercise test with a 12-lead ECG and expired gas analysis on a treadmill. These tests were performed twice at baseline and after completing the exercise program. Expired gases were analyzed continuously (model 2900 U; SensorMedics; Yorba Linda, CA; or TrueMax 2400 ParvoMedics; Sandy, UT). The protocol used consisted of 2-min stages, increasing the workload by approximately one metabolic equivalent per stage. The same protocol and same metabolic cart was used before and after training in each subject. The last 40 s were averaged to determine peak O2. All groups had an average peak respiratory exchange ratio ≥ 1.17 at baseline and ≥ 1.12 after exercise training.

Exercise Training
Subjects were randomized via computer program into one of four groups differing in exercise intensity and amount (caloric expenditure). The exercise groups were as follows: (1) high amount/high intensity (HAHI), the caloric equivalent of jogging approximately 32 km/wk at 65 to 80% of peak O2; (2) low amount/high intensity (LAHI), jogging approximately 19 km/wk at 65 to 80% of peak O2; (3) low amount/moderate intensity (LAMI), walking approximately 19 km/wk at 40 to 55% of peak O2; or (4) a nonexercising control group. For the HAHI group, the specific prescription was to expend 23 kcal/kg of body weight per week, which is the caloric equivalent of approximately 32 km of walking or jogging for a 90-kg person.20 For the LAHI and LAMI groups, the prescription was 14 kcal/kg of body weight per week, the caloric equivalent of 19 km/wk. To ensure a clear separation of exercise exposures between exercise groups for this categorical variable, only data from subjects with adherence ≥ 74% and ≤ 115% were used. Details on the exercise training protocol have previously been described.19

Initially, 282 subjects were randomized. Data from 133 subjects who completed the training and testing and had usable data are presented. Ninety-four subjects (33%) dropped out of the study, and data from 55 subjects (19%) were not usable. Data were considered unusable if exercise training compliance was < 75%, respiratory exchange ratio was < 1.05, mechanical error (eg, poor seal on mouthpiece/nose clip), or the termination of the cardiopulmonary exercise test was due to reasons other than volitional fatigue (eg, orthopedic limitation).

All studies were performed under research protocols approved by the Institutional Review Board of the Duke University Medical Center in accordance with the recommendations found in the Helsinki Declaration of 1975. Each subject was informed of testing protocols and the potential risks and benefits of participation. All subjects provided written consent prior to participation.

Statistical Analysis
Analysis of variance with Bonferroni post hoc testing was used to test for demographic differences between groups. Paired t tests were used to compare intragroup differences between baseline and after training or baseline to after control. Analysis of variance with Bonferroni post hoc testing was used to test relative (percentage) change scores between groups. The reported significance values are corrected for multiple testing. All tabular data are presented as mean ± SD, and all data in Figure 1 are presented as mean ± SE. A corrected p value of < 0.05 was considered significant for all tests.



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  		Figure 1. Percentage changes between groups from before exercise to after training (mean ± SE). Top, A: Absolute peak O2 (*p < 0.02, control vs LAHI and HAHI, **p < 0.02, LAMI vs HAHI, ***p < 0.02, LAHI vs HAHI). Center, B: Relative peak O2 (*p < 0.01, control vs LAHI and HAHI, **p < 0.01, LAMI vs HAHI, ***p < 0.01, LAHI vs HAHI). Bottom, C: TTE (*p < 0.001, control vs all exercise groups).

 

   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Exercise Training
Baseline characteristics of age (control, 52.2 ± 7.1 years; LAMI, 53.7 ± 5.2 years; LAHI, 52.0 ± 6.9 years; and HAHI, 50.9 ± 5.4 years), body mass index (control, 30.8 ± 5.2 kg/m2; LAMI, 30.08 ± 3.5 kg/m2; LAHI, 30.23 ± 3.2 kg/m2; and HAHI, 29.4 ± 2.4 kg/m2), weight (control, 87.7 ± 14.6 kg; LAMI, 86.6 ± 10.0 kg; LAHI, 87.5 ± 13.8 kg; and HAHI, 88.2 ± 12.7 kg), absolute and relative O2, and TTE were not different between groups. Table 1 depicts the actual training protocol of individuals within each of the different training protocols, including subject compliance. Table 2 compares pretraining and posttraining fitness values within groups. The control subjects did not change peak O2 or weight but decreased TTE (p < 0.05). All exercise groups had significantly improved absolute and relative peak O2 (p ≤ 0.001) and TTE (p < 0.001). Body mass was reduced in the LAHI and HAHI groups (p < 0.05) but remained unchanged in the LAMI group. Although all exercise groups lost an average of 1.3 kg (range, 0.8 to 2.1 kg) following exercise, this body mass loss was not different between the three exercise groups.


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  		Table 1. Exercise Training Protocols*

 

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  		Table 2. Within-Group Comparison at Baseline and After Training

 
Figures 1 illustrates the percentage changes of absolute peak O2, relative peak O2, and TTE between groups following exercise training. Findings were similar, only differing slightly in significance, for absolute peak O2 and relative peak O2 (Fig 1, top, A, and center, B) demonstrated that improvements in O2 were greater in the LAHI and HAHI groups compared to the control group (p < 0.02); HAHI group improvements were greater than the LAMI group (p < 0.02) and the LAHI group (p < 0.02). Figure 1, bottom, C, shows that the percentage change in TTE for all exercise groups was higher compared to the control group (p < 0.001). Heart rate recovery at 1 min was > 13 beats/min vs peak heart rate in all groups, indicating a low risk for a sudden cardiac event in this population. Heart rate recovery at 1 min improved in all groups but only reached significance in the LAMI group (– 3.7 ± 4.3; p = 0.001) and the HAHI group (– 5.5 ± 7.6; p = 0.002). There was no difference detected between the groups for heart rate recovery at 1 min after exercise training.


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
There is a clear link between cardiovascular health and fitness.2122 However, limited data are available on how exercise dose (amount and intensity) relates to increases in fitness for individuals at risk for CVD. The three most important findings regarding exercise prescription and fitness from the present study are as follows: (1) based on before/after values of the LAMI group, an exercise prescription of 19 km/wk at 40 to55% of peak O2 is adequate to elicit significant increases in both absolute and relative peak O2 and TTE; (2) when comparing all groups together, the amount of exercise appears to be more important than intensity for increasing peak O2; this conclusion is drawn from our data showing that increasing the intensity from 40 to 55% to 65 to 80% of peak O2 (at a controlled amount of 19 km/wk) did not significantly improve peak O2; however, increasing the amount of exercise from 19 to 32 km/wk (at a controlled intensity of 65 to 80% of peak O2) did improve peak O2; and (3) although no statistically significant difference was detected between LAMI and LAHI, a trend toward both a separate and combined effect of exercise intensity and amount on increasing peak O2 does exist between the groups.

It is well accepted that sedentary individuals who begin a regular routine of aerobic exercise increase their fitness, as measured by peak O2.232425 Most exercise interventions have traditionally prescribed a frequency of three to four times per week at an intensity of 65 to 80% of peak HR or O2 for 30 to 40 min per session. The design of this protocol controlled the amount of exercise between the LAMI and LAHI groups and the intensity of exercise between the LAHI and HAHI groups (Table 1). This design allowed for distinguishing the differences between amount and intensity in improving clinical measurements of peak O2 and TTE. The data demonstrate a significant improvement in both absolute and relative peak O2 and TTE in all three exercise groups following training (Table 2). Of interest, even exercise at the caloric equivalent of approximately 19 km/wk at 40 to 55% of peak O2 improved peak O2 and TTE compared to pre-exercise values.

Figure 1, top, A, and center, B, show a trend for peak O2 improvement across groups, although the LAMI group was not different from the LAHI group (p = 0.14 and p = 0.16, respectively). This suggests increasing the intensity from 40 to 55% of peak O2 to 65 to 80%, at a controlled amount of exercise (19 km/wk), is not a strong stimulus to significantly improve peak O2 further. However, the additional amount of exercise (19 km/wk vs 32 km/wk) prescribed in the HAHI group vs the LAHI group at a controlled intensity of 65 to 80% of peak O2 did result in a greater increase in peak O2 (Fig 1, top, A, and bottom, B). These findings taken together suggest that amount of exercise may be more important than intensity in achieving increases in peak O2.

Since direct measurement of peak O2 in a clinical setting is often cost or time prohibitive and requires technical expertise, it is very practical for clinicians to measure TTE as a surrogate marker of aerobic fitness. In this study, TTE increased in all three exercise groups and decreased in the control group. Interestingly, the LAMI group did not increase peak O2 compared to the control group (p = 0.079 and p = 0.215 for relative and absolute changes, respectively) but did improve TTE vs the control group (Fig 1, bottom, C). Therefore, this stimulus, although not as pronounced as the LAHI and HAHI groups for increasing peak O2, was an adequate exercise stimulus to improve aerobic capacity as measured by the fitness marker of TTE, a much more accessible measure in the clinical setting, where gas exchange analysis is not readily available. While all exercise groups were superior to the control group in improvements in TTE, the LAMI and LAHI groups were not significantly different, nor were the LAHI and HAHI groups. These findings would indicate that TTE is a less sensitive marker than direct measurement of peak O2 changes for measuring the improvements in aerobic capacity between exercise groups. Although not statistically significant, the increased amount of exercise demonstrated a graded increase in TTE between groups. The importance of our finding that mild exercise improves TTE without improving peak O2 compared to the control subjects is further substantiated by several other studies22627 showing increases in TTE with or without a concomitant improvement in peak O2 resulted in decreased cardiovascular risk, improved plasma lipoproteins, and body composition. Furthermore, Blair et al21 demonstrated that increased time on a treadmill test leads to reductions in mortality.

The limitations of this study merit discussion. We report data only for those subjects who completed the exercise training within the parameters (intensity or amount) of their assigned protocol. This study was not designed to account for responders vs nonresponders to an exercise training program. From this perspective, it should be viewed as an efficacy and not effectiveness study (in the latter instance an intent-to-treat analysis would be considered standard). In our analytical approach, there may be a bias in the findings. There is a wide range of responses to a given exercise regimen. It is possible that that some of the dropouts may have been low responders, thereby biasing the results in favor of the high responders. Second, it is important to point out that this trial evaluated the effects of 7 to 9 months of accrued exercise (the last 6 months at a specific dose). Most exercise intervention trials have been 3 to 4 months in duration. Therefore, it is unknown if these results would be reproduced in a shorter time period of 3 months or 4 months. It is possible that short-term and long-term improvements in peak O2 are affected differently by amount and intensity.

In conclusion, this study shows an exercise dose response to two clinical markers previously shown to predict cardiovascular morbidity and mortality: peak O2 and TTE. Exercise amount appears to be more important than exercise intensity for eliciting gains in cardiovascular fitness. However, since there is a trend for a stepwise increase in all three clinical outcomes between groups (Fig 1), we believe that our data imply that there are separate and combined effects of exercise intensity and amount on improvements in cardiovascular fitness. Further, the data demonstrate that exercising at a level of 19 km/wk at 40 to 55% of peak O2 is sufficient to increase aerobic fitness levels significantly above those of sedentary individuals. Increasing either exercise intensity or amount beyond these parameters appear to yield additional separate and combined effects on markers of aerobic fitness. Therefore, it is appropriate to recommend to the lay public a minimum of 19 km/wk of moderate exercise (40 to 55% of peak O2) for individuals intending to simultaneously improve fitness and reduce cardiovascular risk, yet encourage higher intensities and amounts for additional benefit.


   Footnotes
 
Abbreviations: CVD = cardiovascular disease; HAHI = high amount/high intensity; kcal = kilocalorie; km = kilometer; LAHI = low amount/high intensity; LAMI = low amount/moderate intensity; TTE = time to exhaustion; O2 = oxygen consumption

This study was supported by National Institutes of Health grant HL-57353.

Received for publication February 1, 2005. Accepted for publication March 8, 2005.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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