According to recent guidelines from the American College of Sports Medicine (ACSM), cardiac patients should exercise above a minimum intensity to achieve a cardiorespiratory training effect, i.e., a “threshold” intensity (10). Furthermore, these guidelines suggest that the threshold for cardiac patients is most likely between 40% and 50% of oxygen uptake reserve (V̇O2R). However, the value for this threshold is based upon the ACSM’s 1998 position stand that reviewed studies performed on healthy subjects (24). Thus, there is a need to determine whether a threshold training intensity exists in cardiac patients and, if so, its value.
V̇O2 reserve is the difference between resting and maximal oxygen uptake. Studies in healthy individuals (30,31) and in cardiac patients (3) have shown that percentages of heart rate reserve (HRR) more accurately reflect %V̇O2R than %V̇O2max. Consequently, %V̇O2R is now preferred over %V̇O2max for prescribing exercise intensities that are based on oxygen uptake (10,24).
Recently, the authors analyzed previous training studies of healthy subjects to determine whether a threshold intensity exists in that population, and identified a threshold at 45% V̇O2R for individuals with initial aerobic capacities of at least 40 mL·min−1·kg−1, but no threshold for individuals with lower capacities, although the lowest training intensities examined were approximately 30% V̇O2R (29). Given that the threshold in healthy subjects with low fitness levels, if one exists, is less than 30% V̇O2R, it seems likely that any threshold in the typically deconditioned cardiac population would be no more than this value. The purpose of the current study was to analyze previous training studies of cardiac patients, to translate the reported intensity of training into %V̇O2R units, and to determine whether there is a threshold for improvement in aerobic capacity.
Studies that evaluated the effect of aerobic training on the peak V̇O2 of cardiac patients were identified from a comprehensive 1995 review of exercise-based cardiac rehabilitation performed by the U.S. Department of Health and Human Services (34), from a MEDLINE search for studies published thereafter, and by checking the reference lists of all reports obtained in the first two steps. There were several cases in which two or more investigations identified in the initial search used a single data set, publishing different aspects of the results of training in separate papers. In these cases, only one study was cited. Also, there were instances where a study was published and later added more subjects in a subsequent publication. In such cases, only the most recent, i.e., most complete, study was cited.
Only studies that measured pre- and post-training V̇O2peak by using gas exchange techniques were included. This eliminated numerous studies that evaluated the effects of training on the estimated functional capacity of cardiac patients. For the purposes of this research, cardiac patients were those diagnosed with coronary artery disease, in most cases having experienced a myocardial infarction, but also including those having undergone coronary revascularization (14), those with left ventricular dysfunction (heart failure) (5,18,20,28), and those demonstrating significant (≥1.5 mm), exercise-induced, ST-segment depression (6). The greatest V̇O2 attained during exercise testing is referred to in this analysis as V̇O2peak rather than V̇O2max because true maximal values are often not attained during symptom-limited tests of cardiac patients.
Exercise intensities in the training studies were originally reported as percentages of V̇O2peak, percentages of peak heart rate (HRpeak), percentages of HRR, or percentages of peak workload. These measures of exercise intensity were converted to %V̇O2R units by the methods described in a related study on healthy subjects (29) and are summarized below.
In those studies reporting training intensity as %V̇O2peak (6–9,13,16,22,28,32), this percentage was multiplied by the reported mean initial V̇O2peak to yield the gross exercise V̇O2 in mL·min−1·kg−1. Then, %V̇O2R was calculated from the following formula: %V̇O2R = (gross exercise V̇O2 −3.5)/(V̇O2peak −3.5), where 3.5 mL·min−1·kg−1 was assumed to be the average resting V̇O2 of the subjects.
In those studies reporting training intensity as %HRpeak (1,5,12,17,23,25,26), this was converted to %V̇O2R using the formula: %V̇O2R = 1.667(%HRpeak) −70%. As described previously (29), this formula was derived independently from two different HR/V̇O2 data sets in healthy adults. The two data sets yielded nearly identical formulas, and the aerobic capacity of the subjects had only a minor effect on the relationship. Because patients with heart disease exhibit the same highly linear relationship between HR and V̇O2 across the range of rest to maximum exercise as do healthy subjects, even in the presence of beta-blockers and/or calcium antagonists (3,4,15), this formula should provide a reasonable estimate of %V̇O2R in the cardiac population.
For studies reporting training intensity as %HRR (2,14,18,19,21,27), these were assumed to provide equivalent values in %V̇O2R units, as previously shown for healthy adults (30,31) and cardiac patients (3). Similarly, one study reported the training intensity as a percentage of peak workload (20), and this value was assumed to be equivalent to %V̇O2R.
Table 1 presents a summary of the 23 studies that were analyzed. All but seven of the studies utilized a sedentary control group. One of the studies compared a group of subjects on beta-blockade with a group not on beta-blockade, and reported similar responses to training (32). Four other studies, described below, compared groups of subjects at two different intensities. Thus, a total of 28 subject groups were evaluated. The range of durations, frequencies, and length of programs (i.e., in weeks) was too diverse to allow an analysis of these factors.
As seen in Table 1, three of the training groups failed to demonstrate statistically significant increases in V̇O2peak, although they exhibited numerically greater values after training (by 3%, 8%, and 9%) and had small numbers of subjects (8, 11, and 11, respectively). These three studies utilized exercise intensities ranging from 47% to 55% of V̇O2R. Six other studies that utilized similar training intensities (from 42% to 55% of V̇O2R) reported significant increases in V̇O2peak. The initial mean V̇O2peak values of the three groups that did not show improvement were 18.7, 21.2, and 29.4 mL·min−1·kg−1, which overlapped the six groups that did show improvement (13.2, 21.8, 22.5, 23.5, and 24.2 mL·min−1·kg−1, and one group with 1.2 L·min−1, body mass not provided). Thus, the failure of three groups to demonstrate statistically significant improvements is most likely due to their small sample size, rather than being an indication of a threshold intensity.
The mode of exercise and the duration (minutes per session), frequency (sessions per week), and length (number of weeks) of training varied greatly among the 23 studies, precluding any conclusions regarding the influence of these variables. Four studies each utilized two groups of different training intensities, making it possible to compare the effects of intensity on improvements in aerobic capacity. Three of these studies reported a significant difference between groups for the increase in V̇O2peak, and in each case the higher intensity group exhibited the greater relative improvement. However, in each of these studies the two groups used the same exercise duration; consequently, the higher intensity group performed a greater total amount of training.
This analysis found no evidence of a threshold intensity for aerobic training of cardiac patients, i.e., there was not an intensity that could be identified as a minimum intensity for eliciting improvement in peak oxygen uptake. Because the lowest intensities used in any of the studies approximated 45% of V̇O2R, it is possible that intensities below this value are capable of improving V̇O2peak. However, it is also possible that a threshold exists at or below 45% of V̇O2R. Consequently, until further research is conducted using lower training intensities, 45% of V̇O2R should be considered the minimal effective intensity for eliciting improvements in cardiorespiratory fitness in patients with coronary heart disease.
Most of the studies included in this analysis had little or no criteria for the attainment of V̇O2max. Generally, incremental exercise tests were stopped due to volitional fatigue or when patients demonstrated adverse signs or symptoms. Their results were included in the studies’ data despite the fact that criteria for V̇O2max, such as a plateau in V̇O2 or the attainment of a respiratory exchange ratio (RER) of 1.10 or more, were not achieved. This commonly occurs when exercise testing cardiac patients and is why their highest achieved V̇O2 is often referred to as V̇O2peak in contradistinction to V̇O2max. This has two consequences to the current analysis: interpreting the increase in aerobic capacity following training, and expressing the exercise intensity during training as a percentage of maximum capacity.
True V̇O2max was often not attained during testing, as indicated in some studies by significant posttraining increases in peak RER or peak HR. Thus, the increase in aerobic capacity after training could be due in part to greater effort by the patients, a reduction in their symptoms, or both, as opposed to an increase in aerobic capacity per se. Keteyian et al. (18) specifically addressed this issue, and attributed 46% of the posttraining increase in V̇O2peak in their study to the increase in HRpeak. On the other hand, it seems reasonable to conclude that some physiological increase in aerobic capacity does occur with training in cardiac patients (e.g., 54% of the increase in V̇O2peak in Keteyian et al.’s study). Some of the studies in this analysis had strong physiological indicators of maximal effort. In Ehsani et al.’s 1986 study (8), 15 of 25 subjects achieved a plateau in oxygen uptake. By using an unconventionally high exercise intensity during training (up to ∼90% of V̇O2R), a 39% increase in true V̇O2max was reported among the 15 subjects who exhibited plateaus. Furthermore, Ehsani et al. reported significant improvements in left ventricular function, such as a greater ejection fraction during maximal exercise. Four studies reported mean maximal RERs above 1.10, and three of these obtained significant increases in aerobic capacity (18,27,28), whereas the fourth reported a trend (P = 0.15) for an 8% increase (26). Therefore, although not all of the increase in V̇O2peak in the studies included in this analysis can be attributed to a physiological increase in aerobic power, properly performed aerobic training clearly increases true V̇O2max in cardiac patients.
Because a true maximal effort was probably not attained in many of the studies, the reported exercise intensities are likely overestimates of the actual ranges, e.g., if a study reported an exercise intensity as 70% of HRpeak, this value is likely higher than the corresponding percentage of HRmax. The translated values in %V̇O2R units are also likely to be overestimated. Consequently, the minimal effective intensity identified in this analysis, 45% of V̇O2R, must be considered in light of the fact that maximal V̇O2 was not known. If a true V̇O2max were known, then this value would probably be much lower.
In a recent analysis of training studies performed with healthy adults, the authors found that 45% of V̇O2R was a threshold intensity for individuals with initial V̇O2max values of at least 40 mL·min−1·kg−1, whereas 30% of V̇O2R was the minimal effective intensity for those with lower initial capacities (29). The lower fit subjects did not demonstrate a threshold per se, as no studies used intensities below 30% of V̇O2R. The current analysis in cardiac patients, with initial V̇O2peak values ranging from 13.0 to 29.4 mL·min−1·kg−1, found no threshold intensity, consistent with the finding in healthy subjects with low initial fitness, although the lowest intensities evaluated in cardiac patients approximated only 45% of V̇O2R.
Finally, we recognize that training effects in the present analysis were narrowly defined to signify improved cardiorespiratory fitness, rather than global health outcomes. Accordingly, substantial health benefits may still be achieved at exercise levels that are below the minimal effective training intensity identified here (i.e., < 45% V̇O2R), provided that the frequency and duration of training are appropriate. Research has shown that numerous health benefits can be derived at more moderate exercise intensities, that is, at intensities below those commonly prescribed for cardiorespiratory conditioning. These include favorable changes in bone density, glucose tolerance, and coronary risk factors, as well as a reduction in cardiovascular-related mortality (11). There are also intriguing data to suggest that small, insignificant group increases in aerobic fitness (i.e., 3 to 9%) may, on an individual basis, be associated with meaningful reductions in subsequent coronary events, especially in cardiac patients with low baseline V̇O2peak (33).
Our analysis suggests that 45% of V̇O2R should currently be considered the minimal effective intensity for improving aerobic capacity in cardiac patients. In studies using cardiac patients, V̇O2 reserve is generally the difference between resting and peak V̇O2 rather than resting and maximal V̇O2. Thus, 45% of V̇O2R may overestimate the minimal effective intensity if true V̇O2max is known. Studies that used higher versus lower intensities of training generally obtained greater improvements in V̇O2peak with the higher intensities; however, the total amount of work was not equated between groups. Future research with some groups exercising at less than 45% of V̇O2R, with total work equated between groups, and with criteria established for the attainment of maximal effort for pre and post testing, should help to clarify these issues.
Address for correspondence: David P. Swain, Ph.D., FACSM, Wellness Institute and Research Center, Old Dominion University, Norfolk, VA, 23529-0196; E-mail: email@example.com.
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