1. Lavie, Carl J. MD, FACC, FACP, FCCP
  2. Milani, Richard V. MD, FACC

Article Content

Why would one care to know or measure a resting metabolic equivalent or MET? The MET is a practical means of quantifying the energy cost of a particular physical activity or workload and, especially in exercise stress testing, is a means of quantifying the work performed at various stages of exercise intensity.1,2 One MET of energy expenditure was originally defined as the resting level of oxygen uptake of a healthy man weighing 70 kg while sitting, or 3.5 mL O2 [middle dot] kg-1 [middle dot] min-1.3 Therefore, any physical activity can be typically viewed as a multiple of this measure, with threshold requirements identified in individuals who perform unique activities. In this issue of Journal of Cardiopulmonary Rehabilitation and Prevention, however, Savage et al4 raise several issues regarding the determination of the MET, which adds insight into problems that we and others have raised in the past.



The evaluation of functional capacity is an important component of the exercise stress test, providing data that have both prognostic and diagnostic implications and are the foundation for developing an exercise prescription. Functional capacity is related to the maximal (or peak) ventilatory oxygen uptake (VO2max), which represents the greatest amount of oxygen transported and used in cellular metabolism and is the best index of exercise capacity. VO2max is seldom directly measured in most clinical stress testing laboratories and is generally estimated by linear regression equations, although these equations tend to be population specific and nonlinear and often do not apply to patients with chronic conditions.1-3 We have demonstrated, however, that these formulas grossly overestimate the true exercise capacity, more so in younger patients, and even more so after an exercise training program.3,5 For example, 2 individuals of similar weights and percent body fat may both exercise for 9 minutes on a Bruce protocol treadmill test, and both would have a peak estimated exercise capacity of 10 METs. However, on cardiopulmonary assessment, 1 patient may have a peak oxygen consumption of 17.5 mL O2 [middle dot] kg-1 [middle dot] min-1 (or 5 METs), whereas the other patient has 24.5 mL O2 [middle dot] kg-1 [middle dot] min-1 (or 7 METs). Although the regression equations overestimated the peak VO2 in both instances, the overestimation was considerably greater for 1 patient than for the other.



Although peak VO2 provides a better assessment of exercise capacity than simply estimating METs by treadmill speed and incline, generally when reporting peak VO2, this parameter is adjusted for total weight as opposed to lean weight, despite the fact that fat is, for practical purposes, aerobically inactive. As Buskirk wrote in a dissertation nearly 50 years ago, "It is concluded that when VO2 is used to examine the performance of the respiratory-cardiovascular system, the value should be expressed as VO2 per kg of fat-free weight."6 Nevertheless, these measures are still typically corrected for total as opposed to lean body mass. We have previously demonstrated that the differences noted between men and women and between obese and lean patients are mostly explained by the differences in percent body fat.7-11 When correcting values for lean body mass, the differences between sexes as well as between obese and lean are essentially eliminated in our studies and in the present report by Savage and colleagues.4 This adjustment is most applicable for the evaluation of patients with advanced heart failure because peak VO2 has been used as a major prognostic discriminator of patients with heart failure and is a major factor in determining listing for heart transplantation. We have demonstrated that correcting peak VO2 for lean as opposed to total weight, as well as correcting oxygen pulse (peak VO2/peak heart rate) for body fat, provides better prognostic stratification for patients with advanced heart failure.9,10



In the present evaluation by Savage and colleagues4 in this issue of the journal, the entire concept of the MET is seriously questioned. Although 3.5 mL O2 [middle dot] kg-1 [middle dot] min-1 has been the accepted definition of a MET for many decades, these investigators demonstrate that the average MET in patients with coronary heart disease is considerably lower than this widely accepted value. Although variations in the "true" MET may be partly explained by differences in percent body fat, which raises the idea that the "true" MET should probably also be adjusted for lean as opposed to total body weight, still even this does not totally explain the discrepancy between the measured values in patients with coronary heart disease and the typical 3.5 mL O2 [middle dot] kg-1 [middle dot] min-1 value, which has been dogma for decades. Recognizing that the original population used for defining METs was a young and healthy one free of disease, other factors accounting for these differences would likely include age, physical conditioning, and effects of chronic disease in determining resting metabolic activity.


Considering these points, how should we proceed? The concepts illustrated in the study by Savage and colleagues4 provide important insights for future investigators to consider in studies using exercise cardiopulmonary metabolism. However, at the present time, the current data probably raise more questions than provide answers. For example, should peak exercise capacity be described as a peak VO2 in mL O2 [middle dot] kg-1 [middle dot] min-1, or should this be corrected for the patients true basal resting VO2 (which will not be known for most patients), or an average baseline basal resting VO2? In other words, would peak VO2 be more important, or would peak VO2/basal resting VO2 be superior? Obviously, the present data and studies in the near future will not answer these potentially important questions.


At the present time, when performing cardiopulmonary exercise assessments, we would advise reporting the data in mL O2 [middle dot] kg-1 [middle dot] min-1, preferably correcting for lean as opposed to total weight, as opposed to simply reporting METs. A simple estimation of percent body fat by the sum of the skin-fold method is a fast, reliable, and inexpensive method readily available to determine lean body mass. When using routine treadmill testing without cardiopulmonary assessment, investigators and clinicians must recognize the limitations in this crude assessment and thus report these data as estimated METs (as opposed to VO2 in mL O2 [middle dot] kg-1 [middle dot] min-1). Nevertheless, numerous investigators have demonstrated the prognostic impact of estimated METs obtained from treadmill speed and incline,12,13 and at present, this "inflated" value should remain a major part of current cardiovascular medicine.




1. Milani RV, Lavie CJ, Mehra MR. Cardiopulmonary exercise testing: how do we differentiate the cause of dyspnea? Circulation. 2004;110:e27-e31. [Context Link]


2. Milani RV, Lavie CJ, Mehra MD, Ventura HO. Understanding the basics of cardiopulmonary exercise testing. Mayo Clin Proc. 2006;81:1603-1611. [Context Link]


3. Milani RV, Lavie CJ, Spiva H. Limitations of estimating metabolic equivalents in exercise assessment in patients with coronary artery disease. Am J Cardiol. 1995;75:940-942. [Context Link]


4. Savage PD, Toth MJ, Ades PA. A reexamination of the metabolic equivalent (MET) concept in individuals with coronary heart disease. J Cardiopulm Rehabil Prev. 2007;27:143-148. [Context Link]


5. Lavie CJ, Milani RV. Disparate effects of improving aerobic exercise capacity and quality of life after cardiac rehabilitation in young and elderly coronary patients. J Cardiopulm Rehabil. 2000;20:235-240. [Context Link]


6. Buskirk R, Taylor HL. Maximal oxygen intake and its relation to body composition, with special reference to chronic physical activity and obesity. J Appl Physiol. 1957;11:72-78. [Context Link]


7. Lavie CJ, Milani RV. Effects of cardiac rehabilitation and exercise training on peak aerobic capacity and work efficiency in obese patients with coronary artery disease. Am J Cardiol. 1999;83:1477-1480. [Context Link]


8. Richards DR, Mehra MR, Ventura HO, et al. Usefulness of peak oxygen consumption in predicting outcome of heart failure in women versus men. Am J Cardiol. 1997;80:1236-1238. [Context Link]


9. Osman AF, Mehra MR, Lavie CJ, Nunez E, Milani RV. The incremental prognostic importance of body fat adjusted peak oxygen consumption in chronic heart failure. J Am Coll Cardiol. 2000;36:2126-2231. [Context Link]


10. Lavie CJ, Milani RV, Mehra MR. Peak exercise oxygen pulse and prognosis in chronic heart failure. Am J Cardiol. 2004;93:588-593. [Context Link]


11. Lavie CJ, Milani RV, Ventura HO, Mehra MR. Peak oxygen consumption and heart failure prognosis in women. J Am Coll Cardiol. 2007;49:375. [Context Link]


12. Lavie CJ, Milani RV. Cardiac rehabilitation and exercise training programs in metabolic syndrome and diabetes. J Cardiopulm Rehabil. 3005;25:59-66. [Context Link]


13. Blair SN, Church TS. The fitness, obesity and health equation. Is physical activity the common denominator? JAMA. 2004;292:1232-1234. [Context Link]