Importance of Assessing Cardiorespiratory Fitness in Clinical Practice

The American Heart Association has released an important scientific statement entitled, “Importance of Assessing Cardiorespiratory Fitness in Clinical Practice: The Case for Fitness as a Clinical Vital Sign.”¹ This statement reviews the epidemiological evidence linking lower levels of cardiorespiratory fitness (CRF) with increased risk for cardiovascular disease, all-cause mortality, and mortality from breast and intestinal tract cancers. The statement emphasizes that a low CRF level is a risk factor for cardiovascular disease and that low CRF is associated with increased cardiovascular risks numerically similar to those attributable to cigarette smoking, hypertension, elevated cholesterol levels, and type 2 diabetes mellitus. The statement also notes that the biggest reductions in risk in epidemiological studies occur with small increments in CRF and, most importantly, going from the lowest to the next lowest level of CRF.

It is well-known that exercise and exercise training increase CRF, but the statement recognizes the role of genetic factors in CRF. It notes that approximately 50% of an individual’s CRF appears to be genetically determined, and also that approximately 50% of an individual’s increase in CRF with exercise training appears to be genetically influenced. The document argues for including cardiorespiratory fitness as a standard part of all clinical encounters or as a “vital sign." CRF can be determined most accurately with formal cycle or treadmill exercise testing with or without actual measurement of respiratory gas exchange and maximal oxygen uptake.

This is an important document because it summarizes key studies linking increased cardiorespiratory fitness with decreased adverse health effects. This makes sense because CRF is a single parameter but measures multiple aspects of the metabolic response to exercise, including the cardiac, pulmonary, vascular, hematological, muscular, and mitochondrial responses to exertion. Among ostensibly healthy individuals, CRF is a surrogate marker for cardiac output and ventricular function. Those individuals with higher baseline exercise capacity have a superior metabolic chain and can sustain insults to the individual elements and still maintain reasonable health…and survive.

Increased CRF is not a direct measure of habitual physical activity. Exercise training and physical activity increase CRF, but some individuals with higher CRF levels may simply be better genetically endowed or “heartier” than comparison individuals and therefore have reduced risks and better survival. Interestingly, reduced CRF in animal models is associated with higher cardiovascular disease risk factors. Rats bred for low CRF produce a strain of rats with increased risk factors for the metabolic syndrome.²

The document recommends that CRF be added to vital signs that clinicians routinely obtain from patients. Such information could affect how aggressively clinicians address other risk factors because highly fit individuals have better survival and less risk. Individuals with low CRF levels should be encouraged to engage in more physical activity and probably have their other risk factors more aggressively managed. Hopefully, this document will not lead to a routine increase in formal exercise testing. Such testing could have the untoward consequence of finding false-positive ECG results, leading to potentially inappropriate additional testing and interventions in asymptomatic people. CRF can be estimated without formal exercise testing by inquiring what physical tasks a patient can perform. Indeed, an exercise history and an estimate of exercise capacity should be a routine part of every clinician’s evaluation, as should a routine recommendation that patients get more habitual physical activity to increase CRF and reduce their cardiac risk.

References

1. Ross R, Blair SN, Arena R, et al. Importance of assessing cardiorespiratory fitness in clinical practice: a case for fitness as a clinical vital sign: a scientific statement from the American Heart Association [published online November 21, 2016]. Circulation doi: 10.1161/CIR.0000000000000461. http://circ.ahajournals.org/content/early/2016/11/21/CIR.0000000000000461.long
2. Wisløff U, Najjar SM, Ellingsen O, et al. Cardiovascular risk factors emerge after artificial selection for low aerobic capacity. Science. 2005;307(5708):418-420. http://science.sciencemag.org/content/307/5708/418.long 

We are constantly trying to identify which patients are at higher risk so that we can intervene to protect them. We started with age and gender and then we moved on to single risk factors like hypertension, cholesterol, smoking, and diabetes. We then realized that merging them together in a Framingham-type risk calculation could give us even better risk prediction ability.

All of these risk factors are accelerators for the disease process, but they do not tell us how badly the system is damaged or affected. So, perhaps a test of functionality of the systems would give us even more information. It’s like checking out a used car. You look at the age, maintenance schedule, and so on; but, in the end, you have to start it up and take it for a test drive. CRF is like a test drive for our patients.

This article summarizes the current knowledge around CRF. Basically, CRF testing assesses the body’s ability to pull oxygen from the air and use it to generate energy at the end organs such as muscles. CRF is a test of the lungs, heart, circulation, and oxygen extraction by the muscles all at the same time. So, whereas smoking is a risk factor for CV disease, CRF testing tells us how the system has been affected by the smoking. Is there damage or not, and is that damage affecting the overall function of the patient?

In fact, low CRF (<5 METs) is a strong predictor of mortality and high CRF (>8 METs) is associated with increased survival. Interestingly, even a slight increase in CRF by 1 or 2 METs can lead to a 10% to 30% reduction in CV events. Reduced CRF also predicts other outcomes such as stroke and heart failure, and predicts surgical risk. If we identify these higher surgical–risk patients and we do “prehabilitation” on the patient, we can actually improve the surgical outcomes. In other words, we can make a difference once we have identified these patients.

The CRF, when added the traditional risk scores such as Framingham risk score, can enhance the risk prediction accuracy. Serial measurement of CRF can detect deterioration or improvement of the patient and, hence, testing CRF should be done periodically.

The best way to measure CRF is with an exercise stress test during which we also measure the VO2 to see how much oxygen is used and how much CO2 is generated. However, even though this is the gold standard, it is not available for all. Another option is the 6-minute walk test (6MWT); a walks fewer than 350 meters signals risk. Also, 50-meter changes up or down are considered significant in the 6MWT. This test is not perfect, but it does give some idea of the patient’s overall CRF, and it is easily accessible to all patients who are mobile.

There are also many equations that try to calculate the CRF without exercising the patient. These equations are derived from patient population studies. They include multiple parameters such as age, gender, smoking, weight, BMI, and activity level, just to name a few. There is no single standard parameter that has been chosen by any of the guidelines. Perhaps we need a study that tells us which equation is the best for estimating CRF.

I think, overall, this document makes a compelling argument that we should be using CRF measurements to help identify patients at risk. But, more importantly, we should also help patients improve their CRF. So, perhaps statins, RAAS blockers, and antiplatelets are very important, but we also need to spend some time helping our patients increase their CRF. Let’s get them moving and let’s keep them moving.