A guest blog by Dr. Bob Ross with introduction by Dr. Stephen Archer
Introduction by Dr Archer: As a cardiologist I am often in the position of prescribing medications. One of my routine prescriptions is for exercise. Newton’s First Law of Motion states that “a body at rest will remain at rest unless an outside force acts on it, and a body in motion at a constant velocity will remain in motion in a straight line unless acted upon by an outside force”. This law of physics applies to human beings as well. Both sedentary and active lifestyles tend to be self-sustaining once begun. Change from one to the other often requires an external force.
As physicians our conversation with the patient reminds them that exercise is important to their health; important enough that we took the time to discuss it and to prescribe a dose of exercise. Our conversation can be the outside force that Newton refers to as a change agent for the motion of bodies, even those that are less than celestial.
Over the years the nature of my exercise prescriptions has evolved from general encouragement to stay active, to exercising 30 minutes a day at least 5 days per week to the current advice which comes in the form of two questions. The first question is, “What is the most active thing you do in the course of a day?”. The second question is, “Do you try and get 10,000 steps/day?”.
In this guest blog written by Dr. Bob Ross. Professor of Kinesiology at Queen’s University, we learn about the science underlying the recommendation to improve cardiorespiratory fitness (CRF). Bob is a passionate proponent of exercise as a medicine, an accomplished educator and successful researcher. He is also has been lead author on an important scientific statement published on behalf of the American Heart Association, entitled Importance of Assessing Cardiorespiratory Fitness in Clinical Practice: A Case for Fitness as a Clinical Vital Sign
The article below reminds us we can achieve cardiorespiratory fitness but we must, as the Nike advertisement says, Just Do It. The good news is that CRF at baseline can be improved dramatically by regular physical activity. In addition, he outlines that even mild-moderate physical activity is beneficial.
Assessing Cardiorespiratory Fitness in Clinical Practise to Help Manage Patients
Dr. Bob Ross
Cardiovascular disease (CVD) has been the leading cause of death among North American men and women for decades. Long-standing, established risk factors for CVD include cigarette smoking, hypertension, obesity, and abnormal blood cholesterol level. Over the past three decades low levels of cardiorespiratory fitness (CRF) has emerged as a strong and independent predictor of all-cause, CVD, and cancer mortality; an observation that remains true for those with CVD, as well as those with comorbid conditions such as obesity, type 2 diabetes, and hypertension. In fact, numerous reports confirm that low CRF is a more powerful predictor of mortality risk than the aforementioned ‘traditional’ risk factors. Despite these strong associations, CRF remains the only major risk factor that is not routinely assessed in clinical practice.
Given the large body of epidemiological and trial evidence continuing to demonstrate not only that CRF is a potentially stronger predictor of mortality than established risk factors, but that the addition of CRF to traditional risk factors significantly improves the reclassification of risk for adverse outcomes, the AHA decided to convene an international group of experts to review the evidence and to decide whether CRF should be a vital sign in clinical practise.
I was privileged to accept the request to select and Chair the writing group, and to spearhead the development of an AHA Scientific Statement. The underlying premise of the statement is that the addition of CRF for risk classification presents health professionals with unique opportunities to improve patient management and to encourage lifestyle-based strategies designed to reduce cardiovascular risk. In this blog we summarise some of the key findings of the Statement and provide an approach by which practitioners might feasibly incorporate CRF into clinical practice.
What is CRF?
CRF reflects the integrated ability to transport oxygen from the atmosphere to the mitochondria to perform physical work. It therefore quantifies the functional capacity of an individual and is dependent on a linked chain of processes that accommodate and efficiently transport blood from the heart to precisely match oxygen requirements, and the ability of the myocyte to receive and use the oxygen and nutrients delivered. CRF is thus directly related to the integrated function of numerous systems and is a reflection of total body health. About half of the variance in CRF is attributable to heritable factors; similarly, the contribution of inherited factors to the response of CRF to physical activity approximates 45% to 50%. These heritability estimates are similar in magnitude to other CVD risk factors including, for example, insulin, glucose, lipoproteins, blood pressure, and high-sensitivity C-reactive protein. Of importance, there is no correlation between baseline, intrinsic CRF level, and its response to regular exercise, with an r2 in the order of 1%. In other words, intrinsic CRF is independent of its responsiveness to regular physical activity.
Does CRF improve risk assessment?
Although the evidence that CRF is inversely associated with mortality is strong and convincing, it does not necessarily mean that CRF directly enhances CVD mortality risk prediction. For CRF to truly be a novel risk marker, it must improve risk prediction beyond traditional markers. Recent studies suggest that the net reclassification improvement (NRI) and the integrated discrimination improvement can provide important insights beyond traditional statistical tools (eg, hazard ratios, odds ratios, C-index) when estimating risk for adverse outcomes.
These tools more directly address the extent to which a given risk marker adds to existing markers to predict adverse outcomes. NRI indicates whether the addition of a biomarker correctly and significantly alters risk classification; it is defined as the net change in risk among those who do and do not experience an event. Indeed, several recent studies have used these metrics and provide compelling evidence reinforcing the additive value of CRF to traditional risk markers (Table 3 above). In summary, the addition of CRF to traditional risk factors significantly improves reclassification of risk for adverse health outcomes and traditional risk scores (such as Framingham Risk Score) are enhanced by adding CRF. Together these observations suggest that the addition of CRF improves risk classification and hence, helps the practitioner manage their patients.
Dose-Response Association between CRF and Health Outcomes
One of the major observations of the statement is that exceptionally high CRF levels are not necessary to provide significant health benefits. Individuals with a CRF level <5 METs (1 MET is defined as 1 kcal/kg/hour and is roughly equivalent to the energy cost of sitting quietly) tend to have a particularly high risk for mortality, whereas many epidemiological studies have observed that CRF levels >8 to 10 METs are associated with relative protection.
Of particular importance is the observation that the largest benefits occur between the least fit and the next least fit group of individuals studied. Stated differently, health benefits are most apparent at the low end of the CRF continuum. Although studies vary, this is generally the case for both all-cause and CVD mortality. This is an important public health message, because one need not be athletic to gain substantial health benefits from improvements in CRF. This point is illustrated in the Figure above, in which more than half the reduction in all-cause mortality occurs between the least fit group and the next least fit group.
Measurement of CRF in Clinical Settings
Measurement of CRF (VO2peak) using the gold standard approach requires the participant to perform a maximal treadmill/bike test with simultaneous measurement of oxygen consumption. This method requires specialized equipment and appropriately trained personnel and it is impractical for most clinical settings. CRF can also be accurately estimated using a submaximal exercise test (treadmill/bike/step test) without direct measures of oxygen consumption. Although this method can be used in clinical settings at minimal cost and is recommended as a pragmatic alternative to maximal exercise testing, direct measurement of CRF in many clinical settings remains a challenge.
Non-exercise based equations or models offer an alternative and are available to conveniently estimate CRF without performing a maximal or submaximal exercise test. This approach uses variables commonly assessed in clinical settings to provide a rapid and inexpensive way of estimating CRF in public health and clinical settings. The website (https://www.worldfitnesslevel.org/#/) provided to both the practitioner and patient can be used to estimate CRF in minutes. Although direct measurement of CRF using submaximal methods is preferred, non-exercise estimations of CRF are easily implemented in practise and offers the practitioner a simply way of counselling the patient regarding the importance of increasing physical activity to increase CRF. In this way the practitioner adds her/his voice to the long list of allied health practitioners who advocate and encourage all adults to increase physical activity as a means of attenuation health risk.
How much exercise is required to increase CRF?
The statement provides an extremely thorough review of the evidence linking an increase in physical activity/exercise with improvements in CRF. In general, exercise consistent with current guidelines (150 minutes / week of moderate intensity exercise) is associated with clinically relevant improvements (e.g. 1 MET) in CRF for most adults. Clinicians can obtain user friendly ‘Exercise Prescription and Referral’ information from Exercise is Medicine Canada (see Figure) that they can use with their patients to help describe current physical activity guidelines.
As with all cardiometabolic traits the CRF response to increasing exercise will vary substantially across patients and thus serial measurements of CRF are required to determine treatment efficacy. It may be that for some participants an increase in either exercise amount (minutes) or intensity (percent of maximum) may be required to improve CRF. That a single exercise strategy may not provide benefit for all patients is not unusual in clinical practise. The good news is that measurement of CRF provides the practitioner with the opportunity to discuss the benefits of physical activity with his/her patients and may act to motivate the patient to not only adopt physical activity, but to sustain the behaviour because s/he knows that the physician will measure CRF again next visit. Imagine clinicians routinely measuring (estimating) CRF to help ensure the patient is taking his/her ‘medication’ much like the clinician would do to manage blood pressure. This represents an exciting and feasible opportunity with no down side.
CRF should be measured in clinical practice if it can provide additional information that influences patient management. Indeed, decades of research have produced unequivocal evidence that CRF provides independent and additive morbidity and mortality data that when added to traditional risk factors significantly improves CVD risk prediction. On the basis of these observations alone, not including CRF measurement in routine clinical practice fails to provide an optimal approach for stratifying patients according to risk. Estimates of CRF using nonexercise algorithms have pragmatic importance and provide values for CRF that enhance risk prediction when direct CRF measures are not feasible. Of crucial importance is the repeated observation that one does not need to be highly fit to gain benefit from improvements in CRF. More than half the reduction in all-cause and CVD mortality generally occurs when moving from the least fit group to the next least fit group. For many people, this can be achieved by routine, moderate intensity exercise consistent with consensus guidelines; lower levels of physical activity may be all that is needed to derive a clinically significant benefit in habitually sedentary individuals. This has implications for physical activity counselling, given that considerable benefits are likely to occur by encouraging the most sedentary or low-fit individuals to engage in modest amounts of physical activity accumulated throughout the day. Although gaps in knowledge remain, and refinement of CRF targets for risk reduction across age and sex need further investigation, the evidence reviewed within the statement suggests that the measurement of CRF improves patient management and that its omission from routine clinical practice for the vast majority of patients is hard to justify.
It is hoped by all the writing group members that the AHA Statement will at the very least stimulate conversation with the hope that CRF will finally be recognized as a vital sign that must be measured in clinical practise. We need to find ways to incorporate the importance of CRF and physical activity into medical school curriculum in a way that adds value and improves patient management. We need all practitioners to join the team and to advocate for the importance of CRF and physical activity prescription at all levels of clinical medicine. Hopefully the findings reported in this AHA Statement provide a stepping stone to that reality. It would be nice for Queen’s to lead the way.