Maximal Heart Rate And Peak Heart Rate

Since the 1930s, the maximal heart rate of an individual has been shown to approximate a value equal to subtracting one's age from 220 beats per minute (beats-min-1) (Christensen, 1931; Robinson, 1938; Astrand and Rhyming in Astrand, et al., 2003). More recently, Tanaka, et al., (2001) reported that 220 minus age underestimated maximal heart rate in older adults, which would be relevant to cardiac populations. Nevertheless, with age as the main predictor of maximal heart rate in all the above studies, this does not filter out the more individualised factors of autonomic regulation that influence heart rate from rest up to maximal exertion. Astrand and Christensen (1964) and Astrand, et al. (1973) cautioned that the error around the prediction of maximal heart rate based on age had a standard deviation of +/- 10 beats-min-1.This means that

Heart rate (HR) and ejection fraction (EF) response curves

Heart rate (HR) and ejection fraction (EF) response curves

Younger, Healthier, Athletic Populations Cardiac populations

Figure 3.2. Myocardial performance to increase exercise intensities. The left panel demonstrates that in the healthy individual ejection fraction plateaus at 50-60% of VO2max and the increase in heart rate has a turn-point in the region of 60-80% VO2max before it reaches maximal levels (dotted line). This turn point has been hypothesised to be associated with the lactate threshold.

The right panel shows that at similar relative intensities, myocardial performance begins to deteriorate in cardiac populations, where there is a loss of stroke volume associated with a decreased ejection fraction; heart rate rises in an accelerating fashion in an attempt to compensate and to preserve cardiac output.

(Adapted from Conconi, et al., 1982 and Pokan, et al., 1998.)

Younger, Healthier, Athletic Populations Cardiac populations

Figure 3.2. Myocardial performance to increase exercise intensities. The left panel demonstrates that in the healthy individual ejection fraction plateaus at 50-60% of VO2max and the increase in heart rate has a turn-point in the region of 60-80% VO2max before it reaches maximal levels (dotted line). This turn point has been hypothesised to be associated with the lactate threshold.

The right panel shows that at similar relative intensities, myocardial performance begins to deteriorate in cardiac populations, where there is a loss of stroke volume associated with a decreased ejection fraction; heart rate rises in an accelerating fashion in an attempt to compensate and to preserve cardiac output.

(Adapted from Conconi, et al., 1982 and Pokan, et al., 1998.)

in some individuals their actual maximal heart rate could be as much as 20 beats • min-1 above or below the age-estimated maximum. For a healthy individual an error in over-prescribing a target heart rate would result in the discomfort of overexertion. However, for the cardiac patient such an error could be enough to trigger an event of ischaemia, an arrhythmia or a failure of cardiac output to match the systemic circulatory demands of vigorous exercise (Figure 3.2).

It is likely, however, that such individuals will have been through an appropriate ETT (exercise tolerance test), which is assumed to provide a safe upper heart rate limit. It is important to acknowledge that even when an ETT is carried out it is possible that neither a true maximal heart rate will have been attained nor a conclusive intensity identified where a clinical cardiac change occurred. The typical clinical changes include ST-segment displacement (e.g. ST-segment depression suggestive of ischaemia), onset of arrhythmias or tachycardias, or a failure of increases in cardiac output to match increases in exercise intensity (recognised via blood pressure monitoring) (ACSM, 2000).

If an individual completes an ETT without any key clinical events, the highest heart rate attained may need to be described as a 'peak heart rate'. This is because in many cases the criteria for a true maximal test have not been met (ACSM, 2000). Many ETTs are stopped when the patient attains their age-estimated maximal heart rate. If the patient is clearly not at a point of volitional fatigue, their true maximal heart rate will actually be above this level. Subsequent exercise programming based on the heart rate at test termination could be under-prescribed in terms of intensity. This does, however, leave a margin of safety. In this case it is better to describe the prescribed intensity in relation to a peak heart rate (HRpeak). The same holds true when using the Karvonen (1957) heart rate reserve formula. If all exercise leaders on the rehabilitation team have a clear understanding of the differences between HRmax and HRpeak, then it will be clear whether the patient is exercising relative to their maximal capacity or a level which was determined relative to a clinical event or some other limiting factor (e.g. musculoskeletal problems) highlighted during the test. If, on the other hand, a patient stops due to true volitional fatigue, then whatever heart rate they were at (regardless of it being less than 220 minus age) would be a true maximum. This is often the case when the patient being tested is on beta-blocking medication and completes the test without any clinical events, representing a true beta-blocked maximal heart rate.

Tests may be terminated inconclusively, when neither a maximum heart rate nor a heart rate corresponding to a clinical event is determined. This leaves the exercise leader with limited knowledge of what constitutes a safe training heart rate. This problem often relates to factors influenced by the testing protocol or mode of testing (e.g. treadmill) (Myers and Froelicher, 1993). Such factors include changes in the speed and/or gradient of the treadmill, which are too much for the patient who is either limited by neuro-musculoskeletal mobility problems, pulmonary pathology, circulatory pathology (e.g. peripheral vascular disease) or fear and anxiety. The exercise leader often has to use a process of trial and error, or rely on RPE to determine an appropriate intensity based on patient comments, symptoms and visual observation. This may be the only possible option, but it needs to consider two issues:

• The patient may suffer from silent ischaemia, exercise-induced arrhythmias or failure to increase cardiac output at heart rates that could have occurred at levels not much above where the test was prematurely terminated;

• The patient's progress may be hindered (physiologically and psychologically), due to the clinicians taking a more cautious approach.

With regard to patients having undergone percutaneous coronary interventions (PCI) or revascularisation procedures (coronary angioplasty, stenting or bypass graft surgery), it is uncommon in the UK for these patients subsequently to have an exercise ETT. These patients (especially PCI) may, however, have been through an exercise test recently, prior to their revascu-larisation and hence these data (if recent) will still have some valuable information reflecting functional capacity for exercise intensity prescription purposes. Communication with the relevant physician or surgeon is required to qualify the success of the procedure in terms of rectification of exertion-related ischaemia, arrhythmias or myocardial performance. In the absence of an exercise ETT, sub-maximal tests can be used to assess functional capacity and subsequently set target intensity, including heart rate. Such tests are limited as a valid means for risk stratification, diagnosis or prognosis. If a PCI or revascularised patient does develop symptoms over time associated with ischaemia, arrhythmias or myocardial dysfunction, an exercise stress test and other related tests are advisable.

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