The parameters of greatest interest to cardiologists from the exercise stress test are typically ST changes and exercise duration. However, other overlooked factors can provide important insight into the autonomic nervous system (ANS) and help predict patients' likelihood of survival.

Measures of the activity of the ANS reflect the balance between the sympathetic nervous system and the parasympathetic nervous system and have been shown to be powerful predictors of mortality. A review in Circulation Research links abnormal tone of the ANS to cardiac arrhythmias, including atrial and ventricular fibrillation, and to sudden cardiac death.

Calculating Heart Rate Recovery

Heart rate recovery (HRR) is the rate of decline in heart rate (HR) after the cessation of exercise. The most common HRR calculation involves measuring the HR 1 minute after exercise is stopped and subtracting that number in beats per minute from the peak exercise HR. Investigators have also looked at HRR over post-exercise durations of 10 seconds to 2 minutes.

Unlike heart rate variability, no high-tech devices are needed to make this simple but highly reproducible measurement. The gold-standard measurement is HR taken from ECG with the stress standardized during a standardized exercise test protocol observed by a clinician. However, measurements from consumer wearable devices can also provide HRR assessments—albeit with inferior accuracy due to the inherent limitations of the photoplethysmography technique utilized. Lacking a measurement device, individuals can also measure pulse the old-fashioned way by putting a finger on the carotid or radial artery and counting the beats.

What happens to HR during exercise is thought to be the result of a combination of parasympathetic withdrawal and sympathetic activation. The fall in HR immediately after exercise has been shown to be a function of the reactivation of the parasympathetic nervous system. It is accelerated in athletes and blunted in patients with heart failure, according to a study in the Journal of the American College of Cardiology (JACC).

The early increase in HR during exercise is thought to be due to withdrawal of the resting physiological vagal tone, whereas subsequent increases in HR as exercise progresses have been attributed to increased sympathetic tone, as exhibited by research in Circulation: Heart Failure. After exercise, sympathetic withdrawal contributes primarily to early HRR, whereas parasympathetic reactivation predominates in later stages, increasing HRR.

Heart Rate Recovery as a Predictor of Mortality

The seminal study on HRR was published in 1999 in the New England Journal of Medicine. It found that abnormally low HRR doubled the risk of dying over 6 years. The study examined outcomes in 2428 consecutive adults (mean age of 57 years, 63% men) without significant prior cardiac disease who were referred to the Cleveland Clinic cardiac lab for nuclear stress testing. Patients underwent symptom-limited exercise on a treadmill using a standard or modified Bruce protocol.

HR was recorded at peak exercise, and then patients walked upright at a speed of 1.5 miles per hour at a grade of 2.5%. Their HR was checked again 1 minute later. Median HRR was 17 beats/min, with a range from the 25th to the 75th percentile of 12 to 23 beats/min. Abnormally low HRR was selected as ≤12 beats/min and was found in 639 patients (26%).

After adjustment for multiple confounding factors, including age and exercise capacity, patients with HRR ≤12 beats/min had a two-fold risk of dying.

In a follow-up study published in the Journal of the American Medical Association, this same Cleveland Clinic group looked at 9454 patients undergoing treadmill ECG testing and found HRR ≤12 beats/min doubled the 5-year risk of death. Five-year mortality jumped markedly as HRR dropped below 13, and quite dramatically if <10 beats/min.

While 1-minute HRR is the most widely studied parameter, other studies have found prognostic value in post-exercise HRR durations from 10 seconds to 2 minutes.

A British study published in the Journal of the American Heart Association (JAHA) of 40,727 individuals free of cardiovascular disease found that HRR at 10 seconds was superior to subsequent HRR durations in predicting all-cause mortality at a median of 6 years.

A 2001 JACC paper determined that a 2-minute HRR <22 beats/min provided a better cut-point than 1-minue HRR <13 beats/min in predicting mortality at 7 years in male veterans. Individuals underwent maximal treadmill followed by lying down, and those with an abnormal HRR were 2.6 times more likely to die. The HRR was equivalent to age and exercise capacity in predicting death.

More recently, the independent power of HRR to predict outcomes has been confirmed by Mayo Clinic researchers publishing in JAHA. They examined the ability of conventional cardiac risk factors and exercise ECG treadmill test parameters to predict mortality in 6546 patients without documented heart disease.

Functional aerobic capacity (FAC) and abnormal HRR (<12 beats/min at 1 minute) were highly associated with overall mortality and more powerful predictors than ECG ST segment changes. Poor exercise tolerance in the form of FAC and abnormal HRR were independent predictors of death after adjusting for conventional cardiovascular risk factors during a follow‐up period of approximately 10 years. The multivariable model used both these parameters as continuous variables and found a linear relationship with mortality.

In summary, these studies indicate 1-minute HRR <13 beats/min and 2-minute HRR <22 beats/min are bad prognostic signs.

To learn more about the power of the ECG in today's clinical landscape, browse our Diagnostic ECG Clinical Insights Center.

The Potential for Altering Heart Rate Recovery

Several studies have suggested that exercise training during cardiac rehabilitation can improve HRR, resulting in improved survival. A Circulation study of 1,070 patients undergoing phase 2 cardiac rehabilitation training found a significant improvement in HRR at 1 minute from 13.2 to 16.6 beats/min. Of the 544 patients with abnormal HRR (≤12 beats/min) at baseline, 41% normalized their HRR after training. Mortality at median 8.1 year follow-up was independently associated with exit HRR, but not with entrance HRR.

A recent study published in Heart Rhythm further adds to the intriguing possibility that modification of HRR can improve prognosis. Between 1996 and 2007, 386 consecutive patients with recent MI underwent symptom-limited treadmill testing at baseline and after exercise training, and were prospectively followed.

The patients' HRR after 8 weeks of exercise training improved from 17.5 ± 10.0 beats/min to 19.0 ± 12.3 beats/min, P=.011. Independent predictors of cardiac death after an average of 79 months of follow-up included:

Diabetes
Statin use
Baseline HR ≥ 65 beats/min
Post-training HRR <12 beats/min (hazard ratio of 2.49)
LVEF ≤30%

Patients who did not improve HRR from <12 beats/min to ≥12 beats/min after exercise training had significantly higher mortality (hazard ratio of 6.2; 95% CI 1.3–29.2).

A Simple, Powerful, and Intuitive Measure of Autonomic Tone

HRR, unlike heart rate variability, is a simple parameter that is easy to understand and measure. It yields information on vagal/parasympathetic tone and has been proven to be a powerful and independent predictor of overall mortality.

Patients who have been sedentary and are deconditioned or overweight can consider an abnormal HRR as a wake-up call to modify their lifestyle and thereby improve their mortality, as preliminary evidence suggests that increasing HRR with exercise training may lower mortality substantially.

For healthy, asymptomatic individuals, HRR can serve as a marker for overall cardiovascular fitness. It can be monitored along with exercise capacity, peak heart rate, and resting heart rate to raise awareness of how exercise is influencing overall ANS balance.

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