Monitoring health by counting heartbeats

It's often the case that high-intensity workouts (like Fran or Tabata sprints) cause your heart rate to skyrocket in order to meet the metabolic demands of active muscle. Remarkably, the flow of blood to active muscles may increase to four or five times that of resting cardiac output. Just as remarkable is the fact that your heart rate will typically drop 40% five minutes after exercise completion. These dramatic changes in heart rate are controlled by the sympathetic and parasympathetic components of the autonomic nervous system; sympathetic activation increases cardiac acceleration, contractility and coronary constriction whereas parasympathetic activation promotes cardiac deceleration and coronary dilation. Your heart rate response to exercise is largely determined by the balance of these two systems.

Being a sucker for numbers, I'm always on the lookout for simple, predictive physiological measures. There are a few based on heart rate that are strongly predictive of mortality and turn out (not surprisingly) to be modifiable by training. The first is resting heart rate, which the American Heart Association suggests should be between 60-80 beats per minute (bpm). A fast heart rate is associated with an increased risk of death from cardiovascular as well as noncardiovascular causes (Hjalmarson, 2007; Palatini, 1999). Even within the recommended range (60-80 bpm), a lower resting heart rate is significantly associated with decreased risk of dying from any cause, especially heart attack (Jouven et al., 2005).

The second measure is heart rate reserve, the difference between maximal heart rate and resting heart rate. A smaller dynamic range is associated with increased risk of death from any cause, especially heart attack (Jouven et al., 2005), and a failure to reach predicted peak heart rates during graded exercise is predictive of increased mortality and coronary heart disease incidence (Lauer et al., 1996).

Finally, the last measure is heart rate recovery, the difference between maximal heart rate and heart rate measured some fixed time after cessation of exercise (usually 1 or 2 minutes). The failure to drop at least 30 bpm within 1 minute is associated with increase risk of heart attack. A smaller decrease in heart rate suggests a dysfunction of the parasympathetic system, since the decrease in heart rate immediately following exercise is primarily due to parasympathetic reactivation (Imai et al., 1994; Raymond, 2004).

The above figure bins together all the data below 25 bpm recovery, but if you look more closely at lower ranges, an association with risk of death is even more apparent. For all you stats geeks, below is a conditional trellis plot (click the figure to see a larger version) that illustrates risk of all-cause mortality as a function of age, fitness, peak heart rate and heart rate recovery (Ishwaran et al., 2004). Age is a binary grouping indicated by the orange bars (left column is younger than 45 yo and the right column is older than 45 yo). Fitness is a categorical variable indicated by the green bars (least fit in the top row proceeding to most fit in the bottom row). Peak heart rate and heart rate recovery (measured 1 minute after ceasing exercise) are plotted for each subject for whichever panel they correspond to (age x fitness). That's five freakin variables!

And just for kicks, the figure to the right plots some data from the last time I did 400 meter sprints. There goes (220-age) as a predictor for my maximal heart rate! There are better ways of estimating maximal heart rate (e.g., see Joe Friel's work).

It's worth pointing out that these heart rate measures are not independent (Jouven et al., 2005); in fact they're highly correlated, suggesting that they may be different measures of the same disorder. And while the mechanism(s) underlying the association of these heart rate measures with increased mortality and heart disease remain unknown, the data are consistent with the idea that autonomic system imbalance predisposes people to life-threatening arrythmias (Jouven et al., 2005).

Aside from their utility for predicting death, these measures are also interesting because they can be modified by training. Following training, heart rate recovery is accelerated (Darr et al., 1988; Imai et al., 1994; Sugawara et al., 2001) and resting heart rate is decreased (Wilmore et al., 2008). Changes to maximal heart rate are less clear, with some evidence for a slight decrease following endurance training (Darr et al., 1988; Wilmore et al., 2008). So if you're bored, or looking for another way to track progress, break out the stopwatch or heart rate monitor and start logging! Indeed, Levine (1997) showed that the total number of heartbeats in a lifetime is remarkably constant across a wide range of variation in mammals.If we take seriously the idea that a human heart is physiologically predetermined to beat ~3 billion times in a lifetime, perhaps it wouldn't hurt to make reducing your resting heart rate an objective.