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.

I hate running

Warm-up:
0.5 mi jog

WOD 070830
Run 5k
25:49

2x1 min front planks
3x8 (per arm) windmills (30# KB)

Ran on a treadmill (1% incline, set between 7.1-7.6). I didn't find this fun at all, was really thinking I could stick to a 8'/mi pace. Guess it's time to work more aerobic conditioning in. I wore a heart rate monitor, and it was consistently above 170 bpm, peaking at 202 bpm. This seems abnormally high for such slow running?? Poor efficiency?

Mean heart rates recorded during 10 minutes of recovery after peak exercise, sorted by age and training status. Source: Darr et al., 1988.

Turning back the clock

Figure 1 from a recent paper by Melov et al. (2007) studying gene expression profiles in older adults following resistance training. This figure is not particularly useful, and I included because it looks cool (hmmmm). Don't worry though, the results are actually pretty interesting. Melov et al. were interested in how resistance training alters gene expression profiles in skeletal muscle, and whether any of these changes were consistent with a reversal of age-related muscular impairments. They used microarray technology to map the transcription profiles in skeletal muscle of older adults (~70yo) before and after 6 months of full-body resistance training. Perhaps unsurprisingly, a bunch of genes are differentially expressed when older untrained adults are compared to sedentary younger adults, including some associated with mitochondrial function (see also Zahn et al., 2006). However, after 6 months of resistance training (which resulted in significant strength gains), the gene expression profile for older adults was markedly different. A subset of the genes that showed an age-related difference also showed a change in expression due to exercise. Notably, those genes that were expressed at a level lower than young adults were upregulated while those genes that were expressed at a level higher than young adults were downregulated. As the authors put it, the transcriptional signature of aging was reversed back to that of younger levels. Now, I don't have a good sense of how to interpret expression levels, and the authors tended to plot their data on relative scales, so I can't assess the magnitude of these results, but it's an interesting application of gene profiling technology. Unfortunately, there was no individual level correlation of strength gains with changes in gene expression profile (in those genes significantly associated with age and exercise), although this may be a power issue (I guess people aren't jumping for the chance to get repeated muscle biopsies with a 5mm diameter needle!?).

Melov S, Tarnopolsky MA, Beckman K, Felkey K, Hubbard A (2007) Resistance Exercise Reverses Aging in Human Skeletal Muscle. PLoS ONE 2(5): e465 doi:10.1371/journal.pone.0000465

Zahn JM, Sonu R, Vogel H, Crane E, Mazan-Mamczarz K, et al. (2006) Transcriptional Profiling of Aging in Human Muscle Reveals a Common Aging Signature. PLoS Genet 2(7): e115 doi:10.1371/journal.pgen.0020115

Never again

Warm-up:
10-5-5-5-5 overhead squat (45,65,85,95)

WOD from 062707

3 rounds for time:
50 thrusters (45# bar)
35 pullups

35:50

Heart rate at 204 BPM at the end of last set of thrusters (apparently I still have β-adrenergic receptors on my heart despite my age). Forced to use Gravitron due to total muscular failure (aka pussyarms). Everything hurts.

Should only be done in groups.Source: Higginbotham et al., 1986