A recent study about marine mammals caught my eye. I don’t know much about non-human biology and physiology, but this study on dolphins and seals may shed some light on the problem of fatalities during open water swimming or triathlon events.
A group of investigators headed by Terrie Williams from the University of California at Santa Cruz shared their report, “Exercise at depth alters bradycardia and incidence of cardiac anomalies in deep-diving marine mammals” in the January 16th edition of Nature Communications (1).
This group of investigators has been interested in the physiology of the so-called “dive response” in marine mammals. This is a response that is governed by the involuntary, or autonomic, nervous system, which has two antagonistic components: the parasympathetic nervous system and the sympathetic nervous system. As a group, the marine mammals depend on feeding by chasing pray to depths that can range up to 3,000 m. Even at lesser depths, these mammals must maintain a breath-hold under large hydrostatic pressures while they undergo extreme exertion to catch their pray. During a dive, breath-holding stimulates the parasympathetic nervous system to slow the heart rate (producing bradycardia). At the same time, the exertion required to chase pray stimulates the sympathetic nervous system, producing an increase in the heart rate. The current study offers the first detailed study of the interplay between the components of the autonomic nervous system during routine diving and feeding activity in these animals.
The investigators created an electrocardiograph-accelerometer depth monitor that was deployed on 10 Atlantic bottle-nosed dolphins and 3 Weddell seals. This device allowed high-fidelity recording of the heart rate, ECG, water depth, and swimming stroke frequency (a measure of exertion) during dives. For the dolphins, measurements were made for 74 dives to depths of up to 210 m. For the seals, measurements were made for 91 dives to depths of up to 390 m.
As expected, there was a strong relationship between diving depth and heart rate for both species, with heart rates falling during descent and reaching a minimum at the lowest depth of the dive. Superimposed on this effect was an additional effect of exertion. For the dolphins, the maximum heart rate was 1.7 to 3.7 times greater during periods of extreme exercise compared to gliding alone. For the seals, the maximum heart rate was 1.5 to 1.8 times greater during periods of extreme exercise compared to gliding alone.
The surprising finding was that cardiac arrhythmias occurred in more than 73% of the dives. The investigators defined arrhythmias to include ectopic beats or significantly increased variability in the interbeat interval (IBI). There were apparently no sustained or fatal arrhythmias., but there were discrete examples of “wandering pacemaker” and ventricular premature beats. In the Weddell seals, there were often patterns of alternating periods of tachycardia (fast heart rate) and bradycardia (low heart rate) during periods of constant, intense exertion.
The presence of cardiac arrhythmias was strongly correlated with increased depth of dive (parasympathetic activation) and increased exertion (sympathetic activation). As an example, cardiac arrhythmias occurred in 81% of the dolphin dives to >210 m but in only 26% of dives to <100 m.
The authors concluded that our previous understanding of the dive reflex in marine mammals was not totally correct. Given that these animals depend on diving for their food sources, the development of cardiac arrhythmias during feeding appears to be mal-adaptive. In fact, feeding might actually be dangerous.
At first glance, the physiology of the diving response of dolphins and seals during feeding seems far afield from open water swimming and triathlon. And moreover, we already know about the development of cardiac arrhythmias during submersion in breath-holding humans as well as other marine species. The important observation here, though, is what I might call “irritability” or “instability” in the heart rhythm during periods of intense parasympathetic and intense sympathetic activation….and that’s the possible link to human fatalities during open water swimming or triathlon.
We know from autopsy reports of triathletes who’ve died during the swim portion of an event that there are sometimes only subtle abnormalities of the heart, and often nothing that seems explanatory. That leaves us in a difficult position to explain such deaths. In a previous blog post, I wrote about one very plausible hypothesis. Two UK physiologist,s X and X, proposed the concept of “autonomic conflict,” where a surge in both the parasympathetic and sympathetic stimulation of the heart might lead to a fatal arrhythmia. I’ve been intrigued with this hypothesis because it seems to fit many of the observations made about the swim victims. It is easy to see where exertion, cold water, anxiety, etc. might lead to strong sympathetic activation. And it’s equally easy to see where facial wetting, water entering the mouth/hypopharynx/nasopharynx, and breath-holding, even without diving, might lead to strong parasympathetic activation. In that instant, in an athlete with some sort of susceptible heart, a fatal arrhythmia might occur.
The new observations about the dolphins and seals seem to play into this hypothesis.
1. Williams TM, Fuirman LA, Kendall T, et al. Exercise at depth alters bradycardia and incidence of cardiac anomalies in deep-diving marine mammals. Nature Communications 2015;6:6055.