For some time researchers have noted a strong link between heart rate and survival, an association that holds true for most mammals. Most small mammals have a rapid heart rate and a short life expectancy, while large mammals have a significantly slower heart rate and a correspondingly longer life span. For the majority of mammals, large and small, life expectancy is approximately 1 billion heartbeats.
Investigators have played with this information and successfully prolonged the life span of mice by slowing their heart rate. So where do we humans fit in?
We are no exception. A large epidemiological literature documents the association between heart rate and mortality. Resting rates as low as 75 to 80 beats per minute are associated with significant increases in total mortality and mortality due to coronary heart disease. Beta blockers, agents that are used to decrease heart rate, have proven quite effective in decreasing mortality rates after heart attack. Remarkably, the magnitude of the decrease in mortality is directly proportional to the magnitude of heart rate reduction.
What does all this mean? Is there really a magical number of heart beats and then our time is up? Not quite.
However, our heart rate is one of the most sensitive early markers of the effects of stress, a sort of canary in the coal mine. By stress I mean any environmental (eg. pollution), psychological (eg. living with a sick family member or difficult job situation), or biological (eg. elevated blood pressure or blood sugar or inflammation) phenomenon that impairs health. Such stressors affect the system that controls heart rate. Therefore changes in that system provide one of the earliest measureable signals in the development of disease.
To give you an idea of the exquisite sensitivity of heart rate measurements in revealing early disease, I'll give you some startling examples.
As an individual's blood sugar readings creep up, but before leaving the normal range, indicating the start of a process where insulin sensitivity is decreasing, there are characteristic changes in heart rate testing. The same is true of rising cholesterol levels, blood pressure and body weight.
In other words, simple noninvasive heart rate tests can be more sensitive and provide observable changes earlier than blood testing. As importantly, certain exercises can reverse these changes and prevent the onset of illness. First let's give you the background for this physiology.
In order to understand how heart rate is affected by stressors, we need to review that part of the nervous system that is responsible for adjusting our pulse in response to these cues. Unlike the voluntary nervous system which sends messages from brain to muscle so we can move about, the autonomic nervous system directs the "support functions" so to speak. It changes circulation so you don't pass out when you jump out of bed, raises your heart rate when you run for the bus, and brings it back to a resting rate when you get to your seat on the bus. This branch of the nervous system was called "autonomic" because it was thought to be automatic, requiring not only no thought, but no input from higher neural centers in the brain (not so). The heart and vasculature, lungs, stomach, liver, pancrease, spleen, and gastrointestinal tract are all regulated by the autonomic nervous system thereby controlling digestion, heart rate, blood pressure and many other essential functions.
This part of the nervous system acts through two separate, opposing and therefore alternately activated, subsystems, the sympathetic and parasympathetic branches. The "fight or flight" response is orchestrated by the sympathetic division and the parasympathetic division oversees such things as digestion, energy storage, and growth and repair, sort of peace time activities.
This set up has worked brilliantly, beautifully fine tuned by millions of years of evolution. It has allowed countless zebra to escape the lions' claw as well as primates like us to kill and not be killed, grow and reproduce. So what changed? How did this system designed to get us through stressful situations become maladaptive?
The environment in which evolution crafted our nervous system provided short-lived stressors. A predator approaches, you run, you escape or you're eaten. This scenario might have lasted 10-15 minutes.
Contrast that with typical contemporary stress. You wake up after a night of insufficient sleep because you were anxious about the presentation today that will determine a promotion and the colleague competing for the position is the brother-in-law of your boss, completely incompetent, but will probably beat you on this one, and you could really kill him, not only because he's an idiot and drives you crazy, but because your daughter is about to start college and chose the private (read unaffordable) school over the state one your son attends where you just found out he is on academic probation. You see my point.
Put simply, ongoing stress is a recent invention. And our response to it makes us sick. The epidemic prevalence of stroke, heart attack, obesity, stomach ulcer, irritable bowel syndrome, chronic fatigue syndrome, depression and anxiety, insomnia, infertility, compromised immune function and accelerated aging is largely due to chronic stress.
In my next entry I will speak about how we can prevent these maladies through interventions that directly repair the imbalance that chronic stress causes in the autonomic nervous system.