Type 1, Stress, and the Virtue of Slowing Down

I was today years old when I learned there were two different types of stress.

Adrenergic Stress

The first type, adrenergic stress, is familiar to most of us. It’s the type of stress we feel when we barely avoid a car accident, when we feel like someone is chasing us, or when an angry, out-of-control dog confronts us. Our bodies instantly jerk into fight-or-flight mode, and we can feel our hearts pound faster as we try to figure out how to get out of a bad situation. Meanwhile, our breathing passages gear up for the increased demand for oxygen to the bloodstream, our blood vessels dilate, we get ready to sweat in order to dump excess body heat, and our alertness becomes temporarily increased in order to respond to very small changes in our environment that may have life-or-death consequences.

Biologically, adrenergic stress involves the activation of the sympathetic nervous system and the release of catecholamines like epinephrine (adrenaline) and norepinephrine, which bind to adrenergic receptors triggering a cascade of physiological changes. The liver dumps glycogen and blood sugar rises to meet the anticipated energy needs of “escaping the cheetah.” It’s tempting in situations like this to stop eating and take insulin to try to get our blood sugars down, but that only worsens things.

I blogged about this a while back in my article about Stress, Sympathetic Nervous System Overload and blood sugar, so I won’t beat it to death here.

TL;DR: Our bodies seem to “know” that they can’t go on like this, and when we finally HAVE to stop, adrenergic stress subsides and we head into hypoglycemia at the same time we’re glycogen depleted–a dangerous combination. Severe increases in sweating–part of the adrenergic response triggered by low blood glucose–can FURTHER rob our body of precious electrolytes required to keep the heart beating, leading to dead-in-bed syndrome.

Clearly insulin alone isn’t the answer, and it should be obvious that NOT EATING isn’t the answer either, as our bodies are screaming for energy and doing everything they can to produce it. And paradoxically, despite post-exertional “highs”, our greatest need may actually be replenishing glycogen.

Recovery is a whole ‘nother topic, but cutting to the chase–regardless of what’s causing the stress, controlling adrenergic stress is one of the keys to maintaining healthy blood sugars.

Glucocorticoid Stress

There’s also a second type of stress: glucocorticoid stress. Glucocorticoid stress occurs when we put our bodies through a long-term “grind.” Whether that’s 10 consecutive 100-hour weeks trying to bring a work project back onto its timeline or it’s running across a continent is largely immaterial. The constant low-to-moderate energy demand mobilizes many of the same mechanisms it uses to fuel short-term energy demand, plus a few additional ones involving DIFFERENT stress hormones.

Instead of epinephrine, norepinephrine, and catecholamines, the long-term stress response primarily involves cortisol, CRH, and ACTH. The body is recalibrated to draw on long-term energy stores for a steady supply of energy rather than fast bursts, and fatigue and exhaustion can play significant roles. As the body works its way through short-term energy stores and settles down for the long haul, it begins to tap body fat and muscle protein for energy.

As muscle tissue breaks down, the body’s immune system fails to recognize damaged myoglobin and responds as if it were a virus or other invader. Body temperature rises and capillaries expand to make getting rid of the unwanted material easier. A lot of this damaged material is peed out through the kidneys, stressing them in significant and sometimes unrecoverable ways as rhabdomyolysis sets in. Thinking gets sketchy, then irrational, then perceptual miscues such as mistaking the sound of a windmill for heavy breathing of an imagined pursuer turn into outright visual hallucinations.

And as our cortisol-elevated blood sugars refuse to go down, we skip food, leading the body to consume even MORE of its limited on-board resources, scavenging itself for any spare energy that isn’t coming from food. It doesn’t work. Even if we get insulin to bring sugars down, our bodies continue to try to provide energy from scant resources until they can’t.

The physical wear-and-tear on our bodies that isn’t repaired or replenished by food or sleep takes its toll. Prolonged glucocorticoid stress is accompanied by a deterioration of performance and cognition in the short term, and broader aspects of health in the long term.

But the truth is, over the long term, EITHER type of stress can kill us.

Just not overnight.

Chronic Effects of Stress

Chronic exposure to either type of stress can create a number of unhappy consequences, including insulin resistance, dyslipidemia, inflammation, negative immunological outcomes, and cardiac adaptations that aren’t always helpful or adaptive, or mask more serious symptoms requiring attention.

Abnormal lipids are an important early indicator of cardiovascular health, and especially in type 1, an indicator of the ways in which our cardiovascular systems respond to chronic stress. Over time, cholesterol, which is critical to (re)building cell membranes, can be produced in excess in response to stress, can calcify, and then present as calcified plaques in cardiac arteries, the carotids, and elsewhere.

As type 1s, our innate autoimmune condition, associated inflammation, and dysregulation of blood glucose and blood pressure in response to stress can eventually contribute to greater formation of calcified plaques than in the general population. Cardiac risks are higher, and as athletes, our collateral vascularization and other cardiac adaptations from exercise can sometimes mask the seriousness of cardiac complications, leading clinicians to conclude that compared to everyone else, we’re “doing OK” and should just keep on keeping on.

People with type 1 may also be at risk of other autoimmune disorders that can be aggravated by or suddenly appear after the introduction of significant stressors. There is, for instance, anecdotal evidence in the ultra athlete community of individuals noting the appearance of immune disorders after finishing a particularly grueling 100- or 200-mile ultramarathon. While the cohort is admittedly small, it’s not all that different from the much more common reports of individuals experiencing the appearance of type 1 or other autoimmune conditions following viral infections, most recently Covid-19.

Even in populations not considered at-risk, the chronic stress of extreme and prolonged endurance exercise are not to be ignored. Things like myocardial fibrosis, arrhythmias, and hypertrophic cardiomyopathy are a real possibility, and it may be the case that when you talk to someone about these risk, your symptoms may be EITHER ignored or misinterpreted outside the context of exercise and treated accordingly.

The truth is, we’re NOT the same as the general population. The effect of stress on our bodies is not the same, and no matter how well we’re doing, appearing to be doing better than others shouldn’t be considered a passing grade if there are underlying problems left untreated.

Adapted Doesn’t Mean “OK”

I can recall specifically a day about 10 years ago when I was taken to the hospital by ambulance for an extremely low blood sugar. As I was seizing off-and-on in the gurney, I heard one of the EMTs say that I was bradycardic and needed treatment to speed up my heart rate. Fortunately for me, I was conscious and rational enough in the moment (miraculously, because mostly I wasn’t) to tell him that I was a runner and that a heart rate of 45 BPM was pretty normal for me.

Just this year, I’ve had several cardiologists tell me that I’m “OK” with a chronic total occlusion of one my my main cardiac arteries because I have “good collateral flow”, while two others are telling me I need immediate intervention such as a bypass or stent.

The conflict in opinion appears to lie in whether the cardiologist in question knows I’m an athlete. Those who ARE aware seem willing to write off the fact that my heart function as a 63-yea-old diabetic male is better than that of the average 63-year-old diabetic male.

But it shouldn’t.

AS a 63-year-old diabetic male athlete, I’m both the victim and beneficiary of a unique set of circumstances. I’m already in a high-risk group that would benefit from the coronary adaptations brought on by aerobic exercise, and I have benefited. But adaptation doesn’t mean that everything’s A-OK. Sometimes it’s an indication of how well you’re doing despite a serious problem that still needs to be treated.

For instance, I’ve just become aware of something called “hibernating myocardium.” It’s basically a state where the walls of the heart that do the beating are “managing” with a lower supply of oxygen and glucose, function well at rest, but get unhappy under stress. The good news is that the heart tissue isn’t dead. The bad news is that without bypass or some other intervention, it’s just there breathing slowly and fogging up the glass like Sleeping Beauty, waiting for things to get better.

Which, without intervention, they won’t.

Convincing medical professionals that I would be doing so much better if we just fixed the problem has taken four months so far, and it’s still ongoing.

In the mean time, I’m slowing down.

When Slowing Down Makes More Sense

After 20 years of vigorous exercise, I am learning that I’ve probably done myself a favor by hanging out at the middle or the back of the pack and not “pushing it” like some athletes do; and I’ve learned that when I DID push it–for instance, 223 miles of running on 7 hours of sleep back in 2017 or running a near-Boston-qualifying pace at a quadruple marathon back in 2016–I probably made things worse. In fact, I know I did, because I remember the rhabdo-like symptoms, the hives, the exhaustion, and the hallucinations.

Looking back, I know it was a bridge too far.

For folks like me, I think it’s critical to recognize the role different types of stress play in regulating our bodies and adapting to the situation, but ALSO in making us aware of our physical limitations and when it’s time to slow down.

Perhaps not to surprisingly, I’ve drifted toward longer and longer distances at a slower and slower pace. I like to think that my experiences with both long-term and short-term stress have taught me a lesson: that by giving my body time to adapt, it can deal with MANY things, but not ANYthing.

I’ve got collateral flow because I’ve adapted. But I’ve got heart disease because I’m not Superman.

Stress adaptation is a BUFFER to damage, but an ability to endure stress is NOT bulletproof armor. You take damage from every hit, and if you’re lucky, you live to fight another day.

That’s a noteworthy difference.

The warning signals I’ve received from scans, stress tests, and labs may have been conflicting, odd, or hard to extract an action plan from; but they’re a reminder that action still needs to be taken.

And sometimes that action is to slow down until you can fix the engine.