Acute Versus Chronic Stress

This academic discussion of the various stages of the stress response in a bunch of lab rats is all very interesting (really!), but you're probably asking yourself, "What does this mean for me?" Well, it could mean a great deal—especially when you understand how your own body responds to stress, and whether that stress is encountered acutely or chronically. First, let's take a look at what happens inside the body when stress hits. The body's initial response to a perceived acute stressor is the already mentioned fight-or-flight response that we've lived with since the caveman days. When stress hits, the body's energy reserves (fat, protein, and carbohydrates) are rapidly mobilized (through catabolic breakdown of tissues) to deal with the stressor. Levels of adrenaline and cortisol increase, while levels of DHEA (dehydroepiandrosterone) and testosterone decrease. (The combined effects of sustained high cortisol and low DHEA/testosterone lead to muscle loss and fat gain—more on that later.)

Common health effects of dealing with acute stressors typically include increased heart rate and blood pressure, increased breathing rate, increased body temperature and sweating, feelings of anxiety and nervousness, headaches, heartburn, and irritability; these are the things you'll feel while the hormones and neurotransmitters rage throughout your body. The good news about an acute stressor, however, is that because our energy stores are mobilized to either fight off or get away from the stressor, we can use that energy and heightened alertness to do something good—such as exercise. Unfortunately, if we can't eliminate or escape from the stressor (or use exercise to fool our body into thinking that we're escaping), then the acute stressor quickly becomes a chronic stressor.

As the acute stressor becomes more of a chronic stressor, cortisol levels continue to increase and DHEA/testosterone levels continue to decrease. (There is no rule of thumb for when acute crosses the line into chronic; it differs widely among people.) As mentioned above, the dual effect of high cortisol and low DHEA/testosterone leads to muscle loss and fat gain, but it can also have detrimental effects on bone and other tissues (via accelerated breakdown and delayed repair). Typical symptoms associated with chronic stress may include weight gain, fatigue, fluctuations in blood sugar, increased appetite, carbohydrate cravings, muscle weakness, and reduced immune-system function. The loss of muscle tissue leads to a fall in basal metabolic rate (the number of calories the body burns at rest) and marks the turning point between "early" and "late" chronic stress, sometimes called Stage 2 and Stage 3 stress. The early stages of chronic stress can be considered more of a hypercatabolic situation, characterized by accelerated tissue destruction, whereas the later stages put a person into more of a hypoanabolic state, where the ability to rebuild vital tissues is impaired. At this later stage, much of the damage has already been done—muscle and bone tissues are weaker, sex drive is reduced (because of low DHEA/testosterone, growth hormone, and sex steroids), and the person enters a vicious cycle of increased appetite, reduced caloric expenditure, and accelerated fat accumulation.

Ohio University scientists have suggested that the nature of our modern society often makes chronic stress inescapable. In research studies, they have shown overall exposure to cortisol to be significantly related to the degree of "daily hassles" (more hassles lead to more cortisol) as well as to age (higher age = higher cortisol) and to hours slept (less sleep = more cortisol). Researchers in Boston have suggested that acute or chronic psychological stress is a primary cause not just of cortisol overexposure, but also of inflammatory diseases, including insulin resistance, diabetes, obesity, and heart disease. Inflammation and abdominal fat accumulation are inextricably linked, with cortisol, HSD, and cytokines such as IL-6 combing to promoteing fat storage in a "chicken-and-egg" scenario. (Cytokines are a class of proteins that play a central role in the immune response. Their presence is a marker for inflammation.) These cellular signals lead to obesity, which leads to inflammation, which leads to more obesity. We know that weight loss leads to a fall in markers of inflammation and to a fall in cortisol exposure, and that controlling stress can lead to reduced appetite and weight loss—so it seems that the chicken/egg scenario can run both ways if you know how to nudge the cycle in the right direction.

The bottom line here is that the body can deal with acute stress, and it can do so with great effectiveness as long as the acute stress is dealt with before it progresses into the chronic stages. How? By exercising. As the Nike ads used to say about exercise, "Just do it!"—because doing it will be your best hedge against acute stress slipping into the realm of chronic stress (more on the uses and benefits of exercise is presented in Chapters 7 and 9).

But now let's get real. If we all had the time, resources, and inclination to "Just do it" on a regular basis, there would be a lot fewer people reading this book (or at least a few more reading it while walking or running on their treadmills). However, the reality is that most of us (this author included) cannot simply drop what we are doing and run off to "do it" (exercise, that is) at a moment's notice. So we miss a few (or more than a few) exercise sessions, our acute stressors "build up" in a sense, and we slowly slip into the initial stages of chronic stress.


Shawn Talbott

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