A daily 30-minute exercise can revitalize your health, so exercising twice as much should provide you with two times the health benefits, right?
If only that were true…
In this post, we talk about:
○ The fine line between exercise and too much exercise
○ How excessive exercise can lead to free radical damage
○ Avoiding the trap of overtraining
Let's dive right in!
As most people know, adults are strongly recommended to exercise at least 150 minutes per week consisting of moderate to vigorous intensity physical activity.
That's only about 30 minutes per day.
Regularly exercising this much (or should I say, this little) can greatly reduce your risk of developing chronic diseases like cancer, diabetes, Alzheimer’s disease, arteriosclerosis, and so on.
Physical activity comes with a catch. The "too much of a good thing" kind of catch.
Wait, Exercising Too Much Is A Thing?!
Yes. Believe it or not, there is a thing called exercising too much.
The fancy, scientific name for this is Rhabdomyolysis.
More accurately, it’s the degradation of muscle fibers, leading to muscle tissue death.
But how does this even occur?!
When Exercise Becomes a Double-Edged Sword
Normally, a little tissue trauma is good. If you’ve ever been sore, you know this feeling.
With adequate recovery time, the body adapts and athletic performance improves. This process is known as adaptive microtrauma.
Overtraining / extreme exercise can sabotage our performance and even be detrimental to our health.
Let’s explain what exactly overtraining is.
What is Overtraining Syndrome
Overtraining syndrome (OTS) occurs when intense exercise or prolonged periods of strenuous training supersedes the body’s capabilities. When exercise volume and intensity is abruptly increased and recovery time is short, more severe and chronic tissue trauma occurs.
How can you tell if you’ve reached this point?
First of all, your athletic performance will plateau or even decrease.
Once the body’s capacity to recover is exceeded by the training load, you’ll begin to see negative performance and potentially long-term health issues.
The Link Between Excessive Exercise and Free Radical Damage
But how are excessive exercise and free radical damage related?
Or - you might even be thinking - what the heck is free radical damage? Or, better yet, what is a free radical?
A free radical is essentially a moody teenager desperate to be in a relationship. Just like most teenagers have to have a boyfriend/girlfriend, free radicals are lonely electrons that have to have a mate. Electrons (due to their electromagnetic properties) “like” to be in pairs.
And when they don’t got one, they find one.
For better or for worse.
Excessive exercise and free radical damage are intricately linked, with the latter causing harmful effects on health. There is a proven positive correlation between the two, mainly due to overtraining - affecting the balance (homeostasis) of certain reactions and mechanisms in the body, which ultimately leads to an enhanced formation of free radicals and oxidative stress.
Oxidative stress has been scientifically proven to be linked with inflammation and tumor formation and is considered a precursor for cancer development.
(To learn more about the link between oxidative stress and inflammatory disease, cancer, and aging, check this article).
There are several results of free radical damage in the body, such as an increase in white blood cells (leukocytosis) or a decrease in antioxidant capacity.
In this article, we’ll look at 5 culprits that disrupt the balance of free radicals due to overtraining specifically.
Culprit #1: Calcium
The first perpetrator is…calcium. DUN DUN DUUUUN!
Calcium is stored in the sarcoplasmic reticulum, a membrane-bound structure found in skeletal muscles. Calcium releases from the sarcoplasmic reticulum via a ryanodine receptor 1 (RyR1) which initiates skeletal muscle contraction. When you flex your biceps in the mirror, you’re using your skeletal muscles to contract and relax.
The activation of RyR1 is normal, but what’s not normal is when they become “leaky.” When skeletal muscles age and heat stress occurs, the RyR1 calcium channels inadvertently leak calcium into the bloodstream.
This continuous release of calcium results in decreased tension, reduced exercise capacity, and increased ROS production.
(Sidenote: there are specific types of free radicals, like Reactive Oxygen Species, or ROS, which contain oxygen. Hence the name.)
Consequently, the combination of greater calcium and ROS levels contribute to lowered muscle performance and mitochondrial damage.
Culprit #2: Immune Cells
Immune cells also are a culprit in free radical damage. Although immune/white blood cells like neutrophils and macrophages fight pathogens in the body, they also can produce free radicals. Generally, phagocytosis, engulfment of bacterial fragments, requires the activation of immune cells as well as the respiratory burst. The respiratory burst is the abrupt increase in non-mitochondrial oxidative metabolism, which produces superoxide anions and other ROS.
After intense or long bouts of exercise, ROS-producing immune cells may infiltrate local inflammatory sites of exercise-induced injury in muscles. Thus, for several days after intensive exercise, both neutrophil and macrophage counts are higher than usual counts.
Unfortunately, due to their constant inability to differentiate between host and foreign antigens, they depend on other immune system elements to correctly identify truly infectious agents. If the targeting system is not well-controlled, immune cells form and release these free radicals to healthy tissue, causing inflammation and oxidative stress.
Culprit #3: Iron
The third culprit is free iron, which also plays a significant role in ROS production. Typically, free iron is bound to iron transporters and iron-dependent proteins. However, during high impact endurance sports, red blood cells have high destruction rates. This leads to an increase in free iron levels. This excessive iron is then mobilized to assist in the iron-catalyzed reaction called the Haber-Weiss reaction. This reaction converts the superoxide radical into an immensely reactive hydroxyl radical.
To make matters worse, xanthine oxidase is also a facilitator in this particular reaction, and, as we know now, it has greater production levels during periods of overtraining. This combination contributes to excessive ROS production and subsequent oxidative stress.
Culprit #4: Oxygen
While on the subject of “reactive oxygen species,” it is only fitting to include oxygen on this list. Cause, obviously.
In general, exercise = increased oxygen intake.
More oxygen also = increased flow of electrons in the mitochondria, the powerhouse of the cell.
Oxidative phosphorylation occurs in the mitochondrial inner membranes, which means single electrons are passed on to intermediate molecules containing oxygen and hydrogen. However, “electron leakage” may occur, which leads to some oxygen ending up incompletely reduced (incomplete electron transfer), which is a fancy way of saying they only have 1 electron.
Remember, teenagers...I mean electrons...want to be in pairs. This is how superoxide radicals and hydroxyl radicals are produced.
Culprit #5: Xanthine Oxidase
Last, but not least, we have xanthine oxidase (XO), an enzyme that plays a key role in the conversion of hypoxanthine to uric acid.
Normally, XO acts as a dehydrogenase (fancy way of saying removes hydrogen ions from a molecule); but during exercise, it works as an oxidase, using molecular oxygen to generate superoxide anions. Hence, it is a source of free radicals during exhaustive physical training and metabolic stress.
Furthermore, it is not only associated with aerobic exercise, but also with anaerobic exercises as well as resistance exercises in weightlifting.
To test this out, a group of researchers designed an experiment to see the effect of xanthine oxidase in producing free radical after exercise. Through tests involving an 800m run and a cycling race, they found that plasma hypoxanthine concentrations peaked 20 minutes after each activity ended.
What the heck is plasma hypoxanthine though?
It’s an important chemical structure that is a part of xanthine oxidase. Higher hypoxanthine levels indicate that there are higher levels of xanthine oxidase, therefore, higher levels of free radicals.
There is A New Hope though.
Oops sorry, wrong article. There is hope though. There, that’s better.
Allopurinol, a known XO inhibitor, reduces ROS production and muscle damage after strenuous exercise. In animals, it has been effective in preventing the events of glutathione oxidation and lipoperoxidation, which are both related to exhaustion.
How Not to Fall Into the Trap of Overtraining
With all these possible sources of oxidative stress and their associated negative outcomes, you may start to think that exercise might not be worth the effort (and sweat).
BUT, exercise is healthy and beneficial, especially when it comes to reducing the risk of cardiovascular disease. No doubt about that.
That said, physical training, like most things in the world, requires moderation.
When the duration & intensity of physical activity gradually increases, then there is adequate time for the body to adapt and adjust.
Therefore, when done right, exercise can be considered an antioxidant, as it protects against oxidative stress by increasing the concentration of antioxidant enzymes.
So Next Time You Work Out...
Make sure you exercise within your limits, pay attention to how your body feels, and take breaks between workout sessions.
If you take your workouts seriously and are still concerned about free radical damage, we’re happy to introduce a unique antioxidant, which eliminates only the most harmful free radicals, reduces oxidative stress, and puts the body in balance: Molecular Hydrogen.
On top of reducing overall levels of oxidative stress in the body, Molecular Hydrogen has also been proven to improve exercise performance and even help you get back on your feet after soft tissue injuries.
Let Vital Reaction Hydrogen Tablets help you ramp up your workout and mitigate damage produced by oxidative stress!
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9) Radak, Z., Zhao, Z., Koltai, E., Ohno, H., & Atalay, M. (2013). Oxygen Consumption and Usage During Physical Exercise: The Balance Between Oxidative Stress and ROS-Dependent Adaptive Signaling. Antioxidants & Redox Signaling, 18(10), 1208–1246. https://doi.org/10.1089/ars.2011.4498
10) Tremblay, M. S., Warburton, D. E. R., Janssen, I., Paterson, D. H., Latimer, A. E., Rhodes, R. E., Kho, M.E., Hicks, A., LeBlanc, A.G., Zehr, L., Murumets, K., & Duggan, M. (2011). New Canadian Physical Activity Guidelines. Applied Physiology, Nutrition, and Metabolism, 36(1), 36–46. https://doi.org/10.1139/H11-009
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