In this post, we’ll delve into how optimizing your magnesium levels, an essential mineral that 56% of the U.S. population is deficient in, can help you maximize your mitochondria in order to enhance your performance.1 (Note: Magnesium can be tested by the WellnessFX Performance package.) Your mitochondria are what give you energy through the process of oxidative phosphorylation – the consumption of oxygen to generate ATP, the energetic currency of your cells. They supply fuel to every single type of cell in your body, from muscle to neuron, to keep your cells functioning at their best. Your mitochondrial health is strongly tied to your fitness both in terms of physical performance and even longevity. It is your mitochondria that provide nourishment during injury to speed up wound healing and recovery.

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Oxidative capacity or “ability to consume oxygen”

High-intensity interval training (HIT) has repeatedly proven to be an excellent way to improve exercise performance in both non-athletes and athletes. 2 One of the ways HIT improves performance is by increasing oxidative capacity.3 Oxidative capacity is a term that refers to the ability of muscle to utilize (or consume) oxygen. Oxidative capacity not only depends on the availability of oxygen (this is what most people focus on) but also critically relies on your mitochondria, which are the tiny units inside your muscle cells that actually consume oxygen and produce ATP in the process. This is a critical point that should not be minimized: it’s ultimately the abundant production of ATP that enhances performance and prevents muscle fatigue.

At the level of the mitochondria, there are two ways in which studies have shown you can enhance your oxidative capacity:

Boost your mitochondrial mass (increase quantity) Maximize the efficiency of your existing mitochondria (increase quality).4

Increasing the number or “mass” of your mitochondria

One of the ways HIT increases oxidative capacity — and thus, performance — is by increasing your mitochondrial mass, which is the number of mitochondria per muscle cell. Studies have shown that even just one session of HIT results in mitochondrial biogenesis (the production of new mitochondria) within muscle cells.2

Herein lies the problem: remember how I mentioned that 56% of people in the U.S. are deficient in magnesium? In order to produce new mitochondria each of your existing mitochondria have to synthesize their genome anew (yes, mitochondria have their own genome) and this depends on enzymes that require magnesium as a cofactor to do just that.5,6 If your magnesium levels are inadequate, then your ability to boost mitochondrial number during HIT will be dampened, thus, compromising performance and the mitochondrial mass you would have otherwise gained as a consequence of your hard work and effort.

Increasing your mitochondrial efficiency

The second way you can maximize your mitochondria is by making them more efficient at producing ATP. It is well known that intense exercise induces oxidative stress and damage to your mitochondria, which dampens their ATP production (translation: lower oxidative capacity). But, your mitochondria have the ability to repair damage done to them using the same magnesium-dependent enzymes that I just mentioned.5 This means that if adequate levels of magnesium are not maintained (e.g. you’re part of the 56%), your oxidative capacity will suffer because of a decline in the rate of repair of your existing mitochondria.

Increasing your magnesium levels

The role magnesium plays in mitochondrial health is only one of a multitude of reasons why you should routinely get your magnesium levels tested. When in doubt you should increase your consumption of dark green leafy vegetables such as spinach and kale or almonds, which are all high in magnesium. One other reason that magnesium is good for mitochondria, which I’ll save for a future post, is this: energy production in the form of ATP is critical for nearly all wound-healing processes. Since your mitochondria are the centers of ATP production, then mitochondrial health is key to decreasing wound healing time.

In the next segment, we’ll do a deeper dive into what is causing the magnesium deficiencies we are facing today, what we can do to increase absorption and benefits and drawbacks of supplementation vs. food sources.

References:

1. Ames, B. N. Low micronutrient intake may accelerate the degenerative diseases of aging through allocation of scarce micronutrients by triage. Proc Natl Acad Sci U S A 103, 17589-17594, doi:10.1073/pnas.0608757103 (2006).

2. Jacobs, R. A. et al. Improvements in exercise performance with high-intensity interval training coincide with an increase in skeletal muscle mitochondrial content and function. J Appl Physiol, doi:10.1152/japplphysiol.00445.2013 (2013).

3. Larsen, R. G., Callahan, D. M., Foulis, S. A. & Kent-Braun, J. A. In vivo oxidative capacity varies with muscle and training status in young adults. J Appl Physiol 107, 873-879, doi:10.1152/japplphysiol.00260.2009 (2009).

4. Jacobs, R. A. & Lundby, C. Mitochondria express enhanced quality as well as quantity in association with aerobic fitness across recreationally active individuals up to elite athletes. J Appl Physiol 114, 344-350, doi:10.1152/japplphysiol.01081.2012 (2013).

5. Simsek, D. et al. Crucial role for DNA ligase III in mitochondria but not in Xrcc1-dependent repair. Nature 471, 245-248, doi:10.1038/nature09794 (2011).

6. Taylor, M. R., Conrad, J. A., Wahl, D. & O’Brien, P. J. Kinetic mechanism of human DNA ligase I reveals magnesium-dependent changes in the rate-limiting step that compromise ligation efficiency. J Biol Chem 286, 23054-23062, doi:10.1074/jbc.M111.248831 (2011).

The posts on this blog are for information only, and are not intended to substitute for a doctor-patient or other healthcare professional-patient relationship nor do they constitute medical or healthcare advice of any kind. Any information in these posts should not be acted upon without consideration of primary source material and professional input from one's own healthcare professionals.

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