CBD and Exercise Related Inflammation: Is there something there?

December 23, 2019 0
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Disclaimer: Part of our mission is to always present the latest cannabinoid research; however, none of this is intended to represent the safety or efficacy of our products. These statements and our products have not been evaluated by the FDA, and our products are not intended to diagnose, prevent, treat or cure any disease. You should consult your physician or other health care professional before taking CBD to determine if it is right for your needs.

Currently, there are athletes across the country advocating for the use of products containing CBD following their workouts to help them recover.  Is there any merit to this from a physiological, science-based perspective? 

Written by: Dr. Jonny Lisano, Ph.D.

Exercise and Muscle Soreness

Regardless if you are an elite athlete, fitness fiend or a weekend warrior, odds are that you have experienced localized muscle soreness and swelling in the days following your workouts.  This pain and swelling typically become apparent 24-48 hours following your workout and can last for days (Lewis et al., 2012). This swelling and pain might even have led you to miss a workout or two. This is commonly referred to within the fitness community as DOMS (delayed onset muscle soreness) (Lewis et al., 2012). It’s a common misconception that DOMS is the result of lactic acid accumulation during your workout. While lactic acid is produced in large quantities during intense exercise to help provide quick energy to exercising muscles, it is not the primary perpetrator for your exercise-related muscle soreness. Lactic acid quickly dissociates into lactate and hydrogen (H+). While the lactate is harmless and is transported to the blood and processed quickly by other tissues like the liver, the hydrogen ion can act as a free radical and cause chemical damage to the muscle if not adequately dealt with (Bailey et al., 2004)

Inflammation

The root cause of DOMS is actually the chemical and physical damage to muscle as a result form exercise. Yes, you read that right, when you exercise you cause damage to your muscles (that’s ok because this is actually how your body gets stronger, which we’ll discuss later).  This damage causes the inner contents of cells to be released, which are not normally found outside of the cell. These inner contents along with locally secreted factors known as cytokines and chemokines act as a chemical signal to immune cells, primarily monocytes, circulating in the blood (Peake et al., 2017). These immune cells then follow that combined chemical signal to the site of damage and migrate into those local tissues. It is during this process that some of the monocytes become what are known as M1 macrophages. What M1 macrophages do is they “eat” up and clear any of the damaged cellular debris while simultaneously secreting factors to help recruit more immune cells to the area and make the area more permeable to fluid, which promotes circulation of fluid to bring in nutrients and more immune cells, but also flush out debris and release the immune cell factors that promote migration to the area (Ley 2017)

Now, this is a good, natural process and is needed to clear out the damaged tissue before new tissue growth and repair can be stimulated by M2 macrophages. The M2 macrophages are responsible for stimulating muscle satellite cells “baby muscle cells” to grow and mature (Ley 2017). This not only helps to replace damaged tissue but also, in theory, makes the muscle tissue stronger than it was previously so it can handle more stress for the next bout of exercise. This whole process normally takes a few days from start to finish, with the inflammation and pain subsiding within a couple of days. This is what is known as “acute” inflammation. Acute inflammation is a good thing, it naturally helps promote muscle repair and recovery.  

However, when the inflammation stimulated by exercise-related muscle damage persists for more than a few days it becomes what is known as “chronic” inflammation. Chronic inflammation is not desirable and can result in not only the breakdown and removal of damaged tissue but normal, healthy tissue as well (Dalle et al. 2017).  This issue of chronic-inflammation is actually commonly seen in athletes and is one aspect of what is known as overtraining syndrome. One of the ways overtraining syndrome can be induced is through excessive intense exercise, which we already know can cause acute inflammation. With inadequate time for recovery, this is where acute inflammation turns into chronic inflammation. This ultimately results in loss of muscle mass and strength called sarcopenia. So, how do we manage the balance between acute and chronic inflammation to maximize recovery? 

Well, one common method is through the use of non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen.  These drugs help limit the pro-inflammatory process and can help reduce exercise-related pain. However, when taken chronically or in excessive amounts, NSAIDs can cause damage to organs, like your kidneys (Whelton et al., 1991). Could cannabidiol (CBD) potentially be a natural way to help mitigate excessive inflammation resulting from exercise? 

Cannabidiol (CBD)

As you may know, CBD is one of more than 100+ cannabinoids present in the hemp plant (Cannabis Sativa L.). It exerts its physiological effects by acting on the body’s endocannabinoid system. Receptors like CB1, CB2, and GPR55 are all cannabinoid receptors present in immune tissues and cells. Like monocytes, they have been scientifically observed to have varying interactions with CBD.  

Cannabidiol (CBD) and Inflammation

Surprisingly, there is extremely limited research on how both the acute and chronic use of CBD affect the post-exercise inflammatory process in humans. The most promising research with respect to this area has been performed using cell cultures (i.e. performing experiments on cells that are grown outside of the body in highly sterile, highly controlled conditions.)

As mentioned earlier, cytokines released by immune cells and other local tissues, such as muscle, act as a chemical signal that can either promote or suppress the inflammatory process. When a cytokine promotes inflammation, it is referred to as pro-inflammatory, and when it suppresses inflammation it is classified as anti-inflammatory. Remember we stated earlier that a little bit of inflammation is a good thing, and low levels of pro-inflammatory cytokines, such as interleukin-6 (IL-6), are actually necessary for muscle growth and repair (Kurosaka et al., 2013).  Too much of it, however, can be detrimental (Kurosaka et al.,  2013)

One study, assessing the effects of the pre-treating immune cells with either CBD or delta-9-tetrahydrocannabinol (THC) prior to an immune challenge (which could represent a cold or an intense exercise bout) resulted in the suppression of the immune cell’s release of proinflammatory cytokines, like IL-6 and tumor necrosis factor-alpha (TNFα). Further, it was found that as the dose of these cannabinoids was increased, there was a greater immunosuppressive effect on these cytokines. More interestingly, CBD provided a greater immunosuppressive effect than THC at the same concentrations (Kozela et al. 2010). Meaning that CBD on its own has greater immunosuppressive effects than THC on its own, and could potentially prevent the excessive release of IL-6, which can lead to chronic inflammation.  

In a human study comparing the circulating concentrations of interleukin-17 (IL-17), another pro-inflammatory cytokine, between chronic cannabis users and non-users that were either healthy or had multiple sclerosis (MS), showed that both cannabis user groups (healthy and MS) had significantly lower circulating concentrations of the pro-inflammatory IL-17 cytokine (Sexton et al. 2014). The cytokine IL-17 acts on other immune cells, stimulating them to release chemokines that attract more immune cells like monocytes to the tissue. Keep in mind that this study was not exclusive to CBD and participants were using products that contained both THC and CBD.  

However, while these results are promising for the scientifically observed anti-inflammatory effects of CBD, there is still limited/no evidence of the effects of CBD on exercise-induced inflammation in humans. What is even more interesting, is that recent research published in November 2019 showed that chronic exercise can significantly change the expression of CB1 and CB2 receptors in various types of immune cells. Thus, chronic exercise could change the way your immune cells respond to cannabinoids like CBD (Valencia-Sanchez et al., 2019). Increasing the number of CB1 or CB2 receptors expressed on immune cells would, in theory, make your cells more responsive to cannabinoids like CBD, meaning the anti-inflammatory effects could become more pronounced. On the opposite end of that spectrum, if exercise decreases the number of CB1 or CB2 receptors expressed by immune cells this could limit the anti-inflammatory effects of cannabinoids.  

Yet, this begs the question of are there individuals that are using cannabis products like CBD to help with exercise pain and inflammation? In a survey study that I published during my Ph.D., we asked physically active cannabis users, why they were using cannabis products either before, during or after their exercise. Pain mitigation and recovery were two of the most common reasons for use. With cannabis being used for pain at all three time-points (before, during and after exercise), whereas recovery was only reported after exercise (Lisano et al. 2019). However, it was unclear if the pain they were using cannabis to mitigate was exercise-induced pain or a pre-existing condition like arthritis. More research will be needed to provide a definitive answer on if taking CBD following exercise can help reduce localized inflammation, swelling, and pain associated with exercise. Exercise in itself has anti-inflammatory effects, and it is still unclear if the anti-inflammatory effects of CBD would combine with the anti-inflammatory effects of exercise leading to a greater combined immunosuppressive effect. 

Final Thoughts

Exercise-induced inflammation is a complex process, of which we have only just scratched the surface in this article. You now know that the DOMS experienced following exercise is the result of exercise-related damage to the muscles, which results in localized inflammation (swelling) of the tissue that can result in pain. Cannabinoids, especially CBD, have been observed to have anti-inflammatory effects, which may indicate that the use of CBD following exercise can help mitigate the exercise-associated inflammation and get you back to your workouts in the following days feeling great. More research on this to come. 

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Jonny Lisano, Ph.D

JONNY LISANO, Ph.D.

Jonny received his Ph.D. from the University of Northern Colorado (UNC) in Exercise Physiology.  During his time at (UNC) he and his advisor established the first cannabis and exercise performance laboratory in the nation.  Jonny’s early research pertaining to cannabis focused on the assessment of how the long-term use of cannabis products in physically active individuals affected parameters of overall health and exercise performance.  As he progressed into the field of cannabis research his focused shifted from exercise performance to that of how CBD affects immune function in physically active individuals who are using cannabis products.

Jonny has always been an advocate for living a healthy lifestyle and believes CBD can be an integral part of that.  His focus at 6° Wellness is to provide and explain the most current scientific knowledge pertaining to cannabis in a way everyone can understand, and providing recommendations on how the products we offer can fit into your lifestyle.

In his free time Jonny enjoys training for competitive obstacle course races, hiking the beautiful Colorado backcountry, and partaking in the occasional beer from the local craft beer scene.

References:

Bailey, D.M., Young, I.S., McEneny, J., Lawrenson, L., Kim, J., Barden, J., Richardson, R.S. 2004. Regulation of Free Radical Outflow From an Isolated Muscle Bed in Exercising Humans. Am. J. Physiol. Heart Circ. Physiol., 287(4):H1689-99. 

Dalle, S. Rossmeislova, L., Koppo, K. 2017. The Role of Inflammation in Age-Related Sarcopenia. Front. Physiol., 8: 1045. 

Kozela, E., Pietr, M., Juknat, A., Rimmerman, N., Levy, R., Vogel, Z. 2010. Cannabinoids Delta(9)-tetrahydrocannabinol and Cannabidiol Differentially Inhibit the Lipopolysaccharide-Activated NF-kappaB and interferon-beta/STAT Proinflammatory Pathways in BV-2 Microglial Cells. J. Biol. Chem., 285(3): 1616-26. 

Kurosaka, M., Machida, S., 2013. Interleukin-6-induced Satellite Cell Proliferation Is Regulated by Induction of the JAK2/STAT3 Signalling Pathway Through Cyclin D1 Targeting. Cell Prolif., 46(4): 365-73.

Lewis, P.B., Ruby, D., Bush-Joseph, C.A. 2012. Muscle Soreness and Delayed-Onset Muscle Soreness. Clin Sports Med., 31(2):255-62. 

Ley, K. 2017. M1 Means Kill; M2 Means Heal. J. Immunol., 199(7):2191-2193.

Lisano, J.K., Phillips, K.T., Smith, J.D., Barnes, M.J., Stewart, L.K. 2019. Patterns and Perceptions of Cannabis Use with Physical Activity. Cannabis, 2(2):151-64.

Peake, J.M., Roberts, L.A., Figueiredo, V.C., Egner, I., Krog, S., Aas, S.N., Suzuki, K., Markworth, J.F., Coombes, J.S., Cameron-Smith, D., Raastad, T. 2017. The Effects of Cold Water Immersion and Active Recovery on Inflammation and Cell Stress Responses in Human Skeletal Muscle After Resistance Exercise. J. Physiol., 595(3):695-711. 

Sexton, M., Cudaback, E., Abdullah, R.A., Finnel, J., Mischley, L.K., Rozga, M., Lichtman, A.H., Stella, N. 2014. Cannabis Use by Individuals with Multiple Sclerosis: Effects on Specific Immune Parameters.  Inflammopharmacology, 22(5): 295-303. 

Valencia-Sanchez, S., Nava-Castro, K.E., Palacios-Arreola, M.I., Prospero-Garcia, O., Morales-Montor, J., Drucker-Colin, R. 2019. Chronic exercise modulates the cellular immunity and its cannabinoid receptors expression. PloS One, 14(11): e0220542. 

Whelton, A., Hamilton, C.W., 1991. Nonsteroidal Anti-Inflammatory Drugs: Effects on Kidney Function. J. Clin. Pharmacol., 31(7): 588-98. 

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