October 21, 2019
It is common knowledge that exercise and staying active is an important part of a healthy lifestyle for all ages. Exercising and activity have many health benefits. Unfortunately, my knees seem to disagree. I enjoy day hiking, and I have many opportunities and places to hike where I live that include significant elevation changes. My knees complain the most going downhill. (I wish it was uphill both ways, like when my dad went hiking.) My knees become sore and swollen after an extensive downhill descent. This is an inflammatory response to the stress and injuries I am imposing on them.
Inflammation is the immune system’s response to a harmful stimulus.1 These stimuli can include physical injury, thorns, pathogens, oxidative stress, toxic compounds or irradiation. Acute inflammation responses have a goal of preventing further injury or infection. Certain diseases such as bowel diseases, cardiovascular diseases (CVDs), arthritis, diabetes and cancer have chronic inflammation as a common symptom. Dysregulation of the inflammatory response can also lead to chronic inflammation. Many inflammatory proteins and pathways can be triggered depending on the stimulus.
Exercise causes inflammation in an acute phase. In a study conducted on healthy, young adult males, researchers measured the acute effects of walking exercise on inflammatory markers.2 In 2018, the study, published in The European Journal of Applied Physiology, reported that regardless of whether individuals were participating in high-intensity, intermittent walking or continuous, moderate-intensity walking, interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-a) significantly increased for a period of four hours post-exercise.
Additionally, a review article by Sallam and Laher, showed consistent exercise or activity that increases energy expenditure over the resting condition results in modulation of chronic inflammation.3 Their research showed the control of chronic inflammation associated with aging and CVD as a function of exercise may add to the benefits of regular exercise.
Unfortunately, exercise is only one part of the equation. Proper nutritional intake must also be present to support the effects of exercise. This is particularly true with adequate consumption of minerals. Minerals play key roles in many pathways of inflammatory responses.
Zinc is an essential nutrient for many biochemical processes and for cell growth. In the body, there are homeostatic control mechanisms that maintain plasma zinc concentration within a relatively narrow range. In the event of an acute inflammatory response, zinc concentrations rapidly decline in plasma as the zinc is redistributed within cellular compartments.4 This redistribution supplies additional zinc for zinc-dependent protein synthesis and increased oxidative stress relief.
With age, chronic age-related inflammation is a possibility. Researchers studying the effects of zinc status on markers of inflammation in zinc-deficient, old mice found serum IL-6 (inflammatory cytokine protein) levels were significantly reduced with zinc supplementation for three weeks, suggesting restoring zinc status to normal may overcome chronic inflammation in old age.5
Normal, acute inflammatory response causes a significant level of oxidative stress. A large amount of reactive oxygen species (ROS) is generated by the neutrophils, macrophages and phagocytotic cells.6 To rectify and limit the damage these ROS can do, the body employs an arsenal of enzymatic and non-enzymatic proteins. The chief among those is superoxide dismutase (SOD). Zinc is a cofactor of the zinc/ copper SOD, and this SOD scavenges the ROS and renders them to the less harmful oxygen and peroxide species. In another study, researchers examined the effects of chronic exercise and marginal zinc deficiency on oxidative damage.7 The researchers found oxidative DNA damage significantly increased in the prostate when there was marginal zinc deficiency combined with exercise when compared to zinc-adequate animals.
Selenium is another important mineral to help with the inflammatory process of scavenging ROS. It is typically associated in this process with the glutathione peroxidase family, which reduces hydrogen peroxide to water. However, recent studies suggested selenium deficiency and/or altered selenoprotein transcription may play a role in inflammatory bowel disease and oxidative stress induced inflammatory tumorigenesis.8,9
Finally, magnesium may also play a role in the inflammatory response. In one epidemiological study of 3,713 post-menopausal women, a significant inverse relationship occurred between magnesium intake and inflammatory markers of c-reactive protein (CRP), IL-6 and TNF-a.10 This finding was confirmed in a 20-year longitudinal study related to the incidence of diabetes.11 In this study, researchers found those who developed diabetes during the 20-year period had lower magnesium intake and significant inverse relationships between CRP and IL-6. A recent review article suggested a plausible mechanism is the decreased magnesium intake induces an inflammatory response through multiple pathways.12 Magnesium is a physiological calcium channel blocker, and when there is a deficit of magnesium, cellular calcium increases and may result in a triggering of inflammatory response.
In conclusion, minerals have key roles in proper inflammatory response and maintaining adequate mineral intake through diet and supplementation can help maintain an appropriate inflammatory response. Proper mineral nutrition allows us to maximize the long-term benefits of exercise.
Stephen Ashmead is a senior fellow at Balchem Corp. (balchem.com). His area of specialty is in mineral amino acid chelates and their functions.
1. Chen L et al. “Inflammatory responses and inflammation-associated diseases in organs.” Oncotarget. 2018;9(6):7204-7218.
2. Brown M et al. “The acute effects of walking exercise intensity on systemic cytokines and oxidative stress.” Eu J Appl Physiol. 2018;118:2111-2120.
3. Sallam N, Laher I. “Exercise modulates oxidative stress and inflammation in aging and cardiovascular disease.” Oxidative Medicine Cellular Longevity. 2016: Article ID 7239639.
4. Foster M, Samman S. “Zinc and regulation of inflammatory cytokines: Implications for cardiometabolic disease.” Nutrients. 2012;4:676-694.
5. Wong C, Magnussen K, Ho E. “Increased inflammatory response in aged mice is associated with age-related zinc deficiency and zinc transporter dysregulation.” J Nutr Biochem. 2013;24(1):353-359.
6. Jarosz M et al. “Antioxidant and anti-inflammatory effects of zinc. Zinc-dependent NF-κB signaling.” Inflammopharmacology. 2017;25:11-24.
7. Song Y et al. “Marginal zinc deficiency increases oxidative DNA damage in the prostate after chronic exercise.” Free Rad Biol Med. 2010;48(1):82-88.
8. Kudva A, Shay A, Prabhu K. “Selenium and inflammatory bowel disease.” Am J Physiol Gastrointest Liver Physiol. 2015;309:G71-G77.
9. Barrett CW, Short SP, Williams CS. “Selenoproteins and oxidative stress-induced inflammatory tumorigenesis in the gut.” Cell Mol Life Sci. 2017;74(4):607-616.
10. Chacko S et al. “Relations of dietary magnesium intake to biomarkers of inflammation and endothelial dysfunction in an ethnically diverse cohort of postmenopausal women.” Diabetes Care. 2010;33:304-310.
11. Kim D et al. “Magnesium intake in relation to systemic inflammation, insulin resistance, and the incidence of diabetes.” Diabetes Care. 2010;33:2604-2610.
12. Nielsen FH. “Magnesium deficiency and increased inflammation: current perspectives.” J Inflammation Research. 2018;11:25-34.
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