The Catch-22 of Exercise

Reaping the Rewards While Guarding Against Damage

By Jason E. Barker, ND

Exercise and fitness have well known health benefits ranging from lowered blood pressure and weight to improved memory and longevity, among many others. However, the physiological adaptations that the body undergoes as a result of exercise are based on the principle of overload, which is a gradual tearing down and rebuilding process at the microscopic levels. With this comes “collateral damage”—everything from excess free radical production to wear and tear on the joints to excess inflammation and pain—that left unchecked can prevent greater advancements in fitness. Both the positive adaptations from exercise and the “side effects” occur in all exercisers—everyone from the weekend warrior to the average person just wanting to lose a few pounds, to heavy exercisers. Therefore, this article will address the potentially damaging effects of exercise in order to help keep all levels of exercisers healthy on their journey towards fitness.

Joint Support

First and foremost for exercisers is protection of joint integrity at the cellular level. The intra-articular areas are especially prone to injuries from overuse.^1-2 The majority of exercise occurs while weight bearing; the largest joints of the body absorb nearly continuous force as we walk, run or chase a tennis ball. Some of the most common injuries in athletes are tears of the connective tissue (cartilage, tendons, ligaments).^3-4 Osteoarthritis (OA) is a major cause of joint pain and is one of the most common athletic-related conditions for which care is sought.⁵ The common symptoms of OA include stiffness, limited movement and crepitus (grating, crackling or popping sounds) in addition to pain.

Osteoarthritis, including decreased repair efficacy, occur with increasing frequency as we age.⁶ Several pathologic contributors have been noted among the chondrocytes (the only cells found in cartilage), including decreased ability to manufacture growth factors and age-related increases in matrix metalloproteinases, which are capable of degrading extracellular matrix proteins, the extracellular part of tissue that provides structural support to cells. The extracellular matrix is the defining feature of connective tissue. Other changes include telomere shortening, increased senescence markers and reactive oxygen species (free radicals).⁷

In my practice I see many exercisers of all abilities and intensities. One thing that they all have in common is joint pain, whether it is from an older injury or something more acute from a weekend run. Regardless, I make sure that all of them are taking a combination of joint supportive nutrients to maintain a preventive edge against further connective tissue damage and injury. Addressing joint health through supplementation is of primary importance. Cartilage wear and tear is extremely common and can become quite debilitating for many individuals if not addressed early.

A number of natural substances can be used to support joint health including glucosamine, MSM, chondroitin sulfate and Type II Collagen (all found in Nutri-Joint). Glucosamine is perhaps the best-known cartilage-supporting molecule that exhibits significant anti-inflammatory properties,^8-11 improves joint functionality and prevents joint degeneration.^12-13 Other supportive compounds include Methylsulfonylmethane (MSM), which can further decrease pain and swelling while improving joint function and slowing degenerative joint changes^14-15 and chondroitin sulfate, which can reduce pain and improve joint functionality^16-17 and slow degeneration.^18-19

Type II Collagen is being used increasingly for degenerative joint conditions. It serves by assisting the body in producing regulatory chemicals known as cytokines. One group of cytokines (interleukins 4 and 10) exert anti-inflammatory effects in the joint areas while at the same time the collagen’s effects decrease the expression of other pro-inflammatory cytokines (interleukins 1,2,6,8; tumor necrosis factor alpha and interferon gamma).^20-21

Free Radical Damage

Exercise is most commonly associated with improvements in muscle and cardiorespiratory function.^22-23 However, these changes occur at the cellular level starting with oxidative phosphorylation and the creation of energy. Energy production at the microscopic level creates “pollution” in the form of reactive oxygen species, or free radicals. In fact, the mitochondria, the powerhouses of the cell, are thought to be a major source of free radicals.²⁴ These free radicals are manufactured in the respiratory chain and they can cause oxidation of macromolecules, mutations of mitochondrial DNA, aging and cellular death.²⁵ Additionally, muscular contractions create free radicals, which can damage proteins and lipids in the muscle cells (myocytes); high levels can interfere with contractile mechanisms leading to muscle weakness and fatigue.²⁶ For outdoor exercisers, other forms of cellular pollution come from UV light exposure, the sun and air pollutants.

Free radical damage is insidious, inflicting damage over years. Therefore, protecting the cells from free radicals needs to be an ongoing effort. Because oxidation is such a diverse and widespread process in the body, supplementing with antioxidants is important to reduce the additional free radical burden occurring in exercisers.

Glutathione is one of the body’s most important antioxidant molecules. It assists with the metabolism of toxins and carcinogens, boosts immune system function and promotes DNA synthesis and repair.²⁷ Each of these processes takes on even more importance during exercise, and supplementing with a highly absorbable form of glutathione, such as liposomal glutathione, is recommended.

Other antioxidant compounds (such as those found in Extension Antioxidant) have strong antioxidant effects. Vitamins A, C and E, N-Acetyl Cysteine,^28-29 lutein,^30-31 the botanicals rosemary leaf extract (Rosmarinus officinalis),^32-33 Turmeric (Curcuma longa),³⁴ green tea (Camellia sinensis),³⁵ Bilberry (Vaccinium myrtillus)³⁶ and Grape Seed extract (Vitis vinifera)³⁷ are all potent free radical quenchers.

Hydration

Hydration is an important aspect of training as tight, spasmed muscles due to dehydration are prone to injury.

Sweat and the loss of minerals accompany exercise. Chief among the minerals lost in sweat are iodine,³⁸ calcium, sodium, potassium and magnesium.³⁹ Replacement of lost minerals in exercisers is imperative in the short term for the alleviation of muscle spasms, cramping and rigidity. In fact, in my office, the first symptoms that exercisers present with are cramping and/or tight muscles. Many of these people are helped significantly by full spectrum replacement of minerals. In the past, I only focused on replacing the chief electrolytes (sodium, potassium, calcium and magnesium); however, I have since found broad mineral replacement (such as found in Advanced Essential Minerals) to be the most effective in improving muscle function in heavy exercisers. Iodine (Iodoral®) supplementation also is useful.

Additionally, I use a few general rules for hydration, and they are: 1) “Pre-hydration,” consuming adequate pure water plus minerals in advance of exercise, helping the water to stay within the body before patients become dehydrated and mineral deficient; 2) Having my patients drink their body weight, divided in half, in ounces each day as a minimum; 3) Extra magnesium. We live in a calcium-dependent society where our foods are enriched and everyone is told to take extra calcium for bone health. I do not doubt the merits of this; however, excessive calcium may oppose magnesium absorption. Magnesium acts as a gentle muscle relaxant,⁴⁰ whereas calcium assists in muscle contraction.

Cardiovascular Stamina

As the “engine” that drives the body, the heart never stops working. It beats over 100,000 times per day. Because of its importance, the heart fuels itself first via the coronary arteries. Exercise places additional demand on the heart muscle beyond its “regular” duties performed during sedentary periods. Exercise demands that the heart increase cardiac output and that its oxygen requirements are increased as heart rate, ventricular work and myocardial contractility all increase.⁴¹ As exercise intensity increases, so do the demands placed on the heart muscle. Therefore, ensuring heart fitness is a must.

Additional nutrients play a role in heart-specific nutrition; these include the amino acid D-Ribose and Coenzyme Q10. D-Ribose is a pentose sugar that is a rate limiting nutrient in the hexose monophosphate shunt, a pathway that serves to maintain adenosine triphosphate (ATP) resynthesis.⁴² Replacement of ribose via supplementation seems to improve resynthesis and supply of ATP in the myocardium.⁴³ Exercise significantly lowers muscle ATP levels; supplementation with ribose will attenuate ATP depletion following exercise.⁴⁴

Coenzyme Q10 serves as a cofactor in several metabolic pathways; chief among them is the production of ATP.⁴⁵ Supplementation with CoQ10 improves mitochondrial function (energy production) when oxidative metabolism is impaired. Exercise tolerance is one physiologic function that shows improvement with supplementation.^46-47 Additionally, CoQ10 can lessen fatigue and improve physical performance in exercisers.^48-49 It is also notable that one of CoQ10’s main functions is an antioxidant and can offset exercise-related oxidative damage.

For athletes who engage in more endurance-type exercise (running, swimming, cycling) I often employ the use of D-Ribose, CoQ10 and magnesium starting several weeks before an anticipated competitive event. Many athletes have reported improved stamina and decreased fatigue during and after training. I have seen such benefits clinically that I encourage all of my active patients to use this combination.

Inflammation and Pain

With exercise comes pain from pounding the pavement, from tight and sore muscles and from using seldom-used muscles. The most common post-exercise pain, delayed-onset muscle soreness (DOMS), occurs most often 24-48 hours following exercise and is thought to be caused by an inflammatory reaction to exercise.⁵⁰ Interestingly, this inflammatory response may play a role in the onset, amplification and resolution of exercise-induced muscle injury.⁵¹

Although “inflammation” holds mainly negative connotations in health and medicine today, inflammatory processes are the body’s way of repairing and rejuvenating damage. Miniscule tears occurring in muscle tissue, tendons and ligaments become irritated from excessive movement and joints bear thousands of times the force they normally do on a sedentary day. All of this leads to the body creating inflammatory molecules that signal repair—and pain.⁵²

Fortunately for the sore exerciser, there are several anti-inflammatory, natural products with good supporting evidence including turmeric, boswellia and L-phenylalanine (all found in Back in Action™). Turmeric exerts strong anti-inflammatory effects through the modulation of leukotriene and prostaglandin molecules. It is also a cyclooxygenase-2 enzyme inhibitor.^53-54 Additionally, it shows promise in preventing sports-induced muscle injury.⁵⁵ Another herb, Boswellia serrata, has anti-inflammatory effects in addition to preventing collagen degradation and inhibiting the production of prostaglandin E2, cyclooxygenase-2 and matrix metalloproteins (MMPs).⁵⁶ The amino acid L-phenylalanine helps preserve the body’s natural pain reducing chemicals (enkephalins) thereby raising one’s pain threshold.⁵⁷

Enzymes also play a role in tissue repair and regeneration. Nattokinase (also found in Back in Action) is a proteolytic enzyme that inhibits the inflammatory cascade and production of pain-producing chemicals.⁵⁸

Furthermore, omega-3 fatty acids (contained in fish oil supplements such as Ethyl EPA) demonstrate potent anti-inflammatory effects on the COX-2 (cyclooxygenase) enzyme system and inhibit the production of pro-inflammatory cytokines interleukin 1 alpha (IL-1 alpha) and tumor necrosis factor alpha (TNF-alpha).⁵⁹

Immunity

In regards to the immune system, exercise is a double-edged sword. New exercisers may be more susceptible to illness as their bodies adjust to the stress of exercise. The body releases cortisol and epinephrine in response to exercise; these hormones can temporarily lower immunity.^60-61 Similarly, athletes who perform endurance-type exercise are also more susceptible to respiratory infections. Ninety plus minutes of endurance exercise can leave the immune system depressed for 72 hours, leaving the person more susceptible to respiratory infections.⁶² Heavy training is associated with low plasma levels of the amino acid glutamine, which is theorized to be a possible cause of exercise-induced immune depression and increased susceptibility to infection in athletes.^63-64 Supplementing with L-glutamine during and immediately after exercise may support immune function.

Recovery

Recovery, the period following exercise including sleep, is one of the most important aspects of exercise. Poor recovery will negate the benefits of exercise and can increase the risk of injury, fatigue and illness during future training sessions. Ensuring a good night’s sleep and a healthy diet is important for all of us and most certainly in regular exercisers so that they may reap the full reward of their fitness efforts.

Conclusion

Exercise is the best investment we can make in our health. But that investment comes with a cost in that we must maintain the body’s health as we improve its fitness. Addressing all of the fitness support systems mentioned above has the benefit of allowing us to enjoy great health as a result of regular exercise.

References

1. O’Keeffe SA, Hogan BA, Eustace SJ, et al. Overuse injuries of the knee. Magn Reson Imaging Clin N Am. 2009 Nov;17(4):725-39, vii.

2. Dalton SE. Overuse injuries in adolescent athletes. Sports Med. 1992 Jan;13(1):58-70.

3. Swenson TM, Harner CD. Knee ligament and meniscal injuries. Current concepts. Orthop Clin North Am. 1995 Jul;26(3):529-46.

4. Scoggin JF 3rd. Common sports injuries seen by the primary care physician. Part II: Lower extremity. Hawaii Med J. 1998 May;57(5):502-5.

5. Bijlsma JW, Knahr K. Strategies for the prevention and management of osteoarthritis of the hip and knee. Best Pract Res Clin Rheumatol. 2007 Feb;21(1):59-76.

6. Fukuda K. Progress of research in osteoarthritis. Involvement of reactive oxygen species in the pathogenesis of osteoarthritis. Clin Calcium. 2009 Nov;19(11):1602-6.

7. Martin JA, Buckwalter JA. The role of chondrocyte senescence in the pathogenesis of osteoarthritis and in limiting cartilage repair. J Bone Joint Surg Am. 2003;85-A Suppl 2:106-10.

8. Forster K, Schmid K, Rovati L, et al. Longer-term treatment of mild-to-moderate osteoarthritis of the knee with glucosamine sulfate- a randomized controlled, double-blind clinical study. Eur J Clin Pharmacol 1996;50:542.

9. Qiu GX, Gao SN, Giacovelli G, et al. Efficacy and safety of glucosamine sulfate versus ibuprofen in patients with knee osteoarthritis. Arzneimittelforschung 1998;48:469-74.

10. Herrero-Beaumont G, Ivorra JA, Del Carmen Trabado M, et al. Glucosamine sulfate in the treatment of knee osteoarthritis symptoms: a randomized, double-blind, placebo-controlled study using acetaminophen as a side comparator. Arthritis Rheum 2007;56:555-67.

11. Towheed TE, Maxwell L, Anastassiades TP, et al. Glucosamine therapy for treating osteoarthritis. Cochrane Database Syst Rev 2005;(2):CD002946

12. Poolsup N, Suthisisang C, Channark P, et al. Glucosamine long-term treatment and the progression of knee osteoarthritis: systematic review of randomized controlled trials. Ann Pharmacother 2005;39:1080-7.

13. Bruyere O, Pavelka K, Rovati LC, et al. Total joint replacement after glucosamine sulphate treatment in knee osteoarthritis: results of a mean 8-year observation of patients from two previous 3-year, randomised, placebo-controlled trials. Osteoarthritis Cartilage 2008;16:254-60.

14. Usha PR, Naidu MUR. Randomised, double-blind, parallel, placebo-controlled study of oral glucosamine, methylsulfonylmethane and their combinations. Clin Drug Invest 2004;24:353-63.

15. Kim LS, Axelrod LJ, Howard P, et al. Efficacy of methylsulfonylmethane (MSM) in osteoarthritis pain of the knee: a pilot clinical trial. Osteoarthritis Cartilage 2006;14:286-94.

16. Leeb BF, Schweitzer H, Montag K, et al. A meta-analysis of chondroitin sulfate in the treatment of osteoarthritis. J Rheumatol 2000;27:205-11.

17. Mazieres B, Combe B, Phan Van A, et al. Chondroitin sulfate in osteoarthritis of the knee: a prospective, double blind, placebo controlled multicenter clinical study. J Rheumatol 2001;28:173-81.

18. Verbruggen G, Goemaere S, Veys EM. Systems to assess the progression of finger joint osteoarthritis and the effects of disease modifying osteoarthritis drugs. Clin Rheumatol 2002;21:231-43.

19. Uebelhart D, Thonar EJ, Delmas PD, et al. Effects of oral chondroitin sulfate on the progression of knee osteoarthritis: a pilot study. Osteoarthritis Cartilage 1998;6:39-46.

20. Barnett ML, Kremer JM, St.Clair W, et al. Treatment of rheumatoid arthritis with oral type II collagen. Arthritis Rheum 1998;41:290-7.

21. Barnett ML, Combitchi D, Trentham DE. A pilot trial of oral type II collagen in the treatment of juvenile rheumatoid arthritis. Arthritis Rheum 1996;39:623-8.

22. Kemi OJ, Wisloff U. High-intensity aerobic exercise training improves the heart in health and disease. J Cardiopulm Rehabil Prev. 2010 Jan-Feb;30(1):2-11.

23. Whyte JJ, Harold Laughlin M. The Effects of Acute and Chronic Exercise on the Vasculature. Acta Physiol (Oxf). 2010 Mar 26. [Epub ahead of print]

24. Ott M, Gogvadze V, Orrenius S, et al. Mitochondria, oxidative stress and cell death. Apoptosis. 2007 May;12(5):913-22.

25. Kakkar P, Singh BK. Mitochondria: a hub of redox activities and cellular distress control. Mol Cell Biochem. 2007 Nov;305(1-2):235-53. Epub 2007 Jun 12.

26. Powers SK, Jackson MJ. Exercise-induced oxidative stress: cellular mechanisms and impact on muscle force production. Physiol Rev. 2008 Oct;88(4):1243-76.

27. P. Powers SK, Hamilton K. Antioxidants and exercise. Clin Sports Med 1999;18:525-36.

28. Weinbroum AA, Rudick V, Ben-Abraham R, Karchevski E. N-acetyl-L-cysteine for preventing lung reperfusion injury after liver ischemia-reperfusion: a possible dual protective mechanism in a dose-response study. Transplantation 2000;69:853-9.

29. Kelly GS. Clinical applications of N-acetylcysteine. Altern Med Rev 1998;3:114-27.

30. Fernández-Sevilla JM, Acién Fernández FG, Molina Grima E. Biotechnological production of lutein and its applications. Appl Microbiol Biotechnol. 2010 Mar;86(1):27-40. Epub 2010 Jan 21.

31. Tamimi RM, Colditz GA, Hankinson SE. Circulating carotenoids, mammographic density, and subsequent risk of breast cancer. Cancer Res. 2009 Dec 15;69(24):9323-9.

32. Bakirel T, Bakirel U, Keles OU, et al. In vivo assessment of antidiabetic and antioxidant activities of rosemary (Rosmarinus officinalis) in alloxan-diabetic rabbits. J Ethnopharmacol. 2008 Feb 28;116(1):64-73. Epub 2007 Nov 4.

33. Pérez-Fons L, Garzón MT, Micol V. Relationship between the antioxidant capacity and effect of rosemary (Rosmarinus officinalis L.) polyphenols on membrane phospholipid order. J Agric Food Chem. 2010 Jan 13;58(1):161-71.

34. Singh G, Kapoor IP, Singh P. Comparative study of chemical composition and antioxidant activity of fresh and dry rhizomes of turmeric (Curcuma longa Linn.). Food Chem Toxicol. 2010 Apr;48(4):1026-1031. Epub 2010 Jan 21.

35. Dou QP. Molecular mechanisms of green tea polyphenols. Nutr Cancer. 2009 Nov;61(6):827-35.

36. Burdulis D, Sarkinas A, Jasutiené I, et al. Comparative study of anthocyanin composition, antimicrobial and antioxidant activity in bilberry (Vaccinium myrtillus L.) and blueberry (Vaccinium corymbosum L.) fruits. Acta Pol Pharm. 2009 Jul-Aug;66(4):399-408.

37. Stankovic M, Tesevic V, Vajs V, et al. Antioxidant properties of grape seed extract on human lymphocyte oxidative defence. Planta Med. 2008 Jun;74(7):730-5. Epub 2008 May 21.

38. Mao IF, Chen ML, Ko YC. Electrolyte loss in sweat and iodine deficiency in a hot environment. Arch Environ Health. 2001 May-Jun;56(3):271-7.

39. Palacios C, Wigertz K, Weaver CM. Comparison of 24 hour whole body versus patch tests for estimating body surface electrolyte losses. Int J Sport Nutr Exerc Metab. 2003 Dec;13(4):479-88.

40. Mousain-Bosc M, Roche M, Rapin J, et al. Magnesium VitB6 intake reduces central nervous system hyperexcitability in children. J Am Coll Nutr. 2004 Oct;23(5):545S-548S.

41. Duncker DJ, Bache RJ. Regulation of coronary blood flow during exercise. Physiol Rev. 2008 Jul;88(3):1009-86.

42. Pasque MK, Spray TL, Pellom GL, et al. Ribose-enhanced myocardial recovery following ischemia in the isolated working rat heart. J Thorac Cardiovasc Surg 1982;83:390-8.

43. Geisbuhler TP, Schwager TL. Ribose-enhanced synthesis of UTP, CTP, and GTP from parent nucleosides in cardiac myocytes. J Mol Cell Cardiol 1998;30:879-87.

44.  Dodd SL, Johnson CA, Fernholz K, St Cyr JA. The role of ribose in human skeletal muscle metabolism. Med Hypotheses.2004;62(5):819-24.

45. Turunen M, Olsson J, Dallner G. Metabolism and function of coenzyme Q. Biochim Biophys Acta 2004;1660:171-99.

46. Turunen M, Olsson J, Dallner G. Metabolism and function of coenzyme Q. Biochim Biophys Acta 2004;1660:171-99.

47. Greenberg S, Fishman WH. Coenzyme Q10: A New Drug for Cardiovascular Disease. J Clin Pharmacol 1990;30:596-608.

48. Littarru GP, Tiano L. Clinical aspects of coenzyme Q10: an update. Nutrition. 2010 Mar;26(3):250-4. Epub 2009 Nov 22.

49. Gökbel H, Gül I, Belviranl M, Okudan N. The effects of coenzyme Q10 supplementation on performance during repeated bouts of supramaximal exercise in sedentary men. J Strength Cond Res. 2010 Jan;24(1):97-102.

50. Coudreuse JM, Dupont P, Nicol C. Delayed post effort muscle soreness. Ann Readapt Med Phys. 2004 Aug;47(6):290-8.

51. MacIntyre DL, Reid WD, McKenzie DC. Delayed muscle soreness. The inflammatory response to muscle injury and its clinical implications. Sports Med. 1995 Jul;20(1):24-40.

52. Suzuki K, Nakaji S, Yamada M, et al Systemic inflammatory response to exhaustive exercise. Cytokine kinetics. Exerc Immunol Rev. 2002;8:6-48.

53. Zhang F, Altorki NK, Mestre JR, et al. Curcumin inhibits cyclooxygenase-2 transcription in bile acid- and phorbol ester-treated human gastrointestinal epithelial cells. Carcinogenesis 1999;20:445-51.

54. Menon VP, Sudheer AR. Antioxidant and anti-inflammatory properties of curcumin. Adv Exp Med Biol. 2007;595:105-25.

55. Davis JM, Murphy EA, Carmichael MD, et al. Curcumin effects on inflammation and performance recovery following eccentric exercise-induced muscle damage. Am J Physiol Regul Integr Comp Physiol. 2007 Jun;292(6):R2168-73. Epub 2007 Mar 1.

56. Blain EJ, Ali AY, Duance VC. Boswellia frereana (frankincense) suppresses cytokine-induced matrix metalloproteinase expression and production of pro-inflammatory molecules in articular cartilage. Phytother Res. 2009 Nov 26.

57. Walsh NE, Ramamurthy S, Schoenfeld L, et al. Analgesic effectiveness of D-phenylalanine in chronic pain patients. Arch Phys Med Rehabil 1986;67:436-9.

58. Klein G, Kullich W. Reducing pain by oral enzyme therapy in rheumatic diseases. Wien Med Wochenschr. 1999;149(21—22):577—580.

59. Curtis CL, Hughes CE, Flannery CR, et al. n-3 fatty acids specifically modulate catabolic factors involved in articular cartilage degradation. J Biol Chem 2000;275:721-4.

60. Mignini F, Traini E, Tomassoni D, et al. Leucocyte subset redistribution in a human model of physical stress. Clin Exp Hypertens. 2008 Nov;30(8):720-31.

61. Gleeson M, Nieman DC, Pedersen BK. Exercise, nutrition and immune function. J Sports Sci. 2004 Jan;22(1):115-25.

62. Nieman DC, Pedersen BK. Exercise and immune function. Recent developments. Sports Med. 1999 Feb;27(2):73-80.

63. Gleeson M. Dosing and efficacy of glutamine supplementation in human exercise and sport training. J Nutr. 2008 Oct;138(10):2045S-2049S.

64. Castell LM, Poortmans JR, Newsholme EA. Does glutamine have a role in reducing infections in athletes? Eur J Appl Physiol Occup Physiol. 1996;73(5):488-90.