Advertisement

Does Acute Improvement in Muscle Recovery with Curcumin Supplementation Translate to Long-Term Training?

  • Brian K. McFarlinEmail author
  • Elizabeth A. Tanner
  • Melody A. Gary
  • Asheal A. Davis
  • Erin M. Bowman
  • Richard S. Gary
Review Article

Abstract

Dietary polyphenols, such as curcumin, green tea catechins, and pomegranate extract, may have the ability to enhance the effectiveness of long-term training programs by managing training-induced inflammation. Enhanced recovery may translate to increased capacity to train and perform more effectively. The dietary polyphenol curcumin has been reported to block the action of COX-2 and NF-kB signaling and would allow for increased capacity to train leading to heightened adaptations and the potential for ergogenic outcomes. These actions are very similar to the targeted actions of non-steroidal anti-inflammatory drugs (NSAIDs), but without the side-effects of NSAIDs. This review will compare and contrast the known effects of curcumin and identify common design elements between existing studies. Through this critical review of the existing literature it is our goal to establish a set of best practices that could be applied to an athletic population that is interested in using oral curcumin supplementation as a recovery agent.

Keywords

Exercise-induced muscle injury Inflammatory cytokines Inflammation Soreness Distance running Exercise training 

Introduction

A comprehensive training program includes a variety of exercise modes, intensities, and durations [9, 12, 25, 28, 33, 35]. While using a variety of exercise stimuli may improve training efficiency, greater stimuli should lead to greater potential for harms such as overtraining or incomplete recovery [3]. This is not a fault of the person training as it is often not recognized that a given volume of exercise might be too much until an injury occurs. In turn, these higher levels of inflammation and soreness limit performance in subsequent training sessions or competitive events [14]. Traditional treatments (i.e. cryotherapy, massage, stretching, etc.) lack the evidence-based support to consistently improve recovery time course [16, 31, 36]. Improved recovery time course may be defined as fewer days to recovery, reduced severity of soreness/inflammation during recovery, or a combination of the two. Some regular exercisers turn to NSAIDs to relieve soreness and inflammation associated with an excessive training session, but this approach blunts inflammation, potentially blocking the first stage of healing [1, 32, 37]. Also, despite the perceived benefits of NSAIDs, clinical research demonstrates that NSAIDs do not necessarily restore muscle performance and may hinder recovery [32]. Given the negative effects of habitual NSAID treatment on the central nervous system, long-term use is not advised even if NSAIDs did improve recovery [1]. As regular exercisers continue to push the boundaries of athletic performance, critical research and development is needed to identify substances, such as dietary polyphenols like curcumin, that can limit inflammation and oxidative stress without the negative consequences associated with NSAIDs. This review has been structured to provide the biological mechanism of action for oral curcumin supplementation in the context of exercise recovery. Current literature is limited with regard to the role of curcumin supplementation as a component of a comprehensive training program.

Curcumin is a yellow pigment derived from the root of the turmeric (Curcuma longa) plant. Unfortunately, when consumed orally (in humans) curcumin has low bioavailability in its naturally occurring form, thus it is ideal to use a commercially “optimized” form of curcumin [13, 27]. Naturally occurring curcumin has been administered in doses as high as 8 g/day in humans with no side effects; however, roughly 75% was excreted in feces, indicating poor gut absorption [38]. Furthermore, once absorbed, curcumin has been known to bind to serum proteins and be metabolized by the liver into fragments of curcumin that may not retain biological actions [24]. Research in animal and cell culture models has demonstrated that curcumin has anti-inflammatory actions via suppression of cycloxogenase-2 (COX-2) signaling and prostaglandin formation [2, 5, 7, 17, 19]. Prostaglandins are biological substances that contribute to pain and soreness after training, thus suppression of their formation could favorably impact these symptoms. The biological mechanism of action for curcumin is similar to that of NSAIDs [7, 8, 20, 21, 29], albeit less pronounced and without NSAID side-effects. The only side effects known with curcumin are associated with very high doses (>16 g/day) and include indigestion and development of kidney stones [13]. These symptoms are mild considering that NSAID side effects include liver and central nervous system damage.

Biological Mechanism of Action for Curcumin

As stated above, both NSAIDs and curcumin alter inflammatory processes via several different intracellular targets including direct and indirect inhibition of transcription factors NF-κβ and AP-1 associated with pro-inflammatory cytokine production (IL-1β, IL-6, IL-8, TNF-α, MCP-1) and alterations in COX-2 mediated prostaglandin formation [4, 22, 23, 40]. Typically, in response to muscle injury, COX-2 is up regulated by pro-inflammatory cytokines (IL-1β, IL-6, IL-8, and TNF-α). In vitro treatment of cell cultures with curcumin results in a dose dependent decrease in COX-2 mRNA and protein upon exposure to substances that typically increase COX-2 (e.g. pro-inflammatory cytokines) [6]. COX-2 is the enzyme responsible for the conversion of arachidonic acid into prostaglandins and thromboxane, which are lipid compounds responsible for pain sensations and swelling [37]. The basic mechanism of action for curcumin is demonstrated in Fig. 1. In these ways curcumin exerts anti-inflammatory actions that should limit muscle soreness and inflammatory responses. In the context of exercise training, reduced inflammation has more potential to improve physical performance than reduced soreness, which is generally considered to be an inconvenience rather than a performance inhibitor.
Fig. 1

Curcumin Inhibition of NF-κB Transcriptional Activity. NF-κB activation is dependent upon IKK phosphorylation of IκB and subsequent translocation of the p65 and p50 subunits into the nucleus. Transcription of inflammatory cytokines by p50 and p65 stimulates production of COX-2. Dietary phenols inhibits NF-κB transcriptional activity by preventing IκB phosphorylation by IKK and p50/p65 nuclear translocation. AP-1 activation requires MKK-mediated activation of JNK and p38 for fos and jun transcription. Formation of AP-1 occurs outside of the nucleus and is phosphorylated before c-fos/c-jun nuclear translocation and transcription of inflammatory cytokines. Inflammatory cytokine production by AP-1 increases COX-2 expression. TLR toll-like receptor, NEMO NF-κB essential modulator, IKK IκB kinase, MKK mitogen-activated protein kinase kinase, JNK c-Jun N-terminal kinase, p38 p38 mitogen-activated protein kinase family, TCF ternary-complex factors, SRE serum-response element, ERK extracellular-signal-regulated kinase, AP-1 activator protein 1, NF-κB nuclear factor-kappa B, COX-2 cyclooxygenase 2, DP dietary phenols, PLA2 phospholipase A2, COX-2 cyclooxygenase 2, PGG2 prostaglandin G2, PGH2 prostaglandin H2, PGs prostaglandins, TXA2 thromboxane A2, AP-1 activator protein 1, NF-κB nuclear factor-kappa B, AP-1 activator protein 1, DP dietary phenols

Previous Applications of Curcumin for Muscle Recovery

Due to curcumin’s mechanism of action, curcumin has established itself as a relevant ingredient to support sport nutrition and ergogenic outcomes [7, 8, 19, 20, 26, 28, 32, 39]. Two of these previous studies have used a mouse model system [7, 20] and as such don’t have direct application or translation to exercising humans due to species differences in bioavailability and downstream processing of oral curcumin in the liver. The mice studies are of note because other human studies have used them to justify the dosing selected in humans, which may be problematic because of the previously noted species differences in bioavailability. One design variable that can be gleaned from rodent studies is that in order for curcumin to be successful, it appears to have the best efficacy when the quantity of soreness/inflammation is moderate, but not severe. Excessive soreness/inflammation completely overwhelms the biological system, resulting in changes that are unlikely to be managed with oral curcumin supplementation or any other treatment [11, 30]. Soreness is a difficult result to quantify and accurately assess due to individual differences in perception of pain and soreness [10]. One potential solution that may aid with removal of individual bias is to ensure that studies always include a measurable biological indicator of muscle inflammation (i.e. serum creatine kinase, myoglobin, etc.) that isn’t prone to individual perceptual differences. Unfortunately, the measurement of biological outcomes isn’t practical in field-based training studies. This is a critical gap in the scientific literature that needs to be addressed to provide better means of tracking exercise training recovery and effectiveness.

Of the published human curcumin studies, complete comparison of results is limited due to the differences in the timing of sample collection, curcumin dose, curcumin type (i.e. natural vs. optimized), and/or measurements made [8, 26, 28, 33, 34]. Drobnic et al. [8] reported that when consuming curcumin (5.3 mg/kg body weight/d; total dose = 16 mg/kg body weight) 48 h prior to a bout of downhill running (45 min at − 10% grade) subjects reported significantly less subjective muscle soreness and less muscle damage (as measured by MRI) compared to a placebo. They also reported a significant decrease in serum IL-8 (pro-inflammatory cytokine) at 2 h after exercise, but found no other changes in biological measures of inflammation (CRP or MCP-1). One limitation of the study by Drobnic et al. is that no measurements were made later than 24 h after exercise-induced muscle damage, so this sampling design may not allow for a complete assessment of the muscle recovery profile (which may last up to 96 h). Sciberras et al. [33] reported that 3 day of curcumin consumption (5.7 mg/kg body weight/d; total dose = 17 mg/kg body weight) failed to alter serum inflammatory cytokines (i.e. IL-1RA, IL-6, and IL-10) within 1 h following a 2 h bout of cycle exercise. The authors did report significant improvements in psychological mood following exercise with curcumin, but not placebo supplementation. The lack of change seen in cytokines is not surprising due to the invoked exercise stimuli (minimal eccentric contractions) in this study.

In a study from our laboratory using a leg press muscle injury model (60 repetitions of inclined leg press at 110% of the 1RM, eccentric only) [26], we found that oral optimized curcumin supplementation (Longvida®; 400 mg/day for 2 days prior and 4 days after) resulted in decreased serum creatine kinase (biological muscle damage indicator) and decreased inflammatory cytokines (IL-8 and TNF-α). These biological changes were observed despite numerical decreases in soreness that did not reach statistical significance. Our response are similar to Jager [18] who reported that a higher dose of optimized curcumin (CurcuWIN®; 1000 mg/day) resulted in maintenance of muscle strength following downhill running, while a lower dose (250 mg/day) or placebo resulted in loss of muscle strength. To test our laboratory findings in a field model, we conducted a half-marathon training study to determine if optimized curcumin (Longvida®; 500–1000 mg/day) in combination with another dietary polyphenol (pomegranate extract; Pomella®; 500–1000 mg/day) could manage training-associated changes in inflammation [12, 35]. When compared to a placebo, we found that the treatment allowed for 11% more training mileage and 20% more caloric expenditure despite a similar number of training sessions in the 30 days prior to a half marathon race. Since the later study involved combined curcumin and pomegranate, it is difficult to determine the unique contribution of each component. We also noted that the treatment reduced a variety of inflammation-associated RNA and proteins prior to and after the half marathon race, which is the most likely cause of improved training efficiency.

To summarize, oral optimized curcumin supplementation prior to a single exercise session or during prolonged training reduced biological indices of muscle injury and inflammation. Also, despite a similar volume of exercise, individuals who consumed curcumin had lower serum CK with curcumin, which is indicative of less muscle damage. Unfortunately, the reporting of reduced muscle soreness has been inconsistent, which may be partially explained by subjective individual differences in the perception of soreness [10]. These findings collectively outline the preliminary potential for oral supplementation of optimized curcumin as one part of a comprehensive training program. Future work must continue to explore more research in this area to better understand how dosing and timing of dosing will influence outcomes related to curcumin’s potential to favorably impact exercise outcomes and adaptations.

Future Potential of Curcumin for Long-Term Training?

To date most exercise studies have used curcumin acutely to impact short-term recovery. Given these effects, it is reasonable to speculate that curcumin might be a beneficial addition to a long-term training program. Long-term training is a collection of acute sessions, thus more research is needed to evaluate if the acute effects of curcumin can be sustained over the course of training. We have summarized three main effects directly attributed to oral curcumin supplementation: (1) reduced biological indices of inflammation (i.e. pro-inflammatory cytokines, acute phase proteins, etc.), (2) reduced muscle damage despite similar amount of work (i.e. reduced serum CK, maintenance of muscle torque, or other biological marker), and (3) potential for reduced muscle soreness. Using anecdotal observations from our laboratory experiments, we hypothesize that biological inflammation and quantity of muscle damage that carries over between exercise bouts may have the greatest impact on performance. Similarly, according to previous research [15, 18, 26] perceived soreness may not limit performance to the degree of the previous due to individual differences in perception of pain and soreness. Doses of optimized curcumin that exceed 400 mg/day are likely needed to affect systemic inflammatory, while doses greater than 1000 mg/day may be needed to affect both systemic inflammation and muscle soreness. Another observation from the literature is that observed inflammatory outcomes may be affected by both the quantity of muscle damage from exercise and the dose of curcumin used. Given this effect, it seems reasonable to further speculate that during a long-term training plan, it may be necessary to progressively increase the dose of curcumin supplementation to match the anticipated quantity of muscle injury from exercise (Fig. 2). To our knowledge a comprehensive long-term evaluation of curcumin has not been made; however, it is our hope that the proposed model may serve as a foundation for that future work. Future research should continue to explore the chronic use of curcumin and other dietary polyphenols as a valuable aspect of training. We have proposed a model by which curcumin could be used as one component of a comprehensive training program, as more research is needed to validate these outcomes.
Fig. 2

Potential application of oral curcumin to long-term training. To date research involving oral curcumin supplementation has largely focused on short-term, acute models. Given the mechanism of action for curcumin, it is very reasonable to speculate that it could be an effective component in a long-term training program. In this figure, we have proposed a potential approach for integration of curcumin into a training program. It is clear based on mechanism of action that greater quantities of muscle injury may require larger doses of curcumin. Thus, we have proposed an approach that varies the curcumin dose as a function of training load. Future research should test curcumin as a component of a long-term training program

Notes

Acknowledgements

Some of the research from UNT cited in this article was conducted via a Research Grant Awarded to UNT from Verdure Sciences Corp (Indianapolis, IN). The research team was not directly compensated for this work and Verdure Sciences was not involved with the writing or review of this manuscript.

References

  1. 1.
    Auriel E, Regev K, Korczyn AD. Nonsteroidal anti-inflammatory drugs exposure and the central nervous system. Handb Clin Neurol. 2014;119:577–84.CrossRefGoogle Scholar
  2. 2.
    Avci G, Kadioglu H, Sehirli AO, Bozkurt S, Guclu O, Arslan E, Muratli SK. Curcumin protects against ischemia/reperfusion injury in rat skeletal muscle. J Surg Res. 2012;172(1):e39–46.CrossRefGoogle Scholar
  3. 3.
    Cadegiani FA, Kater CE. Novel causes and consequences of overtraining syndrome: the EROS-DISRUPTORS study. BMC Sports Sci Med Rehabil. 2019;11:21.CrossRefGoogle Scholar
  4. 4.
    Chen JC, Ho FM, Pei-Dawn Lee C, Chen CP, Jeng KC, Hsu HB, Lee ST, Wen Tung W, Lin WW. Inhibition of iNOS gene expression by quercetin is mediated by the inhibition of IkappaB kinase, nuclear factor-kappa B and STAT1, and depends on heme oxygenase-1 induction in mouse BV-2 microglia. Eur J Pharmacol. 2005;521(1–3):9–20.CrossRefGoogle Scholar
  5. 5.
    Chun KS, Keum YS, Han SS, Song YS, Kim SH, Surh YJ. Curcumin inhibits phorbol ester-induced expression of cyclooxygenase-2 in mouse skin through suppression of extracellular signal-regulated kinase activity and NF-kappaB activation. Carcinogenesis. 2003;24(9):1515–24.CrossRefGoogle Scholar
  6. 6.
    Crespo I, Garcia-Mediavilla MV, Gutierrez B, Sanchez-Campos S, Tunon MJ, Gonzalez-Gallego J. A comparison of the effects of kaempferol and quercetin on cytokine-induced pro-inflammatory status of cultured human endothelial cells. Br J Nutr. 2008;100(5):968–76.CrossRefGoogle Scholar
  7. 7.
    Davis JM, Murphy EA, Carmichael MD, Zielinski MR, Groschwitz CM, Brown AS, Gangemi JD, Ghaffar A, Mayer EP. Curcumin effects on inflammation and performance recovery following eccentric exercise-induced muscle damage. Am J Physiol Regul Integr Comp Physiol. 2007;292(6):R2168–73.CrossRefGoogle Scholar
  8. 8.
    Drobnic F, Riera J, Appendino G, Togni S, Franceschi F, Valle X, Pons A, Tur J. Reduction of delayed onset muscle soreness by a novel curcumin delivery system (Meriva(R)): a randomised, placebo-controlled trial. J Int Soc Sports Nutr. 2014;11:31.CrossRefGoogle Scholar
  9. 9.
    Duplanty AA, Levitt DE, Hill DW, McFarlin BK, DiMarco NM, Vingren JL. Resistance training is associated with higher bone mineral density among young adult male distance runners independent of physiological factors. J Strength Cond Res. 2018;32(6):1594–600.CrossRefGoogle Scholar
  10. 10.
    Emerson NM, Zeidan F, Lobanov OV, Hadsel MS, Martucci KT, Quevedo AS, Starr CJ, Nahman-Averbuch H, Weissman-Fogel I, Granovsky Y, Yarnitsky D, Coghill RC. Pain sensitivity is inversely related to regional grey matter density in the brain. Pain. 2014;155(3):566–73.CrossRefGoogle Scholar
  11. 11.
    Gary MA, Tanner EA, Davis AA, McFarlin BK (2018) Combined bead-based multiplex detection of RNA and protein biomarkers: implications for understanding the time course of skeletal muscle injury and repair. Methods.Google Scholar
  12. 12.
    Gary MA, Tanner EA, Davis AA, McFarlin BK. Combined bead-based multiplex detection of RNA and protein biomarkers: implications for understanding the time course of skeletal muscle injury and repair. Methods. 2019;158:92–6.CrossRefGoogle Scholar
  13. 13.
    Gota VS, Maru GB, Soni TG, Gandhi TR, Kochar N, Agarwal MG. Safety and pharmacokinetics of a solid lipid curcumin particle formulation in osteosarcoma patients and healthy volunteers. J Agric Food Chem. 2010;58(4):2095–9.CrossRefGoogle Scholar
  14. 14.
    Haramizu S, Ota N, Hase T, Murase T. Catechins suppress muscle inflammation and hasten performance recovery after exercise. Med Sci Sports Exerc. 2013;45(9):1694–702.CrossRefGoogle Scholar
  15. 15.
    Hirose L, Nosaka K, Newton M, Laveder A, Kano M, Peake J, Suzuki K. Changes in inflammatory mediators following eccentric exercise of the elbow flexors. Exerc Immunol Rev. 2004;10:75–90.PubMedGoogle Scholar
  16. 16.
    Hohenauer E, Taeymans J, Baeyens JP, Clarys P, Clijsen R. The effect of post-exercise cryotherapy on recovery characteristics: a systematic review and meta-analysis. PLoS One. 2015;10(9):e0139028.CrossRefGoogle Scholar
  17. 17.
    Huang WC, Chiu WC, Chuang HL, Tang DW, Lee ZM, Wei L, Chen FA, Huang CC. Effect of curcumin supplementation on physiological fatigue and physical performance in mice. Nutrients. 2015;7(2):905–21.CrossRefGoogle Scholar
  18. 18.
    Jager R, Purpura M, Kerksick CM (2019) Eight weeks of a high dose of curcumin supplementation may attenuate performance decrements following muscle-damaging exercise. Nutrients 11(7).CrossRefGoogle Scholar
  19. 19.
    Kang G, Kong PJ, Yuh YJ, Lim SY, Yim SV, Chun W, Kim SS. Curcumin suppresses lipopolysaccharide-induced cyclooxygenase-2 expression by inhibiting activator protein 1 and nuclear factor kappab bindings in BV2 microglial cells. J Pharmacol Sci. 2004;94(3):325–8.CrossRefGoogle Scholar
  20. 20.
    Kawanishi N, Kato K, Takahashi M, Mizokami T, Otsuka Y, Imaizumi A, Shiva D, Yano H, Suzuki K. Curcumin attenuates oxidative stress following downhill running-induced muscle damage. Biochem Biophys Res Commun. 2013;441(3):573–8.CrossRefGoogle Scholar
  21. 21.
    Kerksick CM, Kreider RB, Willoughby DS. Intramuscular adaptations to eccentric exercise and antioxidant supplementation. Amino Acids. 2010;39(1):219–32.CrossRefGoogle Scholar
  22. 22.
    Khoi PN, Park JS, Kim JH, Xia Y, Kim NH, Kim KK, Jung YD. (−)-Epigallocatechin-3-gallate blocks nicotine-induced matrix metalloproteinase-9 expression and invasiveness via suppression of NF-kappaB and AP-1 in endothelial cells. Int J Oncol. 2013;43(3):868–76.CrossRefGoogle Scholar
  23. 23.
    Kim BH, Choi JS, Yi EH, Lee JK, Won C, Ye SK, Kim MH. Relative antioxidant activities of quercetin and its structurally related substances and their effects on NF-kappaB/CRE/AP-1 signaling in murine macrophages. Mol Cells. 2013;35(5):410–20.CrossRefGoogle Scholar
  24. 24.
    Kim HG, Lee JH, Lee SJ, Oh JH, Shin E, Jang YP, Lee YJ. The increased cellular uptake and biliary excretion of curcumin by quercetin: a possible role of albumin binding interaction. Drug Metab Dispos. 2012;40(8):1452–5.CrossRefGoogle Scholar
  25. 25.
    Levitt DE, Luk HY, Duplanty AA, McFarlin BK, Hill DW, Vingren JL. Effect of alcohol after muscle-damaging resistance exercise on muscular performance recovery and inflammatory capacity in women. Eur J Appl Physiol. 2017;117(6):1195–206.CrossRefGoogle Scholar
  26. 26.
    McFarlin BK, Venable AS, Henning AL, Sampson JN, Pennel K, Vingren JL, Hill DW. Reduced inflammatory and muscle damage biomarkers following oral supplementation with bioavailable curcumin. BBA Clin. 2016;5:72–8.CrossRefGoogle Scholar
  27. 27.
    Mohanty C, Das M, Sahoo SK. Emerging role of nanocarriers to increase the solubility and bioavailability of curcumin. Expert Opin Drug Deliv. 2012;9(11):1347–64.CrossRefGoogle Scholar
  28. 28.
    Nicol LM, Rowlands DS, Fazakerly R, Kellett J. Curcumin supplementation likely attenuates delayed onset muscle soreness (DOMS). Eur J Appl Physiol. 2015;115(8):1769–77.CrossRefGoogle Scholar
  29. 29.
    O’Fallon KS, Kaushik D, Michniak-Kohn B, Dunne CP, Zambraski EJ, Clarkson PM. Effects of quercetin supplementation on markers of muscle damage and inflammation after eccentric exercise. Int J Sport Nutr Exerc Metab. 2012;22(6):430–7.CrossRefGoogle Scholar
  30. 30.
    Prasad S, Gupta SC, Tyagi AK, Aggarwal BB (2014) Curcumin, a component of golden spice: from bedside to bench and back. Biotechnol Adv.Google Scholar
  31. 31.
    Roberts LA, Muthalib M, Stanley J, Lichtwark G, Nosaka K, Coombes JS, Peake JM. Effects of cold water immersion and active recovery on hemodynamics and recovery of muscle strength following resistance exercise. Am J Physiol Regul Integr Comp Physiol. 2015;309(4):R389–98.CrossRefGoogle Scholar
  32. 32.
    Schoenfeld BJ. The use of nonsteroidal anti-inflammatory drugs for exercise-induced muscle damage: implications for skeletal muscle development. Sports Med. 2012;42(12):1017–28.CrossRefGoogle Scholar
  33. 33.
    Sciberras JN, Galloway SD, Fenech A, Grech G, Farrugia C, Duca D, Mifsud J. The effect of turmeric (Curcumin) supplementation on cytokine and inflammatory marker responses following 2 hours of endurance cycling. J Int Soc Sports Nutr. 2015;12(1):5.CrossRefGoogle Scholar
  34. 34.
    Takahashi M, Suzuki K, Kim HK, Otsuka Y, Imaizumi A, Miyashita M, Sakamoto S. Effects of curcumin supplementation on exercise-induced oxidative stress in humans. Int J Sports Med. 2014;35(6):469–75.PubMedGoogle Scholar
  35. 35.
    Tanner EA, Gary MA, Davis AA, McFarlin BK. Combining single molecule counting with bead-based multiplexing to quantify biological inflammation time course following skeletal muscle injury. Methods. 2019;158:77–80.CrossRefGoogle Scholar
  36. 36.
    Tiidus PM. Alternative treatments for muscle injury: massage, cryotherapy, and hyperbaric oxygen. Curr Rev Musculoskelet Med. 2015;8(2):162–7.CrossRefGoogle Scholar
  37. 37.
    Vane JR, Botting RM. Anti-inflammatory drugs and their mechanism of action. Inflamm Res. 1998;47(Suppl 2):S78–87.CrossRefGoogle Scholar
  38. 38.
    Vyas A, Dandawate P, Padhye S, Ahmad A, Sarkar F. Perspectives on new synthetic curcumin analogs and their potential anticancer properties. Curr Pharm Des. 2013;19(11):2047–69.PubMedPubMedCentralGoogle Scholar
  39. 39.
    Warner DC, Schnepf G, Barrett MS, Dian D, Swigonski NL. Prevalence, attitudes, and behaviors related to the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in student athletes. J Adolesc Health. 2002;30(3):150–3.CrossRefGoogle Scholar
  40. 40.
    Yoon JY, Kwon HH, Min SU, Thiboutot DM, Suh DH. Epigallocatechin-3-gallate improves acne in humans by modulating intracellular molecular targets and inhibiting P. acnes. J Invest Dermatol. 2013;133(2):429–40.CrossRefGoogle Scholar

Copyright information

© Beijing Sport University 2019

Authors and Affiliations

  • Brian K. McFarlin
    • 1
    • 2
    Email author
  • Elizabeth A. Tanner
    • 1
    • 2
  • Melody A. Gary
    • 1
    • 2
  • Asheal A. Davis
    • 1
    • 2
  • Erin M. Bowman
    • 1
  • Richard S. Gary
    • 1
  1. 1.Applied Physiology LaboratoryUniversity of North TexasDentonUSA
  2. 2.Department of Biological SciencesUniversity of North TexasDentonUSA

Personalised recommendations