INFLAMAÇÃO NO                           DESPORTONutrição no Exercício Físico e Desporto   Pedro Carrera Bastos, 2013
INFLAMAÇÃO AGUDA                                                                       Perda deCalor     Vermelhidão      ...
24      The Underlying Principles of Human Metabolism                                         Cells of tissue             ...
Main function                       Monocytes                                                                             ...
Main function                       Monocytes                                                                             ...
Main function                       Monocytes                                                                             ...
146     J. Romeo et al.                                                                                         Main funct...
t al.                                                                        Main function J. Romeo etMonocytes           ...
Exercise             24 hours after exercise                            1 day to 2 weeks after exercise  During exercise  ...
ac                                                                               sa                                       ...
The Chemistry of Food – and of Bodies          11                                                                    Chole...
De Caterina R. N Engl J Med 2011
AINES        De Caterina R. N Engl J Med 2011
Coxibs         De Caterina R. N Engl J Med 2011
Nonsteroidal Anti-Inflammatory Drugs                241                       COX-1                                        ...
52 • Exercise-induced muscle damage and inflammation                                           10 Change in force-generati...
Lesão c/ contracçõesexcêntricas em Coelhos                2xdia            Durante 6 dias
Lesão c/ contracçõesexcêntricas em Coelhos                2xdia            Durante 6 dias
Lesão c/ contracçõesexcêntricas em Coelhos                2xdia            Durante 6 dias
ü Células em cultura durante 96 horasü Inibição selectiva da COX-2 diminui   proliferação de células satéliteü Inibição...
MODULATING SKELETAL MUSCLE REPAIR BY MUSCLE DERIVED STEM CELLS AND ANTIFIBROTIC AGENTS 83   Mio D – factor de transcrição ...
J Appl Physiol 103: 425–431, 2007ü 14 atletasü Corrida de 36 Kmü Indometacina (100 mg) vs Placeboü  Ingestão: durante ...
J Appl Physiol 103: 425–431, 2007     Células Satélite23
J Appl Physiol 103: 425–431, 2007     Células Satélite24
J Appl Physiol 103: 425–431, 2007     Células Satélite25
J Appl Physiol 107: 1600–1611, 2009     Células satélite200 contrações excêntricas26NSAID numa perna (antes, durante e até...
Exercise-Induced Muscle Damage     TABLE 1. Summary of human studies investigating the effect of NSAID consumption on sate...
Am J Physiol Cell Physiol 287: C475–C483, 2004Lesão induzida pelo frio                    Inibidor de                     ...
INIBIDOR DA COX-2 EM RATOS APÓS ESTÍMULO                   MUSCULAR:ü  Reduziu Inflamaçãoü  Atenuou o crescimento das mi...
Shen W. Am J Pathol 2005; 167:1105–1117
J. Clin. Endocrinol. Metab. 2001 86: 5067-5070ACETAM   IBUPROF       PLACEBO
Inibidor da COX-2
Am J Physiol Endocrinol Metab 2002; 282: E551–E556ü 24 adultos masculinosü RCT com Placeboü 10-14 series de 10 rep excé...
Am J Physiol Endocrinol Metab 2002; 282: E551–E556     Fractional Synthesis Rate34
35   Am J Physiol Regul Integr Comp Physiol 296: R1132–R1139, 2009.
Exercise             24 hours after exercise                            1 day to 2 weeks after exercise  During exercise  ...
Exercise             24 hours after exercise                            1 day to 2 weeks after exercise  During exercise  ...
Basic & Clinical Pharmacology & Toxicology 2007; 102: 10–14
Ahn KS, Aggarwal BB. Ann N Y Acad Sci. 2005 Nov;1056:218-33            Serhan CN. Annu. Rev. Immunol. 2007. 25:101–37     ...
Ahn KS, Aggarwal BB. Ann N Y Acad Sci. 2005 Nov;1056:218-33            Serhan CN. Annu. Rev. Immunol. 2007. 25:101–37     ...
Chen LC, Ashcroft DM. Pharmacoepidemiol Drug Saf. 2007 Jul;16(7):762-72
De Caterina R. N Engl J Med 2011
Lipooxigenases                                                   Ciclooxigenases   LTA4                                   ...
EPA/DHA E AACalder PC. Am J Clin Nutr 2006;83(suppl):1505S–19S.
Time course relativo à incorporação de EPA e DHA                            INCORPORAÇÃO DE EPA Y DHA NOS                 ...
DHA	                                                        	  Calder PC. Am J Clin Nutr 2006;83(suppl):1505S–19S)
DHA	                                                        	  Calder PC. Am J Clin Nutr 2006;83(suppl):1505S–19S)
RESOLUÇÃO DA INFLAMAÇÃO        Gilroy DW. 2010
SeráadequadoBloquear?            Serhan CN, Chiang N. Rheum Dis Clin N Am 30 (2004) 69–95
Serhan CN, Chiang N. Rheum Dis Clin N Am 30 (2004) 69–95
RESOLUÇÃO DA INFLAMAÇÃO1578    SerhanAJP October 2010, Vol. 177, No. 4                                                    ...
Serhan CN, Chiang N. British Journal of Pharmacology (2008) 153, S200–S215.
Serhan CN, Chiang N. British Journal of Pharmacology (2008) 153, S200–S215.
Serhan, CN. Annu. Rev. Immunol. 2007. 25:101–37
Serhan CN, Chiang N. Rheum Dis Clin N Am 30 (2004) 69–95
DOSES BAIXAS DE ASPIRINAChiang N et al. Aspirin triggers antiinflammatory 15-epi-lipoxin A4 and inhibits thromboxane in a ...
De Caterina R. N Engl J Med 2011
Barnes PJ, Karin M. N Engl J Med. 1997 Apr 10;336(15):1066-71.
NF-kB e Lesão MuscularTidball JG, Villalta SA. Am J Physiol Regul Integr Comp Physiol 2010; 298: R1173–R1187
EPA	  &	  DHA	  Calder PC. Biochimie. 2009 Feb 3. [Epub ahead of print]
ÓMEGA-3 E INFLAMAÇÃOü  17 meta-análises de    RCTs testando os    efeitos de Ómega-3 na    ARü  3-4 meses: redução da   ...
EPA & DHA por cada 100g peixeFedacko. n−3 PUFAs—From dietary supplements to medicines. Pathophysiology 14 (2007) 127–132
CONCENTRAÇÕES DE MERCÚRIO                                 Concentração    Peixe                          Mercúrio         ...
BETA-OXIDAÇÃOACTIVIDADE LIMITADA            ACTIVIDAD            E LIMITADA
VEGANS TÊM NÍVEIS BAIXOS DE AA E DHAFokkema et al. Polyunsaturated fatty acid status of Dutch vegans and omnivores. Prosta...
9 vegans saudáveis suplementados com:ü A: 2.01 g ALA (4 ml óleo de linhaça)ü B: 1.17 g GLA (6 ml óleo borragem)ü A+B
ESSENTIAL FATTY ACID INTAKE IN T                                                                                       FIG...
TABLE 12                                                                             Sources of docosahexaeno             ...
DIET AND RED BLOOD CELL n–6 AND n–3 FATTY ACIDS                                                                       LA d...
RÁCIO ÓMEGA 6/ÓMEGA 3 DE ALGUNS ALIMENTOS           Alimento                                                 Rácio ω6/ω3 O...
Original ResearchSaraswathi Viswanathan PhD, Bruce D. Hammock 2C9 in Mediating thePhD, Purushothaman Meerarani PhD,       ...
tabolites. Cells were; upper trace) for 24ed epoxides and diolsy. These metabolites  without supplemen-  arachidonates wer...
Exercício                                     ã Número de Neutrófilos circulantes  Físico     Fagocitose dos             ...
488                                                                                                        Howatson & van ...
↓ DOMS                                                                                                      ↓ IL-6        ...
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  1. 1. INFLAMAÇÃO NO DESPORTONutrição no Exercício Físico e Desporto Pedro Carrera Bastos, 2013
  2. 2. INFLAMAÇÃO AGUDA Perda deCalor Vermelhidão Inchaço Dor função Delves PJ, Roitt, IM. N Engl J Med. 2000 Jul 6;343(1):37-49.
  3. 3. 24 The Underlying Principles of Human Metabolism Cells of tissue Erythrocytes Capillary O2 CO2 O2 Endothelial cells CO2 from Oxygen use cellular metabolism Extracellular fluid (in mitochondria) in the interstitial spaceFigure 1.12 Diffusion of chemical substances through the interstitial fluid. A typicaltissue is shown (schematically) in cross-section. The diffusion of oxygen from erythrocytes to cells in the Frayn KN. Metabolic Regulation. Blackwell Pub; 2010:384.tissue is shown as an example. Oxygen diffuses down a concentration gradient, from the erythrocytes,via the plasma and the interstitial fluid, into the cells, where its concentration is depleted as it is usedin mitochondrial oxidation. CO2 diffuses back to the plasma in the same way. The interstitial fluidoccupies the space between cells known as the extracellular space; this is not a true empty space, but
  4. 4. Main function Monocytes Phagocytosis Macrophages Innate Neutrophils Granulocytes Basophils Exocytosis, Eosinophils NK lymphocytes Cytotoxicity T Cytotoxic T lymphocytes T Helper Modulation Adaptive (Th1, Th2) B lymphocytes Antibody productionFigure 10.1 Cellular components of Interventions for Arthritis and Related Inflammatory Diseases, 2013 Bioactive Food as Dietary the immune system and their main functions.
  5. 5. Main function Monocytes Phagocytosis Macrophages Innate Neutrophils Granulocytes Basophils Exocytosis, Eosinophils NK lymphocytes Cytotoxicity T Cytotoxic T lymphocytes T Helper Modulation Adaptive (Th1, Th2) B lymphocytes Antibody productionFigure 10.1 Cellular components of Interventions for Arthritis and Related Inflammatory Diseases, 2013 Bioactive Food as Dietary the immune system and their main functions.
  6. 6. Main function Monocytes Phagocytosis Macrophages Innate Neutrophils Granulocytes Basophils Exocytosis, Eosinophils NK lymphocytes Cytotoxicity T Cytotoxic T lymphocytes T Helper Modulation Adaptive (Th1, Th2) B lymphocytes Antibody productionFigure 10.1 Cellular components of Interventions for Arthritis and Related Inflammatory Diseases, 2013 Bioactive Food as Dietary the immune system and their main functions.
  7. 7. 146 J. Romeo et al. Main function 146 J. Romeo etMonocytes al.146 J. Romeo et al. Main function Phagocytosis 146 J.Monocytes Macrophages Romeo et al. Main function Innate Monocytes Neutrophils Main function Phagocytosis Macrophages Monocytes 146 J. Romeo et al. J. Romeo et al. 146 Granulocytes Basophils Innate Neutrophils Phagocytosis Macrophages MainPhagocytosis function function Main Macrophages Exocytosis, Eosinophils Monocytes Innate Monocytes Neutrophils Basophils Granulocytes NK lymphocytes Cytotoxicity Innate Neutrophils Exocytosis, Basophils Eosinophils Granulocytes Cytotoxic Phagocytosis Phagocytosis T Macrophages Macrophages T lymphocytes NK lymphocytes Granulocytes Basophils Cytotoxicity T Helper Exocytosis, Innate Eosinophils Modulation Neutrophils Adaptive Innate (Th1, Th2) Neutrophils Exocytosis, T Cytotoxic Cytotoxicity Antibody Eosinophils NK B lymphocytes lymphocytes T lymphocytes production NK lymphocytes Cytotoxicity Basophils Granulocytes Granulocytes Basophils T Helper Modulation Figure 10.1 Cellular components ofTthe immune system and their main functions. Adaptive Cytotoxic (Th1, Th2) T lymphocytes T Cytotoxic Antibody Exocytosis, B lymphocytes immune response is required. This response is more complex and sophisticated production and its key Exocytosis, T Helper T lymphocytes Eosinophils Eosinophils Modulation Adaptive (Th1, Th2) feature is to be specifically effective forNK lymphocytes that triggered the response. The adap- Cytotoxicity Cytotoxicity those antigens T Helper Figure 10.1 Cellular components of the immune system and their main functions. NK lymphocytes Modulation Adaptive Antibody tive response is mainly mediated by lymphocytes and classified into two types: humoral and B lymphocytes (Th1, Th2) production cellular. immune response is required. This response is T Cytotoxic B lymphocytes whileand its key In general terms, the humoral response involves mainly B lymphocytesmore complex and sophisticated T Antibody T Cytotoxic Figure 10.1 in charge of the cell-mediated immune and their main functions. Both responses production cells arefeature iscomponents of theeffective for those antigens(Figure 10.1). the response. The adap- Cellular to be specifically immune system response T lymphocytes T lymphocytes triggered that are linked and togetherFigure mediated bycomponents T and classifiedsystem andtypes:main functions. tive response is mainly 10.1a Cellular effective antigen-driven Helper two their humoral and result in highly of the immune specific immune re- immune response is required. This response islymphocytesHelper sophisticated and its key Modulation Modulation Adaptive more complex and T into Adaptive response involves mainly B lymphocytes while T sponse. T helper In h) lymphocytes the characterized by(Th1, Th2) cellular. (T general terms, are humoral their capacity to produce cytokines triggered the(Th1, Th2) complex and feature is to be specifically effective for those antigens thatThis responseresponse. The adap- sophisticated and its key and participate inin charge of theresponse is required. immune response. Th1 cells pro- Antibody immune B lymphocytes B the is more the initiation and developmentimmune response (Figure 10.1). Both responses of lymphocytes Antibody tive response is are cells mainly mediated by lymphocytes and classified into two types: humoral and production cell-mediated feature is to be specifically effective humoral antigens that triggered the response. The adap- for those response. Several dis- production mote the cell-mediated response result in ha highly effective antigen-driven specific while T 2 stimulate the cellular. In general terms,togetherCellular components of themainly Bsystem and theirwhileimmune re- humoral and are linked and the humoral response involves mediated immune lymphocytes main into two T eases aresponse. T helpertivehresponse is mainlyor activityby lymphocytes and classified functions. types: Figure 10.1 Figure 10.1 Cellular components of the immune system and their main related to the inadequate activation characterized by their capacity to produce cytokines functions. (T ) lymphocytes are response (Figureimmune responses, and of the cells are in charge of the cellular. In general terms, the humoral response Both responses B lymphocytes while T cell-mediated immune 10.1). involves mainly they appear to be associatedinitiationisand developmenttowardsiseither Th1 or Th2hsophisticated and immune inwithchargeresponse antigen-driven more response (Figure 10.1). inappropriate bias of the re- are linkedand participate result are ainhighlyrequired. cell-mediated immunecomplex andcomplex and Bothits key and its key and together in the response effective This response immune response. T 1 cells pro- sophisticated specific immune re- mentioned that a genetic Th2 stimulate This response is more it cells immune of the is required. sponses.mote the be feature is to be specifically effective for thoseexists forthatresponse. Several dis- The adap- It must cell-mediated response while predispositionthe humoral triggered the response. antigens this bias, and responses sponse. T helper (Th) lymphocytes are characterizedresult in capacity to produceantigen-driven specific immune re- adap- are linked and together by their a highly for those antigens that triggered the response. The feature is to be specifically effective effective cytokines
  8. 8. t al. Main function J. Romeo etMonocytes al. al. Main function Phagocytosis Monocytes Macrophages Main function nnate Monocytes Neutrophils Phagocytosis Macrophages Granulocytes Basophils Innate Neutrophils Phagocytosis Macrophages Exocytosis, Eosinophils ate Neutrophils Basophils Granulocytes 146 Cytotoxicity al. J. Romeo et NK lymphocytes Exocytosis, Basophils Eosinophils Granulocytes Cytotoxic Main function T T lymphocytes NK lymphocytes Cytotoxicity Monocytes 146 Exocytosis,al. J. Romeo et al. J. Romeo et 146 T Helper Modulation daptive Eosinophils (Th1, Th2) T Cytotoxic Cytotoxicity Antibody NK B lymphocytes lymphocytes MainPhagocytosis function function Main T lymphocytes production Macrophages T Helper Monocytes Monocytes 0.1 Cellular components ofTthe immune system and their main functions. Modulation Adaptive Cytotoxic (Th1, Th2) T lymphocytes Innate Neutrophils B lymphocytes Antibodye response is required. This response is more complex and sophisticated production T Helper Modulation and its key Phagocytosis Phagocytosis ptive (Th1, Th2) Macrophages Macrophages s to be specifically effective for those antigens that triggered the response. The adap- Figure 10.1 Cellular components of the immune system and their main functions. Granulocytes Basophils Antibody onse is mainly mediated by lymphocytes and classified into two types: humoral and B lymphocytes production In general terms, the humoral response involves mainly B lymphocytes while T Innate immune response is required. This response is more complex and sophisticated and its key Innate Neutrophils Neutrophils1 in charge of the cell-mediated immune and their main functions. Both responses Cellular components of the immune system response (Figure 10.1). Exocytosis, feature is to be specifically effective for those antigens that triggered the response. The adap- Eosinophils ed and together result mediated by lymphocytes and classifiedspecific immune re- lymphocytes tive response is mainly in a highly effective antigen-driven into two types: humoral Granulocytes Cytotoxicity esponse is required. This response is more complex and sophisticated and its key NK and Basophils Granulocytes Basophils T helper In h) lymphocytes the characterized by their capacity to produce cytokineswhile T cellular. (T general terms, are humoral response involves mainly B lymphocytes o be specifically effective for those antigens that triggered the response. The adap- cells mainly mediated by cell-mediated immune response (Figure Th1 cells pro- icipate in the initiation and development of the immune response. 10.1). Both nse is are in charge of thelymphocytes and classified into two types: humoral and responses T Cytotoxic Exocytosis, Exocytosis, e cell-mediated together result in ha highly effective antigen-driven specific immune re- are linked and response while T 2 stimulate the humoral response. Several dis- T lymphocytes Eosinophils Eosinophils n general terms, the humoral response involves mainly B lymphocytes while T Cytotoxicity Cytotoxicityesponse. T helper (Th) lymphocytes are or activity of by their capacity to produce cytokines NK lymphocytes related to the inadequate activation characterized the immune responses, NK and n charge of the cell-mediated immune response (Figure 10.1). Both responses lymphocytes Adaptive T Helper Modulation pearparticipate in the initiation and developmenttowardsimmuneTh1 or Th2h1 cells pro- and to be associated with inappropriate antigen-driveneither response. T re- bias of the (Th1, Th2) and together result in a highly effective specific immune re- Antibody It must mentioned that a genetic T exists for this bias, and it B lymphocytesT Cytotoxic T Cytotoxic mote the belymphocytesresponse while predispositionthe humoral response. Several dis- helper (Thcell-mediated are characterized h2 stimulate ) by their capacity to produce cytokines productionmonlyare related antigen-presentation sensitive genes. of the immune responses, and T lymphocytes eases linked to to the inadequate activation immune response. T 1 cells pro- lymphocytes T ipate in the initiation and development of the or activity Figure 10.1 Cellular components T Helper h of the immune system and their main functions. they appear to be associatedT 2 stimulate the humoraltowards either Thdis- Th2 re- Modulation cell-mediated response while with inappropriate bias response.Adaptive 1 or Several Adaptive (Th1, Th2) T Helper Modulation mune-Related Diseases h sponses. It must be mentioned that a activity of the immuneexists for response isand it (Th1, Th2) genetic predisposition immune this bias, required. This response is more complex and sophisticated and its key elated to the inadequate activation or responses, and Antibody Antibody to antigen-presentation sensitive disease, 1 or is to re- lymphocytesB lymphocytes is commonly linked with inappropriate the etiology ofeither T most conditions B h there are plenty of factors involved in bias towards genes. feature Th2 be specifically effective for those antigens that triggered the response. The adap-ear to be associated production production h t mustthe mentioned that athey frequently being infectious, this10.1 Cellularitcomponents of the by lymphocytesand their main functions. types: humoral and ed to be immune system, genetic predisposition exists for inflammatory, or Figure bias, Figure mainly mediated immune system and classified into two tive response is 10.1 Cellular components and 1.2 linked to antigen-presentation sensitive genes. viruses, bacteria, parasites, terms, the humoral of the immune system and their main functions.muneImmune-Related Diseases are caused byonly processes. Infectious diseases cellular. In general response involves mainly B lymphocytes while T Although there are plenty of factors involved in the etiology ofcellsimmune are in chargeresponsecell-mediated is more complex andcomplex and Bothits key and its key disease, immune of the is required. This response is more sophisticated and responses response is required. This response immune response (Figure 10.1). sophisticated most conditionsmune-Related Diseases system, they frequently being infectious, be specifically orresult in a highly for those triggered the response. The adap- re- are related to the immune feature is to inflammatory,effective for those antigens that antigens that triggered the response. The adap- feature is to be specifically effective effective antigen-driven specific immune are linked and together
  9. 9. Exercise 24 hours after exercise 1 day to 2 weeks after exercise During exercise After exercise Recovery mechanical damage to muscle after exerciseinfiltration Exercise 24 hours • leukocyte • proliferation of satellite cells 1 day to 2 weeks after exercise tissue • inflammation • acquisition of protective effectDuring exercise After exercise Recoverymechanical damage to muscle • leukocyte infiltration • proliferation of satellite cells blood circulationtissue • inflammation • acquisition of protective effect priming adhesion molecules PMN monocytesblood circulation CK adhesion molecules endothelial cells priming MbPMN Inflammation and eccentric exercise • 77 monocytes CK CK cytokines Mb macrophages endothelial cells Mb chemoattractants cytokines Inflammation and eccentric exercise • 77 growth factorscytokines Mb ROS CK macrophages phagocytosis chemoattractants enzymescytokines growth phagocytosis factors damaged muscle tissue muscle tissue regenerated muscle fibres fragments ROS fragments phagocytosis satellite cells muscle fibres enzymes Figure 1 Exercise-induced muscle damage and subsequent muscle inflammation and regeneration process phagocytosis (PMN, polymorphonuclear leucocyte; Mb, myoglobin; CK, creatine kinase; ROS, reactive oxygen species) damaged muscle tissue muscle tissue regeneratedmuscle fibres fragments fragments satellite cells muscle fibres Figure 1 Exercise-induced muscle damage and subsequent muscle inflammation and regeneration process (PMN, polymorphonuclearJ, Nosaka K, Suzuki K. Exerc Immunol Rev. 2005;11:64-85 Peake leucocyte; Mb, myoglobin; CK, creatine kinase; ROS, reactive oxygen species)
  10. 10. ac sa in ha op pa na co si R (C tio in th fo FIGURE 2. Diagrammatic representation of the movement of leukocytesthrough the endothelium and the subsequent generation of inflammatory anmediators. Calder PC. Am J Clin Nutr 2006;83(suppl):1505S–19S)   an
  11. 11. The Chemistry of Food – and of Bodies 11 Cholesterol Aqueous (polar) environment molecules outside cell Non-polar (hydrophobic) region within membrane Phospholipid molecule Intrinsic protein Aqueous (polar) environment (e.g. sugar carrier, inside cell hormone receptor)Figure 1.5 Structure of biological membranes in mammalian cells. Cell membranesand intracellular membranes such as the endoplasmic reticulum are composed of bilayers of phos-pholipid molecules with their polar head-groups facing the aqueous environment on either side andtheir non-polar ‘tails’ facing inwards, forming a hydrophobic center to the membrane. The membranealso contains intrinsic proteins such as hormone receptors, ion channels, and sugar transporters, and Frayn KN. Metabolic Regulation. Blackwell Pub; 2010:384.molecules of cholesterol which reduce the ‘fluidity’ of the membrane. Modern views of cell mem-brane structure emphasize that there are domains, known as ‘rafts,’ in which functional proteinsco-locate, enabling interactions between them. These lipid rafts are characterized by high concentra-
  12. 12. De Caterina R. N Engl J Med 2011
  13. 13. AINES De Caterina R. N Engl J Med 2011
  14. 14. Coxibs De Caterina R. N Engl J Med 2011
  15. 15. Nonsteroidal Anti-Inflammatory Drugs 241 COX-1 COX-2 Coxibs AINES “Side pocket” NSAID binding space Intracellular membrane F S F Br CHCO2H SO2CH3 Bulky grouping CH3 COX-1 inhibitor COX-2 inhibitor Flurbiprofen DuP697Figure 18.2. Serhan CN, Ward PA, Gilroy DW, editors. Fundamentals of Inflammation. Cambridge Univ Pr; 2010: 234-243.
  16. 16. 52 • Exercise-induced muscle damage and inflammation 10 Change in force-generating capacity (%) 0 -10 -20 -30 -40 -50 Mild damage Moderate damage Severe damage -60 -24 0 24 48 72 96 120 144 168 Time (hours after exercise)Figure 2. Recovery of the force-generating capacity of subjects that have performed heavyresistance exercise or G, Mikkelsen UR, Raastad T, Peake JM. Exerc(subjects from several studies are com- Paulsen maximal eccentric exercise Immunol Rev. 2012;18:42-97bined: (230,248-251), as well as unpublished data). The subjects are organized so thatthose who recover their force-generating capacity within 48 hours are represented as mild
  17. 17. Lesão c/ contracçõesexcêntricas em Coelhos 2xdia Durante 6 dias
  18. 18. Lesão c/ contracçõesexcêntricas em Coelhos 2xdia Durante 6 dias
  19. 19. Lesão c/ contracçõesexcêntricas em Coelhos 2xdia Durante 6 dias
  20. 20. ü Células em cultura durante 96 horasü Inibição selectiva da COX-2 diminui proliferação de células satéliteü Inibição de COX-1 e COX-2 reduz diferenciação e fusão de células satélite Muscle Nerve 30: 497–500, 2004
  21. 21. MODULATING SKELETAL MUSCLE REPAIR BY MUSCLE DERIVED STEM CELLS AND ANTIFIBROTIC AGENTS 83 Mio D – factor de transcrição responsável pela activação das células satélite e subsequente proliferação dos mioblastosFigure 1. Generalized scheme of myogenic differentiation. Other markers are used by different investigators. (Adapted from Deasyet al., 2001, Blood Cells Mol Dis, 27, 924–933) Gharaibeh B, et al. Birth Defects Res C Embryo Today. 2012 Mar;96(1):82-94.fibers, as previously mentioned. genetic disease (such as Duch- skeletal muscle is limited and veryThese cells have also been used enne muscular dystrophy [DMD]), often, fibrotic tissue forms, delay-
  22. 22. J Appl Physiol 103: 425–431, 2007ü 14 atletasü Corrida de 36 Kmü Indometacina (100 mg) vs Placeboü  Ingestão: durante 4 dias antes da corrida até à data da última biópsia RESULTADOS:
  23. 23. J Appl Physiol 103: 425–431, 2007 Células Satélite23
  24. 24. J Appl Physiol 103: 425–431, 2007 Células Satélite24
  25. 25. J Appl Physiol 103: 425–431, 2007 Células Satélite25
  26. 26. J Appl Physiol 107: 1600–1611, 2009 Células satélite200 contrações excêntricas26NSAID numa perna (antes, durante e até 4,5 h depois) e a outra como controlo
  27. 27. Exercise-Induced Muscle Damage TABLE 1. Summary of human studies investigating the effect of NSAID consumption on satellite cell activity.* Study Subjects NSAID/dosage Results Bondesen et al. (16) Rodents SC-560/3 mgÁkg21Ád21 Significant blunting of satellite cell SC-236 /6 mgÁkg21Ád21 activity in NSAID compared with placebo Bondesen et al. (17) Rodents SC-236 /6 mgÁkg21Ád21 Significant blunting of satellite cell activity in NSAID compared with placebo Mackey et al. (91) Humans Indomethacin/100 mg Significant blunting of satellite cell activity in NSAID compared with placebo Mikkelsen et al. (100) Humans Indomethacin/45 mg Significant blunting of satellite cell activity in NSAID compared with placebo Paulsen et al. (117) Humans Celcoxib/400 mg No significant differences in satellite cell activity between groups *NSAIDs = nonsteroidal anti-inflammatory drugs.protein accretion seen in eccentric protocols. Other studies, generally less compared with those performed concentri-however, seem to refute whether a reversal of the size cally. This paradox was demonstrated by Grabiner et al. (55),principle actually does occur. An extensive review of the who found that the maximum EMG of the vastus lateralis Schoenfeld BJ. J Strength Cond Res. 2012 eccentric knee extension was only 84 6 41% of thatliterature by Chalmers (26) concluded that the preponder- during May;26(5):1441-53.ance of evidence does not support selective recruitment of obtained concentrically. Hence, although the potential tofast-twitch fibers during eccentric contractions. These results exert peak force is greater with eccentric exercise, most find itheld constant in 9 out of 10 studies deemed suitable to extremely difficult to achieve the maximum force during
  28. 28. Am J Physiol Cell Physiol 287: C475–C483, 2004Lesão induzida pelo frio Inibidor de COX-2
  29. 29. INIBIDOR DA COX-2 EM RATOS APÓS ESTÍMULO MUSCULAR:ü  Reduziu Inflamaçãoü  Atenuou o crescimento das miofibrilhasü  Reduziu a activação e proliferação das células satélite
  30. 30. Shen W. Am J Pathol 2005; 167:1105–1117
  31. 31. J. Clin. Endocrinol. Metab. 2001 86: 5067-5070ACETAM IBUPROF PLACEBO
  32. 32. Inibidor da COX-2
  33. 33. Am J Physiol Endocrinol Metab 2002; 282: E551–E556ü 24 adultos masculinosü RCT com Placeboü 10-14 series de 10 rep excéntricas RM DIMINUIÇÃO (24h): Fractional synthesis rate Sem efeitos na dor comparado com placebo
  34. 34. Am J Physiol Endocrinol Metab 2002; 282: E551–E556 Fractional Synthesis Rate34
  35. 35. 35 Am J Physiol Regul Integr Comp Physiol 296: R1132–R1139, 2009.
  36. 36. Exercise 24 hours after exercise 1 day to 2 weeks after exercise During exercise After exercise Recovery mechanical damage to muscle after exerciseinfiltration Exercise 24 hours • leukocyte • proliferation of satellite cells 1 day to 2 weeks after exercise tissue • inflammation • acquisition of protective effectDuring exercise After exercise Recoverymechanical damage to muscle • leukocyte infiltration • proliferation of satellite cells blood circulationtissue • inflammation • acquisition of protective effect priming adhesion molecules PMN monocytesblood circulation CK adhesion molecules endothelial cells priming MbPMN Inflammation and eccentric exercise • 77 monocytes CK CK cytokines Mb macrophages endothelial cells Mb chemoattractants cytokines Inflammation and eccentric exercise • 77 growth factorscytokines Mb ROS CK macrophages phagocytosis chemoattractants enzymescytokines growth phagocytosis factors damaged muscle tissue muscle tissue regenerated muscle fibres fragments ROS fragments phagocytosis satellite cells muscle fibres enzymes Figure 1 Exercise-induced muscle damage and subsequent muscle inflammation and regeneration process phagocytosis (PMN, polymorphonuclear leucocyte; Mb, myoglobin; CK, creatine kinase; ROS, reactive oxygen species) damaged muscle tissue muscle tissue regeneratedmuscle fibres fragments fragments satellite cells muscle fibres Figure 1 Exercise-induced muscle damage and subsequent muscle inflammation and regeneration process (PMN, polymorphonuclearJ, Nosaka K, Suzuki K. Exerc Immunol Rev. 2005;11:64-85 Peake leucocyte; Mb, myoglobin; CK, creatine kinase; ROS, reactive oxygen species)
  37. 37. Exercise 24 hours after exercise 1 day to 2 weeks after exercise During exercise After exercise Recovery mechanical damage to muscle after exerciseinfiltration Exercise 24 hours • leukocyte • proliferation of satellite cells 1 day to 2 weeks after exercise tissue • inflammation • acquisition of protective effectDuring exercise After exercise Recoverymechanical damage to muscle • leukocyte infiltration • proliferation of satellite cells blood circulationtissue • inflammation • acquisition of protective effect priming adhesion molecules PMN monocytesblood circulation CK adhesion molecules endothelial cells priming MbPMN Inflammation and eccentric exercise • 77 monocytes CK CK cytokines Mb macrophages endothelial cells Mb chemoattractants cytokines Inflammation and eccentric exercise • 77 growth factorscytokines Mb ROS CK macrophages phagocytosis chemoattractants enzymescytokines growth phagocytosis factors damaged muscle tissue muscle tissue regenerated muscle fibres fragments ROS fragments phagocytosis satellite cells muscle fibres enzymes Figure 1 Exercise-induced muscle damage and subsequent muscle inflammation and regeneration process phagocytosis (PMN, polymorphonuclear leucocyte; Mb, myoglobin; CK, creatine kinase; ROS, reactive oxygen species) damaged muscle tissue muscle tissue regeneratedmuscle fibres fragments fragments satellite cells muscle fibres Figure 1 Exercise-induced muscle damage and subsequent muscle inflammation and regeneration process (PMN, polymorphonuclearJ, Nosaka K, Suzuki K. Exerc Immunol Rev. 2005;11:64-85 Peake leucocyte; Mb, myoglobin; CK, creatine kinase; ROS, reactive oxygen species)
  38. 38. Basic & Clinical Pharmacology & Toxicology 2007; 102: 10–14
  39. 39. Ahn KS, Aggarwal BB. Ann N Y Acad Sci. 2005 Nov;1056:218-33 Serhan CN. Annu. Rev. Immunol. 2007. 25:101–37 Roubenoff R. Nutr Rev. 2007 Dec;65(12 Pt 2):S208-12 Tidball JG, Villalta SA. Am J Physiol Regul Integr Comp Physiol 2010; 298: R1173–R1187Inflamação Aguda Regeneração Inflamação Crónica Lesão e Dor Crónica Catabolismo muscular e ósseo Síndrome de Morte Súbita Doenças Metabólicas39 e Neurodegenativas
  40. 40. Ahn KS, Aggarwal BB. Ann N Y Acad Sci. 2005 Nov;1056:218-33 Serhan CN. Annu. Rev. Immunol. 2007. 25:101–37 Roubenoff R. Nutr Rev. 2007 Dec;65(12 Pt 2):S208-12 Tidball JG, Villalta SA. Am J Physiol Regul Integr Comp Physiol 2010; 298: R1173–R1187Inflamação Aguda AA   Regeneração Inflamação Crónica Lesão e Dor Crónica Catabolismo muscular e ósseo Síndrome de Morte Súbita Doenças Metabólicas40 e Neurodegenativas
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  43. 43. Lipooxigenases Ciclooxigenases LTA4 TXA2 LTB4 PGE2 LTC4 Ácido Araquidónico 20:4 n-6 PGF2α LTD4 PGD2 LTE4 PGI2 12-HETE LTA5 TXA3 LTB5 Ácido Eicosapentaenóico PGE3 LTC5 (EPA) PGF3 α LTD5 20:5 n-3 PGD3 LTE5 PGI3 Bastos P. An Nutr Esp Func 2007; 7(36): 17-24
  44. 44. EPA/DHA E AACalder PC. Am J Clin Nutr 2006;83(suppl):1505S–19S.
  45. 45. Time course relativo à incorporação de EPA e DHA INCORPORAÇÃO DE EPA Y DHA NOS em fosfolipídios de membrana de células mononucleares FOSFOLÍPIDOS DE CÉLULAS MONONUCLEARES DHA in mononuclear cell PL (%) EPA in mononuclear cell PL (%) 4 4 3 3 2 1 2 0 1 0 4 8 12 20 0 4 8 12 20 Time (weeks) Time (weeks) Indivíduos saudáveis: 2,1 g EPA + 1,1 g DHA/dia/12 semanas Eur. J. Clin. Invest. 30, 260-274, 2000Eur. J. Clin. Invest. 30, 260-274, 2000
  46. 46. DHA    Calder PC. Am J Clin Nutr 2006;83(suppl):1505S–19S)
  47. 47. DHA    Calder PC. Am J Clin Nutr 2006;83(suppl):1505S–19S)
  48. 48. RESOLUÇÃO DA INFLAMAÇÃO Gilroy DW. 2010
  49. 49. SeráadequadoBloquear? Serhan CN, Chiang N. Rheum Dis Clin N Am 30 (2004) 69–95
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  51. 51. RESOLUÇÃO DA INFLAMAÇÃO1578 SerhanAJP October 2010, Vol. 177, No. 4 Lipoxinas! Serhan CN. Am J Pathol. 2010 Oct;177(4):1576-91!
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  55. 55. Serhan CN, Chiang N. Rheum Dis Clin N Am 30 (2004) 69–95
  56. 56. DOSES BAIXAS DE ASPIRINAChiang N et al. Aspirin triggers antiinflammatory 15-epi-lipoxin A4 and inhibits thromboxane in a randomized human trial. PNAS 2004. 101; 42
  57. 57. De Caterina R. N Engl J Med 2011
  58. 58. Barnes PJ, Karin M. N Engl J Med. 1997 Apr 10;336(15):1066-71.
  59. 59. NF-kB e Lesão MuscularTidball JG, Villalta SA. Am J Physiol Regul Integr Comp Physiol 2010; 298: R1173–R1187
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  61. 61. ÓMEGA-3 E INFLAMAÇÃOü  17 meta-análises de RCTs testando os efeitos de Ómega-3 na ARü  3-4 meses: redução da dor articular, minutos de rigidez matutina, número de articulações com dor e menor uso de AINES Goldberg RJ, Katz J. Pain 129 (2007)
  62. 62. EPA & DHA por cada 100g peixeFedacko. n−3 PUFAs—From dietary supplements to medicines. Pathophysiology 14 (2007) 127–132
  63. 63. CONCENTRAÇÕES DE MERCÚRIO Concentração Peixe Mercúrio (ppm) Peixe-espada 0,97 Arenque 0,35 Atum 0,12 Bacalhau 0,11 Salmão 0,01 Adaptado: FDA (EUA) 66
  64. 64. BETA-OXIDAÇÃOACTIVIDADE LIMITADA ACTIVIDAD E LIMITADA
  65. 65. VEGANS TÊM NÍVEIS BAIXOS DE AA E DHAFokkema et al. Polyunsaturated fatty acid status of Dutch vegans and omnivores. Prostaglandins, Leukotrienes and Essential FattyAcids (2000)
  66. 66. 9 vegans saudáveis suplementados com:ü A: 2.01 g ALA (4 ml óleo de linhaça)ü B: 1.17 g GLA (6 ml óleo borragem)ü A+B
  67. 67. ESSENTIAL FATTY ACID INTAKE IN T FIGUR supply fr indicated FIGURE 4. Regression Blasbalg TL, et for the availability of linoleic acid (LA) analysis al. Am J Clin Nutr. 2011 line, and nbetween 1909 and 1999. The linear relation [LA percentage of energy line. 190(en%) = 2115.4221 + 0.0617 · x] was significant at P , 0.000001 with data are
  68. 68. TABLE 12 Sources of docosahexaeno Food category Poultry Shellfish Eggs Finfish Beef Game Total 1 NA, not applicable. lipids (37), presumab dietary intakes of LA account for the poten However, because LA effects may be nonlin A randomized trial t with high LA (6.7% of Blasbalg TL, et al. Am J Clin Nutr. 2011 FIGURE 8. Omega-3 tissue highly unsaturated fatty acid (HUFA)predictions over the 20th century. Solid arrows indicate the percentage of
  69. 69. DIET AND RED BLOOD CELL n–6 AND n–3 FATTY ACIDS LA diminui DHA na membrana dos eritrócitos N= 105 Mulheres (Canadá) Grávidas (com 36semanas de LA diminui gestação) EPA na membrana dos eritrócitos Friesen RW, Innis SM. Am J Clin Nutr. 2010 Jan;91(1):23-31.
  70. 70. RÁCIO ÓMEGA 6/ÓMEGA 3 DE ALGUNS ALIMENTOS Alimento Rácio ω6/ω3 Ovo convencional 19,4 Ovo de Creta 1,3 Carne (músculo) bovina 5,19 alimentada com cereais Carne (músculo) bovina 2,2 alimentada a pasto Simopoulos AP. J Nutr. 2001 Nov;131(11 Suppl):3065S-73S. Review Cordain L et al. European Journal of Clinical Nutrition 2002; 56:181 – 191.
  71. 71. Original ResearchSaraswathi Viswanathan PhD, Bruce D. Hammock 2C9 in Mediating thePhD, Purushothaman Meerarani PhD, Involvement of CYP PhD, John W. Newman, Proinflammatory Effects of Linoleic Acid in VascularMichal Toborek MD, PhD, and Bernhard Hennig PhD, FACN Endothelial CellsMolecular and Cell Nutrition Laboratory, College of AgricultureJournal ofP.M., B.H.), Department of Surgery 502–510 (2003) (S.V., the American College of Nutrition, Vol. 22, No. 6, (M.T.), University ofKentucky, Lexington, KY, 40546-0215, and PhD, Bruce D. Hammock Entomology and UC CancerMeerarani PhD, Saraswathi Viswanathan Department of PhD, John W. Newman, PhD, Purushothaman Center (B.D.H., J.W.N.), University ofCalifornia, Davis, CA, USA.Michal Toborek MD, PhD, and Bernhard Hennig PhD, FACN Molecular and Cell Nutrition Laboratory, College of Agriculture (S.V., P.M., B.H.), Department of Surgery (M.T.), University ofKey words: linoleic acid, CYP 2C9, leukotoxin, leukotoxin diol, oxidative stress Kentucky, Lexington, KY, 40546-0215, and Department of Entomology and UC Cancer Center (B.D.H., J.W.N.), University of California, Davis, CA, USA. Key words: linoleic acid, CYP 2C9, leukotoxin, leukotoxin diol, oxidative stress Objective: Polyunsaturated Polyunsaturated fattysuchsuch aslinoleic are well are well lipids that may be Objective: fatty acids acids as linoleic acid acid known dietary known dietary lipids that may be atherogenic by activating vascular endothelial cells. In the liver, fatty acids can be metabolized by cytochrome atherogenic by activating vascular endothelial cells. In of theseliver, fatty acids can be metabolized by cytochrome P450 (CYP) enzymes, but little is known about the role the enzymes in the vascular endothelium. CYP 2C9 P450 (CYP) enzymes, butinvolved inis knownepoxygenation, androle of product ofenzymesisin the vascular endothelium. CYP 2C9 is little linoleic acid about the the major these this reaction leukotoxin (LTX). We investigated the role of CYP-mediated mechanisms of linoleic acid metabolism in endothelial cell activation by is involved in linoleic acid epoxygenation, and oxidizedmajor product of leukotoxin diol (LTD). is leukotoxin (LTX). We examining the effects of linoleic acid or its the metabolites such as LTX and this reaction Methods: The effect of linoleic acid on CYP 2C9 gene expression was studied by RT-PCR. Oxidative stress investigated the role of CYP-mediated mechanismsand intracellular glutathione levels, and electrophoretic mobility was monitored by measuring DCF fluorescence of linoleic acid metabolism in endothelial cell activation by examining the effects of linoleicwas carriedto studyliquid chromatography/massstress sensitive transcription factors. and leukotoxin diol (LTD). shift assay was carried out oxidized lipids acid or its the activation of oxidative spectrometry. as LTX Analysis of out by oxidized metabolites such Methods: The effect of linoleic acid on CYP 2C9increased the expression of CYP 2C9studied by RT-PCR. Oxidative stress Results: Linoleic acid treatment for six hours gene expression was in endothelial cells. Linoleic acid-mediated increase in oxidative stress and activation of AP-1 were blocked by sulfaphenazole, a was monitored by measuring inhibitor of CYP 2C9. The linoleic acid metabolites LTX and LTD increased oxidative stress and electrophoretic mobility specific DCF fluorescence and intracellular glutathione levels, and activation of transcription factors only at high concentrations. shift assay was carried out to study the show that CYP 2C9 plays a key role in linoleic acid-induced oxidative stress and Conclusion: Our data activation of oxidative stress sensitive transcription factors. Analysis of subsequent proinflammatory events in vascular endothelial cells by possibly causing superoxide generation oxidized lipids was carried out by liquid chromatography/mass spectrometry. through uncoupling processes. Results: Linoleic acid treatment for six hours increased the expression of CYP 2C9 in endothelial cells. INTRODUCTION Linoleic acid-mediated increase in oxidative stress and activation of AP-1 were blockedlipids play an in sub-endothelial regions. These biologically active by sulfaphenazole, a important role in the development of atherosclerosis. Polyunsatu- specific inhibitor of CYPis 2C9. The a chronic inflammatory Atherosclerosis believed to be linoleic acid metabolites LTX and LTD increased oxidative stress and rated fatty acids and/or their metabolites can have potent biolog- disease, and the earliest event of coronary atherosclerosis is activation of characterized by endothelial activation at high concentrations.Evidence suggeststypes by functioning as signaling mol- transcription factors only and dysfunction [1]. ical effects in various cell ecules. that linoleic acid, a major dietary Conclusion: Our data show Several factors are implicated that CYP 2C9 plays a key role inacid in the American diet, has proinflammatory in the initiation of endothelial unsaturated fatty linoleic acid-induced oxidative stress and dysfunction of which the formation of reactive oxygen species and proatherogenic effects by causing endothelial cell activation subsequent proinflammatory events in this process [2,3]. is believed to play a critical role during vascular endothelial cells by possibly causingis superoxide generation [4]. Linoleic acid-induced endothelial activation considered to Endothelial cells are continuously exposed to circulating through uncoupling processes. be mediated through oxidative stress [4,5]. However, the precise lipids (e.g., dietary fatty acids) and to lipids that have accumulated mechanism involved in linoleic acid-induced oxidative stress andINTRODUCTION in sub-endothelial regions. These biologically active lipids play an Address reprint requests to: Bernhard Hennig, PhD, RD, FACN, Molecular and Cell Nutrition Laboratory, College of Agriculture, 213 Garrigus Building, University of Kentucky, Lexington, KY 40546-0215. E-mail: bhennig@uky.edu
  72. 72. tabolites. Cells were; upper trace) for 24ed epoxides and diolsy. These metabolites without supplemen- arachidonates werea not shown). Results aliquots analyzed by fatty acids may beTo examine if the Fig. 8. Proposedthe American College of mechanism of linoleic (2003) (LA)- Journal of model for the Nutrition, Vol. 22, No. 6, 502–510 acido oxidative stress, mediated endothelial cell activation. LA treatment results in CYP 2C9
  73. 73. Exercício ã Número de Neutrófilos circulantes Físico Fagocitose dos Migração para resíduos celulares local da lesão Libertação de lisoenzimas e radicais de oxigénioApós o exercício excêntrico são observados maiores ã nos neutrófilos do que após o exercício concêntrico CANNON JG. ORENCOLE SF. FIELDING RA. et al. Am J Physiol, 259(6 Pt 2): R1214-9, 1990. SMITH JK. GRISHAM MB. GRANGER DN. KORTHUIS RJ. Am J Physiol, 256(3 Pt 2): H789-93, 1989.
  74. 74. 488 Howatson & van Someren VITAMINA CTable I. Studies reporting effects of antioxidant supplementation on markers of exercise-induced muscle damageStudy Supplementation Exercise protocol Effects post-exercise (compared with control group)Bryer and Goldfarb[70] Vit C (3000 mg/d) for 14 d prior and 70 elbow flexor eccentric ↓ CK 4 d post-exercise contractions ↓ DOMS ↓ Glutathione ratio ↔ Muscle force ↔ ROMKaminsky and Boal[71] Vit C (3000 mg/d) for 3 d prior and 15 min cyclic plantar flexion and ↓ DOMS 4 d post-exercise extensionThompson et al.[72] Vit C (400 mg/d) for 12 d prior 90 min intermittent shuttle ↔ CK, Mb running ↔ MDA ↔ Muscle force ↓ DOMS ↓ IL-6 ↔ CRPConnolly et al.[73] Vit C (3000 mg/d) for 3 d prior and 40 elbow flexor eccentric ↔ DOMS 5 d post-exercise contractions ↔ Muscle force ↔ ROMChilds et al.[74] Vit C (12.5 mg/kg/d) and NAC 30 elbow flexor eccentric ↑ CK (10 mg/kg/d) for 7 d post-exercise contractions ↑ LDH ↔ DOMS ↔ ROM ↔ IL-6Close et al.[75] Vit C (1000 mg/d) 2 h prior and 14 d 30 min downhill running ↓ MDA post-exercise ↓ Muscle force ↔ DOMSSacheck et al.[76] Vit E (1000 IU/d) for 12 wk prior 45 min downhill running ↓ CK in younger men Howatson G, van Someren KA. Sports Med. 2008;38(6):483-503. ↓ iPF(2α) in older menMcBride et al.[77] Vit E (1200 IU/d) for 14 d prior Whole-body resistance exercise ↓ CK ↔ MDA
  75. 75. ↓ DOMS ↓ IL-6 ↔ CRPConnolly et al.[73] 5 d post-exercise VITAMINA E eccentric Vit C (3000 mg/d) for 3 d prior and 40 elbow flexor contractions ↔ DOMS ↔ Muscle force ↔ ROM488 Howatson & van SomerenChilds et al.[74] Vit C (12.5 mg/kg/d) and NAC 30 elbow flexor eccentric ↑ CK (10 mg/kg/d) for 7 d post-exercise contractions ↑ LDH ↔ DOMS ↔ ROMTable I. Studies reporting effects of antioxidant supplementation on markers of exercise-induced muscle ↔ IL-6 damageClose et al.[75] Vit C (1000 mg/d) 2 h prior and 14 d 30 min downhill running ↓ MDAStudy Supplementation Exercise protocol Effects post-exercise post-exercise ↓ Muscle force (compared with control group) ↔ DOMSBryer and Goldfarb[70] Vit C (3000 mg/d) for 14 d prior and 70 elbow flexor eccentric ↓ CKSacheck et al.[76] 4 d E (1000 IU/d) for 12 wk prior Vit post-exercise 45 min downhill running contractions ↓ CK ↓ DOMSin younger men ↓ iPF(2α) in older ↓ Glutathione ratio menMcBride et al.[77] Vit E (1200 IU/d) for 14 d prior Whole-body resistance exercise ↔↓ CK force Muscle ↔↔ MDA ROMKaminsky and Boal[71] Vit C (3000 mg/d) for 3 d prior and ↔ DOMS 15 min cyclic plantar flexion and ↓ DOMSBeaton et al.[78] 4 d E (1200 IU/d) for 30 d prior exerciseextension flexor and extensor Vit post-exercise 240 knee ↔ CKThompson et al.[72] Vit C (400 mg/d) for 12 d prior 90 min intermittent shuttle eccentric contractions ↔↔ Muscle force CK, Mb running ↔↔ Z-band disruption MDA ↔↔ DOMS Muscle force ↓ DOMSShafat et al.[79] Vit C (500 mg/d) and vit E (1200 IU/d) 300 knee extensor eccentric ↓ Decline in torque during ↓ IL-6 for 30 d prior and 7 d post-exercise contractions exercise ↔ CRP ↑ Muscle forceConnolly et al.[73] Vit C (3000 mg/d) for 3 d prior and 40 elbow flexor eccentric ↔↔ DOMS DOMS 5 d post-exercise contractions ↔ Muscle forceGoldfarb et al.[80] Vit C (1000 mg/d) and vit E (400 IU/d) 48 elbow flexor eccentric ↔↓ MDA ROM for 14 d prior and 2 d post-exercise contractions ↓ Plasma protein carbonylsChilds et al.[74] Vit C (12.5 mg/kg/d) and NAC 30 elbow flexor eccentric ↑ CK ↔ Glutathione status (10 mg/kg/d) for 7 d post-exercise contractions ↑ LDHMastaloudis et al.[81] Vit C (1000 mg/d) and vit E (300 mg/d) 50 km ultramarathon run ↔↔ CK DOMS for 6 wk prior ↔↔ LDH ROM Howatson G, van Someren KA. Sports Med. 2008;38(6):483-503. ↔ Muscle force ↔ IL-6Petersen al.[75] [82]Close et et al. Vit C (1000 mg/d) and prior and 14 d Vit C (500 mg/d) 2 h vit E (400 mg/d) 30 min downhill running 90 min downhill running ↔ IL-6 ↓ MDA post-exercise and 7 d post-exercise for 14 d prior ↓ Muscle force ↔ CK

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