Artigo Revisado por pares

Last Word on Point:Counterpoint: Estrogen and sex do/do not influence post-exercise indexes of muscle damage, inflammation, and repair

2009; American Physiological Society; Volume: 106; Issue: 3 Linguagem: Inglês

10.1152/japplphysiol.00013.2009

ISSN

8750-7587

Autores

Peter M. Tiidus, Deborah L. Enns,

Tópico(s)

Muscle Physiology and Disorders

Resumo

POINT-COUNTERPOINTLast Word on Point:Counterpoint: Estrogen and sex do/do not influence post-exercise indexes of muscle damage, inflammation, and repairPeter M. Tiidus and Deborah L. EnnsPeter M. Tiidus and Deborah L. EnnsPublished Online:01 Mar 2009https://doi.org/10.1152/japplphysiol.00013.2009MoreSectionsPDF (29 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations to the editor: It is clear that considerable work remains to be done to fully clarify the effects of estrogen and/or sex on skeletal muscle. As a number of commentators noted, it is important to continue to develop the most appropriate human and animal models and measures to further establish the extent of estrogen influence on muscle damage, inflammation, and repair. In addition, some comments focused on possible methodological confounds in studies showing positive effects of estrogen on muscle damage, which we will respond to. Drs. Warren and Lowe's comments (5) raised the possibility of lower body weights as a factor in female or estrogen-supplemented animals exhibiting less post-exercise muscle damage. Unfortunately the one paper cited to support animal weight as a factor in indexes of post-exercise muscle damage (4) is confounded by large age and exercise volume differences between the all male weight groups as well as a lack of statistical analysis. Hence the potential for weight differences as a factor in the attenuated post-exercise muscle damage that is consistently seen in estrogen supplemented male or female animals, whether exercised by uphill or downhill running (2, 6), while worth investigating, is entirely speculative. Other comments (4) noted the potential variability and clearance rate confounds inherent in the use of blood CK as an in vivo indicator of estrogen attenuated muscle damage. Nevertheless, at least one study using an in vitro isolated muscle preparation has clearly demonstrated that post-exercise CK release specifically from muscle is attenuated by estrogen (1). Other post-exercise damage indexes such as muscle β-glucuronidase activities have also consistently been attenuated by estrogen (2). The commentaries also focused more on the potential effects of estrogen/sex on muscle damage and less on its potential effects on post-damage inflammation and repair. Hence, Dr. Stupka's comments (5) are particularly relevant as they cite the types of dynamic muscle inflammation and repair related processes that are influenced by estrogen as well as noting that to gain a more complete understanding there is a need to assess these measures at multiple post-exercise time points. As an initial attempt to assess these possibilities we have reported evidence of enhanced repair processes such as post-exercise satellite cell activation and proliferation occurring in estrogen-supplemented versus unsupplemented ovariectomized rodents, despite the former having lower indexes of muscle damage and macrophage infiltration and demonstrated that this effect is manifested through muscle estrogen receptors (2). We have also reported 96-h time courses of these events (3). Commentators such as Dr. Sipila (5) corroborated our suggestion that the most relevant information may be gleaned by further investigating the possibilities of enhanced muscle repair and related health and muscle functional benefits, specifically in post-menopausal human women with or without hormone replacement. These and other suggestions put forward in the comments can help formulate future human and animal research in this regard and serve to stimulate interest and research into the potential for estrogen to influence muscle damage, inflammation, and repair and that future research will continue add further insights.REFERENCES1 Amelink GJ, Koot GJ, Erich WBM, Van Gijn PR, Bar J. Sex-linked variation in creatine kinase release and its dependence on oestrogen can be demonstrated in an in-vitro rat skeletal muscle preparation. Acta Physiol Scand 138: 115–123, 1990.Crossref | PubMed | Google Scholar2 Enns DL, Iqbal S, Tiidus PM. Oestrogen receptors mediate oestrogen-induced increases in post-exercise rat skeletal muscle satellite cells. Acta Physiol 194: 81–93, 2008.Crossref | PubMed | ISI | Google Scholar3 Enns DL, Tiidus PM. Time course of skeletal muscle satellite cell response following eccentric exercise. Appl Physiol Nutr Metabol 31: S23, 2006.Google Scholar4 Kasperek GJ, Snider RD. The susceptibility to exercise-induced muscle damage increases as rats grow larger. Experientia 41: 616–617, 1985.Crossref | Google Scholar5 Pizza F, Clark BC, DeMeersman RE, Phillips SM, Stupka N, Sipila S, Kovanen V, Suominen H, Warren GL, Lowe DA, Miles MP, Sorichter S, Walterspacher S, Sayers S, Savage KJ. Comments on Point:Counterpoint: Estrogen and sex do/do not influence post-exercise indexes of muscle damage, inflammation, and repair. J Appl Physiol; doi:10.1152/japplphysiol.00004.2009.Link | ISI | Google Scholar6 Tiidus PM, Holden D, Bombardier E, Zajchowski S, Enns D, Belcastro A. Estrogen effect on post-exercise skeletal muscle neutrophil infiltration and calpain activity. Can J Physiol Pharmacol 79: 400–406, 2001.Crossref | PubMed | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation Cited ByThe Effect of Gender and Menstrual Phase on Serum Creatine Kinase Activity and Muscle Soreness Following Downhill Running23 February 2017 | Antioxidants, Vol. 6, No. 1Sex Differences in Exercise-Induced Muscle Pain and Muscle DamageThe Journal of Pain, Vol. 13, No. 12Increased fat deposition in injured skeletal muscle is regulated by sex-specific hormonesMatthew J. McHale, Zaheer U. Sarwar, Damon P. Cardenas, Laurel Porter, Anna S. Salinas, Joel E. Michalek, Linda M. McManus, and Paula K. Shireman1 February 2012 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 302, No. 3 More from this issue > Volume 106Issue 3March 2009Pages 1021-1021 Copyright & PermissionsCopyright © 2009 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00013.2009History Published online 1 March 2009 Published in print 1 March 2009 Metrics

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