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To the Editor:
OF RODENTS & (WO)MEN
General viewpoint
Of Rodents and Humans
To the Editor
To the Editor
To the editor
Estrogen and Sex Do Not Influence Primary Muscle Damage and Do Influence Secondary Muscle Damage
Hormonal irritations?
Gender differences do exist in high responders to eccentric exercise
A Matter of Model
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Francis X Pizza, Professor University of Toledo
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francis.pizza{at}utoledo.edu Francis X Pizza
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Interpretations on the effect of estrogen/sex should be based on direct measures of muscle injury and subsequent repair/regeneration (i.e., improvements in muscle structure and function after injurious exercise). The inclusion of indices of the inflammatory response (e.g., accumulation of neutrophils and/or macrophages) and inflammation (e.g., edema) into the discussion seems to make interpretations ambiguous (2,6). We reported that neutrophils and/or macrophages can accumulate in rodent skeletal muscle in the absence of histological and functional signs of injury after either passive stretching, isometric contractions, or concentric contractions (4,5). These findings support our belief that neutrophil and/or macrophage accumulation in skeletal muscle after exercise should not be used as markers of muscle injury nor repair/regeneration. As mentioned by Tiidus and Enns (6), neutrophils may exacerbate contraction- induced injury; whereas, macrophages appear to aid muscle repair/regeneration. Recent evidence in rodents however, indicates that neutrophils and/or macrophages also contribute to skeletal muscle hypertrophy (1,3). Thus, neutrophil and/or macrophage accumulation in skeletal muscle is not contingent on the presence of an injury nor does their function in skeletal muscle after exercise appear to be restricted to events that follow an injury. Commonly used measures of edema (e.g., arm circumference, arm volume, and gapping between myofibers) tend to show a high degree of inter-subject variability, have a low degree of sensitivity, and have a poor temporal resolution to histological and functional signs of injury and thus, they have limited value when interpreting the influence of estrogen/sex on muscle injury and repair/regeneration. References 1. DiPasquale DM, Cheng M, Billich W, Huang SA, van Rooijen N, Hornberger TA, and Koh TJ. Urokinase-type plasminogen activator and macrophages are required for skeletal muscle hypertrophy in mice. Am J Physiol Cell Physiol 293: C1278-1285, 2007. 2. Hubal MJ & Clarkson PM. Estrogen and sex do not influence post-exercise indices of muscle damage, inflammation and repair. J Appl Physiol, in press 2009. 3. Marino, JS, Tausch BJ, Dearth CL, Manacci MV, McLoughlin TJ, Rakyta SJ, Linsenmayer MP, Pizza FX. 2 integrins contribute to skeletal muscle hypertrophy in mice. Am J Physiol Cell Physiol 295: C1026 -C1036, 2008 4. McLoughlin, TJ., Mylona E, Hornberger TA, Esser KA, Pizza FX. Inflammatory cells in rat skeletal muscle are elevated after electrically stimulated concentric contractions. J Appl Physiol 94: 876-882, 2003. 5. Pizza, FX, Koh TJ, McGregor SJ, and Brooks SV. Muscle inflammatory cells following passive stretches, isometric contractions, and lengthening contractions. J Appl Physiol 92: 1873-1878, 2002. 6. Tiidus PM & Enns DL. Estrogen and sex do influence post- exercise indices of muscle damage, inflammation and repair. J Appl Physiol, in press 2009. |
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Brian C. Clark, Assistant Professor Ohio University
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clarkb2{at}ohio.edu Brian C. Clark
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Tiidus and Enns make a compelling argument that estrogen attenuates exercise-induced muscle damage (EIMD) (1), while Hubal and Clarkson present data suggesting that sex does not influence EIMD (2). In fact, everyone seems to agree that animal experiments indicate estrogen minimizes EIMD, but that human studies do not reliably demonstrate differences in EIMD between men and women. What neither of the commentaries fully address, as indicated by the series title inextricably linking 'estrogen and sex', is why there is a discrepancy between the effect of estrogen observed in animals and the lack of differences between the sexes in human experiments. In integrating both of these arguments, it seems an understated interpretation is that there are other influential biological, psychological and social factors that exert a larger magnitude of effect on the EIMD response than sex-based differences in estrogen alone. It is hard to argue with Tiidus and Enns assertion as they present strong experimental evidence that estrogen administration diminishes beta- glucuronidase activity post-exercise (3, 4). In examining their data, it appears that estrogen exerts a large effect on attenuating EIMD in type I muscle (eta-squared ~0.50 [calculated from their reported means/SD]) (3,4), but that it may have a more attenuated effect on type II muscle (eta-squared ~0.07) (3). Accordingly, because human myofiber type is heterogeneous (5), it is probable that the magnitude of the estrogen- mediated effect is insufficient to result in more global 'sex differences' in EIMD particularly when one considers the numerous other factors regulating the EIMD response. References 1. Tiidus PM & Enns DL. Estrogen and sex do influence post- exercise indices of muscle damage, inflammation and repair. J Appl Physiol, in press 2009. 2. Hubal MJ & Clarkson PM. Estrogen and sex do not influence post-exercise indices of muscle damage, inflammation and repair. J Appl Physiol, in press 2009. 3. Enns DL & Tiidus PM. Estrogen influences satellite cell activation and proliferation following downhill running in rats. J Appl Physiol 104: 347-353, 2008. 4. Enns DL, Iqbal S & Tiidus PM. Oestrogen receptors mediate oestrogen-induced increases in post-exercise rat skeletal muscle satellite cells. Acta Physiologica 194: 81-93, 2008. 5. Staron RS, Hagerman FC, Hikida RS, Murray TF, Hostler DP, Cril MT, Ragg KE & Toma K. Fiber type composition of the vastus lateralis muscle of young men and women. J Histochem Cytochem 48: 623-629, 2000. |
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Ronald E. De Meersman, Professor Teachers College, Columbia University, Departments of Biobehavioral Sciences and Rehabilitation Med.
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red13{at}columbia.edu Ronald E. De Meersman
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General Viewpoint: Ronald E. De Meersman, Ph.D. Professor, Teachers College, Columbia University, NYC, NY 10025. Upon reviewing the two posted studies and others by these and other authors (1-3) I am struck by the failure of these studies to correct for plasma volume shifts for the blood chemistry parameters. Prior work with resistance training has clearly shown substantial plasma volume changes (PV) in the order of 13.3%, 14.3% and 10.1% respectively (4-6). Failure to correct for these fluids shifts while indicating an awareness of these shifts, referred to in the posted papers as swelling of the tissues, makes data interpretation spurious and debates superfluous. References: 1. Nosaka K, Clarkson PM. Muscle damage following repeated bouts of high force eccentric exercise. Med Sci Sports Exerc. 1995 Sep;27(9):1263-9. 2. Nosaka K, Clarkson PM. Changes in indicators of inflammation after eccentric exercise of the elbow flexors. Med Sci Sports Exerc. 1996 Aug;28(8):953-61 3. Smith, L., A. Anwar, M. Fragen, C. Rananto, R. Johnson, D. Holbert. Cytokines and cell adhesion molecules associated with high-intensity eccentric exercise. European Journal of Applied Physiology, Volume 82, Numbers 1-2 (May 2000), pp. 61-67, 4. Kraemer RR, Kilgore JL, Kraemer GR. Plasma volume changes in response to resistive exercise. J Sports Med Phys Fitness. 1993 Sep;33(3):246-51. 5. Collins MA, Hill DW, Cureton KJ, DeMello JJ. Plasma volume change during heavy-resistance weight lifting. Eur J Appl Physiol Occup Physiol. 1986;55(1):44-8. 6. Ahmadizad S, El-Sayed MS The acute effects of resistance exercise on the main determinants of blood rheology. J Sports Sci. 2005 Mar;23(3):243-9. |
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Stuart M Phillips, Professor McMaster University
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phillis{at}mcmaster.ca Stuart M Phillips
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Reading the point-counterpoint exchange of Tiidus and Enns vs. Hubal and Clarkson (5) is reminiscent of the title of John Steinbecks 1937 novella Of Mice and Men; however, an appropriate renaming to this exchange should perhaps be Of Rodents and Humans? Much of the work cited by Tiidus and Enns as evidence in favour of estrogen as a protective agent against lengthening contraction-induced muscle damage comes from rodents (4, 6). Clarkson and Hubal argue that when this estrogenic protection is tested in humans the results are far more equivocal (2, 3). There are a number of other instances in physiological research where animal and human data do not line up so is this simply a case where rodents and humans are different? Tiidus and Enns argue that a valid approach would be study women during the menopause since the withdrawl of estrogen during that time would provide a model of estrogen withdrawl in humans (5). However, hormonal changes during the menopause are gradual, often take years, and involve hormones other than estrogen. It might be more valid to study women who had surgical ovariectomy pre- and post-surgery? Alternatively, women on hormone replacement therapy post-menopause would also be of interest to study compared to those that are not. In addition, there is at least one report of oral contraceptive use influencing creatine kinase release (1). An intriguing possibility would also be to assess males who are receiving a sex-change, a procedure that involves extensive and often high dose estrogen therapy. Reference List 1. Carter A, Dobridge J and Hackney AC. Influence of estrogen on markers of muscle tissue damage following eccentric exercise. Fiziol Cheloveka 27: 133-137, 2001. 2. Clarkson PM and Hubal MJ. Are women less susceptible to exercise- induced muscle damage? Curr Opin Clin Nutr Metab Care 4: 527-531, 2001. 3. Sewright KA, Hubal MJ, Kearns A, Holbrook MT and Clarkson PM. Sex differences in response to maximal eccentric exercise. Med Sci Sports Exerc 40: 242-251, 2008. 4. Tiidus PM. Oestrogen and sex influence on muscle damage and inflammation: evidence from animal models. Curr Opin Clin Nutr Metab Care 4: 509-513, 2001. 5. Tiidus PM, Enns DL, Hubal MJ and Clarkson PM. Point: Counterpoint: Estrogen and sex do / do not influence post-exercise indices of muscle damage, inflammation and repair. J Appl Physiol 2008. 6. Tiidus PM, Holden D, Bombardier E, Zajchowski S, Enns D and Belcastro A. Estrogen effect on post-exercise skeletal muscle neutrophil infiltration and calpain activity. Can J Physiol Pharmacol 79: 400-406, 2001. |
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Nicole Stupka, NHMRC Postdoctoral Research Fellow Deakin University, Victoria, Australia
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nstupka{at}deakin.edu.au Nicole Stupka
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Muscle weakness following menopause (3) and the deleterious effects of ovariectomy on strength (2) and muscle mass recovery following unloading (4) in rodents, as well as the positive effects of estrogen supplementation, provide compelling support for its role in muscle health and function. If estrogen and gender do influence muscle damage, inflammation and repair, then this has implications for training adaptations in women and maintaining muscle mass and strength post- menopause. Whilst increased estrogen levels may be associated with lower serum CK activity post exercise, this not a consistent finding (1) and CK is a poor marker of muscle damage. Function is a better indicator of damage, which should be assessed routinely post exercise and during recovery. Unlike CK, most human studies report no gender differences in force deficit and recovery following strenous exercise (1), which fits well with our observation that post eccentric leg exercise the extent of Z -disk streaming was similar in young, healthy males and females (5). Furthermore, in ovariectomised mice estrogen supplementation did not protect EDL muscles from eccentric contraction-induced injury in vitro (2). Estrogen may not protect muscle from injury per se, but it may regulate the repair process by modulating the inflammatory response, satellite cell dynamics or muscle protein synthesis (4; 6). To assess this, careful time course studies are needed, as it is difficult to draw conclusions about the effects of estrogen on dynamic processes such as inflammation and satellite cell activation, proliferation and/or differentiation based on a single time point. 1. Hubal MJ and Clarkson PM. Counterpoint: Estrogen and sex do not significantly influence post-exercise indices of muscle damage, inflammation and repair. J Appl Physiol In press: 2008. 2. Moran AL, Nelson SA, Landish RM, Warren GL and Lowe DA. Estradiol replacement reverses ovariectomy-induced muscle contractile and myosin dysfunction in mature female mice. J Appl Physiol 102: 1387-1393, 2007. 3. Phillips SK, Rook KM, Siddle NC, Bruce SA and Woledge RC. Muscle weakness in women occurs at an earlier age than in men, but strength is preserved by hormone replacement therapy. Clin Sci 84: 95-98, 1993. 4. Sitnick M, Foley AM, Brown M and Spangenburg EE. Ovariectomy prevents the recovery of atrophied gastrocnemius skeletal muscle mass. J Appl Physiol 100: 286-293, 2006. 5. Stupka N, Yardley N, Tarnopolsky MA and Phillips SM. Cellular adaptation to repeated eccentric exercise-induced muscle damage. J Appl Physiol 91: 1669-1678, 2001. 6. Tiidus PM and Enns DL. Point: Estrogen and sex do influence post- exercise indices of muscle damage, inflammation and repair. J Appl Physiol In press: 2008. |
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Sarianna Sipila, Research director Department of Health Sciences, University of Jyvaskyla, Finland, Vuokko Kovanen, Harri Suominen
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sarianna.sipila{at}jyu.fi Sarianna Sipila, et al.
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Current literature on the influence of estrogens on human skeletal muscle shows conflicting results as also shown by the discussion regarding the influence of sex and estrogen on post-exercise muscle damage, inflammation and repair (1, 2). The discrepancies between the results of different studies are at least partly explained by different study designs and indirect measures used. Studies comparing men and women are confounded by a number of gender related parameters and those comparing pre- and postmenopausal women by the aging associated wide ranging effects on the whole neuromuscular system, endocrinology and immunology in general (3, 4).When investigating the role of estrogens on skeletal muscle in humans, comparisons should be made between groups of people with same sex and mean age but with notable and consistent difference in circulating estrogen levels. This can be achieved, e.g., by comparing postmenopausal women on estrogen replacement therapy (ERT) with those without therapy or by randomized controlled trials including ERT as a treatment. Experimental animal studies enable the use of sophisticated study designs (5) and representative muscle specific biological markers (6). These studies show that indicators of post-exercise muscle damage and repair are affected by estrogen in either estrogen receptor dependent (satelite cell activation) or non-dependent manner (β-glucuronidase activity, number of leucocytes) (5). In conclusion, we believe that estrogens have influence on skeletal muscle damage, inflammation and regeneration/repair after exercise. More studies of good quality are, however, needed to demonstrate the significance of the adaptive/protective effect of estrogens in muscles among women. 1. Tiidus P. & Enns D. Estrogen and sex do influence post- exercise indices of muscle damage, inflammation and repair. J Appl Physiol; doi:10.1152/japplphysiol.90848.2008 2. Hubal MJ & Clarkson PM. Estrogen and sex do not influence post -exercise indices of muscle damage, inflammation and repair. J Appl Physiol; doi:10.1152/japplphysiol.90848.2008 3. Ryall JG, Schertzer JD, Lynch GS. Cellular and molecular mechanisms underlying age-related skeletal muscle wasting and weakness. Biogerontology. 2008 9:213-28. Epub 2008 Feb 26. 4. Lamberts SW, van den Beld AW, van der Lely AJ. The endocrinology of aging. Science. 1997;278:419-24. 5. Enns DL, Iqbal S, Tiidus PM. Oestrogen receptors mediate oestrogen -induced increases in post-exercise rat skeletal muscle satellite cells. Acta Physiol (Oxf). 2008;194:81-93. 6. Salminen A, Kihlstrm M. Lysosomal changes in mouse skeletal muscle during the repair of exercise injuries. Muscle Nerve. 1985;8(4):269 -79. |
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Gordon L. Warren, Professor Georgia State University, Dawn A. Lowe, Assistant Professor, University of Minnesota
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gwarren{at}gsu.edu Gordon L. Warren, et al.
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We contend that estrogen has not been consistently demonstrated to provide protection against muscle injury (1, 5). The evidence for a protective effect is mostly based on use of the rodent downhill running model and blood levels of creatine kinase (CK). There are problems with both. First, injury following downhill running is greater in larger rats (3) and estrogen deficiency causes weight gain in rodents. Also, estrogen markedly influences physical activity of rodents (4) and it is known that exercise provides protection against contraction-induced injury. Thus, observations that estrogen-deficient rodents exhibit greater injury susceptibility may be due to greater body weight and/or reduced activity rather than loss of a direct protective effect of estrogen on muscle. Second, the use of blood CK as a marker of injury is problematic because it is influenced by the rate of CK release into the bloodstream as well as the rate of CK removal. Though many believe the former process to dictate blood CK level, alterations in the latter process are important (e.g., 2). Also, autoantibodies against CK can enhance CK removal from the bloodstream (6). The CK autoantibody level in women is almost double that in men, which could account for enhanced CK clearance in females (6). Finally, because muscles function is to produce force, we assert that contractile function should be the standard by which estrogen effects are judged. There is little evidence that estrogen protects muscle from losing force-generating capacity or that estrogenic influences on inflammation translate to changes in function. References 1. Hubal MJ and Clarkson PM. Estrogen and sex do not influence post- exercise indices of muscle damage, inflammation and repair. J Appl Physiol, in press 2009. 2. Hyatt JP and Clarkson PM. Creatine kinase release and clearance using MM variants following repeated bouts of eccentric exercise. Med Sci Sports Exerc 30: 1059-1065, 1998. 3. Kasperek GJ and Snider RD. The susceptibility to exercise-induced muscle damage increases as rats grow larger. Experientia 41: 616-617, 1985. 4. Lightfoot JT. Sex hormones' regulation of rodent physical activity: a review. Int J Biol Sci 4: 126-132, 2008. 5. Tiidus PM and Enns DL. Estrogen and sex do influence post-exercise indices of muscle damage, inflammation and repair. in press 2009. 6. Warren GL, O'Farrell L, Rogers KR, Billings KM, Sayers SP, and Clarkson PM. CK-MM autoantibodies: prevalence, immune complexes, and effect on CK clearance. Muscle Nerve 34: 335-346, 2006. |
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Mary P Miles, Associate Professor Montana State University
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mmiles{at}montana.edu Mary P Miles
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Evidence presented in the Point: Counterpoint argument regarding the influence of sex and estrogen on muscle damage, inflammation and repair (2, 5) suggests that sex and estrogen do not influence primary muscle damage and do influence secondary muscle damage. According to Faulkner et al., primary damage consists of focal disruptions to sarcomere architecture caused by mechanical forces, and secondary muscle damage consists of damage extension in preparation for repair caused by inflammatory processes (1). Hubal and Clarkson present evidence that there is no difference between men and women in damage to muscle ultrastructure and loss of muscle function. Recovery of muscle function, e.g. strength, begins before the secondary damage caused by inflammation occurs (1), is not associated with inflammation measures after eccentric exercise (3), and appears to be independent of sex and estrogen exposure (2). Tiidus and Enns provide evidence that plasma membrane stability and muscle regeneration after damage are improved, while inflammation and oxidative damage are attenuated by sex and estrogen exposure (5). These differences are consistent with the attenuation of inflammation and secondary muscle damage by sex and estrogen exposure. Estrogen exposure also decreases enzyme efflux in various muscle damage models in the rat (5). In humans, the influence of sex or estrogen exposure on enzyme efflux and pain or soreness after eccentric exercise is more difficult to measure, perhaps because these measures are influenced by additional factors, such as previous exposure to high mechanical forces in muscle (4). 1. Faulkner JA, Brooks SV, and Opiteck JA. Injury to skeletal muscle fibers during contractions: conditions of occurrence and prevention. Phys Ther 73: 911-921, 1993. 2. Hubal MJ and Clarkson PM. Point: Counterpoint: Estrogen and sex do not influence post-exercise indices of muscle damage, inflammation and repair. J Appl Physiol, 2008. 3. Miles MP, Andring JM, Pearson SD, Gordon LK, Kasper C, Depner CM, and Kidd JR. Diurnal variation, response to eccentric exercise, and association of inflammatory mediators with muscle damage variables. J Appl Physiol 104: 451-458, 2008. 4. Nosaka K and Clarkson PM. Muscle damage following repeated bouts of high force eccentric exercise. Med Sci Sports Exerc 27: 1263-1269, 1995. 5. Tiidus PM and Enns DL. Point: Counterpoint: Estrogen and sex do influence post-exercise indices of muscle damage, inflammation and repair. J Appl Physiol, 2009. |
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Stephan Sorichter, Prof. Dept. of Pneumology, University Hospital of Freiburg, Germany, Stephan Walterspacher
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stephan.sorichter{at}uniklinik-freiburg.de Stephan Sorichter, et al.
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Epidemiological data provide evidence that premenopausal females are protected from various diseases, i.e. high arterial blood pressure (1) or sleep apnea (6). This may also suspect a positive effect of sex on the human muscles regarding injury or damage. Tidius and Enns provide fascinating data on this note in animal studies; however, so far, these findings could not be clearly attributed to human studies as described by Hubal and Clarkson. All authors discussed the diverse findings of sex differences in CK levels. However, there are several observations on the variability of CK activity after comparable, histologically quantified exercise-induced muscle damage in humans (2) and animals (3), which preclude a simple interpretation of increased CK activity, especially with regard to the magnitude of injury. These limitations could be reduced by using more specific parameters for future studies, such as skeletal Troponin I (5). A study by our group did so far not provide any difference in muscle injury between males and females after downhill running (4). Appreciating the findings of Tidius et al of estrogen effects on muscle membrane stability and fiber regeneration, a provocative assumption may be postulated: The lacking difference of indicators of muscle injury in men and women might be attributed to recurrent hormonal effects, equalizing differences between both sexes which might become apparent in the absence of estrogen in women. However, the modifiable factors such as pre- and post-exercise levels or nutrition may outweigh the single effect of estrogen on the muscle cell in humans. Literature: 1 Anonymous. (2008). The Framingham study. http://www.framinghamheartstudy.org/ (last access: 21.12.2008) 2 Fielding, RA, Manfredi, TJ, Ding, W, Fiatarone, MA, Evans, WJ, Cannon, JG. Acute phase response in exercise. III. Neutrophil and IL-1 beta accumulation in skeletal muscle. Am J Physiol 1 Pt 2: R166-72, 1993. 3 Komulainen, J, Takala, TE, Vihko, V. Does increased serum creatine kinase activity reflect exercise-induced muscle damage in rats? Int J Sports Med 3: 150-4, 1995. 4 Sorichter, S, Mair, J, Koller, A, Calzolari, C, Huonker, M, Pau, B, Puschendorf, B. Release of muscle proteins after downhill running in male and female subjects. Scand J Med Sci Sports 1: 28-32, 2001. 5 Sorichter, S, Mair, J, Koller, A, Gebert, W, Rama, D, Calzolari, C, Artner-Dworzak, E, Puschendorf, B. Skeletal troponin I as a marker of exercise-induced muscle damage. J Appl Physiol 4: 1076-82, 1997. 6 Stradling, JR, Davies, RJO. Sleep. 1: Obstructive sleep apnoea/hypopnoea syndrome: definitions, epidemiology, and natural history. Thorax 1: 73-8, 2004. |
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Stephen P. Sayers, Assistant Professor Department of Physical Therapy, University of Missouri
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sayerss{at}missouri.edu Stephen P. Sayers
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Tiidus & Enns (6) and Hubal & Clarkson (2) present an intriguing point/counterpoint regarding the effect of estrogen on post- exercise muscle damage in animals and humans, respectively. The argument against gender differences in muscle damage after eccentric exercise (2), however, is confounded by differences reported among men and women who exhibit extreme responses to eccentric exercise (1). In our first report on this topic, we detailed 6 high responders who exhibited combinations of prolonged strength loss, profound swelling, elevated creatine kinase activity, and extreme soreness after eccentric exercise, all of whom were men (5). In a second report on prolonged strength loss after eccentric exercise (3), we found that although a greater number of women had large strength losses immediately post-exercise, they demonstrated a faster recovery compared to men possibly from an estrogen-related attenuation of secondary damage from inflammation. Moreover, the most prolonged strength losses reported in this study (47, 61 and 89 days) were observed in men (3). In a final study on profound swelling after eccentric exercise, 3 of 4 high responders described were men (4). Raw data from these published studies indicate a 3% incidence of prolonged strength loss and/or profound swelling in men (6 of 204 [5]; 5 of 153 [4]) and less than a 1% incidence in women (1 of 153 [4]). Although difficult to study because of the sample sizes required, future research could examine older men and post- menopausal women high responders to determine whether gender differences persist in the absence of estrogen. References 1. Clarkson PM and Sayers SP. Intersubject variability in developing exertional muscle damage. In: Muscle Damage and Repair, edited by Tiidus, PM. Champaign, IL: Human Kinetics, 2008, p. 185-191. 2. Hubal MJ and Clarkson PM. Estrogen and sex do not influence post- exercise indices of muscle damage, inflammation and repair. J Appl Physiol, in press 2009. 3. Sayers SP and Clarkson PM. Force recovery after eccentric exercise. Eur J Appl Physiol 84: 122-126, 2001. 4. Sayers SP and Clarkson PM. Metabolic response to light exercise after exercise-induced rhabdomyolysis. Eur J Appl Physiol 86: 280-282, 2002. 5. Sayers SP, Clarkson PM, Rouzier PA, and Kamen G. Adverse events associated with eccentric exercise protocols. Med Sci Sports Exerc 31: 1697-1702, 1999. 6. Tiidus PM and Enns DL. Estrogen and sex do influence post-exercise indices of muscle damage, inflammation and repair. J Appl Physiol, in press 2009. |
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Kathleen J Savage, Post-doctoral Fellow NIDDK/NIH
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savagek{at}niddk.nih.gov Kathleen J Savage
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To the Editor: Based on the plethora of studies cited in the Point: Counterpoint of estrogen/genders influence on muscle damage and repair, one would have to agree that the evidence supports that estrogen and/or sex have an effect in rodents but not in humans in this regard (1,3). The use of rodent models has several advantages over studies on humans, least of which are controlling potential confounding effects and subject variability. Controlling variability factors in human studies is admittedly difficult but ideally could be controlled by using a with-in subjects design. For example, Tiidus and Enns' suggestion of comparing pre- versus post-menopausal women may be better controlled by using a with -in subjects design. This would mean studying middle-aged women before they start menopause and again soon after menopause, about 10 years later, an age similar to those used by Sipila et al.(2). Clearly results from rodent studies and human studies seem to lead to very different conclusions regarding estrogen and sexs influences on exercise and muscle damage. Although rodent studies are generally a useful model for human disease and conditions and have been used as such for human muscle damage and recovery, if the results are not in line with studies in humans the utility of such a model is circumspect. The real question therefore shouldnt be why estrogens positive effects are not seen in human studies; but rather, is there a better experimental model for estrogen/sex influence on EIMD and recovery in humans? 1. Hubal MJ, and Clarkson PM. Estrogen and sex do not influence post-exercise indices of muscle damage, inflammation and repair. J Appl Physiol, in press 2009. 2. Sipila S, Taaffe DR, Cheng S, Puolakka J, Toivanen J, and Suominen H. Effects of hormone replacement therapy and high-impact physical exercise on skeletal muscle in post-menopausal women: a randomized placebo-controlled study. Clin Sci (Lond) 101: 147-157, 2001. 3. Tiidus PM, and Enns DL. Estrogen and sex do influence post- exercise indices of muscle damage, inflammation and repair. J Appl Physiol, in press 2009. |
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