Indirect evidence of human skeletal muscle damage and collagen breakdown after eccentric muscle actions
ABSTRACT This metadata relates to an electronic version of an article published in Journal of sports sciences, 1999, vol. 17, no. 5, pp. 397-402. Journal of sports sciences is available online at informaworldTM at http://www.informaworld.com/smpp/content~db=all~content=a713776150?words=indirect|evidence&hash=2313990694 Indirect markers of muscle damage and collagen breakdown were recorded for up to 9 days after a bout of concentric, followed by a bout of eccentric, muscle actions. Nine untrained participants performed two bouts of 50 maximum effort repetitions on an isokinetic dynamometer (angular velocity 1.05 rad.s-1, range of motion 1.75 rad). An initial concentric bout of muscle actions was followed by an eccentric bout 21 days later, using the same knee extensors. Concentric actions induced no changes in maximum voluntary isometric contraction force (MVC),nor induced any changes in the serum enzyme activities of creatine kinase, a lactate dehydrogenase isoenzyme (LDH-1), or alkaline phosphatase. Similarly, concentric actions induced no change in markers of collagen breakdown,namely plasma hydroxyproline and serum type 1 collagen concentration.In contrast,eccentric actions induced a 23.5 +/- 19.0% (mean +/- s) decrease in MVC immediately post-exercise (P< 0.05), and increased the serum enzyme activities of creatine kinase and LDH-1 to 486 +/- 792 and 90 +/- 11 IU.l-1 respectively on day 3 post-exercise, and to 189 +/- 159 and 96 +/- 13 IU.l-1 respectively on day 7 post-exercise (all P < 0.05). Eccentric actions induced no significant changes in plasma hydroxyproline, but increased collagen concentration on days 1 and 9 post-exercise (48.6% and 44.3% increases above pre-exercise on days 1 and 9 respectively; both P < 0.05). We conclude that eccentric but not concentric actions may result in temporary muscle damage, and that collagen breakdown may also be affected by eccentric actions. With caution, indices of collagen breakdown may be used to identify exercise-induced damage to connective tissue.
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ABSTRACT: Introduction Tendons are metabolically active structures, and their biochemical, biomechanical and structural properties adapt to chronic exercise. However, abnormal adaptations may lead to the development of tendinopathy and pain. Acute and subacute adaptations might contribute to tendon pathology. Sources of data A systematic search of peer-reviewed articles was performed using a wide range of electronic databases. A total of 61 publications were selected. Areas of agreement Exercise induces acute responses in collagen turnover, blood flow, glucose, lactate and other inflammatory products (e.g. prostaglandins and interleukins). Mechanical properties are influenced by activity duration and intensity. Acute bouts of exercise affect tendon structure, with some of the changes resembling those reported in pathological tendons. Areas of controversy Given the variation in study designs, measured parameters and outcomes, it remains debatable how acute exercise influences overall tendon properties. There is discrepancy regarding which investigation modality and settings provide optimal assessment of each parameter. Growing points There is a need for greater homogeneity between study designs, including subject consortium and age, exercise protocols and time frames for parameter assessing. Areas timely for developing research Innovative methods, measuring each parameter simultaneously, would allow a greater understanding of how and when changes occur. This methodology is key to revealing pathological processes and pathways that alter tendon properties according to various activities. Optimal tendon properties differ between activities: more compliant tendons are beneficial for slow stretch shortening cycle (SSC) activities such as countermovement jumps, whereas stiffer tendons are considered beneficial for fast SSC movements such as sprinting.British Medical Bulletin 01/2012; 103:169-202. · 4.36 Impact Factor
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ABSTRACT: Rugby league is a team sport in which players engage in repeated high-intensity exercise involving frequent collisions. Recent research, much of which has involved global positioning system (GPS) technology, has provided coaches and sport scientists with a deeper understanding of match demands, particularly at the elite level. This has allowed for the development of training programmes that prepare players for the most intense contact and running demands likely to be experienced in competition. At the elite level, rugby league players have well-developed aerobic and anaerobic endurance, muscular strength and power, reactive agility, and speed. Upper- and lower-body strength and aerobic power are associated with a broad range of technical and sport-specific skills, in addition to a lower risk of injury. Significant muscle damage (as estimated from creatine kinase concentrations) and fatigue occurs as a result of match-play; while muscle function and perceptual fatigue generally return to baseline 48 h following competition, increases in plasma concentrations of creatine kinase can last for up to 5 days post-match. Well-developed physical qualities may minimise post-match fatigue and facilitate recovery. Ultimately, the literature highlights that players require a broad range of physical and technical skills developed through specific training. This review evaluates the demands of the modern game, drawing on research that has used GPS technology. These findings highlight that preparing players based on the average demands of competition is likely to leave them underprepared for the most demanding passages of play. As such, coaches should incorporate drills that replicate the most intense repeated high-intensity demands of competition in order to prepare players for the worst-case scenarios expected during match-play.Sports medicine (Auckland, N.Z.). 04/2014;
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ABSTRACT: Exercise-induced muscle damage is an important topic in exercise physiology. However several aspects of our understanding of how muscles respond to highly stressful exercise remain unclear In the first section of this review we address the evidence that exercise can cause muscle damage and inflammation in otherwise healthy human skeletal muscles. We approach this concept by comparing changes in muscle function (i.e., the force-generating capacity) with the degree of leucocyte accumulation in muscle following exercise. In the second section, we explore the cytokine response to 'muscle-damaging exercise', primarily eccentric exercise. We review the evidence for the notion that the degree of muscle damage is related to the magnitude of the cytokine response. In the third and final section, we look at the satellite cell response to a single bout of eccentric exercise, as well as the role of the cyclooxygenase enzymes (COX1 and 2). In summary, we propose that muscle damage as evaluated by changes in muscle function is related to leucocyte accumulation in the exercised muscles. 'Extreme' exercise protocols, encompassing unaccustomed maximal eccentric exercise across a large range of motion, generally inflict severe muscle damage, inflammation and prolonged recovery (> 1 week). By contrast, exercise resembling regular athletic training (resistance exercise and downhill running) typically causes mild muscle damage (myofibrillar disruptions) and full recovery normally occurs within a few days. Large variation in individual responses to a given exercise should, however be expected. The link between cytokine and satellite cell responses and exercise-induced muscle damage is not so clear The systemic cytokine response may be linked more closely to the metabolic demands of exercise rather than muscle damage. With the exception of IL-6, the sources of systemic cytokines following exercise remain unclear The satellite cell response to severe muscle damage is related to regeneration, whereas the biological significance of satellite cell proliferation after mild damage or non-damaging exercise remains uncertain. The COX enzymes regulate satellite cell activity, as demonstrated in animal models; however the roles of the COX enzymes in human skeletal muscle need further investigation. We suggest using the term 'muscle damage' with care. Comparisons between studies and individuals must consider changes in and recovery of muscle force-generating capacity.Exercise immunology review 01/2012; 18:42-97. · 7.05 Impact Factor