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.
- Analytical Chemistry - ANAL CHEM. 04/2002; 35(12).
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ABSTRACT: Exercise for which a skeletal muscle is not adequately conditioned results in focal sites of injury distributed within and among the fibres. Exercise with eccentric contractions is particularly damaging. The injury process can be hypothesised to occur in several stages. First, an initial phase serves to inaugurate the sequence. Hypotheses for the initial event can be categorised as either physical or metabolic in nature. We argue that the initial event is physical, that stresses imposed on sarcolemma by sarcomere length inhomogeneities occurring during eccentric contractions cause disruption of the normal permeability barrier provided by the cell membrane and basal lamina. This structural disturbance allows Ca++ to enter the fibre down its electrochemical gradient, precipitating the Ca++ overload phase. If the breaks in the sarcolemma are relatively minor, the entering Ca++ may be adequately handled by ATPase pumps that sequester and extrude Ca++ from the cytoplasm ('reversible' injury). However, if the Ca++ influx overwhelms the Ca++ pumps and free cytosolic Ca++ concentration rises, the injury becomes 'irreversible'. Elevations in intracellular Ca++ levels activate a number of Ca(++)-dependent proteolytic and phospholipolytic pathways that are indigenous to the muscle fibres, which respectively degrade structural and contractile proteins and membrane phospholipids; for instance, it has been demonstrated that elevation of intracellular Ca++ levels with Ca++ ionophores results in loss of creatine kinase activity from the fibres through activation of phospholipase A2 and subsequent production of leukotrienes. This autogenetic phase occurs prior to arrival of phagocytic cells, and continues during the inflammatory period when macrophages and other phagocytic cells are active at the damage site. The phagocytic phase is in evidence by 2 to 6 hours after the injury, and proceeds for several days. The regenerative phase then restores the muscle fibre to its normal condition. Repair of the muscle fibres appears to be complete; the fibres adapt during this process so that future bouts of exercise of similar type, intensity, and duration cause less injury to the muscle.Sports Medicine 10/1991; 12(3):184-207. · 5.24 Impact Factor
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ABSTRACT: Protein leakage from type I skeletal muscle cells and collagen synthesizing cells were studied during a 24-h cross-country skiing relay in eight men using serum carbonic anhydrase III (S-CA III) and serum galactosylhydroxylysyl glucosyltransferase (S-GGT) as the respective specific marker proteins. Serum aminoterminal propeptide of type III procollagen (S-Pro(III)-N-P) was used as an indicator of type III collagen synthesis and serum creatine kinase (S-CK) as a nonspecific muscular marker. S-CK, S-CA III, and S-GGT were increased immediately following the skiing relay by 870%, 640%, and 40%, respectively. No significant change was observed in the concentration of S-Pro(III)-N-P following the exercise. A high positive correlation (rs = 0.92, P less than 0.01) was found between the increase in S-CA III and S-CK, whereas no correlation was observed between these muscular markers and S-GGT. The results suggest leakage from type I skeletal muscle cells and collagen synthesizing cells as a consequence of prolonged cross-country skiing, but there seems to exist no dependence between acute responses in muscular and connective tissue cells to exercise.Medicine & Science in Sports & Exercise 11/1989; 21(5):593-7. · 4.48 Impact Factor