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      The relationship of creatine kinase variability with body composition and muscle damage markers following eccentric muscle contractions

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          Abstract

          [Purpose]

          The purpose of the study was to investigate the relationship between CK variability and body composition and muscle damage markers following eccentric exercise.

          [Methods]

          Total 119 healthy male subjects were recruited to perform 50 eccentric contractions consisted of 2 sets of 25 contractions. Then, blood creatine kinase (CK) activity was analyzed to divide into three groups based on their CK activity levels. Maximum isometric strength (MIS), muscle soreness (SOR) and body composition data were obtained before and after exercise.

          [Results]

          The results showed that high CK responders had a significant decrease in MIS ( p<0.001) and greater SOR ( p<0.01) following eccentric exercise compared to low CK responders. Percent body fat was also higher in high responders compared to low responders ( p=0.014). Peak CK activity was significantly correlated with MIS and SOR but no correlation with % body fat, muscle mass, and body mass index.

          [Conclusion]

          CK variability following eccentric exercise is closely related to MIS and SOR and % body fat may be a potent factor for CK variability.

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          Delayed onset muscle soreness : treatment strategies and performance factors.

          Patria Hume, Jackie K. Cheung, Linda Maxwell (2002)
          Delayed onset muscle soreness (DOMS) is a familiar experience for the elite or novice athlete. Symptoms can range from muscle tenderness to severe debilitating pain. The mechanisms, treatment strategies, and impact on athletic performance remain uncertain, despite the high incidence of DOMS. DOMS is most prevalent at the beginning of the sporting season when athletes are returning to training following a period of reduced activity. DOMS is also common when athletes are first introduced to certain types of activities regardless of the time of year. Eccentric activities induce micro-injury at a greater frequency and severity than other types of muscle actions. The intensity and duration of exercise are also important factors in DOMS onset. Up to six hypothesised theories have been proposed for the mechanism of DOMS, namely: lactic acid, muscle spasm, connective tissue damage, muscle damage, inflammation and the enzyme efflux theories. However, an integration of two or more theories is likely to explain muscle soreness. DOMS can affect athletic performance by causing a reduction in joint range of motion, shock attenuation and peak torque. Alterations in muscle sequencing and recruitment patterns may also occur, causing unaccustomed stress to be placed on muscle ligaments and tendons. These compensatory mechanisms may increase the risk of further injury if a premature return to sport is attempted.A number of treatment strategies have been introduced to help alleviate the severity of DOMS and to restore the maximal function of the muscles as rapidly as possible. Nonsteroidal anti-inflammatory drugs have demonstrated dosage-dependent effects that may also be influenced by the time of administration. Similarly, massage has shown varying results that may be attributed to the time of massage application and the type of massage technique used. Cryotherapy, stretching, homeopathy, ultrasound and electrical current modalities have demonstrated no effect on the alleviation of muscle soreness or other DOMS symptoms. Exercise is the most effective means of alleviating pain during DOMS, however the analgesic effect is also temporary. Athletes who must train on a daily basis should be encouraged to reduce the intensity and duration of exercise for 1-2 days following intense DOMS-inducing exercise. Alternatively, exercises targeting less affected body parts should be encouraged in order to allow the most affected muscle groups to recover. Eccentric exercises or novel activities should be introduced progressively over a period of 1 or 2 weeks at the beginning of, or during, the sporting season in order to reduce the level of physical impairment and/or training disruption. There are still many unanswered questions relating to DOMS, and many potential areas for future research.
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            Muscle function after exercise-induced muscle damage and rapid adaptation.

            Gary B. Braun, John Clarkson, K Nosaka (1992)
            This brief review focuses on the time course of changes in muscle function and other correlates of muscle damage following maximal effort eccentric actions of the forearm flexor muscles. Data on 109 subjects are presented to describe an accurate time course of these changes and attempt to establish relationships among the measures. Peak soreness is experienced 2-3 d postexercise while peak swelling occurs 5 d postexercise. Maximal strength and the ability to fully flex the arm show the greatest decrements immediately after exercise with a linear restoration of these functions over the next 10 d. Blood creatine kinase (CK) levels increase precipitously at 2 d after exercise which is also the time when spontaneous muscle shortening is most pronounced. Whether the similarity in the time courses of some of these responses implies that they are caused by similar factors remains to be determined. Performance of one bout of eccentric exercise produces an adaptation such that the muscle is more resistant to damage from a subsequent bout of exercise. The length of the adaptation differs among the measures such that when the exercise regimens are separated by 6 wk, all measures show a reduction in response on the second, compared with the first, bout. After 10 wk, only CK and muscle shortening show a reduction in response. After 6 months only the CK response is reduced. A combination of cellular factors and neurological factors may be involved in the adaptation process.
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              Characterization of inflammatory responses to eccentric exercise in humans.

              Jonathan Peake, Katsuhiko Suzuki, Kazunori Nosaka (2004)
              Eccentric exercise commonly results in muscle damage. The primary sequence of events leading to exercise-induced muscle damage is believed to involve initial mechanical disruption of sarcomeres, followed by impaired excitation-contraction coupling and calcium signaling, and finally, activation of calcium-sensitive degradation pathways. Muscle damage is characterized by ultrastructural changes to muscle architecture, increased muscle proteins and enzymes in the bloodstream, loss of muscular strength and range of motion and muscle soreness. The inflammatory response to exercise-induced muscle damage is characterized by leukocyte infiltration and production of pro-inflammatory cytokines within damaged muscle tissue, systemic release of leukocytes and cytokines, in addition to alterations in leukocyte receptor expression and functional activity. Current evidence suggests that inflammatory responses to muscle damage are dependent on the type of eccentric exercise, previous eccentric loading (repeated bouts), age and gender. Circulating neutrophil counts and systemic cytokine responses are greater after eccentric exercise using a large muscle mass (e.g. downhill running, eccentric cycling) than after other types of eccentric exercise involving a smaller muscle mass. After an initial bout of eccentric exercise, circulating leukocyte counts and cell surface receptor expression are attenuated. Leukocyte and cytokine responses to eccentric exercise are impaired in elderly individuals, while cellular infiltration into skeletal muscle is greater in human females than males after eccentric exercise. Whether alterations in intracellular calcium homeostasis influence inflammatory responses to muscle damage is uncertain. Furthermore, the effects of antioxidant supplements are variable, and the limited data available indicates that anti-inflammatory drugs largely have no influence on inflammatory responses to eccentric exercise. In this review, we compare local versus systemic inflammatory responses, and discuss some of the possible mechanisms regulating the inflammatory responses to exercise-induced muscle damage in humans.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Exerc Nutrition Biochem
                Journal ID (iso-abbrev): J Exerc Nutrition Biochem
                Journal ID (publisher-id): JENB
                Title: Journal of Exercise Nutrition & Biochemistry
                Publisher: Korean Society for Exercise Nutrition
                ISSN (Print): 2233-6834
                ISSN (Electronic): 2233-6842
                Publication date (Print): June 2015
                Publication date (Electronic): 30 June 2015
                Volume: 19
                Issue: 2
                Pages: 123-129
                Affiliations
                College of Physical Education, Kookmin University, Seoul, Republic of Korea
                Author notes
                [* ] Corresponding author: Joohyung Lee, Tel. 82-2-910-4782, Email. jolee@ 123456kookmin.ac.kr
                Article
                Publisher ID: jenb-19-2-123
                DOI: 10.5717/jenb.2015.15061910
                PMC ID: 4523802
                PubMed ID: 26244131
                SO-VID: 39b621c5-cb09-459d-8e4d-6861b6247b49
                Copyright © ⓒ2015 The Korean Society for Exercise Nutrition
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 15 May 2015
                Date revision received : 8 June 2015
                Date accepted : 19 June 2015
                Categories
                Subject: Original Article

                Keywords: ck variability,muscle damage,muscle soreness
                Data availability:
                Keywords: ck variability, muscle damage, muscle soreness

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