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      Preconditioning by light-load eccentric exercise is equally effective as low-level laser therapy in attenuating exercise-induced muscle damage in collegiate men

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          Previous studies have already reported an independent effect of light-load eccentric exercise (10% eccentric exercise contraction [EEC]) and low-level laser therapy (LLLT) as a protective measure against more strenuous eccentric exercise. However, the difference between these two interventions is largely unknown. Therefore, the present study aimed to compare the preconditioning effect of 10% EEC vs. LLLT on subjective, physiological, and biochemical markers of muscle damage in elbow flexors in collegiate men.


          All 36 enrolled subjects were randomly assigned to either 10% EEC or LLLT group. Subjects in 10% EEC group performed 30 repetitions of an eccentric exercise with 10% maximal voluntary contraction strength 2 days prior to maximal eccentric exercise bout, whereas subjects in LLLT group were given LLLT. All the indirect markers of muscle damage were measured pre-exercise and at 24, 48, and 72 hours after the exercise-induced muscle damage protocol.


          The muscle soreness was reduced in both groups ( p = 0.024); however, soreness was attenuated more in LLLT group at 48 hours (33.5 vs. 42.7, p = 0.004). There was no significant difference between the effect of 10% EEC and LLLT groups on other markers of muscle damage like a maximum voluntary isometric contraction ( p = 0.47), range of motion ( p = 0.16), upper arm circumference ( p = 0.70), creatine kinase ( p = 0.42), and lactate dehydrogenase ( p = 0.08). Within-group analysis showed both interventions provided similar protection over time.


          This study indicated that light-load eccentric exercise confers similar protective effect against subsequent maximal eccentric exercise as LLLT. Both the treatments could be used reciprocally based on the patient preference, costs, and feasibility of the equipment.

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          Most cited references 33

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          Biphasic dose response in low level light therapy.

          The use of low levels of visible or near infrared light for reducing pain, inflammation and edema, promoting healing of wounds, deeper tissues and nerves, and preventing cell death and tissue damage has been known for over forty years since the invention of lasers. Despite many reports of positive findings from experiments conducted in vitro, in animal models and in randomized controlled clinical trials, LLLT remains controversial in mainstream medicine. The biochemical mechanisms underlying the positive effects are incompletely understood, and the complexity of rationally choosing amongst a large number of illumination parameters such as wavelength, fluence, power density, pulse structure and treatment timing has led to the publication of a number of negative studies as well as many positive ones. A biphasic dose response has been frequently observed where low levels of light have a much better effect on stimulating and repairing tissues than higher levels of light. The so-called Arndt-Schulz curve is frequently used to describe this biphasic dose response. This review will cover the molecular and cellular mechanisms in LLLT, and describe some of our recent results in vitro and in vivo that provide scientific explanations for this biphasic dose response.
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            Delayed onset muscle soreness : treatment strategies and performance factors.

            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 damage from eccentric exercise: mechanism, mechanical signs, adaptation and clinical applications.

               U Proske,  D Morgan (2001)
              In eccentric exercise the contracting muscle is forcibly lengthened; in concentric exercise it shortens. While concentric contractions initiate movements, eccentric contractions slow or stop them. A unique feature of eccentric exercise is that untrained subjects become stiff and sore the day afterwards because of damage to muscle fibres. This review considers two possible initial events as responsible for the subsequent damage, damage to the excitation-contraction coupling system and disruption at the level of the sarcomeres. Other changes seen after eccentric exercise, a fall in active tension, shift in optimum length for active tension, and rise in passive tension, are seen, on balance, to favour sarcomere disruption as the starting point for the damage. As well as damage to muscle fibres there is evidence of disturbance of muscle sense organs and of proprioception. A second period of exercise, a week after the first, produces much less damage. This is the result of an adaptation process. One proposed mechanism for the adaptation is an increase in sarcomere number in muscle fibres. This leads to a secondary shift in the muscle's optimum length for active tension. The ability of muscle to rapidly adapt following the damage from eccentric exercise raises the possibility of clinical applications of mild eccentric exercise, such as for protecting a muscle against more major injuries.

                Author and article information

                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                11 September 2017
                : 10
                : 2213-2221
                [1 ]Centre for Physiotherapy and Rehabilitation Sciences, Jamia Millia Islamia, New Delhi, India
                [2 ]Faculty of Dentistry, Jamia Millia Islamia, New Delhi, India
                [3 ]Rehabilitation Research Chair, College of Applied Medical Sciences, King Saud University, Riyadh, Saudi Arabia
                [4 ]Dr. D. Y. Patil College of Physiotherapy, Dr. D. Y. Patil Vidyapeeth, Pune, India
                Author notes
                Correspondence: Jamal Ali Moiz, Centre for Physiotherapy and Rehabilitation Sciences, Jamia Millia Islamia, New Delhi 110025, India, Tel +91 11 2698 1717, Email jmoiz@ 123456jmi.ac.in
                © 2017 Nausheen et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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