**1. Introduction**

Muscle injury has been related to resistance exercise and prolonged endurance exercise paradigms both leading to significant local mechanical constraints followed by focal disorders such as sarcolemmal damage and leakage of intracellular proteins, oedema, myofibrillar disorganization and microtrauma-triggered inflammation. These unfavorable events lead to variable soreness, swelling, loss in muscle strength and function with reduced range of motion.

To date strategies finalized to minimize exercise-induced muscle injury are scarce and often not adequately supported by research studies.

Based on the notion that dietary supplementations may exert a variety of beneficial effects on the skeletal muscle, in the last 20 years there has been a great deal of interest in nutritional strategies aiming to attenuate signs and symptoms of exercise induced muscle injuries. Anyhow a large number of variables influences the muscular outcome of nutritional supple‐ ments, strongly depending on nutrient type, genotype, age, and regulation of nutrient sensing pathways.

Overall there is a paucity of studies on the topic, partly related to the high number of supple‐ ments to be considered and their combined use. In general nutrients as vitamins (as vitamin C), N-acetyl-cysteine, L-carnitine, creatine, and branched chain amino acids (BCAA) may exert a potential beneficial role but the underlying cellular mechanism, the optimal dosage and the duration of the pretreatment/treatment period are currently unknown.

This chapter addresses the current knowledge on the potential use of nutritional supplements in preventing and/or minimizing muscle injuries due to resistance or endurance exercise training.

© 2013 D'Antona; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

"If the soreness then, be caused by the same conditions which produce fatigue, namely the presence of diffusible waste products of activity we should expect to find, as we do find, that it takes the course described above, passing away within few hours of the work itself" [1]

Importantly the early mechanical and metabolic mechanisms can promote biochemical changes within the affected area, leading to the generation of a secondary muscle damage including disruption of intracellular calcium homeostasis, local accumulation of inflammatory cytokines such as tumor necrosis factor-a, interleukin (IL)-1b, IL-6, and IL-1 receptor antagonist (IL-1ra) [17], *de facto* mimicking the sequential release of cytokines after trauma [18], and reactive oxygen species (ROS) that may further degrade muscle proteins and increase the local expression of cytokines [19, 20]. This condition may contribute to persistence of signs and

Nutritional Interventions as Potential Strategy to Minimize Exercise-Induced Muscle Injuries in Sports

http://dx.doi.org/10.5772/56590

65

Although it is widely accepted that high intensity eccentric exercise is the fundamental exercise paradigm resulting in muscle damage and subsequent adaptation, structural and functional damage may also arise following long lasting endurance exercise paradigms as demonstrated by the appearance of ultrastructural alterations, as fibers necrosis, sarcolemmal disruption, Z discs streaming, contracture knots, and inflammatory infiltration in endurance athletes even before a race [21]. Anyhow even though the extent and location of damage may greatly vary according to the exercise paradigm and the previous conditioning of the muscoloskeletal system, the extent of damage observed with low intensity and long duration endurance exercise is often less pronounced than with higher intensities. This is the main reason of why most of works finalized to the identification of the physiological mechanisms that regulate the response to exercise-induced stress in skeletal muscle and the possible countermeasures, including the approach based on nutrient supplementation, have been focused on strength

**2. Nutritional intervention to minimize exercise-induced muscle injury**

For decades, dietary supplementation has been proposed in various physiological or patho‐ logical conditions. Based on the recent progress in our understanding of the cell signaling and *in vivo* metabolism of nutrients and on accumulating experimental results, the concept that dietary supplementation might have effects in prevention or treatment of several disorders is experiencing a new revival. To date several investigations have been focused on accumulating experimental evidence aiming to extend the use of specific nutritional supplements in the prevention and/or treatment of exercise induced muscle injuries. Anyhow available outcomes on potentially efficacious supplements are mixed and often conflicting and confident conclu‐ sions cannot be drawn. Several variables may concur to contradictory results including the wide number of supplements to be considered, their combined use, their dose and timing of administration. Furthermore the choice of the proper indexes to be analyzed is certainly a major bias for several published studies on the topic as a misinterpretation of results may follow the analysis of indirect instead of direct signs of muscle injury. Thus, although many nutrients are potentially able to impact on the mechanisms underlying the appearance of muscle damage following exercise, the final efficacy and safety of their supplementation deserves future

The present chapter discusses the potential role of antioxidants, creatine, carnitine and

branched chain amino acids on exercise induced muscle damage.

symptoms of injury.

training exercise.

rigorous investigation.

In 1900 Theodore Hugh first described that exercise induced muscle injury is not a fatigue phenomenon but the consequence of mechanical overload followed by structural and func‐ tional muscular changes [1].

Cycles of repetitive eccentric and concentric contractions represent a fundamental source of mechanical stress for active skeletal muscle and vulnerability of skeletal muscle fibers appears to be particularly evident in unaccustomed individuals. In fact conditioning of the muscle through prior similar activity may minimize damage appearance (so called "repeated bout effect") [2]. Overall the process appears as a fundamental step for the arising of exerciseinduced plastic response as it is followed by muscle remodeling and adaptation [3]. However muscle damage may delay muscle recovery from exercise and performance thus reducing the athletes compliance to exercise programmes.

The direct consequence of mechanical stress on active skeletal muscle fibers is the appearance of soreness (delayed onset muscle soreness, DOMS), stiffness and reduced force production. This is particularly the case as a consequence of strenuous physical work involving heavy resistance exercise including eccentric (i.e. lengthening) actions [4-6]. In these conditions force loss appears immediately post-exercise whereas soreness becomes evident within 24-48 hours after and, as the force impairment, may last several days depending of the extent of damage [7]. At the microscopic and submicroscopic level fibers damage, which preferentially involves fast twitch fibers [8], is already evident within minutes from the mechanical insult [9] displays throughout individual fibers (i.e. focal injury), and includes plasma membrane disruption accompanied by the loss of muscle proteins in the serum (i.e. creatine kinase (CK), myoglobin, lactate dehydrogenase (LDH), aldolase, troponin), myofibrillar disorders as streaming and broadening of the Z-lines, loss of sarcomeres register, the appearance of regions of overex‐ tended sarcomeres, regional disorganization of the myofilaments, subsarcolemmal lipofuscin granules accumulation, alterations of the proteoglycan components, increased interstitial space, and capillary damage [10-15]. Interestingly dramatic changes in the organization of the membrane systems involved in excitation-contraction coupling have been also found follow‐ ing eccentric contractions [16]. The most commonly identified alterations include disorders of the T tubule, changes in the direction and spatial orientation of the triads, and the appearance of caveolar clusters, pentads and heptads (close apposition of two or three T tubule elements with three or four elements with three or four elements of terminal cisternae of sarcoplasmic reticulum).

Apart mechanical stress, other mechanisms may contribute to muscle damage. In particular a metabolic impairment has been proposed as a result of ischemia or hypoxia during prolonged and intense resistance exercise. This insult leads to changes in ion concentration, accumulation of metabolic wastes, and adenosine triphosphate (ATP) deficiency which contribute to soreness and impaired function.

Importantly the early mechanical and metabolic mechanisms can promote biochemical changes within the affected area, leading to the generation of a secondary muscle damage including disruption of intracellular calcium homeostasis, local accumulation of inflammatory cytokines such as tumor necrosis factor-a, interleukin (IL)-1b, IL-6, and IL-1 receptor antagonist (IL-1ra) [17], *de facto* mimicking the sequential release of cytokines after trauma [18], and reactive oxygen species (ROS) that may further degrade muscle proteins and increase the local expression of cytokines [19, 20]. This condition may contribute to persistence of signs and symptoms of injury.

"If the soreness then, be caused by the same conditions which produce fatigue, namely the presence of diffusible waste products of activity we should expect to find, as we do find, that it takes the course described above, passing away within few hours of the work itself" [1]

In 1900 Theodore Hugh first described that exercise induced muscle injury is not a fatigue phenomenon but the consequence of mechanical overload followed by structural and func‐

Cycles of repetitive eccentric and concentric contractions represent a fundamental source of mechanical stress for active skeletal muscle and vulnerability of skeletal muscle fibers appears to be particularly evident in unaccustomed individuals. In fact conditioning of the muscle through prior similar activity may minimize damage appearance (so called "repeated bout effect") [2]. Overall the process appears as a fundamental step for the arising of exerciseinduced plastic response as it is followed by muscle remodeling and adaptation [3]. However muscle damage may delay muscle recovery from exercise and performance thus reducing the

The direct consequence of mechanical stress on active skeletal muscle fibers is the appearance of soreness (delayed onset muscle soreness, DOMS), stiffness and reduced force production. This is particularly the case as a consequence of strenuous physical work involving heavy resistance exercise including eccentric (i.e. lengthening) actions [4-6]. In these conditions force loss appears immediately post-exercise whereas soreness becomes evident within 24-48 hours after and, as the force impairment, may last several days depending of the extent of damage [7]. At the microscopic and submicroscopic level fibers damage, which preferentially involves fast twitch fibers [8], is already evident within minutes from the mechanical insult [9] displays throughout individual fibers (i.e. focal injury), and includes plasma membrane disruption accompanied by the loss of muscle proteins in the serum (i.e. creatine kinase (CK), myoglobin, lactate dehydrogenase (LDH), aldolase, troponin), myofibrillar disorders as streaming and broadening of the Z-lines, loss of sarcomeres register, the appearance of regions of overex‐ tended sarcomeres, regional disorganization of the myofilaments, subsarcolemmal lipofuscin granules accumulation, alterations of the proteoglycan components, increased interstitial space, and capillary damage [10-15]. Interestingly dramatic changes in the organization of the membrane systems involved in excitation-contraction coupling have been also found follow‐ ing eccentric contractions [16]. The most commonly identified alterations include disorders of the T tubule, changes in the direction and spatial orientation of the triads, and the appearance of caveolar clusters, pentads and heptads (close apposition of two or three T tubule elements with three or four elements with three or four elements of terminal cisternae of sarcoplasmic

Apart mechanical stress, other mechanisms may contribute to muscle damage. In particular a metabolic impairment has been proposed as a result of ischemia or hypoxia during prolonged and intense resistance exercise. This insult leads to changes in ion concentration, accumulation of metabolic wastes, and adenosine triphosphate (ATP) deficiency which contribute to

tional muscular changes [1].

64 Muscle Injuries in Sport Medicine

reticulum).

soreness and impaired function.

athletes compliance to exercise programmes.

Although it is widely accepted that high intensity eccentric exercise is the fundamental exercise paradigm resulting in muscle damage and subsequent adaptation, structural and functional damage may also arise following long lasting endurance exercise paradigms as demonstrated by the appearance of ultrastructural alterations, as fibers necrosis, sarcolemmal disruption, Z discs streaming, contracture knots, and inflammatory infiltration in endurance athletes even before a race [21]. Anyhow even though the extent and location of damage may greatly vary according to the exercise paradigm and the previous conditioning of the muscoloskeletal system, the extent of damage observed with low intensity and long duration endurance exercise is often less pronounced than with higher intensities. This is the main reason of why most of works finalized to the identification of the physiological mechanisms that regulate the response to exercise-induced stress in skeletal muscle and the possible countermeasures, including the approach based on nutrient supplementation, have been focused on strength training exercise.
