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Given the major role that oxidants play in cellular damage, and the recent focus on antioxidants as treatment for muscle injuries, the aim of this study was to examine the effect of short-term postinjury grape seed-derived polyphenol supplementation on muscle inflammation and repair processes after contusion injury. Experimental injury of the right gastrocnemius muscle was achieved by drop-mass method (200 g from a height of 50 cm), after which rats were gavaged with either 0.9% saline (placebo-PLA) or 20 mg·kg⁻¹·d⁻¹ of proanthocyanidolic oligomer (PCO) from 2 h after contusion injury, for up to 14 d after injury. Blood samples and injured muscle were collected at 4 h and at days 1, 3, 5, 7, and 14 after injury. Compared to an uninjured control group, PCO supplementation resulted in an earlier peak in number of activated satellite cells in contusion-injured muscle tissue (4 h for PCO vs day 3 for PLA, n = 4 per time point per group) and fetal myosin heavy chain expression (day 5 for PCO, P < 0.01 with no change in PLA, n = 3 per time point per group), indicative of quicker muscle regeneration. PCO supplementation limited neutrophil infiltration and facilitated earlier macrophage infiltration into the injured area (n = 4 per group). PCO also resulted in an earlier return toward control levels of muscle proinflammatory cytokines on day 3 (P < 0.01 for interleukin 6 and P < 0 05 for tumor necrosis factor α, both n = 3 per group). Data show that short-term postinjury PCO supplementation was able to quicken muscle regeneration by facilitating earlier recruitment of activated satellite cells and to modulate the immune system in favor of an anti-inflammatory status.
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... In the current study, quantitative morphological markers of muscle damage included the presence of pale cytoplasm, extracellular leukocytes, intracellular leukocytes, and centrally-located myonuclei, as previously described (Koh and Brooks, 2001;Tsivitse et al., 2003). In general, our histological observations are supported by previous IIMD studies of overt muscle fiber damage, edema and subsequent infiltration of leukocytes (Crisco et al., 1994;Kruger and Smith, 2012;Myburgh et al., 2012;Xiao et al., 2016) and essentially aligns with the typical time course that follows after skeletal muscle trauma (Tidball, 2017). ...
... Two-hours post-IIMD both WBHS and NBT groups had pronounced fiber disruption and edema. The presence of fiber disruption and edema at the 2-hour time point is consistent with previous studies (Crisco et al., 1994;Kruger and Smith, 2012;Myburgh et al., 2012). The percentage of damaged fibers did not differ between treatment groups (Figure 4). ...
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Impact-induced muscle damage (IIMD) is a common sports injury, often resulting in acute skeletal muscle contractile dysfunction. Whole-body heat shock (WBHS) is reported to attenuate skeletal muscle atrophy in animal models. The purpose of this study was to determine if WBHS prior to IIMD will attenuate subsequent muscle damage and accelerate recovery of contractile function. Skeletal muscle contractile function of the anterior crural muscle group was measured in adult male mice in vivo. Body temperature was then raised to 41°C (WBHS) or maintained at 37°C (normal body temperature, NBT) for 30 min. Twenty-four hours later a single impact was delivered to the tibialis anterior. Following 2-hours, 2-days, or 5-days of normal cage activity, contractile function was measured and the tibialis anterior was then excised and mounted for histological analysis. Two-hours post-IIMD contractile function was ~50% lower than pre-IIMD (p < 0.001, both groups), however, the WBHS group had greater maximal contractile function (p = 0.048). Two-days post-IIMD, the WBHS group had recovered (p = 0.090), but the NBT group had not recovered (p < 0.0001) contractile function. Five-days post-IIMD, WBHS group had fully recovered (p = 0.901), however the NBT group had not recovered (p < 0.0001) contractile function. Histological evaluation suggests less visible damage, and accelerated inflammatory response in the WBHS group. Immunohistochemistry results suggest IIMD increases HSP72 expression and this response is enhanced by prior WBHS. WBHS treatment prior to IIMD confers a degree of protection to skeletal muscle function 2-hours post-IIMD, attenuates muscle damage, and accelerates the rate of recovery of in vivo skeletal muscle contractile function within the 2-day and 5-day recovery period.
... The influence of ROS-induced cellular processes on myogenic programming is complex as ROS present in concentrations below a threshold (that is largely unknown though) are implicated in signal transduction, SCs viability and differentiation while they result in inhibition of myogenesis through apoptotic and necrotic pathways such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) when their levels surpass this threshold [19]. Recently, in vitro and in vivo studies that used antioxidant compounds to quench excess ROS production in skeletal muscle during the repair process following aseptic myotrauma have provided evidence of accelerated muscle recovery process via upregulation of the myogenic potential, viability, maintenance and activity of the resident SCs [20][21][22]. However, to this date literature lacks evidence on a redox-dependent regulation of SCs following aseptic myotrauma and inflammation in the human skeletal muscle and to what extent, antioxidant supplementation can affect activity of SCs and muscle's regeneration. ...
... In an attempt to ameliorate the detrimental effects of ROS-induced oxidative damage in muscle tissue and to enhance the myogenic potential as well as the capacity of skeletal muscle to promote healing, a number of in vivo and in vitro studies have utilized antioxidant and antiinflammatory supplementation both in basal conditions and following myotrauma (Table 3). In regards to antioxidant manipulation two studies showed that administration of 20 mg/kg/day of proanthocyanidolic oligomer (PCO) orally for 14 days pre-and post-contusion injury resulted in increased SCs number and fetal myosin fibers (MHCf + ), improved muscle ultrastructural recovery, enhanced antioxidant capacity and reduced TNF-α levels compared to placebo in adult male Wistar rats [21,22]. In vitro and in vivo ursolic acid (UA) supplementation at rest (in vitro: 10 μM UA + DMSO; in vivo: 200 mg/kg) for 7 days resulted in increased Pax7 + and myogenin + cells, increased myonuclei and myofiber content and reduced SCs apoptosis while cell death was evident [20]. ...
Article
Skeletal muscle satellite cells (SCs) are indispensable for tissue regeneration, remodeling and growth. Following myotrauma, SCs are activated, and assist in tissue repair. Exercise-induced muscle damage (EIMD) is characterized by a pronounced inflammatory response and the production of reactive oxygen species (ROS). Experimental evidence suggests that SCs kinetics (the propagation from a quiescent to an activated/proliferative state) following EIMD is redox-dependent and interconnected with changes in the SCs microenvironment (niche). Animal studies have shown that following aseptic myotrauma, antioxidant and/or anti-inflammatory supplementation leads to an improved recovery and skeletal muscle regeneration through enhanced SCs kinetics, suggesting a redox-dependent molecular mechanism. Although evidence suggests that antioxidant/anti-inflammatory compounds may prevent performance deterioration and enhance recovery, there is lack of information regarding the redox-dependent regulation of SCs responses following EIMD in humans. In this review, SCs kinetics following aseptic myotrauma, as well as the intrinsic redox-sensitive molecular mechanisms responsible for SCs responses are discussed. The role of redox status on SCs function should be further investigated in the future with human clinical trials in an attempt to elucidate the molecular pathways responsible for muscle recovery and provide information for potential nutritional strategies aiming at performance recovery.
... A second aim was to assess the sensitivity of this model to reflect preventative efficacy of a grapederived polyphenol antioxidant with demonstrated antioxidant and anti-inflammatory effect. (Bagchi et al. 2000;Kruger and Smith 2012;Myburgh et al. 2012;Kruger et al. 2014;Petersen et al. 2018;Oyenihi et al. 2019). Of particular reference to the topic of accelerated ageing, the ability to modulate oxidative stress and low-grade inflammation may present a broadly applicable preventative strategy for agerelated disease and a novel application of this grapederived polyphenol. ...
... Coupled with its ability to reduce free radical levels, grape seed antioxidants also have significant metal chelating properties which serve to reduce lipid peroxidation (Shi et al. 2003;Xia et al. 2010;Aybast et al. 2018), thus preventing MDA formation. The grape seed polyphenol investigated in this study has also previously been studied and shown to have significant antioxidant and anti-inflammatory properties by increased oxygen radical absorption capacity (ORAC)-indicative of an ascorbic acid-like quenching of hydroxyl ions by donation of hydrogen protons-in a rodent model of muscle damage (Kruger 2007;Kruger and Smith 2012;Myburgh et al. 2012;Kruger et al. 2014). ...
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Considering that the phenomenon of accelerated ageing contributes to early onset of various chronic diseases, modelling of the relevant dysregulated systems or responses is vital for research aimed at identification of potential therapeutic targets. Here, we aimed to establish a model capable of simulating the redox and inflammatory changes of accelerated ageing—specifically, the aim was early phase accelerated ageing, which would allow therapeutic intervention in a preventative approach prior to clinical disease manifestation. A secondary aim was to evaluate the sensitivity of the model to reflect preventative treatment efficacy. Daily d-galactose injections (250 mg/kg body mass/day) for 8 weeks in 9-week-old male Wistar rats induced a model of early accelerated ageing (decreased plasma FRAP; P < 0.05 and altered inflammatory signalling) and an aged profile in lymph node ultrastructure, but did not yet result in telomere shortening. Preventative daily oral antioxidant administration (grape seed-derived polyphenol, 100 mg/kg body mass) prevented tissue ageing, beneficially modulated the inflammatory response, including neutrophil chemokinetic capacity, and tended to increase absolute telomere length. Data suggests that using a mild model of d-galactose administration than those employed to induce neurodegeneration, simulated the point where oxidative stress starts to overwhelm the endogenous antioxidant response and where a pro-inflammatory phenotype switch manifests. Furthermore, despite the expected small effect size, the model was sufficiently sensitive to reflect benefits of preventative antioxidant treatment in the context of ageing. This model presents a practical model for use in drug discovery, particularly in the context of preventative medicine aimed at limiting oxidative stress-associated ageing. Since this starting point of accelerated ageing as illustrated by current data, is not expected to reflect major ageing-associated changes yet, we recommend that future preventative drug discovery studies employ a longitudinal study design in order to clearly demonstrate the delay of this starting point by preventative strategies.
... For example, the performance nutrition and medical team provide targeted nutrition, pain management or other strategies depending on the class of injury, supporting optimal adaptation to exercise for specific tissues. [33][34][35][36][37] management principle 3 Involve the coach and athlete in shared decision-making British Athletics apply an integrated performance health and coaching model and a shared decision-making process when managing injuries in elite track and field athletes. 32 38 This model aligns the health and coaching departments to a defined performance goal. ...
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Rationale Hamstring injuries are common in elite sports. Muscle injury classification systems aim to provide a framework for diagnosis. The British Athletics Muscle Injury Classification (BAMIC) describes an MRI classification system with clearly defined, anatomically focused classes based on the site of injury: (a) myofascial, (b) muscle–tendon junction or (c) intratendinous; and the extent of the injury, graded from 0 to 4. However, there are no clinical guidelines that link the specific diagnosis (as above) with a focused rehabilitation plan. Objective We present an overview of the general principles of, and rationale for, exercise-based hamstring injury rehabilitation in British Athletics. We describe how British Athletics clinicians use the BAMIC to help manage elite track and field athletes with hamstring injury. Within each class of injury, we discuss four topics: clinical presentation, healing physiology, how we prescribe and progress rehabilitation and how we make the shared decision to return to full training. We recommend a structured and targeted diagnostic and rehabilitation approach to improve outcomes after hamstring injury.
... 5,6 Two previous studies have reported that GSE supplementation reduces muscle damage and promotes muscle regeneration. 7,8 However, both of these were animal studies, and human studies on GSE supplementation and muscle damage are lacking. In addition, muscle damage in the abovementioned two studies was not caused by eccentric exercise, but by contusion. ...
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Background/objective High intensity eccentric exercise causes muscle damage. Polyphenol supplementation is one nutritional intervention available to limit muscle damage, but there is a lack of published data concerning the use of polyphenol-rich grape seed extract (GSE). This study investigated the effect of acute GSE supplementation on muscle damage markers after eccentric exercise. Methods Sixteen healthy male university students (mean age: 20.3 ± 0.4 years, height: 176.1 ± 4.7 cm, weight: 69.9 ± 10.2 kg) were included. Participants were randomly assigned to GSE group (n = 8) or placebo group (n = 8); 300 mg/day of GSE or placebo was consumed from the time of eccentric exercise to 72 h after exercise. For the eccentric exercise, the elbow flexor muscle was activated using a modified preacher curl machine at 25 repetitions for 2 sets. For the muscle damage markers, maximal muscle strength, muscle soreness, and creatine kinase (CK) level were measured. Results There was no difference in maximal muscle strength and muscle soreness between groups in the recovery stage after eccentric exercise (p > 0.05); CK level, a marker of cell membrane damage, was significantly decreased 96 h after exercise in the GSE group compared with the placebo group (p < 0.05). Conclusion Acute GSE supplement can be an effective way to decrease cellular membrane damage after eccentric exercise. These results could be helpful in the application of GSE supplementation as a nutritional intervention to reduce muscle damage after high intensity strength training, especially in the early stage of a new strength training program. However, a larger scale study is necessary to validate these results.
... Cocoa polyphenolic extract influences MF metabolism by promoting oxidative pathways and M2 polarization in human MF in vitro (79). Pomegranate and its polyphenols promote M1-to-M2 switch in murine MF (2), and grape seed-derived polyphenols (proanthocyanidolic oligomers) accelerate muscle regeneration in rats by activating SCs and by promoting an anti-inflammatory switch (165). Interestingly, polyamines are able to drive M2 polarization in murine MF (354) and also to promote repair, fibrosis, and tissue remodeling in mice (272). ...
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Skeletal muscle plays a crucial role in motor function, respiration, and whole-body energy homeostasis. How to regulate the development and function of skeletal muscle has become a hot research topic for improving lifestyle and extending life span. Numerous transcription factors and nutritional factors have been clarified are closely associated with the regulation of skeletal muscle development, regeneration and function. In this article, the roles of different dietary factors including green tea, quercetin, curcumin (CUR), eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and resveratrol (RES) in regulating skeletal muscle development, muscle mass, muscle function, and muscle recovery have been summarized and discussed. We also reviewed the potential regulatory molecular mechanism of these factors. Based on the current findings, dietary factors may be used as a potential therapeutic agent to treat skeletal muscle dysfunction as well as its related diseases.
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Rheumatoid arthritis is prevalent in more than 1% of the global population, with the highest occurrence between ages 35 and 50, which places a huge burden on the economy. Drug discovery for the prevention of this chronic disease is; therefore, a priority. It is known that subclinical progression of many chronic non-communicable diseases is exacerbated via accelerated ageing, a pro-inflammatory phenotype shift. However, rheumatoid arthritis additionally has significant humoral immune activation, inflammatory signalling—and thus the accelerated ageing profile—may differ from other chronic inflammatory diseases. The current study simulated inflammatory arthritis onset in a collagen-induced arthritis (CIA) rodent model, to characterise the redox and inflammatory profile at the onset of clinical symptoms, in different tissues, in the presence and absence of preventative antioxidant treatment. The data illustrate that an increased free radical level are evident already very early on in RA disease progression. Furthermore, oxidative stress seems to somewhat precede a significant pro-inflammatory state, perhaps due to humoral immune activation. Our data across different compartments further suggest that the compensatory increase in endogenous antioxidant activity is gradually exhausted at a different pace, with the liver showing the first signs of oxidant damage, even before significant evidence exist in circulation. The current data further suggest that preventative antioxidant intervention may have a sparing effect on endogenous antioxidant mechanisms and preserve telomere length to delay disease progression—or at least the accelerated ageing known to exacerbate RA symptoms—although it did not seem to have a significant direct effect on the autoimmune activity.
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