How Does Altering the Volume-Load of Plyometric Exercises Affect the Inflammatory Response, Oxidative Stress, and Muscle Damage in Male Soccer Players?

Incorporating plyometric exercises (PE) into soccer players' conditioning routines is vital for boosting their performance. Nevertheless, the effects of PE sessions with diverse volume loads on inflammation, oxidative stress, and muscle damage are not yet clearly understood. This study aimed to examine the effects of altering the volume-loads of PE on indicators of oxidative muscle damage and inflammation. The study involved forty young male soccer players who were randomly assigned to three different volume-loads of PE (Low volume-load [100 jumps]: LVL, n = 10; Moderate volume-load [150 jumps]: MVL, n = 10; and High volume-load [200 jumps]: HVL, n = 10) and a control group (CON = 10). The levels of various biomarkers including delayed onset muscle soreness (DOMS), serum lactate dehydrogenase (LDH), creatine kinase (CK), 8-hydroxy-2-deoxyguanosine (8-OHdG), malondialdehyde (MDA), protein carbonyl (PC), leukocytes, neutrophils, interleukin-6 (IL-6), and C-reactive protein (CRP) were measured at different time points. These measurements were taken at rest, immediately after completion of PE, and 24-, 48-, and 72-hours post-PE. The CK, LDH, DOMS, 8-OHdG, MDA, and PC levels were significantly increased (p < 0.05) after the PE protocol, reaching their peak values between 24 to 48 hours post-PE for all the volume-loaded groups. The levels of leukocytes, neutrophils, and IL-6 also increased after the PE session but returned to resting values within 24 hours post-PE. On the other hand, CRP levels increased at 24 hours post-PE for all the treatment groups (p < 0.05). The changes observed in the indicators of muscle damage and inflammation in response to different volume-loads of PE was not significant. However, the HVL and MVL indicated significant differences compared to LVL in the 8-OHdG (at 48-hour) and MDA (at 72-hour). Athletes engaging in higher volume-loads demonstrated more pronounced responses in terms of biochemical variables (specifically, LVL < MVL < HVL); however, these changes were not statistically significant (except 8-OHdG and MDA).

Abnormal myosin post-translational modifications and ATP turnover time associated with human congenital myopathy-related RYR1 mutations.

AIM: Conditions related to mutations in the gene encoding the skeletal muscle ryanodine receptor 1 (RYR1) are genetic muscle disorders and include congenital myopathies with permanent weakness, as well as episodic phenotypes such as rhabdomyolysis/myalgia. Although RYR1 dysfunction is the primary mechanism in RYR1-related disorders, other downstream pathogenic events are less well understood and may include a secondary remodeling of major contractile proteins. Hence, in the present study, we aimed to investigate whether congenital myopathy-related RYR1 mutations alter the regulation of the most abundant contractile protein, myosin. METHODS: We used skeletal muscle tissues from five patients with RYR1-related congenital myopathy and compared those with five controls and five patients with RYR1-related rhabdomyolysis/myalgia. We then defined post-translational modifications on myosin heavy chains (MyHCs) using LC/MS. In parallel, we determined myosin relaxed states using Mant-ATP chase experiments and performed molecular dynamics (MD) simulations. RESULTS: LC/MS revealed two additional phosphorylations (Thr1309-P and Ser1362-P) and one acetylation (Lys1410-Ac) on the ß/slow MyHC of patients with congenital myopathy. This method also identified six acetylations that were lacking on MyHC type IIa of these patients (Lys35-Ac, Lys663-Ac, Lys763-Ac, Lys1171-Ac, Lys1360-Ac, and Lys1733-Ac). MD simulations suggest that modifying myosin Ser1362 impacts the protein structure and dynamics. Finally, Mant-ATP chase experiments showed a faster ATP turnover time of myosin heads in the disordered-relaxed conformation. CONCLUSIONS: Altogether, our results suggest that RYR1 mutations have secondary negative consequences on myosin structure and function, likely contributing to the congenital myopathic phenotype.

The impact of dietary protein supplementation on recovery from resistance exercise-induced muscle damage: A systematic review with meta-analysis.

BACKGROUND: It is unknown whether dietary protein consumption can attenuate resistance exercise-induced muscle damage (EIMD). Managing EIMD may accelerate muscle recovery and allow frequent, high-quality exercise to promote muscle adaptations. This systematic review and meta-analysis examined the impact of peri-exercise protein supplementation on resistance EIMD. METHODS: A literature search was conducted on PubMed, SPORTDiscus, and Web of Science up to March 2021 for relevant articles. PEDro criteria were used to assess bias within included studies. A Hedges' g effect size (ES) was calculated for indirect markers of EIMD at h post-exercise. Weighted ESs were included in a random effects model to determine overall ESs over time. RESULTS: Twenty-nine studies were included in the systematic review and 40 trials were included in ≥1 meta-analyses (16 total). There were significant overall effects of protein for preserving isometric maximal voluntary contraction (MVC) at 96 h (0.563 [0.232, 0.894]) and isokinetic MVC at 24 h (0.639 [0.116, 1.162]), 48 h (0.447 [0.104, 0.790]), and 72 h (0.569 [0.136, 1.002]). Overall ESs were large in favour of protein for attenuating creatine kinase concentration at 48 h (0.836 [-0.001, 1.673]) and 72 h (1.335 [0.294, 2.376]). Protein supplementation had no effect on muscle soreness compared with the control. CONCLUSION: Peri-exercise protein consumption could help maintain maximal strength and lower creatine kinase concentration following resistance exercise but not reduce muscle soreness. Conflicting data may be due to methodological divergencies between studies. Standardised methods and data reporting for EIMD research are needed.

Influence of Alpha-Actinin-3 R577X Polymorphism on Muscle Damage and the Inflammatory Response after an Acute Strength Training Session.

The objective of this study was to verify the influence of the ACTN3 R577X polymorphism on muscle damage and the inflammatory response after an acute strength training (ST) session. Twenty-seven healthy male individuals (age: 25 ± 4.3 years) participated in the study, including 18 RR/RX and 9 XX individuals. The participants were divided into two groups (RR/RX and XX groups) and subjected to an acute ST session, which consisted of a series of leg press, leg extension machine, and seated leg curl machine. The volunteers were instructed to perform the greatest volume of work until concentric muscle failure. Each volunteer's performance was analyzed as the load and total volume of training, and the blood concentrations of C-C motif chemokine ligand 2 (CCL2), interleukin-8 (IL-8), creatine kinase (CK), lactate dehydrogenase (LDH), myoglobin, testosterone, and cortisol were measured before the ST session and 30 min and 24 h postsession. The ACTN3 R577X polymorphism effect was observed, with increased concentrations of CCL2 (p < 0.01), IL-8 (p < 0.01), and LDH (p < 0.001) in XX individuals. There was an increase in the concentration of CK in the RR/RX group compared to XX at 24 h after training (p > 0.01). The testosterone/cortisol ratio increased more markedly in the XX group (p < 0.001). Regarding performance, the RR/RX group presented higher load and total volume values in the training exercises when compared to the XX group (p < 0.05). However, the XX group presented higher values of delayed onset muscle soreness (DOMS) than the RR/RX group (p < 0.05). The influence of ACTN3 R577X polymorphism on muscle damage and the inflammatory response was observed after an acute ST session, indicating that the RR/RX genotype shows more muscle damage and a catabolic profile due to a better performance in this activity, while the XX genotype shows more DOMS.

CD3+/CD56+ NKT-like Cells Show Imbalanced Control Immediately after Exercise in Delayed-Onset Muscle Soreness.

The purpose of the study was to carry out an immunophenotypical characterization with a special focus on natural killer cells of junior swimmers from the Hungarian National Swim Team before and after an intensive acute exercise. Nineteen swimmers, ten females and nine males, completed the exercise protocol. Sixteen swimmers experienced delayed-onset muscle soreness. Most of our findings substantiated earlier results, such as the increase in the percentage of the CD3-/CD56+ natural killer cells and the CD3-/CD56dim+ NK cells, and the decrease in the percentage of CD3+ T cells among lymphocytes after the exercise protocol. The drop of natural killer cell activity back to the pre-exercise level was in line with earlier findings. Interestingly, the percentage of CD3+/CD56+ NKT-like cells did not change significantly in those three swimmers who did not report delayed-onset muscle soreness. On the contrary, the percentage of CD3+/CD56+ NKT-like cells among lymphocytes increased in fourteen and decreased in two swimmers reporting delayed-onset muscle soreness. This study for the first time demonstrated a link between the delayed-onset muscle soreness and the imbalanced control of CD3+/CD56+ NKT-like cells among lymphocytes. However, validation of this association in a larger sample size study will be necessary.

Acute physiological and perceptual responses to a netball specific training session in professional female netball players.

The 24 h responses to professional female netball-specific training were examined. British Superleague players (n = 14) undertook a 90-min on-court training session incorporating key movement, technical, and scenario-specific match-play drills. Perceptual (mood, fatigue, soreness), neuromuscular (countermovement jump peak power output [PPO], PPO relative to mass [PPOrel], jump height [JH]), endocrine (salivary cortisol [C], testosterone [T] concentrations) and biochemical (creatine kinase concentrations [CK]) markers were assessed at baseline (immediately before; Pre), and immediately, two and 24 hours after (+0h, +2h, +24h) training. Session (sRPE) and differential (dRPE) ratings of perceived exertion were recorded at +0h. Identification of clear between time-point differences were based on the 95% confidence interval (CI) for mean differences relative to baseline values not overlapping. At +0h, C (raw unit mean difference from baseline; 95% CI: 0.16; 0.06 to 0.25 µg·dl-1), T (32; 20 to 45 pg⋅ml-1), CK (39; 28 to 50 u·L-1), PPOrel (2.4; 0.9 to 3.9 W·kg-1) and PPO (169; 52 to 286 W) increased. At +2h, fatigue (15; 7 to 24 AU), CK (49; 38 to 60 u·L-1), and soreness (14; 3 to 25 AU) increased, while T (-24; -37 to -11 pg⋅ml-1) and mood (-20; -27 to -12 AU) reduced. At +24h, CK increased (25; 13 to 36 u·L-1) whereas PPOrel (-1.6; -3.2 to -0.1 W·kg-1) and JH (-0.02; -0.03 to -0.08 m) reduced. Responses were variable specific, and recovery of all variables did not occur within 24h. The residual effects of the prior stimulus should be accounted for in the planning of training for professional female netball players.

The effects of collagen peptide supplementation on body composition, collagen synthesis, and recovery from joint injury and exercise: a systematic review.

Collagen peptide supplementation (COL), in conjunction with exercise, may be beneficial for the management of degenerative bone and joint disorders. This is likely due to stimulatory effects of COL and exercise on the extracellular matrix of connective tissues, improving structure and load-bearing capabilities. This systematic review aims to evaluate the current literature available on the combined impact of COL and exercise. Following Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines, a literature search of three electronic databases-PubMed, Web of Science and CINAHL-was conducted in June 2020. Fifteen randomised controlled trials were selected after screening 856 articles. The study populations included 12 studies in recreational athletes, 2 studies in elderly participants and 1 in untrained pre-menopausal women. Study outcomes were categorised into four topics: (i) joint pain and recovery from joint injuries, (ii) body composition, (iii) muscle soreness and recovery from exercise, and (iv) muscle protein synthesis (MPS) and collagen synthesis. The results indicated that COL is most beneficial in improving joint functionality and reducing joint pain. Certain improvements in body composition, strength and muscle recovery were present. Collagen synthesis rates were elevated with 15 g/day COL but did not have a significant impact on MPS when compared to isonitrogenous higher quality protein sources. Exact mechanisms for these adaptations are unclear, with future research using larger sample sizes, elite athletes, female participants and more precise outcome measures such as muscle biopsies and magnetic imagery.

Is "Delayed Onset Muscle Soreness" a False Friend? The Potential Implication of the Fascial Connective Tissue in Post-Exercise Discomfort.

Strenuous and unaccustomed exercise frequently lead to what has been coined "delayed onset muscle soreness" (DOMS). As implied by this term, it has been proposed that the associated pain and stiffness stem from micro-lesions, inflammation, or metabolite accumulation within the skeletal muscle. However, recent research points towards a strong involvement of the connective tissue. First, according to anatomical studies, the deep fascia displays an intimate structural relationship with the underlying skeletal muscle and may therefore be damaged during excessive loading. Second, histological and experimental studies suggest a rich supply of algogenic nociceptors whose stimulation evokes stronger pain responses than muscle irritation. Taken together, the findings support the hypothesis that DOMS originates in the muscle-associated connective tissue rather than in the muscle itself. Sports and fitness professionals designing exercise programs should hence consider fascia-oriented methods and techniques (e.g., foam rolling, collagen supplementation) when aiming to treat or prevent DOMS.

Reduced concentrations of vaginal metabolites involved in steroid hormone biosynthesis are associated with increased vulvar vestibular pain and vaginal muscle tenderness in provoked vestibulodynia: An exploratory metabolomics study.

Provoked vestibulodynia (PVD) is a chronic vulvar pain disorder characterized by hypersensitivity and severe pain with pressure localized to the vulvar vestibule. Knowledge regarding pathophysiological mechanisms contributing to the etiology and production of symptoms in PVD remains incomplete but is considered multifactorial. Using a cross-sectional observational study design, data from untargeted metabolomic profiling of vaginal fluid and plasma in women with PVD and healthy women was combined with pain testing and brain imaging in women with PVD to test the hypotheses that women with PVD compared to healthy women show differences in vaginal and plasma metabolites involved in steroid hormone biosynthesis. Steroid hormone metabolites showing group differences were correlated with vulvar vestibular pain and vaginal muscle tenderness and functional connectivity of brain regions involved in pain processing in women with PVD to provide insight into the functional mechanisms linked to the identified alterations. Sensitivity analyses were also performed to determine the impact of hormonal contraceptive use on the study findings. Women with PVD compared to healthy controls had significant reductions primarily in vaginal fluid concentrations of androgenic, pregnenolone and progestin metabolites involved in steroidogenesis, suggesting localized rather than systemic effects in vagina and vulvar vestibule. The observed reductions in androgenic metabolite levels showed large effect size associations with increased vulvar vestibular pain and vulvar muscle tenderness and decreases in androgenic and progestin metabolites were associated with decreased connectivity strength in primary sensorimotor cortices. Women with PVD showed symptom-associated reductions in vaginal fluid concentrations of metabolites involved in the biosynthesis of steroid hormones previously shown to affect the integrity of vulvar and vaginal tissue and nociceptive processing. Deficiency of certain steroids may be an important mechanism contributing to the pathophysiology of symptoms in PVD may provide potential diagnostic markers that could lead to new targets for therapeutic intervention.

Post Orgasmic Illness Syndrome (POIS) and Delayed Onset Muscle Soreness (DOMS): Do They Have Anything in Common?

Post orgasmic illness syndrome is a rare, mysterious condition with an unknown pathomechanism and uncertain treatment. The symptoms of post orgasmic illness syndrome last about 2-7 days after an ejaculation. The current hypothesis proposes that the primary injury in post orgasmic illness syndrome is an acute compression proprioceptive axonopathy in the muscle spindle, as is suspected in delayed onset muscle soreness. The terminal arbor degeneration-like lesion of delayed onset muscle soreness is theorized to be an acute stress response energy-depleted dysfunctional mitochondria-induced impairment of Piezo2 channels and glutamate vesicular release. The recurring symptoms of post orgasmic illness syndrome after each ejaculation are suggested to be analogous to the repeated bout effect of delayed onset muscle soreness. However, there are differences in the pathomechanism, mostly attributed to the extent of secondary tissue damage and to the extent of spermidine depletion. The spermidine depletion-induced differences are as follows: modulation of the acute stress response, flu-like symptoms, opioid-like withdrawal and enhanced deregulation of the autonomic nervous system. The longitudinal dimension of delayed onset muscle soreness, in the form of post orgasmic illness syndrome and the repeated bout effect, have cognitive and memory consequences, since the primary injury is learning and memory-related.

Acetaminophen Exerts an Analgesic Effect on Muscular Hyperalgesia in Repeated Cold-Stressed Rats through the Enhancement of the Descending Pain Inhibitory System Involving Spinal 5-HT3 and Noradrenergic α2 Receptors.

Musculoskeletal and psychological complaints have increased with the widespread use of visual display terminals, and musculoskeletal pain is known to be closely related to stress. One method of experimentally inducing persistent muscle pain is repeated cold stress (RCS), and animals exposed to such stress exhibit a dysfunction in the descending pain inhibitory system. Acetaminophen (N-acetyl-p-aminophenol; APAP) is widely used to relieve several types of pain, including musculoskeletal pain, and is available as an OTC drug. However, the mechanism underlying its analgesic action has not yet been fully elucidated. In this study, we compared the analgesic effect of APAP on RCS-induced muscular hyperalgesia with those of other analgesics to identify its mechanism of action. The daily oral administration of APAP significantly suppressed the decrease in the mechanical withdrawal threshold caused by RCS, similar to the results for neurotropin but not for the cyclooxygenase inhibitor ibuprofen (IBP). Moreover, the intrathecal administration of antagonists of the 5-hydroxytryptamine (5-HT)3 receptor or α2-adrenoceptor significantly abolished the analgesic effect of APAP but not of IBP. These results suggest that the analgesic effect of APAP on RCS-induced muscular pain might be exerted due to the activation of the descending pathways involving the spinal 5-HT3 receptor or α2-adrenoceptor.

Sexual dimorphic role of the glucocorticoid receptor in chronic muscle pain produced by early-life stress.

Fibromyalgia and other chronic musculoskeletal pain syndromes are associated with stressful early life events, which can produce a persistent dysregulation in the hypothalamic-pituitary adrenal (HPA) stress axis function, associated with elevated plasm levels of corticosterone in adults. To determine the contribution of the HPA axis to persistent muscle hyperalgesia in adult rats that had experienced neonatal limited bedding (NLB), a form of early-life stress, we evaluated the role of glucocorticoid receptors on muscle nociceptors in adult NLB rats. In adult male and female NLB rats, mechanical nociceptive threshold in skeletal muscle was significantly lower than in adult control (neonatal standard bedding) rats. Furthermore, adult males and females that received exogenous corticosterone (via dams' milk) during postnatal days 2-9, displayed a similar lowered mechanical nociceptive threshold. To test the hypothesis that persistent glucocorticoid receptor signaling in the adult contributes to muscle hyperalgesia in NLB rats, nociceptor expression of glucocorticoid receptor (GR) was attenuated by spinal intrathecal administration of an oligodeoxynucleotide (ODN) antisense to GR mRNA. In adult NLB rats, GR antisense markedly attenuated muscle hyperalgesia in males, but not in females. These findings indicate that increased corticosterone levels during a critical developmental period (postnatal days 2-9) produced by NLB stress induces chronic mechanical hyperalgesia in male and female rats that persists in adulthood, and that this chronic muscle hyperalgesia is mediated, at least in part, by persistent stimulation of glucocorticoid receptors on sensory neurons, in the adult male, but not female rat.

Urinary N-terminal fragment of titin: A surrogate marker of serum creatine kinase activity after exercise-induced severe muscle damage.

We aimed to evaluate whether changes in the noninvasively assessed urinary N-terminal fragment of titin (U-titin) concentration may be associated with those of serum creatine kinase (CK) activity, transverse relaxation time (T2), maximal voluntary contraction (MVC) torque, range of motion (ROM), and muscle soreness, following high-intensity eccentric exercise. Twenty-eight healthy young men performed 30 maximal isokinetic (120°/s) eccentric elbow flexor contractions using an isokinetic dynamometer. U-titin concentration, serum CK activity, T2, MVC torque, ROM, and muscle soreness were measured before and after a maximum of 4 days. Both U-titin concentration and serum CK activity increased post-exercise in a similar manner, though the former elevated slightly earlier (p < 0.05). The peak values of log U-titin concentration following eccentric exercise were strongly correlated with those of log serum CK activity (r = 0.90, p < 0.05) and T2 (r = 0.84, p < 0.05). There were moderate correlations between peak values of U-titin concentration and those of MVC torque (r = 0.69, p < 0.05) and ROM decline rate (r = 0.45, p < 0.05). These results suggest that in healthy young men, the non-invasive marker, U-titin, may be used as a serum CK surrogate following exercise-induced severe muscle damage.

Nociceptor Overexpression of NaV1.7 Contributes to Chronic Muscle Pain Induced by Early-Life Stress.

Adult rats previously submitted to neonatal limited bedding (NLB), a model of early-life stress, display muscle mechanical hyperalgesia and nociceptor hyperexcitability, the underlying mechanism for which is unknown. Since voltage-gated sodium channel subtype 7 (NaV1.7) contributes to mechanical hyperalgesia in several preclinical pain models and is critical for nociceptor excitability, we explored its role in the muscle hyperalgesia exhibited by adult NLB rats. Western blot analyses demonstrated increased NaV1.7 protein expression in L4-L5 dorsal root ganglia (DRG) from adult NLB rats, and antisense oligodeoxynucleotide (AS ODN) targeting NaV1.7 alpha subunit mRNA attenuated the expression of NaV1.7 in DRG extracts. While this AS ODN did not affect nociceptive threshold in normal rats it significantly attenuated hyperalgesia in NLB rats. The selective NaV1.7 activator OD1 produced dose-dependent mechanical hyperalgesia that was enhanced in NLB rats, whereas the NaV1.7 blocker ProTx-II prevented OD1-induced hyperalgesia in control rats and ongoing hyperalgesia in NLB rats. AS ODN knockdown of extracellular signal-regulated kinase 1/2, which enhances NaV1.7 function, also inhibited mechanical hyperalgesia in NLB rats. Our results support the hypothesis that overexpression of NaV1.7 in muscle nociceptors play a role in chronic muscle pain induced by early-life stress, suggesting that NaV1.7 is a target for the treatment of chronic muscle pain. PERSPECTIVE: We demonstrate that early-life adversity, induced by exposure to inconsistent maternal care, produces chronic muscle hyperalgesia, which depends, at least in part, on increased expression of NaV1.7 in nociceptors.

Salivary Immunoendocrine and Self-report Monitoring Profiles across an Elite-Level Professional Football Season.

PURPOSE: This investigation examined the longitudinal changes and interrelationships of salivary and self-report monitoring measures across a professional football season. METHODS: Measures were collected biweekly from 18 senior professional male players across a 6-wk preseason and eight 5-wk in-season mesocycles and analyzed using a linear mixed-effects model. RESULTS: Analysis identified a small (P = 0.003) cross-season suppression of salivary immunoglobulin A, small reductions to salivary α-amylase (P = 0.047) and salivary cortisol (P = 0.007), and trivial changes to salivary testosterone (P > 0.05). The testosterone/cortisol ratio typically responded inversely to changes in player workload. Self-report measures of fatigue (P = 0.030), sleep quality (P = 0.003), and muscle soreness (P = 0.005) improved (ES = small) across the first half of the season. Fatigue and sleep measures were most consistently related to hormonal measures (R2 = 0.43-0.45). For these relationships, increases in cortisol were associated with compromised self-report responses, whereas increases in testosterone/cortisol were associated with improved responses. Nonlinear relationships were identified for fatigue with immunoglobulin A (P = 0.017; ES = trivial) and testosterone (P = 0.012; ES = trivial), for sleep quality with testosterone (P < 0.001; ES = trivial), for muscle soreness with testosterone (P = 0.012; ES = trivial), and for the self-report inventory sum with testosterone (P = 0.027; ES = trivial). For these relationships, self-report responses were optimal at mean immunoglobulin A and testosterone levels, and very low levels (-2 SD) exerted the most compromising effects. CONCLUSIONS: Players can experience a chronic cross-season suppression of mucosal immunity. Salivary immunoglobulin A, testosterone, cortisol, and testosterone/cortisol measures relate to self-report measures of fatigue, sleep quality, and muscle soreness. In-season reductions in testosterone, cortisol, and testosterone/cortisol or increases in cortisol among elite football players could be used to indicate the need for reduced workload, which might lead to improved well-being.

Prostaglandin 15d-PGJ2 targets PPARγ and opioid receptors to prevent muscle hyperalgesia in rats.

Pharmacological agents directed to either opioid receptors or peroxisome proliferator-activated receptor gamma (PPARγ) at peripheral tissues reduce behavioral signs of persistent pain. Both receptors are expressed in muscle tissue, but the contribution of PPARγ activation to muscle pain and its modulation by opioid receptors remains unknown. To address this question, we first tested whether the endogenous PPARγ ligand 15d-PGJ2 would decrease mechanical hyperalgesia induced by carrageenan administration into the gastrocnemius muscle of rats. Next, we used receptor antagonists to determine whether the antihyperalgesic effect of 15-deoxyΔ-12,14-prostaglandin J2 (15d-PGJ2) was PPARγ- or opioid receptor-dependent. Three hours after carrageenan, muscle hyperalgesia was quantified with the Randall-Selitto test. 15d-PGJ2 prevented carrageenan-induced muscle hyperalgesia in a dose-dependent manner. The antihyperalgesic effect of 15d-PGJ2 was dose-dependently inhibited by either the PPARγ antagonist, 2-chloro-5-nitro-N-phenylbenzamide, or by the opioid receptor antagonist, naloxone. We conclude that 15d-PGJ2 targets PPARγ and opioid receptors to prevent muscle hyperalgesia. We suggest that local PPARγ receptors are important pharmacological targets for inflammatory muscle pain.

Effect of eccentric exercise on markers of muscle damage in patients with chronic obstructive pulmonary disease.

Background: Eccentric exercise may be considered as an attractive alternative to conventional exercise in pulmonary rehabilitation (PR) for patients with chronic obstructive pulmonary disease (COPD). However, due to muscle damage associated with eccentric exercise, there has been reluctance in using this exercise form in PR.Objective: The aim of the present study was to investigate the effect of eccentric exercise on markers of muscle damage in patients with COPD.Methods: We analyzed 14 patients with moderate-severe COPD and 14 age-matched healthy controls. Both groups performed submaximal eccentric exercise of the elbow flexors. Muscle soreness (MS), maximum voluntary isometric contraction (MVC) of the elbow flexors, elbow range of motion (ROM), upper arm circumference (CIR), and biochemical markers such as creatine Kinase (CK) and lactate Dehydrogenase (LDH) were measured at pre-exercise, 24 h, 48 h, and 72 h following submaximal eccentric exercise.Results: There was a significant difference in markers of muscle damage, MS (p = .002), MVC (p < .001), ROM (p = .010), CIR (p < .001), and LDH (p = .001). However, no significant differences were observed in the activity of CK (p = .261) between COPD and control group following eccentric exercise which indicates greater degree of muscle damage in COPD as compared with control.Conclusion: Sub-maximal eccentric exercise causes significantly greater muscle damage in elderly COPD patients than healthy controls. Therefore, initial exercise should be progressed with lower intensities to prevent undue muscle damage in these patients.

Eccentric exercise per se does not affect muscle damage biomarkers: early and late phase adaptations.

PURPOSE: Acute high-intensity unaccustomed eccentric exercise performed by naive subjects is accompanied by disturbances in muscle damage biomarkers. The aim of the study was to investigate whether a causal relationship indeed exists between eccentric exercise and muscle damage. METHODS: Twenty-four men randomly assigned into a concentric only or an eccentric-only training group and performed 10 weeks of isokinetic resistance exercise (one session/week of 75 maximal knee extensors actions). Physiological markers of muscle function and damage (i.e., range of motion, delayed onset muscle soreness, isometric, concentric and eccentric peak torque) were assessed prior to and 1-3 and 5 days post each session. Biochemical markers of muscle damage (creatine kinase) and inflammation (C-reactive protein) were measured prior and 2 days post each session. RESULTS: After the first bout, eccentric exercise induced greater muscle damage compared to concentric exercise; however, during the nine following sessions, this effect progressively diminished, while after the 10th week of training, no alterations in muscle damage biomarkers were observed after either exercise protocol. Additionally, strength gains at the end of the training period were comparable between the two groups and were mode-specific. CONCLUSION: (1) eccentric exercise per se does not affect muscle damage biomarkers; (2) muscle damage occurs as a result of muscle unaccustomedness to this action type; (3) exercise-induced muscle damage is not a prerequisite for increased muscle strength. Collectively, we believe that muscle unaccustomedness to high-intensity eccentric exercise, and not eccentric exercise per se, is the trigger for muscle damage as indicated by muscle damage biomarkers.

Peripheral EphrinB1/EphB1 signalling attenuates muscle hyperalgesia in MPS patients and a rat model of taut band-associated persistent muscle pain.

BACKGROUND: Myofascial pain syndrome (MPS) is an important clinical condition that is characterized by chronic muscle pain and a myofascial trigger point (MTrP) located in a taut band (TB). Previous studies showed that EphrinB1 was involved in the regulation of pathological pain via EphB1 signalling, but whether EphrinB1-EphB1 plays a role in MTrP is not clear. METHODS: The present study analysed the levels of p-EphB1/p-EphB2/p-EphB3 in biopsies of MTrPs in the trapezius muscle of 11 MPS patients and seven healthy controls using a protein microarray kit. EphrinB1-Fc was injected intramuscularly to detect EphrinB1s/EphB1s signalling in peripheral sensitization. We applied a blunt strike to the left gastrocnemius muscles (GM) and eccentric exercise for 8 weeks with 4 weeks of recovery to analyse the function of EphrinB1/EphB1 in the muscle pain model. RESULTS: P-EphB1, p-EphB2, and p-EphB3 expression was highly increased in human muscles with MTrPs compared to healthy muscle. EphB1 (r = 0.723, n = 11, P < 0.05), EphB2 (r = 0.610, n = 11, P < 0.05), and EphB3 levels (r = 0.670, n = 11, P < 0.05) in the MPS group were significantly correlated with the numerical rating scale (NRS) in the MTrPs. Intramuscular injection of EphrinB1-Fc produces hyperalgesia, which can be partially prevented by pre-treatment with EphB1-Fc. The p-EphB1 contents in MTrPs of MPS animals were significantly higher than that among control animals (P < 0.01). Intramuscular administration of the EphB1 inhibitor EphB1-Fr significantly suppressed mechanical hyperalgesia. CONCLUSIONS: The present study showed that the increased expression of p-EphB1/p-EphB2/p-EphB3 was related to MTrPs in patients with MPS. This report is the first study to examine the function of EphrinB1-EphB1 signalling in primary muscle afferent neurons in MPS patients and a rat animal model. This pathway may be one of the most important and promising targets for MPS.

Physiological Response Differences between Run and Cycle High Intensity Interval Training Program in Recreational Middle Age Female Runners.

The aim of this investigation was to compare the changes in endurance running performance and physiological variables after a four-week period of high intensity interval training (HIIT) in either running or cycling in female athletes. Fourteen recreational female runners (age = 42 10 yr, height = 1.67 0.06 m, body mass = 61.6 10.4 kg, body mass index (BMI) = 22.2 3.4 kg.m-2) were randomly allocated to one of two HIIT training groups: running (HIITrun) or cycling (HIITbike). Each group performed two HIIT sessions per week for 4 weeks, which consisted of 6 x 2 min at 95% of maximal heart rate (HRmax) and 4 x 1 min all out efforts. Maximal oxygen consumption (VO2max) in treadmill running increased significantly after the HIITrun (p < 0.01, ES = 0.6) but remained unchanged in HIITbike. However, HIITbike improved average velocity in a 10 km running time trial (TTrun) (p < 0.05, ES = -0.4), whereas, no changes were found for the HIITrun group. Analysing the first and last HIIT sessions, for HIITrun only the average rate of perceived exertion (RPEav) increased significantly, whereas, performance variables such as average heart rate (HRav) and average pace (paceav) remained unchanged. HIITbike enhanced significantly the average speed of HIIT sets (speedav) and the peak power output (PPO) of the session, as well as, the RPEav and delayed onset muscle soreness immediately after HIIT session (DOMSpost) were increased significantly. A regime of HIIT in cycling may evoke increases in female recreational runners' power, which may be related with improvements in a 10 km TTrun independent of changes in aerobic capacity. This may be advantageous in order to avoid overuse running related injuries.