J Strength Cond Res 33(10): 2655-2664, 2019-The purpose of this study was to evaluate indicators of muscle damage and hormonal responses after soccer matches and its relation to alpha-actinin-3 (ACTN3) gene expression (XX vs. RR/RX), considering that the R allele produces alpha-actinin-3 and provides greater muscle strength and power.
The intervention group demonstrated a significant increase in serum 25-hydroxyvitamin D levels (53.93, 10.68 ng/mL, P < 0.0001), which is the best indicator of vitamin D levels in the body, with no change in the circulating markers of muscle damage and CRP (P ˃ 0.05) but showed increased IL-6 (P = 0.034).
Israeli runners of Ethiopian origin had a greater frequency of the PPARD CC + PARGC1A Gly/Gly polymorphism, associated with improved endurance performance, compared with Israeli runners of non-Ethiopian origins (24 vs. 3%, respectively, p < 0.01); a lower frequency of the ACSL AA polymorphism, favoring endurance trainability (8 vs. 20%, respectively, p < 0.05); a greater frequency of the ACTN3 RR polymorphism, associated with sprint performance (35 vs. 20%, respectively, p < 0.05); a greater frequency of the MCT1 AA genotype, associated with improved lactate transport (65 vs. 45%, respectively, p < 0.05); and a lower frequency of IL-6 174C carriers, associated with reduced postexercise muscle damage (27 vs. 40%, respectively, p < 0.01).
The deficiency in dystrophin and drastic reduction in dystrophin-associated proteins appears to trigger (i) enhanced membrane repair involving myoferlin, dysferlin and annexins, (ii) increased protein synthesis and the compensatory up-regulation of cytoskeletal proteins, (iii) the decrease in the scaffolding protein periaxin and myelin PO involved in myelination of motor neurons, (iv) complex changes in bioenergetic pathways, (v) elevated levels of molecular chaperones to prevent proteotoxic effects, (vi) increased collagen deposition causing reactive myofibrosis, (vii) disturbed ion homeostasis at the sarcolemma and associated membrane systems, and (viii) a robust inflammatory response by the innate immune system in response to chronic muscle damage.
Blood samples were collected immediately before, after, 2, and 4 hours after the games to assess muscle damage (creatine kinase [CK] and alpha-actin) and hormonal responses (interleukin-6 [IL-6], cortisol, and testosterone).
Taken together, our findings challenge the long-held perception of eosinophils as cytotoxic in dystrophin-deficient muscle; we show clearly that eosinophil infiltration is not a driving force behind acute muscle damage in the mdx mouse strain.
The ACTN3R577X gene variant results in the absence of the α-actinin-3 protein in ∼18% of humans worldwide and has been associated with athletic performance and increased susceptibility to eccentric muscle damage.
Therefore, to determine the impact of the absence of dystrophin on metabolism, we investigated the metabolic and lipid profile at two different, well-defined stages of muscle damage and stabilization in mdx mice.
Muscle damage in collegiate swimmers was modest and peaked after the first week of training (week 2) for men (CK = 438 ± 259 U/L; P < 0.0001; r = 0.28; myoglobin = 47 ± 18 ng/mL; P = 0.001; r = 0.22) and women (CK = 446 ± 723 U/L; P < 0.01; r = 0.13; myoglobin = 63 ± 140 ng/mL, not significant) with high variability.
Israeli runners of Ethiopian origin had a greater frequency of the PPARD CC + PARGC1A Gly/Gly polymorphism, associated with improved endurance performance, compared with Israeli runners of non-Ethiopian origins (24 vs. 3%, respectively, p < 0.01); a lower frequency of the ACSL AA polymorphism, favoring endurance trainability (8 vs. 20%, respectively, p < 0.05); a greater frequency of the ACTN3 RR polymorphism, associated with sprint performance (35 vs. 20%, respectively, p < 0.05); a greater frequency of the MCT1 AA genotype, associated with improved lactate transport (65 vs. 45%, respectively, p < 0.05); and a lower frequency of IL-6 174C carriers, associated with reduced postexercise muscle damage (27 vs. 40%, respectively, p < 0.01).
The present study investigated the informative value of TMG parameters in correlation with commonly used (creatine kinase, CK; myoglobin, Mb) and novel candidate biomarkers of muscle damage (heart-type fatty acid-binding protein, h-FABP; high-mobility group box 1, HMGB1).
There was a significant correlation between blood lactate concentration (post) and blood CK (P=0.027), Mb (P=0.007) and AST (P=0.024) (48 hours post), which means that higher blood lactate concentration is associated with higher muscle damage values after exercise.
Blood samples were obtained before competition (Pre-Comp.), after competition-in ths case meaning four consecutive matches (End-Comp.), and 24 h after the first match (Next day) for determination of biomarkers of muscle damage (myoglobin and CK), hematological profiles, and hormonal profiles (testosterone and cortisol).
In order to verify the effects of the supplementation protocol markers of muscle damage as lactate dehydrogenase (LDH) and creatine kinase (CK), and inflammatory markers tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were quantified, also triathletes' performance was evaluated by exhaust test on a treadmill.
Muscle strength (MVC), muscle damage (CK), oxidative stress (GPx), inflammation (IL6) and volunteer-reported muscle soreness intensity were assessed pre and post exercise.
In terms of muscle damage and inflammatory markers, we observed an overall moderate decrease in creatine kinase [SMD (95% CI) = -0.37 (-0.58 to -0.16), I<sup>2</sup> = 40.15%] and overall small decreases in interleukin-6 [SMD (95% CI) = -0.36 (-0.60 to -0.12), I<sup>2</sup> = 0%] and C-reactive protein [SMD (95% CI) = -0.38 (-0.59 to-0.14), I<sup>2</sup> = 39%].
Along with enhanced FAO capacity during exhaustive exercise, a KD may also alter IL-6 synthesis and secretion profile, thus contribute to fatty acid mobilization, ketolysis, lipolysis and preventing muscle damage.
Since dystrophin is essential in maintaining the integrity of the sarcolemmal membrane, the absence of the protein leads to muscle damage and DMD disease manifestation.
X-allele triathletes in the ACTN3R577X polymorphism presented greater signs of exercise-induced muscle damage during a half-ironman race than RR homozygotes.
These results suggest that urinary N-ter titin is present at low basal concentrations in normal urine and increases dramatically coincident with muscle damage produced by dystrophin deficiency.