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).
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).
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).
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.
Markers of muscle damage (LDH, CK, and Mb) were significantly elevated following both HV and HI (p < 0.05), while cortisol and IL-6 concentrations were significantly elevated at P-30 min following HV only (p < 0.001 and p < 0.05, respectively).
The main aim of this study was to assess and compare the kinetics of blood brain-derived neurotrophic factor (BDNF), norepinephrine (NE) and cortisol (as stress indicators) and proinflammatory (IL-6) and anti-inflammatory (IL-10) cytokines within 24 hours after metabolically demanding SIE and after muscle damage inducing SSE.
We present an adolescent elite water polo player who despite a genetic predisposition to develop exercise-induced severe muscle damage due to carrying the IL-6 174C allele single-nucleotide polymorphism, developed acute rhabdomyolysis only after a vigorous out-of-water training, suggesting that water polo training may be more suitable for genetically predisposed athletes.
Blood samples were taken from athletes pre-eccentric training, immediately after (post), 2- and 4-h post-eccentric training to determine hormone responses (cortisol and testosterone), muscle damage (CK and α-actin), and inflammatory responses (IL-6).
We evaluated changes in markers of exercise-induced skeletal muscle damage and inflammation [serum creatine kinase (CK), serum lactate dehydrogenase (LDH), and skeletal muscle mRNA expression of IL-6, IL-8, IL-15, and TNF-alpha] in postmenopausal women after a high-intensity resistance exercise bout.