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Purpose: Alpha-actinin-3, encoded by the ACTN3 gene, is an actin-binding protein with an important role in myofibril contraction and muscle force output. In humans, there is a relatively common deficiency of the α-actinin-3 due to homozygosity in a polymorphism of the ACTN3 gene (R577X, rs1815739), that has been related to decreased resistance to strain during voluntary muscle contractions. The purpose of this study was to investigate the influence of the ACTN3 genotype on the level of exercise-induced muscle damage attained by 23 experienced triathletes during an official half-ironman competition., Methods: Before and after the race, a sample of venous blood was obtained and jump height was measured during a countermovement jump. The changes in serum creatine kinase (CK-MM isoform) were measured in the blood samples and muscle pain was measured with a visual analogue scale (0-10 cm). Data from RX heterozygotes and XX mutant homozygotes were grouped as X-allele carriers (n = 13) and compared to RR homozygotes (n = 10)., Results: Race time was very similar between groups (313 ± 31 vs. 313 ± 25 min; P = 0.45); however, pre-to-post-competition reduction in jump height was greater in X-allele carriers than RR homozygotes (-18.4 ± 11.4 vs. -8.2 ± 6.9%; P = 0.04). At the end of the race, X-allele carriers presented higher serum CK-MM concentrations (682 ± 144 vs. 472 ± 269 U/L; P = 0.03), and there was also a tendency for higher self-reported values of lower limb muscle pain (7.7 ± 1.1 vs. 6.3 ± 2.3 cm; P = 0.06)., Conclusions: X-allele triathletes in the ACTN3 R577X polymorphism presented greater signs of exercise-induced muscle damage during a half-ironman race than RR homozygotes.

The aim of this study was to investigate the relationship between changes in serum free amino acids, muscle fatigue and exercise-induced muscle damage during a half-ironman triathlon. Twenty-six experienced triathletes (age = 37.0 ± 6.8 yr; experience = 7.4 ± 3.0 yr) competed in a real half-ironman triathlon in which sector times and total race time were measured by means of chip timing. Before and after the race, a countermovement jump and a maximal isometric force test were performed, and blood samples were withdrawn to measure serum free amino acids concentrations, and serum creatine kinase levels as a blood marker of muscle damage. Total race time was 320 ± 37 min and jump height (-16.3 ± 15.2%, P < 0.001) and isometric force (-14.9 ± 9.8%; P = 0.007) were significantly reduced after the race in all participants. After the race, the serum concentration of creatine kinase increased by 368 ± 187% (P < 0.001). In contrast, the serum concentrations of essential (-27.1 ± 13.0%; P < 0.001) and non-essential amino acids (-24.4 ± 13.1%; P < 0.001) were significantly reduced after the race. The tryptophan/BCAA ratio increased by 42.7 ± 12.7% after the race. Pre-to-post changes in serum free amino acids did not correlate with muscle performance variables or post-race creatine kinase concentration. In summary, during a half-ironman triathlon, serum amino acids concentrations were reduced by > 20%. However, neither the changes in serum free amino acids nor the tryptophan/BCAA ratio were related muscle fatigue or muscle damage during the race.

The aim of this study was to determine the changes in body mass and myoglobinuria concentration in recreational runners during a marathon in a warm environment, and the relation of these changes to muscle fatigue. We recruited 138 amateur runners (114 men and 24 women) for the study. Before the race, leg muscle power output was measured during a countermovement jump on a force platform, body weight was measured, and a urine sample was obtained. Within 3 min of race completion (28 °C; 46% relative humidity), the runners repeated the countermovement jump, body weight was measured again, and a second urine sample was obtained. Myoglobin concentration was determined in the urine samples. After the race, mean body mass reduction was 2.2% ± 1.2%. Fifty-five runners (40% of the total) reduced their body mass by less than 2%, and 10 runners (7.2%) reduced their body mass by more than 4%. Only 3 runners increased their body mass after the marathon. Mean leg muscle power reduction was 16% ± 10%. Twenty-four runners reduced their muscle power by over 30%. No myoglobin was detected in the prerace urine specimens, whereas postrace urinary myoglobin concentration increased to 3.5 ± 9.5 μg·mL(-1) (p < 0.05). Muscle power change after the marathon significantly correlated with postrace urine myoglobin concentration (r = -0.55; p < 0.001), but not with body mass change (r = -0.08; p = 0.35). After a marathon in a warm environment, interindividual variability in body mass change was high, but only 7% of the runners reduced their body mass by more than 4%. The correlation between myoglobinuria and muscle power change suggests that muscle fatigue is associated with muscle breakdown.

Background: To investigate the cause/s of muscle fatigue experienced during a half-iron distance triathlon., Methodology/principal Findings: We recruited 25 trained triathletes (36±7 yr; 75.1±9.8 kg) for the study. Before and just after the race, jump height and leg muscle power output were measured during a countermovement jump on a force platform to determine leg muscle fatigue. Body weight, handgrip maximal force and blood and urine samples were also obtained before and after the race. Blood myoglobin and creatine kinase concentrations were determined as markers of muscle damage., Results: Jump height (from 30.3±5.0 to 23.4±6.4 cm; P<0.05) and leg power output (from 25.6±2.9 to 20.7±4.6 W · kg(-1); P<0.05) were significantly reduced after the race. However, handgrip maximal force was unaffected by the race (430±59 to 430±62 N). Mean dehydration after the race was 2.3±1.2% with high inter-individual variability in the responses. Blood myoglobin and creatine kinase concentration increased to 516±248 µg · L(-1) and 442±204 U · L(-1), respectively (P<0.05) after the race. Pre- to post-race jump change did not correlate with dehydration (r = 0.16; P>0.05) but significantly correlated with myoglobin concentration (r = 0.65; P<0.001) and creatine kinase concentration (r = 0.54; P<0.001)., Conclusions/significance: During a half-iron distance triathlon, the capacity of leg muscles to produce force was notably diminished while arm muscle force output remained unaffected. Leg muscle fatigue was correlated with blood markers of muscle damage suggesting that muscle breakdown is one of the most relevant sources of muscle fatigue during a triathlon.

The purpose of the study was to assess the occurrence of muscle damage after a simulated badminton match and its influence on physical and haematological parameters. Sixteen competitive male badminton players participated in the study. Before and just after a 45-min simulated badminton match, maximal isometric force and badminton-specific running/movement velocity were measured to assess muscle fatigue. Blood samples were also obtained before and after the match. The badminton match did not affect maximal isometric force or badminton-specific velocity. Blood volume and plasma volume were significantly reduced during the match and consequently haematite, leucocyte, and platelet counts significantly increased. Blood myoglobin and creatine kinase concentrations increased from 26.5 ± 11.6 to 197.3 ± 70.2 µg·L−1 and from 258.6 ± 192.2 to 466.0 ± 296.5 U·L−1, respectively. In conclusion, a simulated badminton match modified haematological parameters of whole blood and serum blood that indicate the occurrence of muscle fibre damage. However, the level of muscle damage did not produce decreased muscle performance. [ABSTRACT FROM AUTHOR]