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Kazuyuki Arakawa,1,2 Akihiro Hosono,2 Kiyoshi Shibata,3 Reza Ghadimi,4 Mizuho Fuku,5 Chiho Goto,6 Nahomi Imaeda,7 Yuko Tokudome,8 Hideki Hoshino,9 Mitsuhiro Marumoto,1,2 Masaaki Kobayashi,10 Sadao Suzuki,2 Shinkan Tokudome1,2,11 1Department of Health and Nutrition Policy, 2Department of Public Health, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; 3Department of Public Health and Nutrition, Aichi Gakusen University, Okazaki, Japan; 4Social Determinants of Health Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran; 5Department of Rehabilitation Medicine, Yokohama Stroke and Brain Center, Yokohama, Japan; 6Department of Health and Nutrition, Nagoya Bunri University, Inazawa, Japan; 7Department of Food Science and Nutrition, Nagoya Women’s University, Nagoya, Japan; 8Department of Nutritional Sciences, Nagoya University of Arts and Sciences, Nisshin, Japan; 9Department of Early Childhood Studies, Aichi Bunkyo Women’s College, Inazawa, Japan; 10Department of Orthopaedic Surgery, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; 11National Institute of Health and Nutrition, Tokyo, Japan Abstract: We studied changes in blood markers of 18 nonprofessional, middle-aged runners of a 2-day, 130 km ultramarathon. Blood was sampled at baseline, after the goals on the first and second day, and at three time points (1, 3, and 5/6 days) after the race. Blood indices showed three patterns. First pattern indices showed essentially no changes after the two goals and after the race, including red blood cell indices, gamma-glutamyl transferase, and tumor necrosis factor-α. Second pattern markers, including the majority of indices, were elevated during the race (and also after the race for some parameters) and then returned to baseline afterward, including hemolysis/red blood cell destruction markers (indirect bilirubin) and an iron reservoir index (ferritin), muscle damage parameters (uric acid, creatine kinase, lactate dehydrogenase, and aspartate aminotransferase), renal function markers (creatinine and blood urea nitrogen), liver injury index (alanine aminotransferase), lipid metabolism indices (free fatty acid), reactive oxygen species and inflammation parameters (white blood cells, interleukin-6, and C-reactive protein), and energy production and catecholamines (adrenaline, noradrenaline, and dopamine). Third pattern index of a lipid metabolism marker – triglyceride – decreased during the race periods and started returning to baseline from then onward. Some hormonal markers such as insulin, leptin, and adiponectin showed unique patterns. These findings appeared informative for nonprofessional athletes to know about an optimal physical activity level, duration, and total exercise for elevating physical performance and monitoring physical/mental conditioning as well as for prevention of overtraining and physical injuries. Keywords: long-distance running, blood biochemical markers, anemia, muscle damage, lipid metabolism, inflammation

MOTS-c is a mitochondrial microprotein that improves metabolism. Here, we demonstrate CK2 is a direct and functional target of MOTS-c. MOTS-c directly binds to CK2 and activates it in cell-free systems. MOTS-c administration to mice prevented skeletal muscle atrophy and enhanced muscle glucose uptake, which were blunted by suppressing CK2 activity. Interestingly, the effects of MOTS-c are tissue-specific. Systemically administered MOTS-c binds to CK2 in fat and muscle, yet stimulates CK2 activity in muscle while suppressing it in fat by differentially modifying CK2-interacting proteins. Notably, a naturally occurring MOTS-c variant, K14Q MOTS-c, has reduced binding to CK2 and does not activate it or elicit its effects. Male K14Q MOTS-c carriers exhibited a higher risk of sarcopenia and type 2 diabetes (T2D) in an age- and physical-activity-dependent manner, whereas females had an age-specific reduced risk of T2D. Altogether, these findings provide evidence that CK2 is required for MOTS-c effects., Competing Interests: Pinchas Cohen is an advisor to and stockholder in CohBar Inc. UCLA has licensed the intellectual property on MOTS-c, on which Pinchas Cohen is listed as an inventor, to CohBar. None of the other authors has any conflicts of interest, financial or otherwise, to disclose., (© 2024 The Author(s).)

This study aimed to clarify 1 ) the influence of genetic polymorphisms in the cytochrome P450 aromatase gene ( CYP19A1 ) on circulating estradiol levels in men and 2 ) whether estrogen-related genetic polymorphisms, such as the CYP19A1 rs936306 and estrogen receptor-α ( ESR1 ) rs2234693 polymorphisms, predict exercise-induced serum creatine kinase (CK) activity, which is an index of skeletal muscle membrane disruption. Serum estradiol levels were examined in young men ( n = 167). In a different cohort, serum CK activity was analyzed in a 2-day ultramarathon race: baseline, after the first day, and after the second day (114 males and 25 females). Genetic polymorphisms in CYP19A1 rs936306 C/T and ESR1 rs2234693 T/C were analyzed using the TaqMan SNP Genotyping Assay. Male subjects with the TT genotype of the CYP19A1 polymorphism exhibited significantly higher serum estradiol levels than the C allele carriers. Male runners had significantly higher postrace serum CK activity than female runners. The change in the CK activity during the ultramarathon race was significantly lower in male subjects with the CYP19A1 TT genotype than in those with the CC + CT genotypes and was correlated with the number of C alleles in ESR1 rs2234693 in male subjects. Furthermore, the genotype scores of these two polymorphisms were significantly correlated with changes in serum CK activity during race ( r = -0.279, P = 0.003). The results of this study suggest that genetic polymorphisms in CYP19A1 rs936306 influence serum estradiol levels in men, and genetic polymorphisms in CYP19A1 and ESR1 are associated with serum CK activity in men. NEW & NOTEWORTHY Men with the TT genotype of the CYP19A1 polymorphism exhibited higher circulating estradiol levels than the TC + CC genotype. The TT genotype in the CYP19A1 polymorphism and the C allele of the ESR1 polymorphism, an allele increasing ESR1 expression, were associated with low serum CK activity after the ultramarathon. A combination of these polymorphisms was correlated with changes in the serum CK activity. Therefore, estrogen-related genetic polymorphisms partially predict exercise-induced muscle damage, that is, skeletal muscle membrane disruption.

Objectives: Changes in plasma thioredoxin (TRX) concentrations before, during, and after a 130-km endurance race were measured with the aim of elucidating the relationship between exercise and oxidative stress (OS)., Methods: Blood samples were taken from 18 runners participating in a 2-day-long 130-km ultra-marathon during the 2 days of the race and for 1 week thereafter. There were six sampling time points: at baseline, after the goal had been reached on the first and second day of the endurance race, respectively, and on 1, 3, and 5/6 days post-endurance race. The samples were analyzed for plasma TRX concentrations, platelet count, and blood lipid profiles., Results: Concentrations of plasma TRX increased from 17.9 ± 1.2 ng/mL (mean ± standard error of the mean) at baseline to 57.3 ± 5.0 ng/mL after the first day's goal had been reached and to 70.1 ± 6.9 ng/mL after the second day's goal had been reached; it then returned to the baseline level 1 day after the race. Platelet counts of 21.3 ± 1.2 × 10(4) cell/μL at baseline increased to 23.9 ± 1.5 × 10(4) cells/μL on Day 1 and to 26.1 ± 1.0 × 10(4) cells/μL on Day 2. On Day 7, the platelet counts had fallen to 22.1 ± 1.2 × 10(4) cell/μL. There was a significant positive correlation between plasma TRX and platelet count., Conclusions: These data suggest that plasma TRX is an OS marker during physical exercise. Further studies are needed to determine the appropriate level of exercise for the promotion of health.