Physical performance level in sarcomeric mitochondria creatine kinase knockout mouse model throughout ageing

The objective of the present study was to establish role sarcomeric mitochondrial creatine kinase (Mt-CK) in muscle energy output during exercise a murine model ageing (the Mt-CK knock-out mouse, Mt-CK?/?). Three age groups Mt-CK?/? mice and control male (6, 9, 18 months age) underwent incremental treadmill running tests. maximum speed (Vpeak) maximal oxygen consumption (VO2peak) values were recorded. Urine samples analyzed using metabolomic techniques. skeletal (quadriceps) expression proteins involved mitochondria biogenesis, peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1?) dynamin-related GTPase mitofusin 2 (Mnf2) quantified. VO2 peak (normalized heart weight: HW) 18-month-old (mo) 27% (p < 0.001) lower than 18-mo mice. VO2peak/HW ratio 29% 6-mo 32% 9-mo With 0° slope, Vpeak 10% 0.05) but did not differ when comparing groups. muscles weight normalized on body 13 14% 0.001, p versus control, addition, presence branched-chain amino acids urine suggests an imbalance protein turnover (catabolism rather anabolism) we observe any age-related differences. PGC-1? Mnf2 quadriceps showed that effects more prominent genotype effects. is potentialized by deficiency with regard VO2peak, expression. Our results support undergo physiological adaptations, enabling them survive perform as well wild-type Furthermore, it possible these adaptations have high cost might trigger premature ageing.