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Creatine Kinase and Lactate Dehydrogenase Responses after Different Resistance and Aerobic Exercise Protocols.

ABSTRACT: The aim of this study was to investigate the responses of creatine kinase (CK) and lactate dehydrogenase (LDH) after performing different resistance and aerobic exercise protocols. Twelve recreationally trained men (age, 23.2 ± 5.6 years; body mass, 84.3 ± 9.3 kg; body height, 178.9 ± 4.5 cm; and BMI, 26.3 ± 2.3 kg·m2) volunteered to participate in this study. All subjects were randomly assigned to four experimental protocols (crossover): (a) aerobic training at 60% of VO2max, (b) aerobic training at 80% of VO2max, (c) a resistance exercise (RE) session with a bi-set protocol, and (d) an RE session with a multiple sets protocol. Blood samples were collected before, immediately after and 24 hours following the experimental protocols. After 24 hours, there was a significant increase in CK for the 80% of VO2max protocol vs. the bi-set RE session (p = 0.016). Immediately after the protocols, we observed a significant increase in LDH among certain groups compared to others, as follows: multiple sets RE session vs. 60% of VO2max, bi-set RE session vs. 60% of VO2max, multiple sets RE session vs. 80% of VO2max, and bi-set RE session vs. 80% of VO2max (p = 0.008, p = 0.013; p = 0.002, p = 0.004, respectively). In conclusion, aerobic exercise performed at 80% of VO2max appears to elevate plasma CK levels more than bi-set RE sessions. However, the bi-set and multiple sets RE sessions appeared to trigger greater levels of blood LDH compared to aerobic protocols performed at 60% and 80% of VO2max.

SUBMITTER: Callegari GA

PROVIDER: S-EPMC5548155 | biostudies-other | 2017 Sep

REPOSITORIES: biostudies-other

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Project description:BackgroundMost normal cells in the presence of oxygen utilize glucose for mitochondrial oxidative phosphorylation. In contrast, many cancer cells rapidly convert glucose to lactate in the cytosol, a process termed aerobic glycolysis. This glycolytic phenotype is enabled by lactate dehydrogenase (LDH), which catalyzes the inter-conversion of pyruvate and lactate. The purpose of this study was to identify and characterize potent and selective inhibitors of LDHA.MethodsHigh throughput screening and lead optimization were used to generate inhibitors of LDHA enzymatic activity. Effects of these inhibitors on metabolism were evaluated using cell-based lactate production, oxygen consumption, and 13C NMR spectroscopy assays. Changes in comprehensive metabolic profile, cell proliferation, and apoptosis were assessed upon compound treatment.Results3-((3-carbamoyl-7-(3,5-dimethylisoxazol-4-yl)-6-methoxyquinolin-4-yl) amino) benzoic acid was identified as an NADH-competitive LDHA inhibitor. Lead optimization yielded molecules with LDHA inhibitory potencies as low as 2 nM and 10 to 80-fold selectivity over LDHB. Molecules in this family rapidly and profoundly inhibited lactate production rates in multiple cancer cell lines including hepatocellular and breast carcinomas. Consistent with selective inhibition of LDHA, the most sensitive breast cancer cell lines to lactate inhibition in hypoxic conditions were cells with low expression of LDHB. Our inhibitors increased rates of oxygen consumption in hepatocellular carcinoma cells at doses up to 3 microM, while higher concentrations directly inhibited mitochondrial function. Analysis of more than 500 metabolites upon LDHA inhibition in Snu398 cells revealed that intracellular concentrations of glycolysis and citric acid cycle intermediates were increased, consistent with enhanced Krebs cycle activity and blockage of cytosolic glycolysis. Treatment with these compounds also potentiated PKM2 activity and promoted apoptosis in Snu398 cells.ConclusionsRapid chemical inhibition of LDHA by these quinoline 3-sulfonamids led to profound metabolic alterations and impaired cell survival in carcinoma cells making it a compelling strategy for treating solid tumors that rely on aerobic glycolysis for survival.

Project description:BackgroundIt is unknown whether patients with chronic musculoskeletal pain (CMP) show autonomic dysregulation after exercise, and the interventional effects of exercise on the autonomic dysregulation have not been elucidated. The objectives of this study were to reveal acute autonomic responses after aerobic and resistance exercises and the interventional effects of both exercises on autonomic dysregulation in patients with CMP.MethodsA systematic search using nine electronic databases was performed based on three key search terms: "chronic musculoskeletal pain," "autonomic nervous system," and "exercise." Data were extracted from measurements of the autonomic nervous system and pain.ResultsWe found a total of 1170 articles; 17 were finally included, incorporating 12 observational and five interventional studies. Although a comparator has not been specified, healthy controls were compared to patients with CMP in observational studies. Three of five interventional studies were pre-post study with healthy controls as a comparator or no controls. The other two interventional studies were randomized controlled trial with a different treatment e.g., stretching. There were four good, 10 fair, and three poor-quality articles. The total number of participants was 617, of which 551 were female. There was high heterogeneity among the five disease conditions and nine outcome measures. Following one-time exposure to aerobic and resistance exercises, abnormal autonomic responses (sympathetic activation and parasympathetic withdrawal), which were absent in healthy controls, were observed in patients with CMP. The effects of aerobic and resistance exercise as long-term interventions were unclear since we identified both positive effects and no change in the autonomic activities in patients with CMP.ConclusionsThis study indicates dysfunctional autonomic responses following one-time exposure to exercise and inconsistent interventional effects in the autonomic activities in patients with CMP. Appropriate therapeutic dose is necessary for studying the management of autonomic regulation and pain after exercise.

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Creatine Kinase and Lactate Dehydrogenase Responses after Different Resistance and Aerobic Exercise Protocols.

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