Adenine, guanine and pyridine nucleotides in blood during physical exercise and restitution in healthy subjects

Maximal physical exertion is accompanied by increased degradation of purine nucleotides in muscles with the products of purine catabolism accumulating in the plasma. Thanks to membrane transporters, these products remain in an equilibrium between the plasma and red blood cells where they may serve as substrates in salvage reactions, contributing to an increase in the concentrations of purine nucleotides. In this study, we measured the concentrations of adenine nucleotides (ATP, ADP, AMP), inosine nucleotides (IMP), guanine nucleotides (GTP, GDP, GMP), and also pyridine nucleotides (NAD, NADP) in red blood cells immediately after standardized physical effort with increasing intensity, and at the 30th min of rest. We also examined the effect of muscular exercise on adenylate (guanylate) energy charge—AEC (GEC), and on the concentration of nucleosides (guanosine, inosine, adenosine) and hypoxanthine. We have shown in this study that a standardized physical exercise with increasing intensity leads to an increase in IMP concentration in red blood cells immediately after the exercise, which with a significant increase in Hyp concentration in the blood suggests that Hyp was included in the IMP pool. Restitution is accompanied by an increase in the ATP/ADP and ADP/AMP ratios, which indicates an increase in the phosphorylation of AMP and ADP to ATP. Physical effort applied in this study did not lead to changes in the concentrations of guanine and pyridine nucleotides in red blood cells

Metabolomic Response to Acute Hypoxic Exercise and Recovery in Adult Males

Metabolomics is a relatively new “omics” approach used to characterize metabolites in a biological system at baseline and following a diversity of stimuli. However, the metabolomic response to exercise in hypoxia currently remains unknown. To examine this, 24 male participants completed 1 h of exercise at a workload corresponding to 75% of pre-determined O2max in hypoxia (Fio2 = 0.16%), and repeated in normoxia (Fio2 = 0.21%), while pre- and post-exercise and 3 h post-exercise metabolites were analyzed using a LC ESI-qTOF-MS untargeted metabolomics approach in serum samples. Exercise in hypoxia and in normoxia independently increased metabolism as shown by a change in a combination of twenty-two metabolites associated with lipid metabolism (p < 0.05, pre vs. post-exercise), though hypoxia per se did not induce a greater metabolic change when compared with normoxia (p > 0.05). Recovery from exercise in hypoxia independently decreased seventeen metabolites associated with lipid metabolism (p < 0.05, post vs. 3 h post-exercise), compared with twenty-two metabolites in normoxia (p < 0.05, post vs. 3 h post-exercise). Twenty-six metabolites were identified as responders to exercise and recovery (pooled hypoxia and normoxia pre vs. recovery, p < 0.05), including metabolites associated with purine metabolism (adenine, adenosine and hypoxanthine), the amino acid phenylalanine, and several acylcarnitine molecules. Our novel data provides preliminary evidence of subtle metabolic differences to exercise and recovery in hypoxia and normoxia. Specifically, exercise in hypoxia activates metabolic pathways aligned to purine and lipid metabolism, but this effect is not selectively different from exercise in normoxia. We also show that exercise per se can activate pathways associated with lipid, protein and purine nucleotide metabolism

Sprint training reduces urinary purine loss following intense exercise in humans

The influence of sprint training on endogenous urinary purine loss was examined in seven active male subjects (age: 23.1 ± 1.8 years, weight: 76.1 ± 3.1 kg, VO2peak: 56.3 ± 4.0 ml.kg-1.min-1). Each subject performed a 30s sprint performance test (PT), before and after 7 days of sprint training. Training consisted of fifteen 10s sprints on an air-braked cycle ergometer performed twice per day. A rest period of 50s separated each sprint during training. Sprint training resulted in a 20% higher muscle ATP immediately after PT, a lower IMP (57% and 89%, immediately following and after 10 min recovery from PT, respectively), and inosine accumulation (53% and 56%, immediately following and 10 min after the PT, respectively). Sprint training also attenuated the exercise-induced increases in plasma inosine, hypoxanthine (Hx) and uric acid during the first 120 min of recovery and reduced the total urinary excretion of purines (inosine + Hx + uric acid) in the 24 hours recovery following intense exercise. These results show that intermittent sprint training reduces the total urinary purine excretion after a 30s sprint bout