Physical exercise modifies animal metabolism profoundly. Until recently, biochemical investigations related to exercise focused on a small number of biomolecules. In the present study, we used a holistic analytical approach to investigate changes in the human urine metabolome elicited by two exercise sessions differing in the duration of the rest interval between repeated efforts. Twelve men performed three sets of two 80 m maximal runs separated by either 10 s or 1 min of rest. Analysis of pre- and postexercise urine samples by (1)H NMR spectroscopy and subsequent multivariate statistical analysis revealed alterations in the levels of 22 metabolites. Urine samples were safely classified according to exercise protocol even when applying unsupervised methods of statistical analysis. Separation of pre- from postexercise samples was mainly due to lactate, pyruvate, hypoxanthine, compounds of the Krebs cycle, amino acids, and products of branched-chain amino acid (BCAA) catabolism. Separation of the two rest intervals was mainly due to lactate, pyruvate, alanine, compounds of the Krebs cycle, and 2-oxoacids of BCAA, all of which increased more with the shorter interval. Metabonomics provides a powerful methodology to gain insight in metabolic changes induced by specific training protocols and may thus advance our knowledge of exercise biochemistry.

The present study shows that obese children and adolescents were at greater risk for ID and IDA than their normal-weight peers. Low grade inflammation induced by excessive adiposity may be a reason for the observed low iron levels. This is also strengthened by the elevated serum ferritin levels, comprising an acute phase protein that is plausibly increased in inflammation.

Metabonomics is an established strategy in the exploration of the effects of various stimuli on the metabolic fingerprint of biofluids. Here, we present an application of (1)H NMR-based metabonomics on the field of exercise biochemistry. Fourteen men were assigned to either of two training programs, which lasted 8 weeks and involved sets of 80-m maximal runs separated by either 10 s or 1 min of rest. Analysis of pre- and postexercise serum samples, both at the beginning and end of training, by (1)H NMR spectroscopy and subsequent multivariate statistical techniques revealed alterations in the levels of 18 metabolites. Validated O-PLS models could classify the samples in regard to exercise, the separation being mainly due to lactate, pyruvate, alanine, leucine, valine, isoleucine, arginine/lysine, glycoprotein acetyls, and an unidentified metabolite resonating at 8.17 ppm. Samples were also classified safely with respect to training, the separation being mainly due to lactate, pyruvate, methylguanidine, citrate, glucose, valine, taurine, trimethylamine N-oxide, choline-containing compounds, histidines, acetoacetate/acetone, glycoprotein acetyls, and lipids. Samples could not be classified according to the duration of the rest interval between sprints. Our findings underline the power of metabonomics to offer new insights into the short- and long-term impact of exercise on metabolism.

The delineation of exercise biochemistry by utilizing metabolic fingerprinting has become an established strategy. We present a combined RP-UPLC-MS and (1)H NMR strategy, supplemented by photometric assays, to monitor the response of the human urinary metabolome to short maximal exercise. Seventeen male volunteers performed two identical sprint sessions on separate days, consisting of three 80 m maximal runs. Using univariate and multivariate analyses, we followed the fluctuation of 37 metabolites at 1, 1.5, and 2 h postexercise. 2-Hydroxyisovalerate, 2-hydroxybutyrate, 2-oxoisocaproate, 3-methyl-2-oxovalerate, 3-hydroxyisobutyrate, 2-oxoisovalerate, 3-hydroxybutyrate, 2-hydroxyisobutyrate, alanine, pyruvate, and fumarate increased 1 h postexercise and then returned toward baseline. Lactate and acetate were higher than baseline at 1 and 1.5 h. Hypoxanthine and inosine remained above baseline throughout the postexercise period. Urate decreased at 1 h and increased at 1.5 h before returning to baseline. Valine, isoleucine, succinate, citrate, trimethylamine, trimethylamine N-oxide, tyrosine, and formate decreased at 1 h and/or 1.5 h postexercise and then returned to baseline. Creatinine gradually decreased over the sampling period. Glycine, 4-aminohippurate, and hippurate remained below baseline throughout the postexercise period. Our findings show that even one-half minute of maximal exercise elicited major perturbations in human metabolism, several of which persisted for at least 2 h.

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Throughout adolescence, swimmers begin to carry out demanding endurance and high-intensity training sets, the effect of which on redox status is largely unknown. The aim of the present study was to investigate the effects of 2000-m continuous swimming and 6 × 50-m maximal swimming on the redox status of adolescent swimmers. Fifteen male and 15 female swimmers, aged 14-18 years, provided blood samples before, immediately after, 1 h after, and 24 h after each exercise for the determination of redox status parameters. Oxidative damage was short-lived and manifest as increases in 8-hydroxy-2΄-deoxyguanosine (8-OHdG) 1 h after high-intensity exercise (39%, P < 0.001) and in malondialdehyde immediately after both exercises (65%, P < 0.001). Alterations in antioxidant parameters were sustained during recovery: reduced glutathione decreased 24 h post-exercise (11%, P = 0.001), uric acid increased gradually after high-intensity exercise (29%, P < 0.001) and bilirubin peaked 24 h post-exercise (29%, P < 0.001). Males had higher 8-OHdG (49%, P = 0.001) and uric acid (29%, P < 0.001) concentrations than females. However, females showed higher values of malondialdehyde than males immediately post-exercise (30%, P = 0.039), despite lower pre-exercise values. In conclusion, both endurance and high-intensity exercise perturbed the redox balance without inducing prolonged oxidative damage in trained adolescent male and female swimmers. These swimming training trials were not found to be detrimental to the redox homeostasis of adolescents.

The aim of the present study was to monitor the nutritional status of 9 Greek national top-level swimmers during a competitive season of eight months. The swimmers were assessed through recording of food and supplement intake, blood sampling, and anthropometry at four landmarks: in the beginning of the season (baseline), after completing a phase of intensive and voluminous training (at 10 weeks), at a minor taper (19 weeks), and during the major taper (32 weeks). Energy and macronutrient intake did not change significantly over time, and only a few significant changes were found in micronutrient intakes. Low carbohydrate and high fat intakes (e.g., 36 and 42 % of total energy, respectively, in males), inadequate intake of some micronutrients, and improper use of supplements indicated suboptimal dietary habits. Blood hemoglobin fluctuated significantly during the season. No significant changes in parameters indicative of the iron stores (transferrin saturation and ferritin) were found, although iron intake increased by supplementation with the onset of training. Serum markers of training stress were not significantly altered. In conclusion, Greek top-level swimmers should be guided toward a balanced diet and a rational use of supplements. Monitoring of dietary intakes during a competitive season is highly recommended.

Data on redox balance in response to marathon swimming are lacking, whereas findings from studies using other types of ultraendurance exercise are controversial. The aim of the present study was to investigate the effect of ultramarathon swimming on selective blood oxidative stress markers. Five well-trained male swimmers aged 28.8 (6.0) years participated in the study. Blood samples were obtained before and after the ultramarathon swimming, for full blood count analysis and determination of protein carbonyls, thiobarbituric acid-reactive substances (TBARS), and total antioxidant capacity (TAC). The swimmers swam 19.4 (3.4) hours, covering 50.5 (15.0) km. Hematocrit and erythrocyte count, and leukocyte, neutrophil and monocyte counts were significantly elevated after swimming, whereas protein carbonyls, TBARS and TAC did not significantly change. The findings of the present study indicate that well-trained swimmers were able to regulate a redox homeostasis during ultra-long duration swimming. It is also postulated that the relatively low intensity of marathon swimming may not be a sufficient stimulus to induce oxidative stress in well-trained swimmers. The fact that low-intensity long-duration exercise protocols are not associated with oxidative damage is useful knowledge for coaches and athletes in scheduling the content of the training sessions that preceded and followed these exercise protocols.