Regulation of free radical outflow from an isolated muscle bed in exercising humans.

Depts. of Anesthesiology and Surgery, Colorado Center for Altitude Medicine and Physiology, University of Colorado Health Sciences Center, PO Box 6508, Mail Stop F524, Aurora, CO 80111, USA.
AJP Heart and Circulatory Physiology (Impact Factor: 4.01). 11/2004; 287(4):H1689-99. DOI: 10.1152/ajpheart.00148.2004
Source: PubMed

ABSTRACT Incremental knee extensor (KE) exercise performed at 25, 70, and 100% of single-leg maximal work rate (WR(MAX)) was combined with ex vivo electron paramagnetic resonance (EPR) spectroscopic detection of alpha-phenyl-tert-butylnitrone (PBN) adducts, lipid hydroperoxides (LH), and associated parameters in five males. Blood samples were taken from the femoral arterial and venous circulation that, when combined with measured changes in femoral venous blood flow, permitted a direct examination of oxidant exchange across a functionally isolated contracting muscle bed. KE exercise progressively increased the net outflow of LH and PBN adducts (100% > 70% > 25% WR(MAX), P < 0.05) consistent with the generation of secondary, lipid-derived oxygen (O(2))-centered alkoxyl and carbon-centered alkyl radicals. Radical outflow appeared to be more intimately associated with predicted decreases in intracellular Po(2) (iPo(2)) as opposed to measured increases in leg O(2) uptake, with greater outflow recorded between 25 and 70% WR(MAX) (P < 0.05 vs. 70-100% WR(MAX)). This bias was confirmed when radical venoarterial concentration differences were expressed relative to changes in the convective components of O(2) extraction and flow (25-70% WR(MAX) P < 0.05 vs. 70-100% WR(MAX), P > 0.05). Exercise also resulted in a net outflow of other potentially related redox-reactive parameters, including hydrogen ions, norepinephrine, myoglobin, lactate dehydrogenase, and uric acid, whereas exchange of lipid/lipoproteins, ascorbic acid, and selected lipid-soluble anti-oxidants was unremarkable. These findings provide direct evidence for an exercise intensity-dependent increase in free radical outflow across an active muscle bed that was associated with an increase in sarcolemmal membrane permeability. In addition to increased mitochondrial electron flux subsequent to an increase in O(2) extraction and flow, exercise-induced free radical generation may also be regulated by changes in iPo(2), hydrogen ion generation, norepinephrine autoxidation, peroxidation of damaged tissue, and xanthine oxidase activation.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract 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.
    Journal of Sports Sciences 01/2014; · 2.08 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: This investigation sought to determine if supplementation with polyphenol antioxidant (PA) improves exercise performance in the heat (31.5 °C, 55% RH) by altering the cardiovascular and thermoregulatory responses to exercise. Twelve endurance trained athletes ingested PA or placebo (PLAC) for 7 days. Consecutive days of exercise testing were performed at the end of the supplementation periods. Cardiovascular and thermoregulatory measures were made during exercise. Performance, as measured by a 10 min time trial (TT) following 50 min of moderate intensity cycling, was not different between treatments (PLAC: 292 ± 33 W and PA: 279 ± 38 W, p = 0.12). Gross efficiency, blood lactate, maximal neuromuscular power, and ratings of perceived exertion were also not different between treatments. Similarly, performance on the second day of testing, as assessed by time to fatigue at maximal oxygen consumption, was not different between treatments (PLAC; 377 ± 117 s vs. PA; 364 ± 128 s, p = 0.61). Cardiovascular and thermoregulatory responses to exercise were not different between treatments on either day of exercise testing. Polyphenol antioxidant supplementation had no impact on exercise performance and did not alter the cardiovascular or thermoregulatory responses to exercise in the heat.
    Nutrients 01/2014; 6(3):1273-92. · 3.15 Impact Factor
  • Source