Free radical-mediated lipid peroxidation and systemic nitric oxide bioavailability: implications for postexercise hemodynamics

Karl J New, Michael E Reilly, Kath Templeton, Gethin Ellis, Philip E James, Jane Mceneny, Michael Penney, James Hooper, Dave Hullin, Bruce Davies, Damian M Bailey

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)



The metabolic vasodilator mediating postexercise hypotension (PEH) is poorly understood. Recent evidence suggests an exercise-induced reliance on pro-oxidant–stimulated vasodilation in normotensive young human subjects, but the role in the prehypertensive state is not known.


Nine prehypertensives (mean arterial pressure (MAP), 106±5mm Hg; 50 ± 10 years old) performed 30 minutes of cycle exercise and a nonexercise trial. Arterial distensibility was characterized by simultaneously recording upper- and lower-limb pulse wave velocity (PWV) via oscillometry. Systemic vascular resistance and conductance were determined by MAP/Q˙ and Q˙/MAP, respectively. Venous blood was assayed for indirect markers of oxidative stress (lipid hydroperoxides (LOOH); spectrophotometry), plasma nitric oxide (NO) and S-nitrosothiols (fluorometry), atrial natriuretic peptide (ANP), and angiotensin II (ANG-II) (radioimmunoassay).


Exercise reduced MAP (6mm Hg) and vascular resistance (15%) at 60 minutes after exercise, whereas conductance was elevated (20%) (P < 0.05). The hypotension resulted in a lower MAP at 60 and 120 minutes after exercise compared with nonexercise (P < 0.05). Upper-limb PWV was also 18% lower after exercise compared with baseline (P < 0.05). Exercise increased LOOH coincident with the nadir in hypotension and vascular resistance but failed to affect plasma NO or S-nitrosothiols. Exercise-induced increases in LOOH were related to ANG-II (r = 0.97; P < 0.01) and complemented by elevated ANP concentrations.


These data indicate attenuated vascular resistance after exercise with increased oxidative stress and unchanged NO. Whether free radicals are obligatory for PEH requires further investigation, although it seems that oxidative stress occurs during the hyperemia underlying PEH.

Original languageEnglish
Pages (from-to)126-134
JournalAmerican Journal of Hypertension
Issue number1
Early online date13 Dec 2012
Publication statusPublished - Jan 2013


  • Adult
  • Antioxidants
  • Arterial Pressure
  • Biological Availability
  • Exercise
  • Heart Rate
  • Hemodynamics
  • Humans
  • Lipid Peroxidation
  • Male
  • Middle Aged
  • Nitric Oxide
  • Post-Exercise Hypotension
  • Prehypertension
  • Pulse Wave Analysis
  • S-Nitrosothiols
  • Vascular Resistance
  • Vasodilation


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