European Journal of Applied Physiology

, Volume 100, Issue 2, pp 225–234

The effect of acute aerobic exercise on pulse wave velocity and oxidative stress following postprandial hypertriglyceridemia in healthy men

  • Conor M. Mc Clean
  • Jim Mc Laughlin
  • George Burke
  • Marie H. Murphy
  • Tom Trinick
  • Ellie Duly
  • Gareth W. Davison
Original Articles

DOI: 10.1007/s00421-007-0422-y

Cite this article as:
Mc Clean, C.M., Mc Laughlin, J., Burke, G. et al. Eur J Appl Physiol (2007) 100: 225. doi:10.1007/s00421-007-0422-y

Abstract

Oxidative stress is postulated to be responsible for the postprandial impairments in vascular function. The purpose of this study was to measure pulse wave velocity (PWV) and markers of postprandial oxidative stress before and after an acute bout of moderate exercise. Ten trained male subjects (age 21.5 ± 2.5 years, VO2 max 58.5 ± 7.1 ml kg−1 min−1) participated in a randomised crossover design: (1) high-fat meal alone (2) high-fat meal followed 2 h later by a bout of 1 h moderate (60% max HR) exercise. PWV was examined at baseline, 1, 2, 3, and 4 h postprandially. Blood Lipid hydroperoxides (LOOHs), Superoxide dismutase (SOD) and other biochemical markers were measured. PWV increased at 1 h (6.49 ± 2.1 m s−1), 2 h (6.94 ± 2.4 m s−1), 3 h (7.25 ± 2.1 m s−1) and 4 h (7.41 ± 2.5 m s−1) respectively, in the control trial (P < 0.05). There was no change in PWV at 3 h (5.36 ± 1.1 m s−1) or 4 h (5.95 ± 2.3 m s−1) post ingestion in the exercise trial (P > 0.05). LOOH levels decreased at 3 h post ingestion in the exercise trial compared to levels at 3 h (P < 0.05) in the control trial. SOD levels were lower at 3 h post ingestion in the control trial compared to 3 h in the exercise trial (0.52 ± 0.05 vs. 0.41 ± 0.1 units μl−1; P < 0.05). These findings suggest that a single session of aerobic exercise can ameliorate the postprandial impairments in arterial function by possibly reducing oxidative stress levels.

Keywords

ExercisePostprandial lipaemiaOxidative stressVascular functionLipid hydroperoxides

Abbreviations

CAD

Coronary artery disease

CE

Cholesterol esterase

CO

Cholesterol oxidase

CRP

C-reactive protein

CV

Co-efficient of variation

ECG

Electrocardiograph

HDL-C

High density lipoprotein cholesterol

HSD

Honestly significant difference

LDL-C

Low-density cholesterol

K3EDTA

Potassium ethylenediaminetetraacetic acid

LOOH

Lipid hydroperoxides

NO

Nitric oxide

NO2

Nitrite

NO3

Nitrate

NOS

Nitric oxide synthase

eNOS

Endothelial NOS

NOX

Nitrate/nitrite

ONOO

Peroxynitrite

O2

Superoxide anion

PHTG

Postprandial hypertriglyceridemia

PWV

Pulse wave velocity

ROS

Reactive oxygen species

SOD

Superoxide dismutase

TAG

Triacylglycerols

Copyright information

© Springer-Verlag 2007

Authors and Affiliations

  • Conor M. Mc Clean
    • 1
  • Jim Mc Laughlin
    • 2
  • George Burke
    • 2
  • Marie H. Murphy
    • 1
  • Tom Trinick
    • 3
  • Ellie Duly
    • 3
  • Gareth W. Davison
    • 1
  1. 1.Sport and Exercise Sciences Research Institute, School of Sports StudiesUniversity of UlsterNewtownabbeyUK
  2. 2.School of Electrical and Mechanical EngineeringUniversity of Ulster JordanstownNewtownabbeyUK
  3. 3.Department of MedicineUlster HospitalDundonaldUK