Exercise training, lipid regulation, and insulin action: a tangled web of cause and effect.

Journal Article (Journal Article;Review)

Lipids are a strong mediator of coronary artery disease and cardiovascular risk. Although the effects of exercise to improve high-density lipoprotein (HDL) cholesterol and serum triglycerides (TGs) have been known for some time, the effects of different amounts and intensities of exercise on fasting and postprandial serum lipids are little understood. Normal lipid physiology is perturbed in insulin resistant states, where inhibition of lipolysis is impaired, particularly in the postprandial period when excursions in insulin and serum TGs are particularly high. In our STRRIDE (Studies of a Targeted Risk Reduction Intervention through Defined Exercise) study, three important metabolic cardiovascular risk-related variables were improved more by moderate intensity than vigorous-intensity exercise. Moderate-intensity exercise was significantly more effective at lowering TGs and improving insulin sensitivity than was vigorous exercise. Additionally, a composite score for metabolic syndrome improved significantly with low-amount/moderate, but did not with low-amount/vigorous-intensity exercise. That all three of these strong, independent, cardiovascular risk factors were significantly affected by moderate-intensity exercise suggests that regular walking exercise might be as effective, if not more so, than more vigorous exercise in favorably modifying cardiovascular risk. Despite the impressive effects of regular exercise on fasting lipids and atherogenic dyslipidemia, they are more impressive when compared with the trajectory of changes that occur in individuals that remain inactive, without regular exposure to regular exercise. A scientific priority for future investigations should be to study the independent and combined effects of exercise intensity and amount on exercise responses through a direct comparison between two groups matched on amount but differing in intensity.

Full Text

Duke Authors

Cited Authors

  • Kraus, WE; Slentz, CA

Published Date

  • December 2009

Published In

Volume / Issue

  • 17 Suppl 3 /

Start / End Page

  • S21 - S26

PubMed ID

  • 19927141

Electronic International Standard Serial Number (EISSN)

  • 1930-739X

Digital Object Identifier (DOI)

  • 10.1038/oby.2009.384


  • eng

Conference Location

  • United States