File(s) under permanent embargo
Microvascular blood flow responses to muscle contraction are not altered by high-fat feeding in rats
Aim: Exercise and insulin each increase microvascular blood flow and enhance glucose disposal in skeletal muscle. We have reported that insulin-mediated microvascular recruitment in a diet-induced model of insulin resistance (high-fat feeding for 4 weeks) is markedly impaired; however, the effect of muscle contraction in this model has not been previously explored.
Methods: We fed rats either normal (ND, 10% calories from fat) or high-fat (HFD, 60% calories from fat) diets ad libitum for 4–8 weeks. Animals were then anaesthetized and one hindlimb electrically stimulated to contract at 0.05, 0.1 and 2 Hz (field stimulation, 30 V, 0.1 ms duration) in 15 min stepwise increments. Femoral artery blood flow (Transonic flow probe), muscle microvascular blood flow (hindleg metabolism of 1-methylxanthine and contrast-enhanced ultrasound) and muscle glucose disposal (uptake of radiolabelled 2-deoxy-d-glucose and hindleg glucose disappearance) were measured.
Results: Both ND and HFD rats received the same voltage across the leg and consequently developed the same muscle tension. Femoral artery blood flow in the contracting leg increased during 2 Hz contraction, but not during the lower frequencies and these effects were similar between ND and HFD rats. Muscle microvascular blood flow significantly increased in a contraction frequency-dependent manner, and preceded increases in total limb blood flow and these effects were similar between ND and HFD rats. Muscle glucose disposal was markedly elevated during 2 Hz contraction and was comparable between ND and HFD rats.
Conclusion: Contraction-mediated muscle microvascular recruitment and glucose uptake are not impaired in the HFD insulin resistant rat.
Funding
Australian Research Council
History
Publication title
Diabetes, Obesity and MetabolismVolume
14Issue
8Pagination
753-761ISSN
1462-8902Department/School
Menzies Institute for Medical ResearchPublisher
Blackwell Publishing LtdPlace of publication
9600 Garsington Rd, Oxford, England, Oxon, Ox4 2DgRights statement
Copyright 2012 Blackwell Publishing Ltd.Repository Status
- Restricted