Aerobic interval training vs. continuous moderate exercise in the metabolic syndrome of rats artificially selected for low aerobic capacity.
OBJECTIVE
The recent development of a rat model that closely resembles the metabolic syndrome allows to study the mechanisms of amelioration of the syndrome by exercise training. Here, we compared the effectiveness for reducing cardiovascular risk factors by exercise training programmes of different exercise intensities.


RESULTS
Metabolic syndrome rats were subjected to either continuous moderate-intensity exercise (CME) or high-intensity aerobic interval training (AIT). AIT was more effective than CME at reducing cardiovascular disease risk factors linked to the metabolic syndrome. Thus, AIT produced a larger stimulus than CME for increasing maximal oxygen uptake (VO(2max); 45 vs. 10%, P < 0.01), reducing hypertension (20 vs. 6 mmHg, P < 0.01), HDL cholesterol (25 vs. 0%, P < 0.05), and beneficially altering metabolism in fat, liver, and skeletal muscle tissues. Moreover, AIT had a greater beneficial effect than CME on sensitivity of aorta ring segments to acetylcholine (2.7- vs. 2.0-fold, P < 0.01), partly because of intensity-dependent effects on expression levels of nitric oxide synthase and the density of caveolae, and a greater effect than CME on the skeletal muscle Ca2+ handling (50 vs. 0%, P < 0.05). The two exercise training programmes, however, were equally effective at reducing body weight and fat content.


CONCLUSIONS
High-intensity exercise training was more beneficial than moderate-intensity exercise training for reducing cardiovascular risk in rats with the metabolic syndrome. This was linked to more superior effects on VO(2max), endothelial function, blood pressure, and metabolic parameters in several tissues. These results demonstrate that exercise training reduces the impact of the metabolic syndrome and that the magnitude of the effect depends on exercise intensity.
Haram
Per Magnus
PM
Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Medical Technology Research Centre, Olav Kyrres Gate 9, N-7489 Trondheim, Norway.
Kemi
Ole J
OJ
Lee
Sang Jun
SJ
Bendheim
Marianne Ø
MØ
Al-Share
Qusay Y
QY
Waldum
Helge L
HL
Gilligan
Lori J
LJ
Koch
Lauren G
LG
Britton
Steven L
SL
Najjar
Sonia M
SM
Wisløff
Ulrik
U
D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D008076:Cholesterol, HDL / Q000097:blood; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology; D005081:Exercise Therapy / Q000379:methods*; D054890:Fatty Acid Synthase, Type I / Q000378:metabolism; D050556:Fatty Acid-Binding Proteins / Q000378:metabolism; D007328:Insulin / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D018482:Muscle, Skeletal / Q000378:metabolism; D010101:Oxygen Consumption; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D010766:Phosphorylation; D016601:RNA-Binding Proteins / Q000378:metabolism; D051381:Rats; D011972:Receptor, Insulin / Q000378:metabolism; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism; D014664:Vasodilation
D008076:Cholesterol, HDL; D050556:Fatty Acid-Binding Proteins; D007328:Insulin; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; C501429:Ppargc1a protein, rat; D016601:RNA-Binding Proteins; C493570:Slc27a1 protein, rat; D014157:Transcription Factors; D054890:Fatty Acid Synthase, Type I; D011972:Receptor, Insulin; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases