Divergent outcomes of fructose consumption on exercise capacity of rats: friend or foe
| Autor: | An Huang, Dong Sun, Thomas H. Hintze, Su Song, Angela Sun, Elizabeth Kertowidjojo |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Nitric Oxide Synthase Type III Physiology Vasodilator Agents Fructose intake Fructose 030204 cardiovascular system & hematology Nitric Oxide Nitric oxide 03 medical and health sciences chemistry.chemical_compound Oxygen Consumption 0302 clinical medicine Superoxides Physical Conditioning Animal Physiology (medical) Internal medicine medicine Animals Muscle Skeletal Beneficial effects biology business.industry Exercise capacity Rats Vasodilation Nitric oxide synthase Arterioles Oxidative Stress NG-Nitroarginine Methyl Ester 030104 developmental biology Endocrinology chemistry Vasodilator agents biology.protein Fructose feeding Endothelium Vascular Nitric Oxide Synthase Shear Strength business Research Article |
| Zdroj: | Journal of Applied Physiology. 122:368-375 |
| ISSN: | 1522-1601 8750-7587 |
| Popis: | To test the hypothesis that high fructose (HF) consumption divergently affects exercise capability as a function of feeding duration, rats were fed a normal (as control) diet or a normal caloric diet with HF for 3, 6, 10, and 30 days, respectively, and then were run on a treadmill. Results show that running distance and work were significantly increased, which was associated with greater exercise oxygen consumption in rats fed HF for 3 (HF-3D) and 6 days, but were decreased in rats fed HF for 30 days (HF-30D) compared with rats in their respective control groups. Shear stress-induced vasodilation (SSID) in isolated plantaris muscle arterioles was significantly greater in the HF-3D group than the control group. The difference in SSID between the two groups was abolished by Nω-nitro-l-arginine methyl ester (L-NAME), suggesting a nitric oxide (NO)-mediated response. Expression of phosphorylated/activated endothelial NO synthase (eNOS) and release of nitrite/NO were significantly increased in vessels of animals in the HF-3D group than controls. In contrast, arterioles isolated from the hypertensive rats in the HF-30D group displayed significantly attenuated NO-mediated SSID accompanied with greater production of superoxide compared with vessels of control animals. Additionally, the NO-dependent modulation of myocardial oxygen consumption (MV̇o2) was also impaired in the HF-30D group, and was prevented by blocking superoxide production with apocynin, an inhibitor that also normalized the reduced SSID in the HF-30D group. In conclusion, short-term (3–6 days) HF feeding enhances exercise potential via an increase in endothelial sensitivity to shear stress, which stimulates eNOS to release NO, leading to better tissue perfusion and utilization of oxygen. However, long-term (30 days) HF feeding initiates endothelial dysfunction by superoxide-dependent mechanisms to compromise exercise performance. NEW & NOTEWORTHY The evidence that short-term fructose intake potentiates exercise capacity by nitric oxide-mediated mechanisms yields an optimal fructose feeding frame in which beneficial effects of fructose have been acquired while detrimental effects have not yet been manifested. This highlights the significance of exercise physiology in providing constructive regimens to improve physical performance. |
| Databáze: | OpenAIRE |
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