Sun Angela, Huang An, Kertowidjojo Elizabeth, Song Su, Hintze Thomas H, Sun Dong
Department of Physiology, New York Medical College, Valhalla, New York.
Department of Physiology, New York Medical College, Valhalla, New York
J Appl Physiol (1985). 2017 Feb 1;122(2):368-375. doi: 10.1152/japplphysiol.00767.2016. Epub 2016 Dec 1.
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 -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 (MV̇o) 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. 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.
为了验证高果糖（HF）摄入根据喂养持续时间不同地影响运动能力这一假设，分别给大鼠喂食正常（作为对照）饮食或含HF的正常热量饮食3、6、10和30天，然后让它们在跑步机上跑步。结果显示，与各自对照组的大鼠相比，喂食HF 3天（HF - 3D）和6天的大鼠的跑步距离和做功显著增加，这与更大的运动耗氧量相关，但喂食HF 30天（HF - 30D）的大鼠的跑步距离和做功减少。HF - 3D组离体比目鱼肌小动脉中剪切应力诱导的血管舒张（SSID）显著大于对照组。两组之间SSID的差异被左旋硝基精氨酸甲酯（L - NAME）消除，表明这是一种一氧化氮（NO）介导的反应。与对照组相比，HF - 3D组动物血管中磷酸化/活化的内皮型一氧化氮合酶（eNOS）的表达和亚硝酸盐/NO的释放显著增加。相反，与对照动物的血管相比，从HF - 30D组高血压大鼠分离的小动脉显示出NO介导的SSID显著减弱，同时超氧化物的产生增加。此外，HF - 30D组中NO对心肌耗氧量（MV̇o）的调节也受损，用夹竹桃麻素阻断超氧化物产生可预防这种情况，夹竹桃麻素是一种抑制剂，它也使HF - 30D组降低的SSID恢复正常。总之，短期（3 - 6天）HF喂养通过增加内皮对剪切应力的敏感性来增强运动潜力，这刺激eNOS释放NO，导致更好的组织灌注和氧气利用。然而，长期（30天）HF喂养通过超氧化物依赖性机制引发内皮功能障碍，从而损害运动表现。短期果糖摄入通过NO介导的机制增强运动能力的证据产生了一个最佳果糖喂养框架，在这个框架中，果糖的有益作用已经获得，而有害作用尚未显现。这突出了运动生理学在提供建设性方案以改善身体表现方面的重要性。
