有氧运动和力量训练的减重、降脂和增强抗氧化功能的机理

---本研究发现，运动可以增强机体的抗氧化系统，因而可以有效预防运动产生的氧化应激导致的损伤。译者---

不同的运动方式改善了代谢综合征的标志物，组织甘油三酯的含量和抗氧化的状态。

讨论

每日能量消耗的减少与肥胖个体数量的突然增加密切相关[23]。体育锻炼是控制体重的重要手段[24]。在这项研究中，A组和S组的动物在体重AUC值上与c组相比有所下降，在体育锻炼时，骨骼肌可能会在运动过程中增加100倍的能量消耗[25]。最小乳酸(ML)强度大约相当于最大耗氧量的77% (VO2;VO2max,最大值)。在我们的研究中，A组和A组的动物接受了80% ML强度的训练，大约相当于VO2max的60%[26]。在中等强度下进行长时间运动的能量消耗主要是通过脂质动员，其次是碳水化合物，最后是蛋白质。甘油三酯动员可以解释在研究结束时耐力训练动物的体重减轻。来自S组的动物可能会对这种高强度训练导致的能量消耗和肌肉肥大的增加作出反应[27]。

GIF

改善胰岛素抵抗最佳的方式是有氧运动+力量训练

胰岛素敏感性和葡萄糖耐量是测定碳水化合物代谢效率的重要试验。在本研究中所使用的力量训练练习中，乳酸糖的能量占主导地位。在这个系统中，被细胞捕获的葡萄糖被分解为两个乙酰辅酶a分子[28]，转化为乳酸。这种反应是糖代谢和葡萄糖摄取的一种强有力的激活物，葡萄糖转运蛋白4 (Glut-4)。根据表2中所述的结果，在这方面，运动组和对照组之间没有显著差异。然而，在运动组中发现的葡萄糖耐量和胰岛素敏感性值与其他研究中发现的值有关系[11,29]。此外，在研究结束时，动物的血糖水平没有差异，表明没有发生糖代谢变化。

动物的脂质代谢水平发生变化。与对照组相比，A组和S组的血液高密度脂蛋白胆固醇升高。此外，与对照组相比，运动动物在所有被调查区域的肝脏和脂肪组织中的甘油三酯浓度下降。能量消耗的增加也许可以解释这些脂类物质浓度的降低。在运动过程中，持续1至2小时，肌肉内甘油三酯被消耗，脂肪组织被激活，在脂肪组织中为身体锻炼提供 能量。另外，甘油三酯可能被重新酯化并储存在肌肉组织中以供将来使用[30]。在强度运动中，由于这种训练所产生的肌肉肥大[28]，可能会增加能量消耗和基础代谢[11]。A组肝脂的减少可能与肝功能的改善以及随后的高密度脂蛋白胆固醇的增加有关。几项研究表明，耐力训练大鼠的脂质谱有所改善[31,32,33,34]。在经过训练的动物中，甘油三酯的减少对所有脂肪组织都有显著影响。物理训练和可能的代谢改变引起的能量消耗的增加可能是导致大鼠脂质谱改善的主要原因。类似于先前的研究，涉及不同的运动协议[35,36,37]，这一发现表明，在不同的强度、体积和能量的支配下，体育锻炼是对抗肥胖的重要工具。

观察到的体育锻炼的另一个有益效果与运动动物血液中tbar脂质过氧化标记的浓度有关(A组，AS和S)。这一发现很有趣，因为脂肪氧化的增加也见于肥胖。然而，在这种情况下，脂质过氧化是由自由基的增加引起的[38,39]。长期来看，活性氧的不平衡可能会使抗氧化系统无法减少自由基，导致其失效，降低其活性并阻断其保护作用[40]。体育锻炼可能改善脂质氧化和抗氧化状态的效率,这是诊断通过动物肝脏超氧化物歧化酶活性的组织,和S和过氧化氢酶活性在动物肝脏在A组这些酶存在于所有哺乳动物细胞和抗氧化剂与减少o和过氧化氢,在呼吸链中[41]。

抗氧化机制的维持和活性氧对机体结构损伤的降低对肥胖者非常重要。稳定的高层活性氧状态可能导致细胞结构损伤,这反过来,TNF-α等炎症标记物的浓度增加,白介素6和interferon-γ和降低脂联素的浓度和抗炎白细胞介素(42、43)。炎症的维持会导致代谢综合征的破坏性影响，如内皮功能障碍和胰岛素抵抗[44]。血液低密度脂蛋白胆固醇的过氧化可使粥样斑块积聚在内皮细胞壁上，从而最终分离和阻断重要的小量血管的血流，引起脑血管意外、心肌缺血和梗死[45]。

炎症标志物通过引起胰岛素受体substrate-1 (IRS-1)和胰岛素受体substrate-2 (ir -2)的功能失调，降低胰岛素敏感性，降低葡萄糖的捕捉，从而增加对脂质代谢的依赖[46]。体育锻炼可能会打断整个事件链，使这种不健康的状态回归[6]。体育锻炼还可以提高脂质氧化的效率和抗氧化酶的活性。

综上所述，体育锻炼对以下方面是有效的:减少动物肝脏和脂肪组织中甘油三酯的储存;减少A组和S组动物的体重;降低A组动物脂质谱;显著增加抗氧化系统的活性;降低脂质过氧化标记的浓度。还需要进一步的研究来确定其他能够在这些标志物中得到改善的运动强度区域。

参考文献

Different exercise protocols improve metabolic syndrome markers, tissue triglycerides content and antioxidant status in rats | Diabetology & Metabolic Syndrome | Full Text  https://dmsjournal.biomedcentral.com/articles/10.1186/1758-5996-3-35

Discussion

The reduction in daily energy expenditure is strongly correlated with the abrupt increase in the number of obese individuals [23]. Physical exercise is an important tool for controlling body weight [24]. In this study, animals in groups A and S exhibited reductions in the body weight AUC values compared to group C. During physical exercise, the skeletal muscle might increase its energy expenditure up to 100 times during physical exercise [25]. Minimum lactate (ML) intensity corresponds to approximately 77% of the maximum oxygen consumption (VO2; VO2max, for maximum value). In our study, animals in groups A and AS were subjected to training at 80% ML intensity, corresponding to approximately60% of VO2max [26]. The energy expenditure during long duration exercise performed at moderate intensity is obtained mostly by lipid mobilization, followed by carbohydrates and finally by proteins. Triglyceride mobilization might explain the weight loss of endurance-trained animals at the end of the study. Animals from group S might have responded to the increase in energy expenditure and muscular hypertrophy caused by this type of high-intensity training [27].

Insulin sensitivity and glucose tolerance are significant tests to determine the efficiency of carbohydrate metabolism. In the strength training exercises used in this study (group S), lactic glycolytic energy predominates. In this system, glucose captured by cells is degraded into two acetyl-CoA molecules that are transformed into lactate, supplying two ATP molecules [28]. This reaction is a powerful activator of carbohydrate metabolism and glucose capture by glucose transporters-4 (Glut-4). According to the results described in Table 2, there were no significant differences between the exercised groups and control in this regard. However, the glucose tolerance and insulin sensitivity values found in the exercised groups approach the values found in other studies [11, 29]. Moreover, no differences were seen in the blood glucose levels of animals at the end of the study, suggesting that no alteration of carbohydrate metabolism occurred.

The lipid metabolism levels of animals were altered. There were increases in blood HDL cholesterol in groups A and S compared to the control group. Moreover, exercised animals exhibited reductions in the concentrations of triglycerides in the liver and fatty tissue in all investigated areas compared to the control. An increase in energy expenditure might explain the reductions in the concentrations of these lipids. During exercise lasting 1 to 2 h, intramuscular triglycerides are consumed, and the lipolysis mechanism is activated in the fatty tissue that supplies carbon skeletons for physical exercise. Alternatively, triglycerides might be re-esterified and stored in the muscle tissue for future use [30]. During strength exercise, there might be an increase in energy expenditure and basal metabolism due to the muscular hypertrophy [28] developed by this type of training [11]. The reduction of liver lipids in group A might be related to an improvement in liver function and the subsequent increase in HDL cholesterol production. Several studies suggest an improvement in the lipid profiles in endurance-trained rats [31, 32, 33, 34]. The reductions of triglycerides were significant in all fatty tissue areas investigated in the trained animals. An increase in energy expenditure caused by physical training and possible metabolic alterations might be the major cause behind the improvements in the lipid profiles of rats. Similar to previous studies involving different exercise protocols [35, 36, 37], this finding shows that at different intensities, volume and energy predominance, physical exercise is an important tool in the fight against obesity.

Another beneficial effect of physical training that was observed is related to the concentrations of TBARS lipid peroxidation markers in the blood of exercised animals (groups A, AS and S). This finding is interesting because an increase in lipid oxidation is also seen in obesity. However, in this condition, lipid peroxidation is caused by the increased production of free radicals [38, 39]. In the long run, this imbalance in reactive oxygen species might make the antioxidant system unable to reduce free radicals, causing its failure, decreasing its activity and blocking its protective role [40]. Physical exercise might have improved the efficiency of lipid oxidation and the antioxidant status, which was diagnosed by means of superoxide dismutase activity in animal livers in groups A, AS and S and catalase activity in the animal livers in group A. These enzymatic antioxidants are present in all mammalian cells and are associated with the reduction of O-and H2O2- in the respiratory chain [41].

Maintenance of the antioxidant mechanism and a decrease in the structural damage caused by reactive oxygen species are very important for obese individuals. A steady high-level reactive oxygen species state could lead to cell structural damage, which, in turn, increases the concentrations of inflammatory markers such as TNF-α, interleukin 6 and interferon-γ and decreases the concentrations of adiponectin and anti-inflammatory interleukins [42, 43]. Maintenance of inflammation leads to the damaging effects present in metabolic syndrome, such as endothelial dysfunction and insulin resistance [44]. Peroxidation of blood LDL cholesterol allows atheromatous plaques to accumulate on the endothelial walls, which might eventually detach and block blood flow in important small-caliber blood vessels, causing cerebrovascular accidents, myocardial ischemia and infarction [45].

Inflammatory markers decrease insulin sensitivity by causing dysfunction of insulin receptor substrate-1 (IRS-1) and insulin receptor substrate-2 (IRS-2), decreasing glucose capture and consequently increasing the dependence on lipid metabolism, thus creating a vicious circle [46]. Physical exercise might interrupt the full chain of events and make this unhealthy status regress [6]. Physical exercise might also increase the efficiency of lipid oxidation and the activity of anti-oxidizing enzymes.

In conclusion, physical exercise was efficient with respect to the following: reducing the storage of triglycerides in animal livers and fatty tissue; decreasing the body weights of animals in groups A and S; decreasing the lipid profiles of animals in group A; significantly increasing the activities of the anti-oxidizing system; and reducing the concentrations of lipid peroxidation markers. Further studies are needed to identify other physical activity intensity zones that can achieve improvement in these markers.