人参皂甙Rg_1促进小鼠力竭游泳后体能恢复的作用

目的 :研究人参皂甙Rg1对力竭运动后小鼠体能恢复的作用 ,并从糖代谢角度探讨其机理。方法 :以小鼠为实验动物 ,测定力竭游泳时间和不同恢复时间点的血糖浓度、肌糖原含量、肝糖原含量及血乳酸浓度。结果 :(1 )人参皂甙Rg1给药组小鼠第二次力竭游泳时间较对照组明显延长。 (2 )力竭游泳后恢复期 ,糖原含量的增加、血乳酸浓度降低比对照组明显加快。结果表明 ,人参皂甙Rg1能促进力竭游泳后体能的恢复 ,其机制可能与其能促进糖原合成及加速乳酸清除有关。     

葛根总黄酮对力竭运动大鼠肝脏部分抗氧化指标和超微结构的影响

目的:探讨补充葛根总黄酮对耐力训练大鼠力竭运动后肝脏部分抗氧化指标、肝糖原含量和超微结构的影响。方法:24只雄性SD大鼠随机分为安静对照组、运动训练组和训练服药组。运动训练组和训练服药组进行7周递增强度耐力训练。训练服药组每天灌服一次葛根总黄酮悬浮液,安静对照组和运动训练组灌服相同体积的蒸馏水。测定运动训练组和训练服药组力竭运动后即刻及安静对照组安静时肝脏超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)的活性与丙二醛(MDA)含量、糖原含量及运动至力竭的时间等指标,并在电镜下观察大鼠肝脏超微结构的变化。结果:(1)训练服药组大鼠力竭时间(116.32±6.20min)显著长于运动训练组(94.82±9.05min)(P<0.05)。(2)运动训练组肝脏组织T-SOD、GSH-Px和CAT活性显著低于安静对照组(P<0.05),CuZn-SOD活性和MDA含量显著高于安静对照组((P<0.05);训练服药组T-SOD、GSH-Px、CAT、铜锌超氧化物歧化酶(CuZn-SOD)活性显著高于运动训练组(P<0.05),而MDA显著低于运动训练组(P<0.05)。训练服药组肝糖原含量显著高于运动训练组(P<0.05)。训练服药组血清谷丙转氨酶(GPT)活性显著低于运动训练组(P<0.05)。(3)电镜观察发现,安静对照组线粒体结构完整;运动训练组线粒体形态变异明显,其膜、嵴均有溶解,断裂现象,甚至整个线粒体崩解,出现空泡化,基质电子密度降低,粗面内质网减少,出现不规则扩张、断裂、扭曲;训练服药组线粒体、粗面内质网发生了损伤,但程度较运动训练组轻。结论:葛根总黄酮可提高肝脏抗氧化酶的活性,促进机体自由基的消除,维护肝细织的正常结构,促进肝糖原合成,具有延缓运动疲劳发生的作用。     

补充复方1,6-二磷酸果糖及谷氨酰胺对训练大鼠游泳运动能力和运动后骨骼肌损伤的影响

目的:探讨补充复方1,6-二磷酸果糖(FDP)和谷氨酰胺对训练大鼠运动能力与运动后骨骼肌损伤的影响。方法:76只雄性Wistar大鼠被随机分为安静对照组、运动对照组、训练组、训练加补充谷氨酰胺组和训练加补充活性糖组。游泳训练6周后,除安静对照组外,其余大鼠进行1次力竭游泳运动,记录力竭时间;检测各组大鼠血浆CK及其同工酶活性变化;取比目鱼肌制备电镜切片,观察骨骼肌细胞Z线变化。结果:训练加补充活性糖组大鼠力竭游泳时间显著长于训练组和训练加补充谷氨酰胺组(P<0.05),训练加补充谷氨酰胺组大鼠运动后即刻比目鱼肌Z线异常率分别显著低于对照组和训练加补充活性糖组(P<0.05),训练组大鼠力竭运动后即刻比目鱼肌Z线异常率亦分别显著低于对照组和训练加补充活性糖组(P<0.05)。结果提示,补充活性糖有助于提高训练大鼠的运动能力;补充谷氨酰胺对于降低运动导致的骨骼肌细胞损伤是否有积极作用尚待进一步探讨。     

补锌对耐力训练、力竭运动大鼠腓肠肌超氧化物岐化酶、谷胱甘肽过氧化物酶、总抗氧化能力以及Bax、Bcl-2 mRNA的影响

目的:探讨补锌对耐力训练、力竭运动大鼠腓肠肌超氧化物岐化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px,简称GPX)、总抗氧化能力(T-AOC)、细胞凋亡诱导和阻遏分子(Bax,Bcl-2)mRNA的影响。方法:将32只雄性SD大鼠随机分成对照组、耐力训练组、耐力训练补锌组和一次性力竭运动补锌组4组,每组8只。补锌方法为在饮用水中溶入ZnSO4.7H2O,[Zn]=227 mg/L。耐力训练组和耐力训练补锌组进行6周游泳耐力训练,每周6天。6周训练结束24小时后取材。一次性力竭运动组取材当日在同一泳池每隔15 min被放入2只大鼠,进行无负重游泳至力竭后取材。测定大鼠腓肠肌SOD、GPX、T-AOC活性,Bax、Bcl-2 mRNA表达。结果:耐力训练补锌组大鼠腓肠肌SOD活性显著高于对照组(P<0.05),GPX活性显著高于对照组和耐力训练组(P<0.05)。力竭运动补锌组大鼠腓肠肌GPX和T-AOC活性显著高于对照组(P<0.05)。耐力训练补锌组大鼠腓肠肌Bax mRNA表达显著低于对照组和耐力训练组(P<0.05),Bcl-2 mRNA表达显著高于对照组和耐力训练组(P<0.05)。力竭运动补锌组大鼠腓肠肌Bax,Bcl-2 mRNA表达均显著高于对照组(P<0.05)。结论:耐力训练提高大鼠腓肠肌GPX活性,增加Bcl-2 mRNA表达,降低大鼠腓肠肌Bax mRNA表达,补锌效果更明显。一次性力竭运动补锌提高大鼠腓肠肌GPX活性和T-AOC活性,增加腓肠肌Bcl-2 mRNA表达,但对Bax mRNA表达影响不明显。     

复方红景天片抗疲劳作用研究

目的研究复方红景天片对小鼠的抗疲劳作用。方法将小鼠随机分为5组：空白对照组,生力胶囊组（0.5g.kg-1.d-1）,复方红景天片低、中、高剂量组（0.5、1.0、2.0 g.kg-1.d-1）。灌胃给药,连续给药30 d后对负重游泳时间、爬杆时间、血清尿素氮（BUN）含量、肝/肌糖原含量、全血乳酸（BLA）等指标测定,观察长时间游泳对小鼠心肌超微结构的影响,评价其抗疲劳作用。结果复方红景天片能明显延长小鼠负重游泳及爬杆时间,提高小鼠肝/肌糖原储量,减少BUN的产生,加速BLA清除,心肌超微结构显示,复方红景天片可减轻长时间运动所导致的心肌损伤。结论复方红景天片具有一定的抗疲劳作用。     

耐力训练和一次性力竭运动对大鼠心肌和骨骼肌硫氧还蛋白还原酶的影响

目的:观察运动对大鼠心肌、骨骼肌硫氧还蛋白还原酶(TR)的影响.方法:SD大鼠30只,随机分成安静对照组、耐力训练组和力竭组.训练组进行6周渐增游泳训练,5次/周.最后1次训练后24小时,断头处死安静对照组和训练组大鼠,力竭组大鼠在一次性力竭运动后即刻处死.DTNB法检测心肌、骨骼肌TR活性,RT-PCR法观察TR mRNA水平变化.结果:6周耐力训练大鼠心肌TR活性显著高于安静对照组,一次性力竭组大鼠心肌TR活性显著低于安静对照组.各组大鼠心肌TR mRNA均无显著性差异.结论:6周耐力训练显著提高大鼠心肌TR活性,而在mRNA水平上无显著性差异.     

补充葛根素对力竭游泳训练大鼠海马细胞凋亡及Bcl-2、P53蛋白表达的影响

目的:观察补充葛根素对力竭性游泳训练造成的大鼠海马细胞凋亡以及Bcl-2和P53表达的影响。方法:2月龄SD大鼠30只随机分为安静对照组、力竭训练组和力竭训练+葛根素补充组,每组10只。对照组不运动,其它两组进行4周的力竭性游泳训练。葛根素补充组每天给予葛根素注射液灌胃(100mg/kg),对照组及单纯力竭运动组给予等量生理盐水。各组大鼠分别于实验结束后麻醉处死,取大鼠海马组织,采用流式细胞仪检测大鼠海马组织细胞凋亡、Bcl-2及P53蛋白表达。结果:与安静对照组相比,力竭训练组海马细胞凋亡率显著升高(P<0.01),细胞增殖指数显著升高(P<0.05),海马神经细胞Bcl-2表达显著下降(P<0.05),P53表达显著升高(P<0.01)。与力竭训练组相比,葛根素补充组海马神经细胞凋亡率显著下降(P<0.01),海马神经细胞Bcl-2表达显著升高(P<0.05),P53表达显著性下降(P<0.05)。结论:补充葛根素对力竭性游泳大鼠海马细胞有保护作用及促进疲劳恢复的作用,可能与葛根素上调凋亡基因Bcl-2及下调P53蛋白表达有关。     

氨基酸维生素制剂的抗疲劳作用研究

目的 探讨氨基酸维生素制剂对力竭运动大鼠的抗疲劳作用,为新型抗疲劳营养补剂的开发提供理论基础.方法 雄性SD大鼠36只,适应性游泳后随机分为胶囊组、对照组和冲剂组,每组12只.采用无负重游泳方式建立大鼠力竭游泳模型.分别给予复方氨基酸胶囊、正常饮用水和氨基酸果糖粉同体饮料.14d后处死、取材,测定大鼠力竭游泳时间、肝糖原和肌糖原含量、血清β-内啡肽(β-EP)、乳酸(LA)、乳酸脱氢酶(LDH)、肌酸激酶(CK)水平.结果 胶囊组和冲剂组大鼠游泳力竭时间显著长于对照组(P＜0.05),肝糖原、肌糖原含量显著高于对照组(P＜0.05),血清β -EP、LDH、CK均明显低于对照组(p＜0.05),血乳酸水平无显著性差异(p＞0.05).结论 复方氨基酸维生素制剂可延长大鼠游泳力竭时间,增加肌糖原和肝糖原含量,减少大鼠疲劳运动时的多种代谢产物生成,从而发挥抗疲劳作用.     

补充强化多肽片对耐力训练大鼠游泳力竭时间、肌糖原及血清T、BU、CK的影响

目的:探讨强化多肽片对耐力训练大鼠运动能力及疲劳恢复的影响。方法:将Wistar大鼠随机分为5组:安静对照组(n=12)、运动对照组(n=11)、高剂量强化多肽片(1.6mg/gBW/d)运动组(n=12)、中剂量强化多肽片(0.8mg/gBW/d)运动组(n=12)、低剂量强化多肽片(0.4mg/gBW/d)运动组(n=12)。采用递增负荷游泳运动方案,每周训练5天,上、下午各一次,游泳时间从第1周的20min/次增加至第6周的85min/次,共训练6周,第6周最后一次训练时令各运动组采用5%体重负荷游泳至力竭,记录力竭游泳时间。24小时后断头取血和股四头肌,检测血睾酮(T)、血尿素(BU)、肌酸激酶(CK)和肌糖原(MG)。结果:(1)中剂量强化多肽片运动组力竭运动时间显著长于运动对照组(P<0.01);高、中、低剂量多肽片运动组MG含量显著高于运动对照组(P<0.01,P<0.05)。(2)与安静对照组相比,运动对照组血T值显著降低(P<0.05),但高、中、低剂量多肽片运动组与安静对照组、运动对照组相比均无显著性差异(P>0.05);运动对照组血BU值显著高于安静对照组(P<0.01),中、低剂量多肽片运动组显著低于运动对照组(P<0.05);运动对照组血CK活性显著高于安静对照组(P<0.01),中、高剂量多肽片运动组较运动对照组显著下降(P<0.01)。结论:补充中剂量强化多肽片能延长大鼠力竭游泳时间,增加骨骼肌糖原含量,降低血清肌酸激酶和尿素水平,提示补充适宜剂量的强化多肽片有提高耐力训练大鼠运动能力和促进疲劳恢复的作用。     

罗汉果提取液对小鼠运动耐力及肝组织抗氧化损伤的影响

目的:探讨罗汉果提取液对小鼠运动耐力及肝组织抗氧化损伤的影响。方法:以60只昆明种雄性小鼠为研究对象,随机分成对照组和罗汉果组两大组,每组又各分为安静组、运动组和恢复组3小组,即:安静对照组、运动对照组、运动+恢复对照组;安静+罗汉果组、运动+罗汉果组、运动+恢复+罗汉果组。以15g.kg-1.d-1的剂量灌服罗汉果提取液结合游泳训练6周,最后进行一次性力竭游泳。测定小鼠力竭游泳时间、Hb、Bla、血清LDH、血清GPT、肝SOD、MDA、GSH-Px等指标。结果:灌服罗汉果提取液小鼠游泳至力竭的时间明显延长;力竭运动后即刻,运动+罗汉果组Hb与肝组织SOD、GSH-Px活性显著高于运动对照组(P<0.05),而运动+罗汉果组Bla、血清LDH、GPT及肝组织MDA含量显著低于运动对照组(P<0.05);恢复24小时后,运动+恢复+罗汉果组Hb与肝组织SOD、GSH-Px活性显著高于运动+恢复对照组(P<0.05),而运动+恢复+罗汉果组Bla、血清LDH、GPT与肝组织MDA显著低于运动+恢复对照组(P<0.05)。结论:罗汉果提取液能提高小鼠运动至力竭的时间,并有效促进机体Hb的合成与肝组织SOD、GSH-Px活性的升高及Bla的清除,提高机体的抗氧化能力。     

游泳训练对大鼠学习记忆和脑内神经递质的影响

目的:探讨8周游泳训练对大鼠学习记忆的影响及其与脑内多巴胺(DA)的关系.方法:本实验选取28只3月龄SD大鼠,随机分成4组:对照组(C组)、无训练运动即刻组(E组)、训练对照组(TC组)、训练运动即刻组(TE组).TC组、TE组进行每周4次的无负重游泳训练,每次1小时,共8周.所有大鼠每周进行一次迷宫实验的测试.E组和TE组在第8周最后一次运动后即刻,与C组、TC组一起迅速断头处死,各组交叉进行,迅速取血液和脑组织(纹状体、海马、前额叶皮层、伏隔核)测试.结果:第7周时,TC组和TE组大鼠迷宫实验的错误次数比C组和E组显著减少,说明7周的游泳训练能显著提高大鼠的学习记忆能力.同时发现游泳训练使大鼠脑内纹状体、海马、前额叶皮层和伏隔核中DA的含量显著增加.提示:游泳训练提高大鼠的学习和记忆能力可能与DA等神经递质的正相调控作用有关.     

正交试验结合血乳酸测定优选淫羊藿苷抗大鼠运动性疲劳方案

目的:优选淫羊藿苷辅助提高运动能力的最佳方案。方法:采用L9(34)正交设计,以游泳时间为指标,以淫羊藿苷的剂量、给药时刻及训练方法为因素,结合血乳酸水平,进行综合分析。结果:力竭游泳时间最长的为100 mg.kg-1、8∶00喂药及负重4%组,游泳时间最短的为30 mg.kg-1、15∶00喂药及负重2%组。血乳酸水平最高的为30 mg.kg-1、20∶00喂药及负重4%组,血乳酸水平最低的为100 mg.kg-1、15∶00喂药及无负重组。结论:优化的方案合理、易操作,为淫羊藿苷抗疲劳研究提供了一定的参考依据。     

The latest on carbohydrate loading: a practical approach

High dietary carbohydrate (CHO) intake for several days before competition (CHO loading) is known to increase muscle glycogen stores, with subsequent ergogenic performance benefits often seen in events longer than 90 min in duration. CHO-loading strategies vary in characteristics such as type and duration of dietary manipulation and the accompanying exercise/training activities. Additionally, glycogen concentration may remain elevated for up to 5 d. This versatility in CHO-loading strategies allows the athlete greater flexibility in tailoring pre-event preparation. Women who attempt to CHO load should be particularly attentive to both total energy intake and relative CHO intake; dietary CHO should exceed 8 g x kg body mass(-1) x d(-1) or 10 g x kg lean body mass(-1) x d(-1). As long as the amount ingested is adequate for loading, the type of CHO is less important, with the exception of 1-d loading protocols where the glycemic index may be an important consideration.     

Effects of exercise training on insulin response to intravenous glucose in pubertal rats.

This study was undertaken to evaluate the effects of exercise training on glucose tolerance and glucose-stimulated insulin response (GSIR) in 55- and 90-day-old peripubertal female rats. Intravenous glucose tolerance tests (0.5 g/kg) were done in: 1) 90-day-old rats exercised in swimming sessions for either 5 or 10 weeks and evaluated 48 h after the last exercise bout; 2) 55-day-old rats exercised for 5 weeks and evaluated either 24 h or 48 h after the last exercise bout and; 3) unexercised 55- and 90-day-old rats. The total area under the GSIR curve was suppressed in 55- and 90-day-old rats exercised since the age of 21 days. However, this decrease was observed 48 and only 24 h after the last exercise bout in the 90- and 55-day-old rats respectively. Exercise did not affect the GSIR curve for the 90-day-old rats subjected to 5 weeks of exercise training (started at 55 days of age) when evaluated 48 h after the last exercise bout. Nor did one single bout of swimming exercise (2 h) in the last 24 h affect the GSIR in unexercised 55-day-old rats. These results suggest that the shorter duration of the residual effects of exercise in the younger rats (55 days) was related to the shorter length of the training programme. Body weight was not significantly reduced with exercise in 55-day-old rats, whereas the same amount of exercise in 90-day-old rats caused body weight reduction of approximately 35 g (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of myocardial ischaemia on left ventricular function and adaptability to exercise training.

PURPOSE: We evaluated the possible interaction between exercise-induced myocardial ischemia and abnormalities in left ventricular function in 72 patients with coronary artery disease at entry and upon discharge from a 6-month exercise training program. METHODS: Twenty-two patients with myocardial ischemia (MIS) defined by electrocardiographic and radionuclide imaging criteria constituted our experimental group (EG). Fifty patients without MIS were assigned to the control group for exercise training (CG-ET) and 31 healthy subjects to the control group for measures of left ventricular function (CG-LV). RESULTS: Both groups EG and CG-ET showed significant and comparable increases in peak oxygen uptake (EG: 25.2 +/- 5.1 to 26.9 +/- 5.4 mL x kg(-1) x min(-1), P < 0.02; CG-ET: 25.1 +/- 0.6 to 27.4 +/- 0.7 mL x kg(-1) x min(-1), P < 0.001) after exercise training, but only CG-ET showed significant reductions in heart rate, systolic blood pressure, and rate-pressure product during submaximal exercise. A significant increase in end-diastolic volume contributed to the increase in cardiac output during exercise in patients with MIS. Heart rate or treadmill time at onset of ST segment depression failed to increase as a result of training, and stroke counts and the product of stroke counts and heart rate showed a trend toward a decrease in response to exercise, suggesting progression of disease. CONCLUSIONS: Patients with myocardial ischemia showed improvements in maximal exercise capacity but failed to elicit physiologic adaptations during submaximal exercise or to increase the threshold for ischemia after exercise training. It is possible that the main emphasis in the management of this type of patient in a cardiac rehabilitation setting should be placed more on coronary risk factor modification to slow progression of disease than on improving cardiovascular efficiency.     

Acute effect of exercise-hypoxia challenge on GLUT4 protein expression in rat cardiac muscle

Altitude training is a frequently used method for enhancing endurance performance in athletes. But its acute effect on carbohydrate metabolism in cardiac muscle is unknown. In this study, we determined the acute effect of an exercise-hypoxia challenge on glycogen storage and GLUT4 protein expression in heart muscle. Sixteen male Sprague-Dawley rats were assigned to one of two groups: control (CTRL) and exercise-hypoxia (EX+HY). The exercise protocol consisted of swimming for 180 min twice, with a 45-min rest interval. Five hours after the exercise, the EX+HY rats were exposed to a 14% O(2) systemic hypoxia under normobaric condition for 12 h. After this hypoxia exposure, the EX+HY and control rats were given glucose orally (1 g/kg body weight) with stomach tube and recovered under normal condition for 16 h. Ventricular portion of the heart was used to determine the levels of glycogen, GLUT4 mRNA, and GLUT4 protein after recovery. We found that myocardial glycogen level was lowered by the exercise-hypoxia challenge (51% below control, p < 0.05), while GLUT4 mRNA was dramatically elevated (approximately 400% of the control level, p < 0.05). The acute exercise-hypoxia treatment did not affect GLUT1 protein level in the same tissue. The novel finding of the study was that the exercise-hypoxia treatment significantly induced GLUT4 gene expression in the cardiac muscle. This acute response appears to be associated with a sustained glycogen depletion of the muscle.     

Carbohydrate availability and muscle energy metabolism during intermittent running

PURPOSE: To examine the influence of ingesting a carbohydrate-electrolyte (CHO-E) solution on muscle glycogen use and intermittent running capacity after consumption of a carbohydrate (CHO)-rich diet. METHODS: Six male volunteers (mean +/- SD: age 22.7 +/- 3.4 yr; body mass (BM) 75.0 +/- 4.3 kg; V O2 max 60.2 +/- 1.6 mL x kg(-1) x min(-1)) performed two trials separated by 14 d in a randomized, crossover design. Subjects consumed either a 6.4% CHO-E solution or a placebo (PLA) in a double-blind fashion immediately before each trial (8 mL x kg(-1) BM) and at 15-min intervals (3 mL x kg(-1) BM) during intermittent high-intensity running to fatigue performed after CHO loading for 2 d. Muscle biopsy samples were obtained before exercise, after 90 min of exercise, and at fatigue. RESULTS: Subjects ran longer in the CHO-E trial (158.0 +/- 28.4 min) compared with the PLA trial (131.0 +/- 19.7 min; P < 0.05). There were no differences in muscle glycogen use for the first 90 min of exercise (approximately 2 mmol of glucosyl units per kilogram of dry matter (DM) per minute). However, there was a trend for a greater use in the PLA trial after 90 min (4.2 +/- 2.8 mmol x kg(-1) DM x min(-1)) compared with the CHO-E trial (2.5 +/- 0.7 mmol x kg(-1) DM x min(-1); P = 0.10). Plasma glucose concentrations were higher at fatigue in the CHO-E than in the PLA trial (P < 0.001). CONCLUSIONS: These results suggest that CHO-E ingestion improves endurance capacity during intermittent high-intensity running in subjects with high preexercise muscle glycogen concentrations. The greater endurance capacity cannot be explained solely by differences in muscle glycogen, and it may actually be a consequence of the higher plasma glucose concentration towards the end of exercise that provided a sustained source of CHO for muscle metabolism and for the central nervous system.     

Serum testosterone responses to continuous and intermittent exercise training in male rats

Serum testosterone (T) were investigated at rest and following exercise during 6 weeks of continuous and intermittent swimming training in male rats, and the regulatory mechanisms of the changes were discussed by evaluating serum luteinizing hormone (LH), and conducting GnRH (gonadotropin releasing hormone, 1.5 microg/kg body weight) or hCG (human chorionic gonadotropin, 25 IU/kg body weight) challenge tests. Relative to the resting level, serum T increased after intermittent exercise (6.47 +/- 1.58 vs 3.08 +/- 2.85 nmol/l), which was followed with the same changes in LH (12.81 +/- 4.21 vs 5.70 +/- 1.56 nmol/l). Serum T was lower after continuous exercise compared to the resting level (2.02 +/- 0.53 vs 10.96 +/- 3.11 nmol/l), while LH level was higher than that in sedentary group (11.23 +/- 5.61 vs 5.00 +/- 1.61 nmol/l). No significant changes were observed in resting T during and after intermittent training. A lower resting T level was shown at the end of 3 weeks of continuous training as compared to the sedentary group (1.88 +/- 0.69 vs 12.36 +/- 2.10 nmol/l), but it increased after 6 weeks of training. Serum T increased significantly in the intermittent training group after hCG treatment as compared to the saline treatment (52.42 +/- 12.10 vs 6.81 +/- 6.22 nmol/l), but insignificantly in the continuous training group. The similar increases in serum LH were observed in all the groups after GnRH treatment.     

Nutritional concerns in the diabetic athlete

The etiology of type I and type II diabetes differs and so do the nutritional challenges during and after exercise. For type I diabetics, exercise may cause hypoglycemia. To avoid hypoglycemia, a carbohydrate-rich meal should be eaten 1 to 3 hours prior to exercise and the insulin dose reduced. During exercise, at least 40 g glucose per hour should be ingested; more if the insulin dose is not reduced. After exercise, it is important to rebuild the glycogen stores to reduce the risk for hypoglycemia. Carbohydrates should always be available during training and in the recovery period. Despite these difficulties, exercise is recommended for type I diabetics and competition at high level is possible. Exercise prevents development of type II diabetes and improves metabolic regulation. For type II diabetics, exercise is normally performed to improve insulin sensitivity and to reduce body weight. Carbohydrates should only be supplied to prevent hypoglycemia.