青少年运动员锌、铜营养状况的评价

<正> 锌、铜作为人体必需的微量元素在运动过程中发挥着重要的作用。许多研究表明:运动可以导致机体中锌、铜的特殊消耗及代谢改变,运动员易发生锌、铜缺乏。青少年运动员由于机体生长发育亦需要锌、铜,因此对锌、铜的需要量可能更高。本研究结合血清、头发中锌、铜水平的测定及膳食中锌、铜摄入量     

运动与锌、铜营养及自由基生物学的研究进展

<正> 近10年来,在运动医学、生理学和生物化学领域内出现了三个新的研究趋势。一是运动对锌铜代谢的影响,二是运动与自由基生物学的关系,三是锌、铜与自由基生物学的关系。但从有关文献看,尚无人将运动、锌铜代谢及自由基生物学一并考虑。鉴于运动与锌、铜及与自由基生物学的密切联系,本文特将以上几方面的研究进展一并进行综述,以期能进一步解释实验结果并澄清有关矛盾。     

服食百臣奶昔与葡锌乳酸奶的生理效应及对运动能力的影响

当前,运动医学领域内出现了三个新的研究动向:一是运动与自由基生物学的基础理论;二是运动对锌铜代谢的影响;三是锌铜与自由基生物学的关系。其主要理论观点可综合为三点:(1)运动员普遍缺锌,而缺锌将直接影响运动成绩的提高;(2)补锌可加速自由基的消除,从而消除疲劳;(3)补锌可以直接提高肌肉力量与耐久力。这些理论是我     

中国优秀运动员血清锌、铜水平的研究

为研究参加系统训练运动员冬春两季的血清锌、铜水平的变化及影响因素,作者对9个运动项目360名优秀运动员测定了血清锌、铜水平。结果表明:运动员在冬训期的血清锌水平偏低、血清铜水平偏高,18岁以下的运动员血清铜低于成年运动员。25名优秀运动员冬春两季血清锌、铜水平配对T检验的数据表明,女运动员在冬季时的血清锌远低于春季时的水平。本文数据为运动员微量元素的合理补充提供了依据。     

运动、锌铜营养与自由基代谢—Ⅴ.锌缺乏对运动小鼠体内自由基生成与清除的影响

离乳Balb/c小鼠48只,按性别体重随机分成缺锌、对饲对照及自由进食对照三大组,每大组又分成运动和不运动两组。6周后进行锌、铜、丙二醛(MDA)、超氧化物歧化酶(SOD)、谷光甘肽过氧化物酶(GSH-Px)及过氧化氢酶(CAT) 的测定,并对肝组织直接进行低温ESR(电子自旋共振)波谱分析。实验结果提示:锌缺乏将导致运动及不运动小鼠体内的自由基生成增加和清除减少;运动训练虽可使正常小鼠体内的自由基防御能力加强,但却对锌缺乏小鼠体内的SOD、GSH-Px和CAT均无显著作用,相反,运动训练还可以使缺锌小鼠肝线粒体内的脂质过氧化产物进一步显著增加。     

睾酮对大鼠肝脏金属硫蛋白诱导合成的作用

本研究主要观察了睾酮对大鼠肝脏金属硫蛋白(Metallothionein,MT)诱导合成的作用,并动态观察了不同锌营养状态的大鼠在急性力竭运动后的恢复期中,肝脏金属硫蛋白诱导合成和锌、铜、铁离子含量的变化,探讨了它们之间的关系.结果显示大鼠皮下注射睾酮能够刺激诱导肝脏MT的合成.锌缺乏引起安静状态下大鼠肝脏MT含量下降,MT下降的原因可能与睾酮低下和锌离子减少有关.睾酮可能是MT在体内的正向调节因子.营养性锌缺乏不仅引起大鼠肝脏MT和锌基础水平的下降,而且导致急性力竭游泳后肝脏MT峰值较晚出现.这表明锌缺乏造成MT对运动的应激能力和合成速率下降,这将不利于运动后自由基的清除和组织的恢复.不管大鼠的锌营养状态如何,力竭游泳后,肝脏锌、铜、铁的含量均出现不同程度的升高或升高趋势.这些金属离子的升高和再分布,可能与MT的升高有关.     

急性白血病患者脑脊液铜、锌测定及其在脑膜白血病和脑膜微小残留病中的意义

本文报告了50例(10例急性淋巴细胞白血病,10例急性粒细胞白血病及30例健康对照)脑脊液中铜、锌含量及比值的变化,并进行了统计学处理.铜、锌变化与正常人比较有显著差异(铜P<0.05、锌P<0.01).治疗缓解前后亦有显著差异(P<0.05).出现脑膜白血病(CNSL)及疑有CNSL无显著差异(P>0.05).这些资料说明,白血病细胞与铜、锌有直接关系.我们初步认为铜明显升高而锌明显下降可能系由脑膜白血病或脑膜残留微小病(MRD)存在而引起.因此脑脊液微量元素铜、锌含量变化可做为观察白血病治疗、CNSL的辅助诊断及间接提示脑膜残留微小病提供了一种简捷的途径.     

儿童血清微量元素锌、铜正常值研究

微量元素锌和铜与儿科某些疾病的发病关系密切.缺锌可引起儿童味觉减退、厌食、异食癖、消瘦、下肢水肿及生长延迟等症状和体征,在排除其他影响因素之后,血锌测定常有确诊价值;缺铜可形成低色素小细胞性贫血、婴儿出生体重减轻、骨胳、心血管及中枢神经系统结构异常或畸形,以至发生多种缺铜性疾病;体内铜过多同样可引起中枢神经系统、肝脏、内分泌等处病变.锌、铜过多可发生急慢性中毒.关于儿童血清锌、铜的正常值的研究在国内很少见到报导,为了解儿童的血锌、血铜的正常值范围,我们对空军总医院幼儿园122名健康儿童血清中的锌和铜浓度进行了调查研究,供临床诊断有关疾病时参考.     

空中晕厥与血清微量元素铜、锌关系的探讨

本对19例空中晕厥飞行员于离心机检查前、离心机检查出现灰视后即刻、30min及48h进行血清铜、锌测定，18例健康飞行员测空腹血清铜、锌作为对照。结果：空中晕厥组离心机检查均为加速度耐力不良，检查前血清锌明显高于对照组(P<0．01)，其中三例高于正常。血清铜／锌比值明显低于对照组(P<0.01)低于正常。据报告血清锌高可诱发癫痫，血清铜／锌比值变小可引起多种疾病。推测空中晕厥可能与血清锌偏高，血清铜／锌比值变小有关。     

运动对体内锌代谢平衡的影响

大鼠运动后血浆锌水平下降、肝脏锌和金属硫蛋白含量明显增加;大鼠腹腔注射肾上腺素和地塞米松后12小时,组织锌代谢变化与运动后锌代谢变化相似。表明运动可以使机体锌产生重新分布;儿茶酚胺和糖皮质激素参与运动调节锌代谢。     

Influence of nitrate supplementation on VO2 kinetics and endurance of elite cyclists

The present study examined if an elevated nitrate intake would improve VO₂ kinetics, endurance, and repeated sprint capacity in elite endurance athletes. Ten highly trained cyclists (72 ± 4 mL O₂/kg/min, mean ± standard deviation) underwent testing for VO₂ kinetics (3 × 6 min at 298 ± 28 W), endurance (120 min preload followed by a 400‐kcal time trial), and repeated sprint capacity (6 × 20 s sprints, recovery 100 s) during two 6‐day periods in randomized order with a daily ingestion of either 0.5 L beetroot (BR) juice to increase nitrate levels or a 0.5 L placebo (PLA) drink with blackcurrant juice. Plasma NOx (nitrate + nitrite) levels were higher (P < 0.01) in BR (147 ± 102 and 159 ± 103 μM after 4 and 6 days of beverage intake, respectively) compared with PLA (41 ± 10 and 40 ± 7 μM). VO₂ kinetics and exercise economy were the same in BR and PLA. Time‐trial performance was similar with an average completion time of 18:20 and 18:37 min:s in BR and PLA, respectively, with average power outputs of 290 ± 43 W in BR and 285 ± 44 W in PLA. Peak and mean power during repeated sprinting were similar in BR and PLA. In contrast to observations in moderately trained subjects intake of BR juice had no effect on VO₂ kinetics and performance in elite cyclists.     

运动员血清中黄体生成素生物活性与免疫活性的研究

对２８名普通男大学生，１４名男竞走运动员和２０名男短跑运动员安静状态的血清免疫活性黄体生成素（ＲＩＡ－ＬＨ）、生物活性黄体生成素（Ｂｉｏ－ＬＨ）及睾酮水平进行了测试，并分析了１４名男子足球运动员急性运动前、后Ｂｉｏ－ＬＨ，ＲＩＡ－ＬＨ和睾酮的变化。结果表明：（１）三组受试者Ｂｉｏ－ＬＨ与ＲＩＡ－ＬＨ呈正相关，三组之间的Ｂ／Ｉ比值和睾酮水平均无显著性差异，表明他们的垂体－性腺轴的分泌功能状况基本一致。（２）竞走运动员的ＲＩＡ－ＬＨ明显高于其他两组，而Ｂｉｏ－ＬＨ无显著性差异。提示：把Ｂｉｏ－ＬＨ和ＲＩＡ－ＬＨ结合起来。能更客观地评价ＬＨ的水平。（３）急性运动后，Ｂｉｏ－ＬＨ明显升高，而ＲＩＡ－ＬＨ变化不明显，表明运动使ＬＨ的成分发生改变。（４）急性运动后血清睾酮的升高，可能与ＬＨ生物活性升高有关。     

Regulation of MAC-1 (CD11b/CD18) expression on circulating granulocytes in endurance runners

PURPOSE: We tested the hypothesis that degranulation of granulocytes and upregulation of the granulocyte integrin MA-1 (CD11b/CD18) are related to exercise duration and/or intensity. We also investigated whether or not the expression of MAC-1 would be influenced by body temperature or dehydration. Moreover, we tested the hypothesis that changes in leukocyte counts and changes in MAC1 expression with endurance exercise are independently regulated. METHODS: In eight amateur runners, MAC-1 (CD11b/CD18) surface expression on granulocytes was determined by fluorescent antibody cell sorting, before and after an incremental maximal treadmill test, a moderate 3-h run, and a competitive marathon race. RESULTS: Expression CD11b on granulocytes was increased by 10+/-9.6% (P < 0.05) after the maximal treadmill test and by 84+/-76% (P < 0.01) after the marathon run. There was no change in CD11b expression after the moderate 3-h run. CD18 expression was not significantly changed after any of the exercise protocols. CONCLUSION: Expression of CD11b on granulocytes is increased with intense endurance exercise, either incremental maximal treadmill testing or competitive marathon running, but not in moderate endurance training. Thus, exhaustive exercise may be one mechanism for the upregulation of integrin adhesive receptors on granulocytes. This phenomenon could be in part responsible for increased adhesion of granulocytes to endothelial cells and could facilitate tissue infiltration after endurance exercise.     

Evidence for an exercise induced increase of TNF‐α and IL‐6 in marathon runners

Regular physical activity of moderate intensity improves cardiovascular risk factors including low‐grade inflammation. However, acute vigorous exercise such as marathon running results in marked increases of circulating pro‐inflammatory markers. Up to now, the origin of this pro‐inflammatory boost is still debated equivocally. We analyzed the change of interleukin‐6 (IL‐6), tumor necrosis factor‐alpha (TNF‐α), and leptin from pre‐ to immediately post‐race in 15 male runners (age 43 ± 10.9 years and body mass index 24.5 ± 2.7 kg/m²) both on the protein level in the plasma and on the messenger ribonucleic acid (mRNA) level in blood mononuclear cells (BMNC). We observed a significant increase of IL‐6 (prerace 2.08 ± 0.10 ng/L and postrace 40.14 ± 24.85 ng/L, P < 0.001) and TNF‐α (prerace 8.14 ± 1.38 ng/L and postrace 12.40 ± 3.15 ng/L, P < 0.001) and a decrease of leptin (prerace 1.64 ± 2.64 μg/L and postrace 0.80 ± 1.70 μg/L, P = 0.04) serum levels after the marathon race. Furthermore, TNF‐α, IL‐6, and leptin were expressed (mRNA level) in BMNC. However no significant differences in mRNA levels were seen before and after the run in these cells. We found an up‐regulation of TNF‐α and IL‐6 in the plasma during vigorous exercise. This increase is not attributable to BMNC. We assume a local production in, or release from, exercised tissues.     

HSP expression in human leukocytes is modulated by endurance exercise

PURPOSE: Temperature increase, oxidative stress, and inflammatory reactions after endurance exercise were expected to stimulate the synthesis of heat shock proteins (HSP) in peripheral blood leukocytes. Furthermore, it was of interest whether regular endurance training influences HSP expression. METHODS: The expression of HSP27, HSP60, HSP70, constitutive HSC70, and HSP90 in the cytoplasma and surface of lymphocytes, monocytes, and granulocytes of 12 trained athletes was analyzed by flow cytometry before and after (0, 3, and 24 h) a half marathon. Twelve untrained persons at rest were included as control. RESULTS: After the race, there was a significantly greater percentage of leukocytes expressing cytoplasmic HSP27, HSP60, and HSP70 (P < 0.01), whereas HSC70 and HSP90 remained unchanged. The fluorescence intensity increased significantly in monocytes for HSP27 (0 and 3 h) and HSP70 (0, 3, and 24 h) and in granulocytes, only 24 h postexercise for HSP70. The percent values of trained athletes at rest were significantly lower compared with untrained persons (P < 0,01). CONCLUSIONS: Strenuous exercise increased HSP expression in blood immediately after the run, indicating a protective function of HSP in leukocytes of athletes to maintain function after heavy exercise. The downregulation of HSP-positive cells in trained athletes at rest seems to be a result of adaptation mechanisms to regular endurance training.     

Running performance and thermal sensation in the heat are improved with menthol mouth rinse but not ice slurry ingestion

The purpose of this study was to compare the effects of a cooling strategy designed to predominately lower thermal state with a strategy designed to lower thermal sensation on endurance running performance and physiology in the heat. Eleven moderately trained male runners completed familiarization and three randomized, crossover 5‐km running time trials on a non‐motorized treadmill in hot conditions (33 °C). The trials included ice slurry ingestion before exercise (ICE), menthol mouth rinse during exercise (MEN), and no intervention (CON). Running performance was significantly improved with MEN (25.3 ± 3.5 min; P = 0.01), but not ICE (26.3 ± 3.2 min; P = 0.45) when compared with CON (26.0 ± 3.4 min). Rectal temperature was significantly decreased with ICE (by 0.3 ± 0.2 °C; P < 0.01), which persisted for 2 km of the run and MEN significantly decreased perceived thermal sensation (between 4 and 5 km) and ventilation (between 1 and 2 km) during the time trial. End‐exercise blood prolactin concentration was elevated with MEN compared with CON (by 25.1 ± 24.4 ng/mL; P = 0.02). The data demonstrate that a change in the perception of thermal sensation during exercise from menthol mouth rinse was associated with improved endurance running performance in the heat. Ice slurry ingestion reduced core temperature but did not decrease thermal sensation during exercise or improve running performance.     

The effect of compression socks worn during a marathon on hemostatic balance

Introduction. Marathon running evokes parallel increases in markers of coagulation and fibrinolysis (i.e. hemostatic activation) immediately following strenuous, endurance exercise such that hemostatic balance is maintained. However, other factors incident to marathon running (i.e. dehydration, travel) may disproportionately activate the coagulatory system, increasing blood clot risk after an endurance event in otherwise healthy individuals. We investigated the effect of compression socks on exercise-induced hemostatic activation and balance in endurance athletes running the 2013 Hartford Marathon. Methods. Adults (n = 20) were divided into compression sock (SOCK; n = 10) and control (CONTROL; n = 10) groups. Age, anthropometrics, vital signs, training mileage and finishing time were collected. Venous blood samples were collected 1 day before, immediately after and 1 day following the marathon for analysis of coagulatory (i.e. thrombin–antithrombin complex [TAT] and D-dimer) and fibrinolytic (i.e. tissue plasminogen activator [t-PA]) factors. Results. Plasma D-dimer, TAT and t-PA did not differ between groups at baseline (p > 0.16). There were no significant group · time interactions (all p ≥ 0.17), however, average t-PA was lower in SOCK (8.9 ± 0.7 ng/mL) than CONTROL (11.2 ± 0.7 ng/mL) (p = 0.04). Average TAT also tended to be lower in SOCK (2.8 ± 0.2 µg/L) than CONTROL (3.4 ± 0.2 µg/L) (p = 0.07). Conclusions. Our results suggest that overall hemostatic activation (both coagulation and fibrinolysis) following a marathon tended to be lower with compression socks. Thus, compression socks do not adversely influence markers of hemostasis, appear safe for overall use in runners and may reduce exercise-associated hemostatic activation in individuals at risk for deep vein thrombosis.     

Inflammation and atrial remodeling after a mountain marathon

Endurance athletes have an increased risk of atrial fibrillation. We performed a longitudinal study on elite runners of the 2010 Jungfrau Marathon, a Swiss mountain marathon, to determine acute effects of long‐distance running on the atrial myocardium. Ten healthy male athletes were included and examined 9 to 1 week prior to the race, immediately after, and 1, 5, and 8 days after the race. Mean age was 34.9 ± 4.2 years, and maximum oxygen consumption was 66.8 ± 5.8 mL/kg*min. Mean race time was 243.9 ± 17.7 min. Electrocardiographic‐determined signal‐averaged P‐wave duration (SAPWD) increased significantly after the race and returned to baseline levels during follow‐up (128.7 ± 10.9 vs. 137.6 ± 9.8 vs. 131.5 ± 8.6 ms; P < 0.001). Left and right atrial volumes showed no significant differences over time, and there were no correlations of atrial volumes and SAPWD. Prolongation of the SAPWD was accompanied by a transient increase in levels of high‐sensitivity C‐reactive protein, proinflammatory cytokines, total leucocytes, neutrophil granulocytes, pro atrial natriuretic peptide and high‐sensitivity troponin. In conclusion, marathon running was associated with a transient conduction delay in the atria, acute inflammation and increased atrial wall tension. This may reflect exercise‐induced atrial myocardial edema and may contribute to atrial remodeling over time, generating a substrate for atrial arrhythmias.     

Short-term effects of marathon running: no evidence of cardiac dysfunction.

PURPOSE: The purpose of this study was to analyze the short-term effects of a marathon race (Madrid Marathon) on both markers of cardiac damage and echocardiographic parameters in a group of 22 runners (17 male and 5 female; 34 +/- 5 yr; VO2max: 55.7 +/- 9.1 mL x kg(-1) x min(-1) with a wide range of fitness levels. METHODS: Venous blood samples were collected from each subject 48 h before the race, at race finish, and 6, 24, and 48 h postexercise for the determination of myoglobin, total creatine kinase catalytic activity (total CK), mass concentration of creatine kinase isoenzyme MB (CK-MB mass), and cardiac isoforms of troponin T and I (TnT-c and TnI-c, respectively). In addition, echocardiographic parameters (M-mode two-dimensional and Doppler analysis) indicative of both left ventricular (LV) systolic and diastolic function were obtained three times from each runner: 2-5 d before the race, at race finish, and 24-36 h after exercise. RESULTS: Except in one subject, levels of TnT-c and TnI-c were within normal limits (<0.1 ng x mL(-1)) in all the samples collected before or after the race. Overall LV systolic function was not altered by marathon running. Finally, LV diastolic function was transiently altered after the race since the ratio between peak early and late transmitral filling velocities (E/A) was significantly reduced at race finish (P < 0.01) and returned to resting levels after 24-36 h. CONCLUSIONS: Our findings suggest that marathon running does not adversely affect the hearts of healthy individuals independently from their training status.