Cardiovascular changes associated with decreased aerobic capacity and aging in long-distance runners

Summary Fifty-five male runners aged between 30 to 80 years were examined to determine the relative roles of various cardiovascular parameters which may account for the decrease in maximal oxygen uptake ( ) with aging. All subjects had similar body fat composition and trained for a similar mileage each week. The parameters tested were , maximal heart rate (HR _max), cardiac output (Q), and arteriovenous difference in oxygen concentration (C _a —C _ˉv) O₂ during graded, maximal treadmill running. Average body fat and training mileage were roughly 12% and 50 km·week⁻¹, respectively. The average 10-km runtime slowed significantly by 6.0%·decade⁻¹ {[10-km run-time (min)=0.323 x age (years)+24.4] (n=49,r=0.692,p<0.001)}. A strong correlation was found between age and {[ (ml·kg⁻¹·min⁻¹)=- 0.439xage+76.5] (n=55,r=-0.768, p<0.001)}. Thus, decreased by 6.9%·decade⁻¹ along with reductions ofHR _max (3.2%·decade⁻¹, p<0.001) andQ (5.8%·decade⁻¹, p<0.001), while no significant change with age was observed in estimated (C _a —C _ˉv) O₂. It was concluded that the decline of with aging in runners was mainly explained by the central factors (represented by the decline ofHR andQ in this study), rather than by the peripheral factor (represented by (C _a —C _ˉv) O₂). This study was supported, in part, by a Research Grant on Aging and Health, Ministry of Health and Welfare, Japan, and by a Research Grant for young researchers, Meiji Life Foundation of Health and Welfare, Japan.     

高压氧抑制一氧化氮生成改善缺血性脑细胞凋亡

目的探讨高压氧对脑缺血再灌流脑皮层一氧化氮(NO)生成的影响及其对脑细胞的保护作用。方法采用沙土鼠双侧颈总动脉夹闭30min再灌流模型。用电化学及免疫细胞化学方法检测脑皮层一氧化氮生成、一氧化氮合酶(NOS)表达及神经细胞凋亡。结果缺血再灌流期沙土鼠脑皮层中NO的含量显著增加，3型NOS均有表达，缺血再灌流第2d，iNOS的表达最为明显，同时NO的生成达到高峰。缺血再灌流第1、2、3d，沙土鼠脑皮层均可见凋亡细胞，以第2、3d更为明显。高压氧暴露能明显抑制iNOS表达，减少NO生成，减轻神经细胞凋亡。结论高压氧能抑制沙土鼠脑缺血再灌流期脑皮层NO生成，减轻神经细胞凋亡，从而起到脑保护作用。     

Physicochemical properties of membranes and functional status of liver mitochondria in rats with an inherited capacity for increased radical formation

Liver mitochondria of inbred W/SSM rats with inherited increased radical formation reveal the following anomalies: inhibition of oxidative phosphorylation, a lowered transmembrane potential, and alterations in protein-lipid interaction. The membrane viscosity and osmotic stability of mitochondria are unaffected. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 119, N ^o 6, pp. 628–631, June, 1995     

Near‐infrared spectroscopy determined brain and muscle oxygenation during exercise with normal and resistive breathing

To elevate effects of carbon dioxide (CO₂) retention by way of an increased respiratory load during submaximal exercise (150 W), the concentration changes of oxy‐ (ΔHbO₂) and deoxy‐haemoglobin (ΔHb) of active muscles and the brain were determined by near‐infrared spectroscopy (NIRS) in eight healthy males. During exercise, pulmonary ventilation increased to 33 (28–40) L min^–1 (median with range) with no effect of a moderate breathing resistance (reduction of the pneumotach diameter from 30 to 14 and 10 mm). The end‐tidal CO₂ pressure (P_ETCO ₂) increased from 45 (42–48) to 48 (46–58) mmHg with a reduction of only 1% in the arterial haemoglobin O₂ saturation (S_aO ₂). During control exercise (normal breathing resistance), muscle and brain ΔHbO₂ were not different from the resting levels, and only the leg muscle ΔHb increased (4 (–2–10) μM , P < 0.05). Moderate resistive breathing increased ΔHbO₂ of the intercostal and vastus lateralis muscles to 6 ± (–5–14) and 1 (–7–9) μM (P < 0.05), respectively, while muscle ΔHb was not affected. Cerebral ΔHbO₂ and ΔHb became elevated to 6 (1–15) and 1 (–1–6) μM by resistive breathing (P < 0.05). Resistive breathing caused an increased concentration of oxygenated haemoglobin in active muscles and in the brain. The results indicate that CO₂ influences blood flow to active skeletal muscle although its effect appears to be smaller than for the brain.     

Adaptive changes in cerebral blood flow and oxygen consumption during ethanol intoxication in the rat

Cerebral blood flow (CBF) and oxygen consumption (CMRO₂) were measured during acute and long-term ethanol intoxication in the rat. The purpose was to investigate whether the adaptive changes (development of tolerance) occurring in the CNS during ethanol intoxication were associated with changes in CBF and/or CMRO₂. Consistent with other studies we found that acute severe ethanol intoxication (median blood alcohol concentration (BAC=5.4 mg/ml)) caused a significant decrease in CBF and CMRO₂. After 3–4 days of severe intoxication (BAC of 6.6 mg/ml) these physiological variables were less affected indicating that functional tolerance had developed: CMRO₂ and CBF during acute ethanol intoxication were 9.3 ml/100 g/min and 60 ml/100 g/min respectively; after the long term intoxication period these variables reached 11.2 ml/100 g/min and 78 ml/100 g/min respectively, i.e. values not significantly lower than those of the control group. After induction of hypercapnia (PaCO₂ about 80 mmHg) CBF increased by 360% in the control group; in the acutely intoxicated group CBF increased by only 127% and in the long term intoxicated group by 203 % indicating that the cerebrovascular CO₂-reactivity had also adapted to the ethanol intoxication. It is concluded that adaptive changes of the CNS to chronic ethanol intoxication comprise alterations in CMRO₂, CBF and cerebrovascular reactivity.     

活性氧对红细胞膜流动性影响的研究

目的 :研究活性氧诱导红细胞发生氧化溶血的机制。方法 :用不同浓度的 H2 O2 作用于离体正常红细胞 ,分别用比色法、硫代巴比妥酸荧光法、荧光偏振法测定红细胞溶血度、红细胞膜脂质过氧化物 (L PO)、红细胞膜微粘度。结果 :5 0 ,10 0 ,12 0 mm ol/ L 浓度的 H2 O2 作用于红细胞后 ,均引起红细胞发生氧化溶血 ,红细胞溶血度、红细胞膜 L PO、红细胞膜微粘度均明显增加 ;H2 O2 在 5 0～ 12 0 mm ol· L- 1浓度范围内 ,红细胞溶血度、红细胞膜 L PO、红细胞膜微粘度的增加与 H2 O2 有明显的量效关系 ;红细胞膜微粘度与红细胞溶血度呈明显正相关 ,红细胞膜 L PO与红细胞膜微粘度呈明显正关。结论 :活性氧引发红细胞膜脂质过氧化导致红细胞膜流动性降低在活性氧诱导红细胞发生氧化溶血的机制中起一定的作用     

玉米浆用量、渗透压和耗糖速率对甘油发酵的影响

Candida krusei发酵生产甘油过程中,菌体生长由玉米浆限制,菌体对玉米浆的得率为1．63g/g,培养其中玉米浆浓度相同时,增加渗透压或通过流加补料限制生长阶段的菌体生长,可使甘油生产阶段的比耗糖速率减慢,比耗糖速率保持在不很高的水平,可以因消耗的葡萄糖用于生长,维持,甘油和副产物形成所占比例的变化而提高甘油得率。     

常压氧治疗胎儿-胎盘循环功能降低疗效的多普勒超声心动图观察

目的评价常压氧在胎儿-胎盘循环功能降低治疗中的疗效.方法应用超声心动图观察52例胎儿胎盘循环功能降低在常压氧治疗前后的变化情况并与45例普通吸氧组及41例未治疗组进行对照.结果52例胎盘循环功能降低胎儿中43倒常压氧治疗后胎盘循环功能恢复正常,有效率82.7%.明显高于对照组(P＜0.01).结论常压氧是治疗胎儿胎盘循环功能降低安全、有效的方法.