Generation of reactive oxygen species after exhaustive aerobic and isometric exercise

Many studies have implicated elevated oxygen consumption (VO2) associated with aerobic exercise as contributing to oxidative stress. Only a few studies have investigated nonaerobic exercise and its relation to pro-oxidant and antioxidant activities. PURPOSE: The purpose of this study was to compare biomarkers of oxidative stress: lipid peroxidation, protein oxidation, and total antioxidants in blood after exhaustive aerobic (AE) and nonaerobic isometric exercise (IE). METHODS: Blood samples were collected from 12 subjects who performed a maximum AE and IE test and were analyzed for thiobarbituric acid (TBARS), carbonyls, lipid hydroperoxides (LH), and oxygen radical absorbance capacity (ORAC). RESULTS: VO2 increased 14-fold with AE compared with 2-fold with IE. Protein carbonyls increased 67% (P < 0.05) pre- to immediately and 1 h post-AE, and 12% pre- to immediately post-IE and returned to baseline 1 h post-IE. TBARS did not increase significantly with either treatment. LH increased 36% above rest during IE compared with 24% during AE (P < 0.05). ORAC increased 25% (P < 0.05) pre- to post-AE, compared with 9% (P < 0.05) pre- to post-IE. CONCLUSION: There was evidence of oxidative stress after both exhaustive aerobic and isometric exercise. Lipid hydroperoxides, protein carbonyls, and total antioxidants increased after both IE and AE. Due to the different metabolic demands of aerobic and isometric exercise, we can rule out a mass action effect of VO2 as the sole mechanism for exercise-induced oxidative stress.     

Moderate exercise and hemodilution during sleep deprivation

The effect of 52 h of sleep deprivation (SD) upon blood constituents was studied in 12 young women aged 21.5 +/- 0.4 years. Subjects were individually isolated without time cues, performing a sequence of cognitive tasks. Significant decreases in hematocrit (p less than 0.002) and red cell count (p less than 0.04) developed, mainly over the first 28 h of SD, reaching a subsequent plateau or partial recovery. The calculated plasma volume also increased by 10.7 +/- 3.1% at 52 h, with recovery to a 6.9 +/- 3.2% increase the following day. About 1 L of water was retained over the first 30 h of SD, with a subsequent partial elimination of this excess. Plasma albumin and total protein concentrations were largely sustained in the face of the plasma expansion. The plasma pH showed a progressive fall from a baseline value of 7.381 +/- 0.014 to 7.332 +/- 0.006 at 52 h, while plasma bicarbonate decreased from a baseline figure of 31.2 +/- 0.7 to 26-27 mM/L (p less than 0.05). After 8 weeks, all subjects repeated the experiment, with the introduction of 30 min of exercise in the 40th h of wakefulness. Hematocrit and plasma volume changes were similar to those of the first experiment up to the time of exercise, but hematocrit decreased and plasma volume increased after the exercise bout, rather than reaching a plateau. Plasma pH increased with exercise, but returned to the previous low level at 52 h. Any arousing effect of the exercise bout was transient. The plasma expansion reflects metabolic and/or respiratory acidosis, plus possible effects of a prolonged period without recumbency.     

Control of oxygen uptake during exercise

Other than during sleep and contrived laboratory testing protocols, humans rarely exist in prolonged metabolic steady states; rather, they transition among different metabolic rates (V O2). The dynamic transition of V O2 (V O2 kinetics), initiated, for example, at exercise onset, provides a unique window into understanding metabolic control. This brief review presents the state-of-the art regarding control of V O2 kinetics within the context of a simple model that helps explain the work rate dependence of V O2 kinetics as well as the effects of environmental perturbations and disease. Insights emerging from application of novel approaches and technologies are integrated into established concepts to assess in what circumstances O2 supply might exert a commanding role over V O2 kinetics, and where it probably does not. The common presumption that capillary blood flow dynamics can be extrapolated accurately from upstream arterial measurements is challenged. From this challenge, new complexities emerge with respect to the relationships between O2 supply and flux across the capillary-myocyte interface and the marked dependence of these processes on muscle fiber type. Indeed, because of interfiber type differences in O2 supply relative to V O2, the presence of much lower O2 levels in the microcirculation supplying fast-twitch muscle fibers, and the demonstrated metabolic sensitivity of muscle to O2, it is possible that fiber type recruitment profiles (and changes thereof) might help explain the slowing of V O2 kinetics at higher work rates and in chronic diseases such as heart failure and diabetes.     

Accumulated oxygen deficit during ramp exercise

This study aimed to compare oxygen deficit during exhaustive ramp exercise (OD ramp and OD lag) with maximal oxygen deficit during a high-intensity constant-power test (MAOD). OD ramp was estimated from the difference between oxygen demand and actual oxygen uptake. OD lag was estimated using a simple equation assuming a linear increase in oxygen uptake lagging behind metabolic requirement. After a first test providing estimation of P peak, 12 healthy males did two 15 W.min(-1) and two 30 W.min(-1) ramp tests to evaluate in duplicate OD ramp and OD lag and an exhaustive exercise at 105% of P peak to evaluate MAOD. OD ramp from the 15 W.min(-1) tests (1.50 +/- 1.83 and 2.60 +/- 2.12 l) and from the 30 W.min(-1) tests (2.41 +/- 1.00 and 2.72 +/- 1.23 l) did not differ from MAOD (2.33 +/- 0.50 l). Contrary to OD lag estimated from the 15 W.min(-1) tests (2.27 +/- 0.30 and 2.31 +/- 0.31 l), OD lag from the 30 W.min(-1) tests (2.51 +/- 0.34 and 2.52 +/- 0.36 l) was significantly greater than MAOD (p < 0.05). The conclusion is that the oxygen deficit would accumulate progressively during a ramp test until attaining the maximal oxygen deficit. This measurement would not however give reliable index of an individual subject due to the elevated test-retest variability.     

Nitric oxide, reactive oxygen species, and skeletal muscle contraction

Nitric oxide (NO) derivatives and reactive oxygen species (ROS) modulate contractile function of respiratory and limb skeletal muscle. The intracellular processes regulated by NO and ROS remain enigmatic, however. Studies of reduced preparations have identified a number of regulatory proteins that exhibit altered function when exposed to exogenous NO or ROS donors ex vivo. The relative importance of these targets in the intact cell is not known and conflicting theories abound regarding the mechanism(s) whereby NO and ROS regulate contraction. This review article provides a personal perspective on the processes regulated by NO and ROS by addressing three major topics: 1) the regulatory mechanisms by which endogenous NO depresses force production, 2) the processes whereby endogenous ROS modulate contraction of unfatigued muscle, and 3) the site(s) of action and reversibility of ROS effects in muscle fatigue.     

Kinetics of induction of reactive oxygen species during the post-irradiation expression of neoplastic transformation in vitro

Purpose : To examine whether the delayed expression of cell death and neoplastic foci in irradiated HeLa ×human skin fibroblast human hybrid cells correlates with the presence of reactive oxygen species (ROS) in the progeny of the irradiated cells. Material and methods : HeLa ×human skin fibroblast human hybrid cells were irradiated and plated as for assay of neoplastic transformation. At regular time intervals during the post-irradiation expression period of 21 days, samples were harvested and assessed for the presence of oxyradical activity by measuring the oxidation of dichlorohydrofluorescein (DCFH) to dichlorofluorescein (DCF) using flow cytometry. This reagent principally detects hydrogen peroxide. The kinetics of production of ROS were compared with those previously measured using the identical experimental protocol for the expression of both cell death and neoplastic foci. Results : The kinetics of production of ROS closely matched those for the onset of delayed cell death and delayed expression of neoplastic transformation. Conclusions : The induction of ROS is associated with delayed cell death and delayed neoplastic transformation in irradiated HeLa ×human skin fibroblast human hybrid cells.     

Aerobic and anaerobic energy conversion during high-intensity exercise

PURPOSE: The aim of the study is to compare data on anaerobic and aerobic energy conversion during exercise of high intensity leading to exhaustion. Several different data sources are used, including data extracted from mathematical analyses of world and Olympic running records, data from laboratory tests, and data based on biochemical information. METHODS: Theoretical relationships are derived and comparisons are made of the ratio of aerobic to total energy contributions as functions of time. RESULTS: The ratio is shown to depend not only on the duration of the high-intensity exercise but also in part on a factor lambda, which governs the rate of anaerobic and aerobic energy release. A further important factor is the value of the parameter Q/lambda, which is the ratio of anaerobic capacity to maximum sustainable aerobic power. Values in the range 55 s < Q/lambda < 72 s and 0.030 s(-1) < lambda < 0.042 s(-1) are shown to provide the best correlation of data. The results indicate that the ratio of maximal anaerobic power to maximum aerobic power lies in the range from 2.0 to 2.6. CONCLUSION: Data extracted from the mathematical models of running are generally more consistent than the body of experimental data. This may indicate that the inherent difficulties of laboratory techniques relating to the measurement of anaerobic energy conversion are giving rise to significant experimental errors.     

Kinetics of induction of reactive oxygen species during the post-irradiation expression of neoplastic transformation in vitro.

PURPOSE: To examine whether the delayed expression of cell death and neoplastic foci in irradiated HeLa x human skin fibroblast human hybrid cells correlates with the presence of reactive oxygen species (ROS) in the progeny of the irradiated cells. MATERIAL AND METHODS: HeLa x human skin fibroblast human hybrid cells were irradiated and plated as for assay of neoplastic transformation. At regular time intervals during the post-irradiation expression period of 21 days, samples were harvested and assessed for the presence of oxyradical activity by measuring the oxidation of dichlorohydrofluorescein (DCFH) to dichlorofluorescein (DCF) using flow cytometry. This reagent principally detects hydrogen peroxide. The kinetics of production of ROS were compared with those previously measured using the identical experimental protocol for the expression of both cell death and neoplastic foci. RESULTS: The kinetics of production of ROS closely matched those for the onset of delayed cell death and delayed expression of neoplastic transformation. CONCLUSIONS: The induction of ROS is associated with delayed cell death and delayed neoplastic transformation in irradiated HeLa x human skin fibroblast human hybrid cells.     

Kinetics of oxygen uptake during decremental ramp exercise

BACKGROUND: The purpose of the present study was to examine the kinetics of oxygen uptake (VO2) during decremental ramp exercises after incremental ramp exercise above the anaerobic threshold. METHODS: Triangle exercise consisting of incremental and decremental exercises, and trapezoid exercise in which a constant load was inserted between incremental and decremental exercises were carried out. RESULTS: Blood lactate (La) increased in incremental phases during triangle and trapezoid exercises, and showed a further increase at constant work during trapezoid exercise. It significantly decreased during decremental exercise. Initial VO2 level during decremental exercise was significantly higher in trapezoid exercise than in triangle exercise. The VO2 level then exponentially decreased and later showed a linear decrease during both exercises. These VO2 kinetics were expressed by an approximate equation. The time constant expressing the exponential manner was about one minute on average in both exercises. The slope of the linearly decreasing phase of VO2 was significantly related to La at 100 watts during the decremental exercise. CONCLUSIONS: VO2 kinetics during decremental exercise after incremental exercise above the anaerobic threshold consists of at least three components: initial level, exponentially decreasing phase, and linearly decreasing phase.     

高压氧联合西酞普兰治疗抑郁症睡眠障碍患者的临床疗效观察

目的:探讨高压氧(HBO)联合西酞普兰治疗抑郁症睡眠障碍患者的临床疗效及其作用机制。方法:收集2016年3月至2019年6月在山西白求恩医院精神卫生科诊治的抑郁症睡眠障碍患者140例,按随机数字表法分为观察组和对照组,每组70例。对照组给予西酞普兰治疗,观察组给予西酞普兰联合HBO治疗,均治疗4周后观察2组患者的治疗效果、抑郁评分、睡眠障碍情况以及血清白细胞介素-1(IL-1)、IL-6、肿瘤坏死因子-α(TNF-α)和皮质醇水平。结果:治疗4周后,观察组患者治疗总有效率(94.29%)显著高于对照组(77.14%),差异有统计学意义( P<0.05);治疗后2组患者睡眠质量、入睡时间、抑郁状态评分均显著低于治疗前,且观察组治疗后下降更显著,差异均有统计学意义( P<0.05或 P<0.01);治疗后2组患者的IL-1、IL-6、TNF-α和皮质醇水平均明显低于治疗前,且观察组治疗后较对照组下降更显著,差异有统计学意义( P<0.05或 P<0.01)。 结论:HBO联合西酞普兰治疗可降低抑郁症睡眠障碍患者血清IL-1、IL-6、TNF-α、皮质醇水平,显著改善抑郁状况和睡眠障碍,有较好的临床疗效。     

Alterations in energy metabolism during exercise and heat stress

Much of the research that has examined the interaction between metabolism and exercise has been conducted in comfortable ambient conditions. It is clear, however, that environmental temperature, particularly extreme heat, is a major practical issue one must consider when examining muscle energy metabolism. When exercise is conducted in very high ambient temperatures, the gradient for heat dissipation is significantly reduced which results in changes to thermoregulatory mechanisms designed to promote body heat loss. This can ultimately impact upon hormonal and metabolic responses to exercise which act to alter substrate utilisation. In general, the literature examining metabolic responses to exercise and heat stress has demonstrated a shift towards increased carbohydrate use and decreased fat use. Although glucose production appears to be augmented during exercise in the heat, glucose disposal and utilisation appears to be unaltered. In contrast, glycogen use has been consistently demonstrated to be augmented during exercise in the heat. This increase in glycogenolysis is observed via both aerobic and anaerobic pathways. Although several hypotheses have been proposed as mechanisms for the substrate shift towards greater carbohydrate metabolism during exercise and heat stress, recent work suggests that an augmented sympatho-adrenal response and intramuscular temperature may be responsible for such a phenomenon.     

Pten基因敲除对过氧化物酶家族表达和活性氧水平的影响

目的:探讨Pten基因敲除后对过氧化物酶家族(Peroxiredoxins,Prdxs)水平和活性氧水平的影响.方法:采用Western印迹和化学/荧光发光分析法分别检测了在Pten / MEF和Pten-/-MEF细胞中PRDXs的表达和细胞内活性氧水平.结果:Western印迹结果显示,与Pten / MEF细胞相比,Pten-/-MEF细胞PRDX Ⅰ,Ⅱ,Ⅴ,Ⅵ蛋白水平下调,PRDX Ⅲ不变,PRDX Ⅳ上调.DCFH探针标记后流式结果显示Pten-/-MEF 细胞活性氧荧光值显著高于对照Pten / MEF细胞(P＜0.05).结论:Pten基因敲除引起数种PRDXs表达下调,细胞内活性氧水平增高.     

Creatine enhances oxygen uptake and performance during alternating intensity exercise

PURPOSE: The main purpose of the present study was to measure the total oxygen consumed, accumulation of blood metabolites, and performance during alternating intensity exercise before and after a period of creatine (Cr) loading in well-trained humans. METHODS: Fourteen males were randomly assigned to two groups of seven males and were tested before and after 5 d of placebo (PL) or Cr monohydrate (CR) loading (20 g x d(-1)). Oxygen uptake was measured using a breath-by-breath system during bicycle exercise alternating every 3 min between bouts at 30%(-30%) and 90% (-90%) of the maximal power output to exhaustion. Blood samples were also obtained at rest, before the end of each cycling load, at exhaustion, and 5-min postexercise. RESULTS: The oxygen consumed during 1-90% (5.08 +/- 0.39 L) and 2-90% (5.32 +/- 0.30 L) was larger after CR (5.67 +/- 0.34 and 5.78 +/- 0.35 L, P < 0.01 and P < 0.05, respectively). Blood ammonia accumulation at the end of 1-90% (23.1 +/- 6.5 micromol x L(-1)) and 3-30% (64.7 +/- 15.2 micromol x L(-1)) was lower after CR (P < 0.05), whereas plasma uric acid accumulation was lower at exhaustion (P < 0.05) and 5-min postexercise (P < 0.01). Time to exhaustion increased (P < 0.05) from 29.9 +/- 3.8 to 36.5 +/- 5.7 min after CR, whereas it remained the same after PL. CONCLUSIONS: The results indicate that Cr feeding increases the capacity of human muscle to perform work during alternating intensity contraction, possibly as a consequence of increased aerobic phosphorylation and flux through the creatine kinase system.     

Inadequate cerebral oxygen delivery and central fatigue during strenuous exercise

Under resting conditions, the brain is protected against hypoxia because cerebral blood flow increases when the arterial oxygen tension becomes low. However, during strenuous exercise, hyperventilation lowers the arterial carbon dioxide tension and blunts the increase in cerebral blood flow, which can lead to an inadequate oxygen delivery to the brain and contribute to the development of fatigue.     

Relationship between leucine oxidation and oxygen consumption during steady-state exercise

PURPOSE: The purpose of this study was to assess the relationship between whole-body leucine oxidation and oxygen consumption during steady-state exercise. Our hypothesis was that leucine oxidation will be responsive to increased whole-body energy needs. METHODS: Sixteen healthy individuals (7 women and 9 men) were infused with a stable isotope of leucine and, for comparison purposes, lysine during 60 min of moderate-intensity exercise. RESULTS: Leucine oxidation was increased (P < 0.05) and nonoxidative leucine disposal was decreased (P < 0.05), whereas leucine and lysine rate of appearance remained unchanged (P = NS) during exercise. Linear regression analysis indicated a modest relationship between leucine oxidation and steady-state oxygen consumption (R = 0.69; P < 0.003) during steady-state exercise. The coefficient of determination (R(2) = 0.49) indicates that approximately half of the variance in whole-body leucine oxidation during exercise can be explained by whole-body oxygen consumption. CONCLUSION: In a statistically appropriate sample size of humans whose dietary intake was controlled, the whole-body rate of leucine oxidation during exercise was only partially influenced by energy demands.     

Mild overcooling increases energy expenditure during endurance exercise

Intensive cooling has been shown to increase energy expenditure (EE) during work as well as to decrease physical performance. Two different levels of moderate cooling (10°C vs 15°C) were studied during light endurance exercise in order to examine the effect of the increased heat loss on EE. Twelve subjects performed a 90-min low intensity exercise (100 W) on a cycle ergometer, wearing a water-cooled calorimeter suit for controlled cooling. The lower temperature resulted in a 4.3±3.8% (mean±SD) higher EE, increased total heat loss and lowered skin temperatures. No differences in central core body temperature, heart rate or respiratory quotient (RQ) were recorded. There was a relation between differences in the rate of heat loss and the corresponding increase in EE. Even a small increase in cooling during endurance exercise increased EE which may be a relevant problem in winter sports.