应《网络安全法》要求，自2017年10月1日起，未进行实名认证将不得使用互联网跟帖服务。为保障您的帐号能够正常使用，请尽快对帐号进行手机号验证，感谢您的理解与支持！

24小时热门版块排行榜    

小木虫论坛-学术科研互动平台» 学术交流区» 论文翻译 » 论文翻译求助完结子版 » 翻译求助
121/2返回列表12下一页
查看: 541  |  回复: 11
只看楼主 @他人 存档 新回复提醒 (忽略) 收藏    在APP中查看
当前主题已经存档。

leiyu6788

新虫 (小有名气)

[交流] 翻译求助

英译汉！麻烦高手们帮忙，谢谢！leiyu6788
leiyu6788
leiyu6788
回复此楼

» 猜你喜欢
1楼 2009-07-27 17:46:11
已阅   回复此楼   关注TA 给TA发消息 送TA红花 TA的回帖

leiyu6788

新虫 (小有名气)
注意：3天有效啊！
赞一下 回复此楼
2楼2009-07-27 17:47:26
已阅   回复此楼   关注TA 给TA发消息 送TA红花 TA的回帖

Y.F.Zhou

木虫 (著名写手)
★ ★
leiyu6788(金币+1,VIP+0): 7-29 15:57
leiyu6788(金币+1,VIP+0): 7-31 16:21
为什么不把内容直接贴出来呢？
赞一下(18人) 回复此楼
风风雨雨，一起走过。
3楼2009-07-27 19:38:54
已阅   回复此楼   关注TA 给TA发消息 送TA红花 TA的回帖

monitor2885

至尊木虫 (职业作家)

队长
★
leiyu6788(金币+1,VIP+0): 7-29 15:57
内容直接贴出来
回复此楼
Retirement
4楼2009-07-27 20:56:20
已阅   回复此楼   关注TA 给TA发消息 送TA红花 TA的回帖

liuth

木虫 (正式写手)
★ ★ ★
telomerase(金币+3,VIP+0):辛苦辛苦！！！ 7-28 09:04
代楼主贴出：
Growth of Fitness-Specific Tissues
The anabolic actions of growth factors are directed to specific tissues, whose increase in size is important in the development of physical fitness as children grow. In the development of aerobic fitness, increased dimensions of the respiratory and circulatory systems, particularly the heart, are instrumental. Improvements in strength and anaerobic fitness, on the other hand, are expected to be tied more closely to increases in muscle bulk.
Growth hormone can profoundly affect the functional capacity of the cardiac, respiratory, and muscular systems in children, as evidenced by observed improvements in physical fitness after its use in clinical settings. Hutler et al. reported the effect of growth hormone treatment on exercise tolerance in 10 prepubertal children with cystic fibrosis (39).The children were randomly assigned to either a control group or a group that received growth hormone treatment for the initial six months and then to the other group for the next six months. Compared with the control condition, growth hor¬mone treatment produced a significant increase in absolute peakVO, (+ 19%), peak ventilation (+ 14%), and peak oxygen pulse (+18%). In this study 71% of the improvement in peak [0, was explained by changes in lean body mass and forced expiratory volume.
Cardiac Growth
Insights into the effect of growth factors on heart size and function have been derived from animal studies as well as investigations of humans-both children and adults-who have deficiencies of growth factors, particularly deficiencies involving the GH/IGF-I axis. This has been the subject of several reviews (15, 48, 73).
There is abundant evidence that both GH and IGF-I stimulate cardiac growth, with associated improvements in both rnyocardial contractility and energy economy. GH also causes peripheral vasodi¬latation, probably via the effect of IGF-I on nitric oxide release.
Cardiac size and contractility are depressed in patients with GH deficiency, conditions that resolve with GH treatment. Cittadini et al. found depressed ventricular ejection fraction, cardiac output, and exer¬cise performance in 11 young adults with childhood¬onset GH deficiency (14). In healthy control subjects, ejection fraction rose from 66% to 76% with exercise, while in the GH-deficient patients, little change was seen from a resting value of 54%. After six months of GH treatment, exercise tolerance rose from 7.2 to 9.4 minutes, and resting ejection fraction increased to 61%, while cardiac output responses to exercise became similar to those of the controls.
Administration of GH to children with GH defi¬ciency does not stimulate cardiac size or function beyond that paralleling total body growth. Rowland et al. found no differences in left ventricular wall thickness or chamber size when related to body size in echocardiograms of 13 children with GH deficiency who had been treated with GH (mean dose 0.17 IU kg' three times per week) for 13 to 46 months (70). Crepaz et al. compared echocardio¬graphic findings in 22 children ages 3 to 17 years with GH deficiency who were given GH for an average of 14 months (19). Compared with size-matched healthy children, no differences were observed in left ventricular chamber size, wall thickness, contractility, diastolic function, cardiac index, or systemic vascular resistance.
赞一下(10人) 回复此楼
寡聚噻吩，传感，Two-photon，SquaraineDye，Porphyrin
5楼2009-07-27 21:31:47
已阅   回复此楼   关注TA 给TA发消息 送TA红花 TA的回帖

liuth

木虫 (正式写手)
Studies of the cardiac effects of GH administered to children without GH deficiency probably serve as a better model for the role of GH in the normal course of cardiac development with somatic growth. Daubeney et al. reported echocardiographic measures of heart size in 15 children with short stature (but no GH deficiency) before and after four years of GH treatment, compared with an untreated group (22). No anthropometric or ventricular-dimension differences were observed between the two groups at baseline. After four years of GH treatment, however, the treated children exhibited greater height, weight, and lean body mass as well as larger left ventricular end-diastolic dimension (41 ± 5 mm vs. 36 ± 5 mm) and left ventricular mass (93 ± 33 g vs. 73 ± 26 g).
Posttreatment left ventricular mass expressed relative to lean body mass was similar to that of the controls, however, suggesting that increases in heart size reflected changes in lean body mass with GH treatment. No alterations in ventricular shortening fraction (an indicator of systolic contractile function) were observed following hormone treatment.
Similar results were observed in short children by Barton et al., who found that increases in cardiac dimensions with GH treatment paralleled those of body size (4).These findings in short but otherwise normal children mimic those in rats with GH-secreting tumors, who show accelerated heart growth in pro¬portion to increases in body dimensions (72). They also simulate empiric observations during the growth of normal children: increasing heart size in relation to body dimensions (particularly lean body mass) without changes in myocardial contractility.
In abnormal hearts, GH increases myocardial function and improves energy efficiency. In the presence of left ventricular hypertrophy and failure, GH administered to both humans and animals causes a shift in myocardial myosin composition (increased V3 isoform and enhanced troponin I and myosin light chain 2), all changes associated with greater efficiency of myocardial contraction. These salutary effects of GH suggest its potential as a therapeutic modality for patients with depressed myocardial function (41). Fazio et al. administered recombinant GH to seven adult patients with idiopathic dilated cardiomyopathy and mild to severe congestive heart failure (29). Serum IGF-I concentrations doubled in response.Ventricular wall thickness increased, and a reduction was observed in end-diastolic dimension. Cardiac output during exercise improved 31 %, while myocardial oxygen uptake at rest fell by one third.
The cardiac effects of IGF-I are similar to those of GH. IGF-I enhances myocardial protein synthe¬sis and contractile function, both in normal hearts and in those with myocardial dysfunction (23). For example, Donath et al. found that IGF-I administered to healthy adults resulted in an 18% rise in cardiac output in association with a 9% increase in ventricu¬lar ejection fraction (23). Maximal oxygen uptake and exercise endurance, however, were not altered.
A host of locally acting growth factors have been identified that can mediate cardiac rnyocyte hypertrophy (at least in vitro), including cytokines, catecholamines, angiotensin II, and IGF-I (36).The increase in heart muscle cell size (i.e., hypertrophy) from such factors in response to hemodynamic over¬load may, however, not be an appropriate model for assessment of increases in cell size that occur with normal growth. Stress-related responses involve specific alteration in gene expression, which alters the phenotypic expression of contractile proteins. The extent to which such alterations occur with normal growth in humans is uncertain. It is of inter¬est, however, that stress-induced changes in forms of myosin are often characterized by a reversal to fetal gene expression.
Increases in contractility in response to IGF-I exposure are dose dependent and reach about 20% to 25% above baseline. Alterations of calcium flux appear to be responsible.This improvement in myo¬cardial contractile function occurs despite absence of change in ATP content or high-energy phosphates, thus indicating greater energy efficiency.
Muscular Growth
Growth of skeletal muscle mass is one of the most firmly established activities of the GH/IGF-I axis (84).While animal studies indicate that GH has some primary effects, IGF-I appears to be predominantly responsible for the growth and development ofmuscle cells seen with exogenous or endogenous exposure to GH.This activity reflects both augmented protein synthesis through increased amino acid transport and inhibited cellular protein degradation.
Short stature is the most common feature of children with growth hormone deficiency, but these patients also demonstrate delayed motor develop¬ment and reduced muscle strength.These conditions are typically reversed by GH treatment. Brat et al. measured isometric muscle force and endurance in a small group of children with GH deficiency before and after 10 and 24 months of GH treatment (8). Before treatment, the muscle force of children with GH deficiency was 56% to 62% of that of matched healthy children. Strength measurements rose to 75% to 78% after 10 months of treatment and to 87% to 93% at 24 months.
A deficiency of GH is not necessary for these treatment effects. Leger et al. (45) assessed the effects of three years of GH treatment (0.2 IU • kg 1• d-') on muscle mass in 14 prepubertal children who were born small for gestational age (SGA). Muscle mass in this study was determined by magnetic resonance imaging. Results were compared with longitudinal measurements of children of normal stature. The increase in muscle cross-sectional area was 72 ± 5 % in the GH-treated SGA children compared with 22 ± 5 % in the controls.
The pharmacologic dose of GH in this study was approximately twice that used for replacement therapy in children who are GH deficient. In a previous publication, Leger et al. described a more rapid change in muscle size in SGA children than in GH-deficient children (46).This caused the authors to suggest that it is possible that the effect of GH on muscle in children is dose dependent.
Paracrine and autocrine factors acting locally and independently of GH may also be important for muscle growth. For example, mechanogrowth factor (MGF), produced in response to muscle stretch, has been demonstrated to stimulate muscle protein synthesis (34).
Adams reviewed data regarding the role of IGF¬I in mediating skeletal muscle adaptations to work stress (1). In rats, IGF-I stimulates muscle protein synthesis, increases amino acid uptake, and sup¬presses protein degradation. Furthermore, IGF-I has a separate action in promoting cell proliferation (mitogenesis) and differentiation in the embryonic development of skeletal muscle. Increasing evidence exists that these same two processes are involved in muscle adaptive responses to increased workload.
These investigations suggest that paracrine or autocrine actions rather than circulating IGF-I stimulate anabolic effects leading to muscle hyper¬trophy with work stress. In addition, IGF-I has been demonstrated to stimulate proliferation of satellite cells: small, mononucleated stem cells that have the capacity to proliferate and differentiate into myoblasts in response to work stress or injury.
Accounting for Interindividual Fitness Differences in Children
So far, the development of physiologic and physical fitness in children has been examined as an out¬come of increases in body size. Somatic maturation is largely responsible for longitudinal changes in exercise functional capacity during the growing years. This analysis, however, does not address fac¬tors that are responsible for individual differences in physical fitness.
If the somatic expression of growth factors was the only determinant of development of physiologic and performance fitness, all children of the same size would exhibit identical levels of fitness.This is clearly not the case. Any physiologic factor varies signifi¬cantly in respect to a given appropriate measure of body size. How can we explain such variations in fitness relative to the same body dimensions in any group of children of even identical chronologic or biologic age? Several possible answers can be con¬sidered.
1. Specific factors, which act independently of determinants of height and weight, may target their effects on the growth of fitness-related tissues. Such agents have been recognized, in fact. A number of peptide growth factors, particularly fibroblast growth factor 6 and epidermal growth factor, have been iden¬tified in cardiac myocytes (7).These factors have been implicated in hypertrophic responses of the heart to systolic overwork (systenuc hypertension) as well as fetal cardiac organogenesis. In any event, they provide evidence that localized, tissue-specific factors exist that can stimulate heart growth.
2. GH receptors may be selectively more popu¬
lous or active in the fitness-related tissues of children who exhibit superior levels of fitness. This would result in disproportionate growth of heart or muscle size, for example, relative to height and weight.
3. Size-independent factors may operate more prominently in children with greater fitness. As noted earlier, the development of size-independent factors may contribute significantly to the evolution of exercise fitness during childhood.The nature and magnitude of these size-independent influences vary among types of fitness. Interindividual variations in fitness could then relate to greater or lesser input from these factors, presumably on a genetic basis.The child with 50-yd dash performance superior to that of another child her own age and size might possess greater glycolytic capacity to provide anaerobically derived energy. A more developed level of neuro¬muscular input to muscles might explain the stronger child. This would not, however, explain differences in aerobic fitness, in which the influence of lung or heart size on VOzmax is predominant.
This issue is a critical one for developmental exercise physiologists, for it bears on the central question of identifying limiting factors to physical and physiologic performance by growing children. Because these interindividual differences in fitness are observed in nontrained youth in populations homogeneous in nutrition, socioeconomic status, and body composition, it is reasonable to conclude that, by whatever phenotypic mechanism, these dif¬ferentiating factors are under genetic control. Much progress has been made in determining specific gene loci that influence physical fitness (65). It is possible that this research will identify specific gene markers that define individual levels of fitness via one or more of the preceding mechanisms.
Effects of Exercise on Growth

还有一半没有贴出
赞一下 回复此楼
寡聚噻吩，传感，Two-photon，SquaraineDye，Porphyrin
6楼2009-07-27 21:32:53
已阅   回复此楼   关注TA 给TA发消息 送TA红花 TA的回帖

liuth

木虫 (正式写手)
★ ★ ★ ★ ★
leiyu6788(金币+5,VIP+0): 7-29 15:55
The previous section addressed the influence of somatic growth and its determinants on children's physiologic responses to exercise. We now turn the arrow around to look at cause and effect in the opposite direction: How might physical activity during child¬hood and adolescence, particularly athletic participa¬tion, affect physical growth?This question is a major concern of parents, coaches, and physical educators alike. Can the stresses of intense physical activity in the growing years impair linear and visceral growth? If so, should limits be placed on young people's par¬ticipation in athletic training programs?
The concept that increased physical stresses might stunt growth arose initially from animal studies in which swim-trained rats demonstrated delayed bone growth and from an early report indicating delayed statural maturation in children undertaking hard labor in poor socioeconomic conditions (3). More recently, the concern has been reinforced by studies suggesting that intense training might delay linear growth in young female gymnasts (83).
At the same time, it is accepted that increased physical activity and musculoskeletal stress are important for promoting growth in children (3, 6). Moreover, children's involvement in sport training might provide particular long-term health benefits (e.g., stimulation of bone growth and density may ameliorate the risk of future osteoporosis). The fol¬lowing discussion focuses on the biologic means by which exercise by children might affect positively or negatively-their normal patterns of growth. For the most part, however, analysis ofhow growth responses to repeated exercise (i.e., sport training) might improve physical fitness and accelerate specific forms of physi¬ologic development is deferred until chapter 11.
Physical activity might influence growth in chil¬dren by three possible mechanisms (6; figure 2.4): (a) Exercise draws on caloric stores and competes（图：4~- FIGURE 2.4 Potential mechanisms for the effects of physical activity on growth.）with the energy demands of normal growth for available nutrients. Through "caloric stealing," physical activity may thus potentially impair growth on a nutritional basis. (b) Physical activity serves as a potent stimulus for production of growth factors. However, the mechanisms behind this action-as well as its implications for positive growth-are not clear. (c) Muscular activity creates local mechanical stresses that trigger musculoskeletal growth. In some cases, intermediary apocrine and autocrine agents may mediate this process.

Competition for Nutrition
During childhood and early adolescence the energy needs of exercise are superimposed on the energy needs for not only homeostasis and tissue repair but also somatic growth. That the requirements for normal growth can lose in this conflict is evidenced by the poor growth seen in active children in nutri¬tionally marginal conditions in underdeveloped countries. This phenomenon may also contribute to the delayed statural maturation associated with negative caloric balance in activities where slender body habitus is important, such as gymnastics and ballet dancing (31, 83).
Undernutrition with negative caloric balance is associated with depression of serum IGF-I levels in male (80) as well as female gymnasts (40). Smith et al. (80) demonstrated a significant decline in IGF-I levels after a seven-day exercise period that put young adult males in a negative caloric balance (causing weight loss of 0.5-2.0 kg). A similar decline in IGF-I was observed when an equivalent caloric imbalance was created by dietary restriction without exercise.Thus, energy deficiency caused by either exercise or diet caused a fall in IGF-I levels.
Roemmich and Sinning demonstrated increases in GH secretion but a decline in growth hormone¬binding protein (GHBP) and IGF-I in undernour¬ished adolescent wrestlers (67). All values quickly reverted to normal at the end of the competitive season. No significant effect was observed on linear bone growth or sexual maturation.

Response of Growth Factors
Acute and chronic exercise trigger alterations in the GH/IGF-I axis and in the production of other growth factors.The extent to which these alterations stimulate growth or reparative processes through anabolic activity or provide metabolic support (e.g., substrate utilization) in children is uncertain.
Growth Hormone
Acute bouts of exercise stimulate the release of GH. In fact, exercise serves as one of the most effective provocative agents for clinically evaluating GH pro¬duction capacity.The rise in GH with acute exercise is not immediate. Levels typically begin to rise 10 to 15 minutes after the beginning of a 30-minute exercise bout and peak at the end of exercise. Level of physical fitness affects this acute GH response. Trained adults demonstrate blunted GH production compared with nontrained individuals, and a three¬to six-week training period has been demonstrated to lower the GH response to acute exercise (90). Interestingly, however, 24-hour GH secretion and amplitude of GH pulses in adult athletes are greater than those of nonathletes.
The extent of GH response depends linearly on the intensity of exercise, but the intensity of exercise necessary to evoke a rise in GH varies considerably between individuals. In general, however, exercise above 50%VOZmax is necessary to trigger a substan¬tial rise. This suggests that some physiologic trigger related to intensity of muscle contraction serves as the stimulus for pituitary GH release.
The neuroendocrine mechanism by which acute exercise triggers and regulates GH is not known. Both alpha- and beta-adrenergic pathways appear to play a role, since pharmacologic beta-blockage enhances GH response to exercise, while phentol¬amine (an alpha-receptor antagonist) depresses GH release. Administration of pyridostigmine, a promoter of the cholinergic system, augments GH response to exercise, probably by inhibiting the action of somatostatin.
A rise in body temperature has been suggested as a mediator of GH release in response to acute exercise (9, 10, 87). Weeke and Gunderson could find no rise in GH secretion when exercise was performed in a cold environment (87). Brennen et al., however, reported no differences in GH response to acute exercise at 40°C and 23°C ambient tem¬perature (9).
Dietary factors appear to strongly alter GH responses to acute exercise. Cappon et al. found that GH responses to exercise bouts following a high-fat drink were 50% lower than those following a placebo (12). Cooper suggested that this might be "a possible mechanism whereby not only the quality and quan¬tity of caloric intake, but also the hormonal response to a particular diet, may play a role in attenuating the protein-anabolic and lipolytic effects of exercise" (16, p. 18).
Hopkins et al. provided evidence that IGF-I activity during prolonged exercise is not related to carbohydrate levels (37). Nineteen-year-old males cycling at 60% VO,max to fatigue demonstrated a fall in serum glucose concentration that was prevented by carbohydrate supplementation during a second trial. IGF-I levels did not change significantly in either trial. IGFBP-I levels rose with exercise, however, and this increase occurred whether or not glucose levels declined.
The biologic meaning of this GH response to exercise is not immediately obvious. Acute bouts of exercise-and repeated exercise, or training pro¬grams-do not result in measurable increases in linear growth (e.g., height). Since the peak of GH release occurs near the end of a brief exercise bout, its role as a metabolic support (such as by increasing the avail¬ability of free fatty acids via lipolysis) seems question¬able. It may be that this GH release is anticipatory of the need for reparative anabolic actions in response to the musculoskeletal stresses of exercise.
The rise of GH seen with acute exercise does not, of course, necessarily imply increases in GH activ¬ity. Such changes could be associated with down¬regulation of GH receptors (16) or with alterations in degradation, clearance, or affinity to circulating binding proteins.
Several reports have described "standardized" exercise protocols for GH provocation in the clini¬cal testing of children (44, 75, 77). Sartorio et al. (75) found that plasma GH levels with acute exercise rose by 600% to 1200% in short children with normal resting GH, while in children with GH deficiency, levels increased by only 94%.
Seip et al. described their observations of 10 healthy children 9 to 15 years old who performed a 15-minute cycle bout at 70% of predicted maximal work rate on two occasions (77). Serum GH concen¬trations rose from 2.2 ± 2.8 to 27.1 ± 6.9 ng • ml-' on the first test and from 6.5 ± 7.8 to 19.9 ± 12.3 ng • ml-' on the second.While this report emphasized the feasibility of such testing, it also demonstrated that considerable variability in GH stimulation might be expected. Such variability has been reported by others (27). Seip et al. suggested that since the work rates in their two tests were equivalent, variation in secretion or pituitary response to GHRH or soma¬tostatin might be responsible (77).
Both peak GH response to exercise and the mag¬nitude of difference between exercise and resting levels are lower in prepubertal children than in those who have achieved sexual maturity. No qualitative or quantitative differences in these responses related to sex have been seen.
Wirth et al. measured blood levels of GH before and after submaximal exercise in 41 swimmers ages 8 to 18 years (91; figure 2.5). Subjects were divided into prepubertal, pubertal, and postpubertal stages of sexual maturation by Tanner staging.The exercise protocol involved pedaling for 15 minutes at 70% VOzmax. As indicated in figure 2.5, both resting and incremental levels of GH in response to exercise were lowest in the prepubertal group, and this was observed in girls and boys equally. Sexually mature adolescents demonstrated a rise in growth hormone at least twice as great in magnitude as that of the prepubertal group; the authors suggested that the greater GH response may be a manifestation of the influence of sex steroids, particularly estrogen, at the time of puberty.
To test this idea, Marin et al. administered a standard treadmill exercise test to 84 healthy boys and girls at all stages of puberty (56). A randomized subset of 11 prepubertal children received ethinyl estradiol-an estrogen-like hormone-for two days prior to testing, while the rest received a placebo. As in the study byWirth et al. (91), GH response to exercise increased with greater pubertal stage. The peak level of GH in Tanner stageV subjects (17.2 ± 14.7 ng • ml-') was three times greater than that of the prepubertal group (5.7 ± 4.1. ng • ml-').
赞一下(10人) 回复此楼
寡聚噻吩，传感，Two-photon，SquaraineDye，Porphyrin
7楼2009-07-27 21:33:29
已阅   回复此楼   关注TA 给TA发消息 送TA红花 TA的回帖

leiyu6788

新虫 (小有名气)
谢谢各位！
回复此楼
8楼2009-07-29 15:56:18
已阅   回复此楼   关注TA 给TA发消息 送TA红花 TA的回帖

leiyu6788

新虫 (小有名气)
急啊！
回复此楼
9楼2009-07-29 16:02:28
已阅   回复此楼   关注TA 给TA发消息 送TA红花 TA的回帖

monitor2885

至尊木虫 (职业作家)

队长
★
leiyu6788(金币+1,VIP+0): 8-14 13:20
我们要看看
回复此楼
Retirement
10楼2009-08-10 16:34:23
已阅   回复此楼   关注TA 给TA发消息 送TA红花 TA的回帖
相关版块跳转 我要订阅楼主 leiyu6788 的主题更新
121/2返回列表12下一页
普通表情 龙 兔 虎 猫 高级回复 (可上传附件)
信息提示
关闭
请填处理意见
关闭