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1.
This study examined whether the ventilatory (V) compensation for metabolic acidosis with increasing O2 uptake (VO2) and CO2 output (VCO2) might be more in accord with the theoretical expectation of a progressive acceleration of proton production from carbohydrate oxidation rather than a sudden onset of blood lactate (BLa) accumulation. The interrelationships between V, VO2, VCO2 and BLa concentration, [BLa], were investigated in 10 endurance-trained male cyclists during incremental (120 +/- 15 W min-1) exercise tests to exhaustion. Regression analyses on the V, VCO2 and [BLa] vs VO2 data revealed that all were better fitted by continuous Y = A.exp.[B.VO2] + C rate laws than by threshold linear rate equations (P < 0.0001). Plots of V vs VCO2 and [BLa] were also non-linear. Ventilation increased as an exponential V = 27 +/- 4.exp.[0.37 +/- 0.03.VCO2] function of VCO2 and as a hyperbolic function of [BLa]. In opposition to the 'anaerobic (lactate) threshold' hypothesis, we suggest these data are more readily explained by a continuous development of acidosis, rather than a sudden onset of BLa accumulation, during progressive exercise.  相似文献   

2.
Nine males cycled at 53% (s = 2) of their peak oxygen uptake (VO(2peak)) for 90 min (dry bulb temperature: 25.4 degrees C, s = 0.2; relative humidity: 61%, s = 3). One litre of flavoured water at 10 (cold), 37 (warm) or 50 degrees C (hot) was ingested 30 - 40 min into exercise. Immediately after the 90 min of exercise, participants cycled at 95%VO(2peak) to exhaustion to assess exercise capacity. Rectal and mean skin temperatures and heart rate were recorded. The gradient of rise in rectal temperature was influenced (P < 0.01) by drink temperature. Mean skin temperature was highest in the hot trial (cold trial: 34.2 degrees C, s = 0.5; warm trial: 34.4 degrees C, s = 0.5; hot trial: 34.7 degrees C, s = 0.6; P < 0.01). Significant differences were observed in heart rate (cold trial: 132 beats . min(-1), s = 13; warm trial: 134 beats . min(-1), s = 12; hot trial: 139 beats . min(-1), s = 13; P < 0.05). Exercise capacity was similar between trials (cold trial: 234 s, s = 69; warm trial: 214 s, s = 52; hot trial: 203 s, s = 53; P = 0.562). The heat load and debt induced via drinking resulted in appropriate thermoregulatory reflexes during exercise leading to an observed heat content difference of only 33 kJ instead of the predicted 167 kJ between the cold and hot trials. These results suggest that there may be a role for drink temperature in influencing thermoregulation during exercise.  相似文献   

3.
Abstract

Nine males cycled at 53% (s = 2) of their peak oxygen uptake ([Vdot]O2peak) for 90 min (dry bulb temperature: 25.4°C, s = 0.2; relative humidity: 61%, s = 3). One litre of flavoured water at 10 (cold), 37 (warm) or 50°C (hot) was ingested 30 – 40 min into exercise. Immediately after the 90 min of exercise, participants cycled at 95%[Vdot]O2peak to exhaustion to assess exercise capacity. Rectal and mean skin temperatures and heart rate were recorded. The gradient of rise in rectal temperature was influenced (P < 0.01) by drink temperature. Mean skin temperature was highest in the hot trial (cold trial: 34.2°C, s = 0.5; warm trial: 34.4°C, s = 0.5; hot trial: 34.7°C, s = 0.6; P < 0.01). Significant differences were observed in heart rate (cold trial: 132 beats · min?1, s = 13; warm trial: 134 beats · min?1, s = 12; hot trial: 139 beats · min?1, s = 13; P < 0.05). Exercise capacity was similar between trials (cold trial: 234 s, s = 69; warm trial: 214 s, s = 52; hot trial: 203 s, s = 53; P = 0.562). The heat load and debt induced via drinking resulted in appropriate thermoregulatory reflexes during exercise leading to an observed heat content difference of only 33 kJ instead of the predicted 167 kJ between the cold and hot trials. These results suggest that there may be a role for drink temperature in influencing thermoregulation during exercise.  相似文献   

4.
The aim of this study was to compare the lactate indices provided by single- and double-breakpoint models with lactate thresholds obtained with conventional methods. Arterial samples for the determination of lactate concentrations were drawn from eight participants at rest and every minute during a ramp test (15 W x min(-1)) on a cycle ergometer. Lactate thresholds were determined from a blood lactate concentration equal to 4 mM (LT(4)), from an increase of 1 mM above the resting level (Delta1 mM), and from indirect methods using ventilatory parameters. Other indices were computed from the modelling of the lactate curve using an exponential function (LSI), a polynomial function (Dmax), a semi-log model (SLog), a parabola plus delay model (Mod P), and a two-breakpoint model (Mod M). Mod P and Mod M showed poor agreement with the other methods. LT(4), Dmax, LSI, and respiratory exchange ratio equal to 1 were correlated with each other (0.81 相似文献   

5.
Abstract

The aim of this study was to compare the lactate indices provided by single- and double-breakpoint models with lactate thresholds obtained with conventional methods. Arterial samples for the determination of lactate concentrations were drawn from eight participants at rest and every minute during a ramp test (15 W · min?1) on a cycle ergometer. Lactate thresholds were determined from a blood lactate concentration equal to 4 mM (LT4), from an increase of 1 mM above the resting level (Δ1 mM), and from indirect methods using ventilatory parameters. Other indices were computed from the modelling of the lactate curve using an exponential function (LSI), a polynomial function (Dmax), a semi-log model (SLog), a parabola plus delay model (Mod P), and a two-breakpoint model (Mod M). Mod P and Mod M showed poor agreement with the other methods. LT4, Dmax, LSI, and respiratory exchange ratio equal to 1 were correlated with each other (0.81 ≤ R ≤ 0.92) and their mean differences ranged from 2.8 to 15 W, with limits of agreement within the range ± 24.6 to ± 42.4 W. These results question the interest in breakpoints models to detect lactate thresholds, knowing that LT4, LSI, Dmax, and respiratory exchange ratio equal to 1 provide indices that occur at similar power outputs.  相似文献   

6.
王国祥 《体育学刊》2004,11(1):45-48
采用等速运动方式 ,以表面肌电图和血乳酸为指标 ,在 10 %、3 0 %和 50 %MVC三种负荷条件下 ,对肘关节屈伸运动时的肱三头肌、肱二头肌和前腕骨肌的表面肌电图和血乳酸浓度的变化进行了比较分析。结果表明 :(1)肘关节屈伸运动时 ,伸展运动的力矩峰值下降幅度大于屈曲运动。 (2 )以 3 0 %和 50 %MVC负荷强度运动时 ,出现了表面肌电图的MF值逐步下降和血乳酸浓度逐渐增加的现象 ;工作肌群MF下降幅度 ,由大到小依次为肱三头肌 >肱二头肌 >前腕骨肌。 (3 )肱三头肌、肱二头肌和前腕骨肌的表面肌电图的MF变化与血乳酸浓度变化相互比较 ,10 %、3 0 %和 50 %MVC三种运动形式都表现出了非常明显的相关性。实验结果可以说明 ,sEMG作为特异性良好的非损伤性检测手段 ,不但能够直观地反映肌肉的收缩活动 ,还与肌肉组织代谢变化有一定的相关关系  相似文献   

7.
研究优秀武术运动员无氧运动强度时肌电信号特征及其与血乳酸指标之间的相关性。研究对象为12名一级武术运动员和12名二级武术运动员。研究方法:肌电指标测试:两组受试对象负重体重的7.5%,在功率自行车上持续运动60s后记录运动中和运动后30s内肌电指标MPF、MF和IEMG;血乳酸测试:采集运动中(20s一次)和运动后3min内的血乳酸浓度。结论:两组受试对象的MPF和MF均呈线性下降,但是对照组下降的斜率始终大于试验组,表明对照组比试验组更容易疲劳;IEMG呈线性上升,随着时间的延长,斜率加大,并且试验组斜率始终大于对照组,表明实验组肌纤维的募集能力要强于对照组;各肌电图指标与血乳酸之间存在着高度的负相关,但是血乳酸的积累并不是引起肌电图指标变化的直接原因。  相似文献   

8.
The aim of this study was to determine the magnitude and pattern of intensity, and physiological strain, of competitive exercise performed across several days, as in adventure racing. Data were obtained from three teams of four athletes (7 males, 5 females; mean age 36 years, s = 11; cycling .VO(2 peak) 53.9 ml . kg(-1) . min(-1), s = 6.3) in an international race (2003 Southern Traverse; 96 - 116 h). Heart rates (HR) averaged 64% (95% confidence interval: +/- 4%) of heart rate range [%HRR = (HR - HR(min))/(HR(max) - HR(min)) x 100] during the first 12 h of racing, fell to 41% (+/-4%) by 24 h, and remained so thereafter. The level and pattern of heart rate were similar across teams, despite one leading and one trailing all other teams. Core temperature remained between 36.0 and 39.2 degrees C despite widely varying thermal stress. Venous samples, obtained before, during, and after the race, revealed increased neutrophil, monocyte and lymphocyte concentrations (P < 0.01), and increased plasma volume (25 +/- 10%; P < 0.01) with a stable sodium concentration. Standardized exercise tests, performed pre and post race, showed little change in the heart rate-work rate relationship (P = 0.53), but a higher perception of effort post race (P < 0.01). These results provide the first comprehensive report of physiological strain associated with adventure racing.  相似文献   

9.
ABSTRACT

This study aimed to analyze the acute effect of inter-repetition rest (IRR) intervals on mechanical and metabolic response during four resistance exercise protocols (REPs). Thirty resistance-trained men were randomly assigned to: continuous repetitions (CR), 10 s (IRR10) or 20 s (IRR20) inter-repetition rest. The REPs consisted of 3 sets of 6, 5, 4 and 3 repetitions against 60, 70, 75 and 80% 1RM, respectively, in the full squat exercise. Muscle fatigue was assessed using: percentage of velocity loss over three sets, percentage of velocity loss against the ~1 m·s?1 load (V1 m·s?1), and loss of countermovement jump (CMJ) height pre-post exercise. Blood lactate was measured before and after exercise. The percentage of velocity loss over three sets and lactate concentration were significantly lower (< 0.05) for IRR groups compared to CR in all REPs. The CR group showed a significantly higher (< 0.05) velocity loss against V1 m·s?1 load and loss of CMJ height pre-post exercise than IRR groups in REP against 60% 1RM. In conclusion, both IRR groups produced a significant lower degree of fatigue compared to CR group. However, no significant differences were found in any measured variables between IRR configurations.  相似文献   

10.
The aim of this study was to assess the responses of blood lactate and pyruvate during the lactate minimum speed test. Ten participants (5 males, 5 females; mean +/- s: age 27.1+/-6.7 years, VO2max 52.0+/-7.9 ml x kg(-1) x min(-1)) completed: (1) the lactate minimum speed test, which involved supramaximal sprint exercise to invoke a metabolic acidosis before the completion of an incremental treadmill test (this results in a 'U-shaped' blood lactate profile with the lactate minimum speed being defined as the minimum point on the curve); (2) a standard incremental exercise test without prior sprint exercise for determination of the lactate threshold; and (3) the sprint exercise followed by a passive recovery. The lactate minimum speed (12.0+/-1.4 km x h(-1)) was significantly slower than running speed at the lactate threshold (12.4+/-1.7 km x h(-1)) (P < 0.05), but there were no significant differences in VO2, heart rate or blood lactate concentration between the lactate minimum speed and running speed at the lactate threshold. During the standard incremental test, blood lactate and the lactate-to-pyruvate ratio increased above baseline values at the same time, with pyruvate increasing above baseline at a higher running speed. The rate of lactate, but not pyruvate, disappearance was increased during exercising recovery (early stages of the lactate minimum speed incremental test) compared with passive recovery. This caused the lactate-to-pyruvate ratio to fall during the early stages of the lactate minimum speed test, to reach a minimum point at a running speed that coincided with the lactate minimum speed and that was similar to the point at which the lactate-to-pyruvate ratio increased above baseline in the standard incremental test. Although these results suggest that the mechanism for blood lactate accumulation at the lactate minimum speed and the lactate threshold may be the same, disruption to normal submaximal exercise metabolism as a result of the preceding sprint exercise, including a three- to five-fold elevation of plasma pyruvate concentration, makes it difficult to interpret the blood lactate response to the lactate minimum speed test. Caution should be exercised in the use of this test for the assessment of endurance capacity.  相似文献   

11.
The aim of this study was to assess the responses of blood lactate and pyruvate during the lactate minimum speed test. Ten participants (5 males, 5 females; mean +/- s: age 27.1 +/- 6.7 years, VO 2max 52.0 +/- 7.9 ml kg -1 min -1 ) completed: (1) the lactate minimum speed test, which involved supramaximal sprint exercise to invoke a metabolic acidosis before the completion of an incremental treadmill test (this results in a ‘U-shaped’ blood lactate profile with the lactate minimum speed being defined as the minimum point on the curve); (2) a standard incremental exercise test without prior sprint exercise for determination of the lactate threshold; and (3) the sprint exercise followed by a passive recovery. The lactate minimum speed (12.0 +/- 1.4 km h -1 ) was significantly slower than running speed at the lactate threshold (12.4 +/- 1.7 km h -1 ) (P < 0.05), but there were no significant differences in VO 2 , heart rate or blood lactate concentration between the lactate minimum speed and running speed at the lactate threshold. During the standard incremental test, blood lactate and the lactate-topyruvate ratio increased above baseline values at the same time, with pyruvate increasing above baseline at a higher running speed. The rate of lactate, but not pyruvate, disappearance was increased during exercising recovery (early stages of the lactate minimum speed incremental test) compared with passive recovery. This caused the lactate-to-pyruvate ratio to fall during the early stages of the lactate minimum speed test, to reach a minimum point at a running speed that coincided with the lactate minimum speed and that was similar to the point at which the lactate-to-pyruvate ratio increased above baseline in the standard incremental test. Although these results suggest that the mechanism for blood lactate accumulation at the lactate minimum speed and the lactate threshold may be the same, disruption to normal submaximal exercise metabolism as a result of the preceding sprint exercise, including a three- to five-fold elevation of plasma pyruvate concentration, makes it difficult to interpret the blood lactate response to the lactate minimum speed test. Caution should be exercised in the use of this test for the assessment of endurance capacity.  相似文献   

12.
This study compares test-retest reliability and peak exercise responses from ramp-incremented (RAMP) and maximal perceptually-regulated (PRETmax) exercise tests during arm crank exercise in individuals reliant on manual wheelchair propulsion (MWP). Ten untrained participants completed four trials over 2-weeks (two RAMP (0–40 W + 5–10 W · min?1) trials and two PRETmax. PRETmax consisted of five, 2-min stages performed at Ratings of Perceived Exertion (RPE) 11, 13, 15, 17 and 20). Participants freely changed the power output to match the required RPE. Gas exchange variables, heart rate, power output, RPE and affect were determined throughout trials. The V?O2peak from RAMP (14.8 ± 5.5 ml · kg?1 · min?1) and PRETmax (13.9 ± 5.2 ml · kg?1 · min?1) trials were not different (P = 0.08). Measurement error was 1.7 and 2.2 ml · kg?1 · min?1 and coefficient of variation 5.9% and 8.1% for measuring V?O2peak from RAMP and PRETmax, respectively. Affect was more positive at RPE 13 (P = 0.02), 15 (P = 0.01) and 17 (P = 0.01) during PRETmax. Findings suggest that PRETmax can be used to measure V?O2peak in participants reliant on MWP and leads to a more positive affective response compared to RAMP.  相似文献   

13.
采用文献资料法,阐述了中等强度运动对氧化应激与血管内皮功能障碍的影响,旨在为利用中等强度运动进行防病治病提供理论依据,同时也为这一领域的进一步研究提供参考.  相似文献   

14.
15.
16.
Exercise has been shown to influence collagen synthesis and degradation. The aim of this study was to determine whether the stimulus for these changes is metabolic or mechanical. Eight healthy adults aged 22 +/- 4 years (mean +/- s) completed two exercise bouts-a 10 km road run and a deep water running session. Blood samples were collected before exercise and on days 1, 2, 3, 6 and 10 after exercise for measurement of creatine kinase activity, type IV collagen antigenicity, and concentrations of matrix metalloproteinase (MMP)- 9, tissue inhibitors of metalloproteinase (TIMP)- 1 and -2, and the MMP-2/TIMP-2 complex. Serum creatine kinase was elevated 24 h after the road run, but unchanged after the deep water running session. Serum collagen IV antigenicity decreased after both the road run and the deep water running session, suggesting suppressed type IV collagen synthesis in response to exercise, although serum MMPs and TIMPs remained unchanged after exercise. These results suggest that collagen IV synthesis is temporarily suppressed after exercise, irrespective of exercise type.  相似文献   

17.
The many important benefits of physical exercise also encompass maintenance or improvement of cognitive functions. Among the various mechanisms underlying the association between physical exercise and brain health, recent evidence attests that neurotrophin receptor signaling may have an important role, because the activation of this pathway leads to growth and differentiation of new neurons and synapses, supports axonal and dendritic growth, fosters synaptic plasticity, and preserves survival of existing neurons. In this review of published evidence, we highlight that a positive relationship exists between physical exercise and circulating brain-derived neurotrophic factor levels and that the postexercise variation of this molecule is associated with improvement of neurocognitive functioning. Less clear evidence has instead been published for other neurotrophins, such as nerve growth factor, neurotrophin-3, and neurotrophin-4. Overall, promotion of adequate volumes and intensities of physical exercise (i.e., approximately 3 months of moderate-intensity aerobic exercise, with 2–3 sessions/week lasting not less than 30 min) may hence be regarded as an inexpensive and safe strategy for boosting brain-derived neurotrophic factor release, thus preserving or restoring cognitive functions.  相似文献   

18.
Abstract

The aim of this study was to determine whether creatine ingested in combination with relatively small quantities of essential amino acids, simple sugars, and protein would stimulate insulin release and augment whole-body creatine retention to the same extent as a large bolus of simple sugars. Seven young, healthy males underwent three randomized, 3-day experimental trials. Each day, 24-h urine collections were made, and on the second day participants received 5 g creatine + water (creatine trial), 5 g creatine + ~95 g dextrose (creatine + carbohydrate) or 5 g creatine + 14 g protein hydrolysate, 7 g leucine, 7 g phenylalanine, and 57 g dextrose (creatine + protein, amino acids, and carbohydrate) via naso-gastric tube at three equally spaced intervals. Blood samples were collected at predetermined intervals after the first and third naso-gastric bolus. After administration of the first and third bolus, serum insulin concentration was increased by 15 min (P < 0.05) in the creatine + carbohydrate and creatine + protein, amino acids, and carbohydrate trials compared with creatine alone, and plasma creatine increased more following creatine alone (15 min, P < 0.05) than in the creatine + carbohydrate and creatine + protein, amino acids, and carbohydrate trials. Urinary creatine excretion was greater with creatine alone (P < 0.05) than with creatine + carbohydrate and creatine + protein, amino acids, and carbohydrate. Administration of creatine + protein, amino acids, and carbohydrate can stimulate insulin release and augment whole-body creatine retention to the same extent as when larger quantities of simple sugars are ingested.  相似文献   

19.
Conconi et al. (1982) reported that an observed deviation from linearity in the heart rate-running velocity relationship determined during a field test in runners coincided with the ‘lactate threshold’. The aim of this study was to assess the validity of the original Conconi test using conventional incremental and constant-load laboratory protocols. Fourteen trained male distance runners (mean ± s : age 22.6 ±3.4 years; body mass 67.6±4.8 kg; peak [Vdot] O 2 66.3 ± 4.7 ml kg -1 min -1) performed a standard multi-stage test for determination of lactate turnpoint and a Conconi test on a motorized treadmill. A deviation from linearity in heart rate was observed in nine subjects. Significant differences were found to exist between running velocity at the lactate turnpoint (4.39 ± 0.20 ms -1) and at deviation from linear heart rate (5.08 ± 0.25 ms -1) (P < 0.01), and between heart rate at the lactate turnpoint (172 ± 10 beats min -1) and at deviation from linearity (186 ± 9 beats min -1) (P < 0.01). When deviation of heart rate from linearity was evident, it occurred at a systematically higher intensity than the lactate turnpoint and at approximately 95% of maximum heart rate. These results were confirmed by the physiological responses of seven subjects, who performed two constant-velocity treadmill runs at 0.14 ms -1 below the running velocity at the lactate turnpoint and that at which the heart rate deviated from linearity. For the lactate turnpoint trial, the prescribed 30 min exercise period was completed by all runners (terminal blood lactate concentration of 2.4 ± 0.5 mM ), while the duration attained in the trial for which heart rate deviated from linearity was 15.9 ± 6.7 min (terminal blood lactate concentration of 8.1 ± 1.8 mM). We concluded that the Conconi test is invalid for the non-invasive determination of the lactate turnpoint and that the deviation of heart rate from linearity represents the start of the plateau at maximal heart rate, the expression of which is dependent upon the specifics of the Conconi test protocol.  相似文献   

20.
In this study, we wished to determine whether the changes in metabolism observed during exercise in the cold are associated with changes in interleukin-6 (IL-6) and/or its soluble receptors. Eight healthy male participants performed 1 h of cycling exercise at 70% VO2max in a control (20 degrees C) and cold (0 degrees C) environment. Plasma concentrations of IL-6, soluble IL-6 receptor (sIL-6R), and sgp130 were measured before exercise, at 30 and 60 min of exercise, and 60 min after exercise. Substrate oxidation was estimated through measures of pulmonary gas exchange recorded between 50 and 55 min of cycling. Exercise in the cold resulted in an increase (P < 0.05) in carbohydrate oxidation (mean 2.58 g.min(-1), s = 0.49 at 20 degrees C vs. 2.85 g.min(-1), s = 0.58 at 0 degrees C) and a decrease (P < 0.05) in fat oxidation (0.55 g.min(-1), s = 0.17 at 20 degrees C vs. 0.38 g.min(-1), s = 0.16 at 0 degrees C) compared with the control trial. Interleukin-6 concentrations were elevated (P < 0.05) after 60 min of exercise in both the cold and control trials, with no differences between trials at any instant. Neither sIL-6R nor sgp130 was affected by exercise or the environment. The alterations in carbohydrate and fat utilization during 1 h of exercise in the cold are not paralleled by changes in plasma concentrations of IL-6 or its soluble receptors.  相似文献   

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