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1.

Objectives

To investigate whether functional overreaching affects locomotor system behaviour when running at fixed relative intensities and if any effects were associated with changes in running performance.

Design

Prospective intervention study.

Methods

Ten trained male runners completed three training blocks in a fixed order. Training consisted of one week of light training (baseline), two weeks of heavy training designed to induce functional overreaching, and ten days of light taper training designed to allow athletes to recover from, and adapt to, the heavy training. Locomotor behaviour, 5-km time trial performance, and subjective reports of training status (Daily Analysis of Life Demands for Athletes (DALDA) questionnaire) were assessed at the completion of each training block. Locomotor behaviour was assessed using detrended fluctuation analysis of stride intervals during running at speeds corresponding to 65% and 85% of maximum heart rate (HRmax) at baseline.

Results

Time trial performance (effect size ±95% confidence interval (ES): 0.16 ± 0.06; p < 0.001), locomotor behaviour at 65% HRmax (ES: ?1.12 ± 0.95; p = 0.026), and DALDA (ES: 2.55 ± 0.80; p < 0.001) were all detrimentally affected by the heavy training. Time trial performance improved relative to baseline after the taper (ES: ?0.16 ± 0.10; p = 0.003) but locomotor behaviour at 65% HRmax (ES: ?1.18 ± 1.17; p = 0.048) and DALDA (ES: 0.92 ± 0.90; p = 0.045) remained impaired.

Conclusions

Locomotor behaviour during running at 65% HRmax was impaired by functional overreaching and remained impaired after a 10-day taper, despite improved running performance. Locomotor changes may increase injury risk and should be considered within athlete monitoring programs independently of performance changes.  相似文献   
2.
BackgroundThere is a clinical need to be able to reliably detect meaningful changes (0.1 to 0.2 m/s) in usual gait speed (UGS) considering reduced gait speed is associated with morbidity and mortality.Research questionWhat is the impact of tester on UGS assessment, and the influence of test repetition (trial 1 vs. 2), timing method (manual stopwatch vs. automated timing), and starting condition (stationary vs. dynamic start) on the ability to detect changes in UGS and fast gait speed (FGS)?MethodsUGS and FGS was assessed in 725 participants on a 8-m course with infrared timing gates positioned at 0, 2, 4 and 6 m. Testing was performed by one of 13 testers trained by a single researcher. Time to walk 4-m from a stationary start (i.e. from 0-m to 4-m) was measured manually using a stopwatch and automatically via the timing gates at 0-m and 4-m. Time taken to walk 4-m with a dynamic start was measured during the same trial by recording the time to walk between the timing gates at 2-m and 6-m (i.e. after 2-m acceleration).ResultsTesters differed for UGS measured using manual vs. automated timing (p = 0.02), with five and two testers recording slower and faster UGS using manual timing, respectively. 95% limits of agreement for trial 1 vs. 2, manual vs. automated timing, and dynamic vs. stationary start ranged from ±0.15 m/s to ±0.20 m/s, coinciding with the range for a clinically meaningful change. Limits of agreement for FGS were larger ranging from ±0.26 m/s to ±0.35 m/s.SignificanceRepeat testing of UGS should performed by the same tester or using an automated timing method to control for tester effects. Test protocol should remain constant both between and within participants as protocol deviations may result in detection of an artificial clinically meaningful change.  相似文献   
3.
The syndrome of senile gait   总被引:1,自引:0,他引:1  
Summary Infrared computed stroboscopic photometry was used to quantify the kinematic profiles of walking in 10 elderly patients with symmetrical neurological disturbances of gait and in 19 age-matched neurologically healthy people. Clinical examination of the patients revealed similar profiles of walking even though their diagnoses were vascular dementia (2), normal pressure hydrocephalus (2), Alzheimer dementia with possible normal pressure hydrocephalus (2), mixed Alzheimer and vascular dementia (1), peripheral neuropathy (1), Alzheimer dementia with parkinsonian features (1), and un determined (1). Quantitatively, the patients' gait kinematics deviated greatly from control values, but these deviations were statistically attributable to reductions in stride. We suggest that many gait disturbances in elderly people are similar, regardless of etiology, because the characteristics of these gait disturbances are heavily veiled by nonspecific stride-dependent changes that comprise the syndrome of senile gait.  相似文献   
4.
Summary The influence of locomotor activity upon neurons in the lateral vestibular nucleus was investigated in precollicularly-postmamillary decerebrate guinea pigs. Out of 95 recorded neurons, 24 were identified as vestibulospinal and 71 had no descending projections. Locomotor activity occurred either spontaneously or was prompted by electrical stimulation of the mesencephalic locomotor region. Natural vestibular stimulation was supplied by tilting the animal about its longitudinal axis. Locomotor rhythmic limb muscle activity was accompanied by an increase in the firing frequency in the vast majority of investigated neurons. The increase in frequency was observed at the beginning of ipsilateral forelimb extensor muscle activity. Only in a few non-vestibulospinal neurons was the spontaneous activity depressed during locomotion. An increase in evoked responses was observed in almost all vestibulospinal neurons and in two thirds of the neurons without descending projections. A decrease in evoked responses was observed in one quarter of non-vestibulospinal neurons. During locomotion, the mean and maximal frequencies of evoked neuronal impulse activity changed, but the phase lag of these changes was not altered significantly. The results suggest an enhancement of vestibulospinal influences during locomotion, thus providing a high level of tonus in antigravitational muscles. This is interpreted as a mechanism to ensure that equilibrium is maintained during motion in different gaits and postures.  相似文献   
5.
The effects of withdrawal from continuous administration of cocaine on behavioral sensitivity to apomorphine and monoamine receptor density were examined in rats. Subdermal minipumps that delivered either saline or 20 mg/kg/day cocaine hydrochloride were implanted for 2 weeks. Apomorphine-induced stereotypy (0.5 mg/kg, SC) was examined in separate groups of rats either 4 hr or 7, 28, or 60 days after removal of the minipumps. Transient enhanced sensitivity to apomorphine-induced stereotypy occurred during the course of withdrawal. Animals withdrawn from cocaine for 4 hours did not differ from controls in their sensitivity to apomorphine, whereas animals withdrawn from cocaine for 7 days exhibited an increase in apomorphine-induced oral stereotypy relative to controls. However, the enhanced stereotypy response was no longer evident in animals withdrawn for 28–60 days. The animals were sacrificed after behavioral testing, and their brains were assayed for changes in monoamine receptor density in the frontal cortex, caudate-putamen, and nucleus accumbens. The density of 3H-SCH-23390-labeled D1 receptors was altered in all three regions examined in a time-dependent manner that paralleled the changes in behavioral sensitivity to apomorphine. There was a transient decrease in D1 receptor density that was evident by 7 days following withdrawal from continuous cocaine administration and was no longer evident 28 or 60 days posttreatment. There were no changes in 3H-spiroperidol-labeled D2 receptors, 125-pindolol-labeled β-adrenergic receptors, or 3H-ketanserin-labeled 5-HT2 receptors in any of the regions examined at both 4 hr and 7 days after termination of the cocaine infusion. These findings are discussed in terms of their relevance to developing pharmacologic treatments for withdrawal from cocaine. © 1994 Wiley-Liss, Inc.  相似文献   
6.
In order to establish the origin of the central coupling between locomotion and respiration which operates in freely moving mammals during galloping, we sought experimental conditions that readily lead to such a coupling in decerebrate and curarised rabbit preparations. In such preparations, stimulation of the mesencephalic locomotor region (MLR) evokes locomotor activities, recorded from hindlimb muscle nerves, that are rarely totally coordinated with phrenic inspiratory activity. However, low doses (0.2 mg/kg i.v.) of MK 801, a non-competitive NMDA antagonist which has been shown to increase the activity of the spinal locomotion generators (Fenaux et al. 1991), dramatically enhanced this coupling during MLR stimulation in most experiments: 1/1 coupling was dominant but 2/1 and 3/1 couplings (i.e. two or three locomotor cycles per respiratory cycle) were also obtained. Compared with spontaneous respiratory activity, which was apneustic under these conditions, the respiratory period was drastically decreased during coupling. However, a further transection of the spinal cord at the C6 or C7 level, which isolated the spinal locomotion generators from the supraspinal levels, totally suppressed this reduction of the inspiratory period during MLR stimulation in the presence of MK 801. In experiments where locomotor activity was simultaneously recorded at forelimb and hindlimb levels, the 1/1 evoked locomotor-respiratory coupling remained after the lumbar cord had been isolated by L1 spinal transection. The present data do show that intact spinal mechanisms are required for entrainment to occur. They suggest either that a common supraspinal drive cannot entrain locomotion and respiration when being depressed, or that respiration is entrained at the locomotor rate by the spinal locomotion generators. If so, this capacity for entrainment does not appear to be limited to the lumbar locomotion generators, but rather, is likely to involve the cervico-thoracic locomotion generators too. MK 801 potentiates this coupling through an increase in rhythmogenesis of the spinal locomotion generators.  相似文献   
7.
The aim was to study firstly, the motor effects of a new 5-HT1A antagonist, NDL-249 [(R)-3-(N-cyclopentyl-N-propylamino)-8-fluoro-3,4-dihydro-2H-1-benzopyran-5-carboxamide hydrochloride] and of the reference 5-HT1A antagonist WAY-100 635 [N-(2-(1-(4-(2-methoxyphenyl)piperazinyl))ethyl)-N-(2-pyridinyl) cyclohexanecarboxamide trihydrochloride], in comparison to the 5-HT1A agonist (±)-8-OH-DPAT [(8-hydroxy-2-(di-N-propylamino) tetralin, hereafter 8-OH-DPAT], in rats acclimatised to the automated activity cages; secondly, to study whether the behavioural effects of NDL-249 and 8-OH-DPAT are sensitive to the 5-HT depleting effects of p-chlorophenylalanine (PCPA); thirdly, to characterise the nature of the antagonist-induced activation seen in the automatic activity cages with the aid of a behavioural observation analysis; fourthly, to examine the interaction between the 5-HT1Areceptors mediating the behavioural effects and dopamine (DA) receptors. NDL-249 was found to bind in vitro to rat hippocampal 5-HT1A receptors with high affinity and selectivity. In second messenger studies, it was devoid of agonist-like effects. In the locomotor activity studies, each antagonist significantly increased the incidence of horizontal activity, peripheral activity and rearing. 8-OH-DPAT, while significantly increasing peripheral and horizontal activities, decreased the incidence of rearing. PCPA blocked the motor effects of NDL-249 but did not affect those of 8-OH-DPAT. Observational analyses indicated that NDL-249 induced significant increases at one or more doses in sniffing, rearing and locomotion together with a significant reduction in stillness. WAY-100 635 significantly increased the incidence of rearing, intense grooming and vacuous chewing. The significant increases in sniffing, grooming and intense grooming and the significant decrease in stillness induced by the DA D1 agonist, SK&F 38393 [(±)-1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol hydrochloride], were not altered by concomitant pre-treatment with NDL-249. Pre-treatment of rats with either the DA D1 antagonist SCH-23390 (2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepin-7-ol) or the DA D2 antagonist, raclopride, blocked the reduced stillness and increased sniffing and rearing induced by NDL-249. In conclusion, 5-HT1A antagonists including the new selective antagonist, NDL-249, induce mild behavioural activation in rats, which is mediated probably indirectly via DA systems. Received: 3 April 1997/Final version: 23 February 1998  相似文献   
8.
Summary Fetal spinal cord transplants placed into the site of a neonatal spinal cord lesion alter the response of immature CNS neurons to injury. The transplants prevent the retrograde cell death of immature axotomized neurons and support the growth of axons into and through the site of injury. In the present experiments we used a battery of locomotor tasks to determine if these transplants are also capable of promoting the recovery of motor function after spinal cord injury at birth. Embryonic (E14) spinal cord transplants were placed into the site of a spinal cord over-hemisection in rat pups. Three groups of animals were used: 1) normal control animals, 2) animals with a spinal cord hemisection only, and 3) animals with a spinal cord transplant at the site of the hemisection. Eight to twelve weeks later, the animals were trained and videotaped while crossing runways requiring accurate foot placement and footprinted while walking on a treadmill. The videotapes and footprints were analyzed to obtain quantitative measures of locomotor function. Footprint analysis revealed that the animals' base of support during locomotion was increased by a neonatal hemisection. The base of support in animals with transplants was similar to control values. Animals with a hemisection rotated their hindlimbs further laterally than did control animals during locomotion. A transplant at the site of injury modified this response. Normal animals were able to cross a grid runway quickly with only a few errors. In contrast, animals with a hemisection took a longer time and made more errors while crossing. The presence of a transplant at the site of injury enabled the animals to cross the grid more quickly and to make fewer errors than the animals with a hemisection only. Animals that received the transplants demonstrated qualitative and quantitative improvements in several parameters of locomotion. Spinal cord transplants at the site of neonatal spinal cord injury result in enhanced sparing or recovery of motor function. We suggest that this transplant induced recovery of function is a consequence of the anatomical plasticity elicited by the transplants.  相似文献   
9.
Nociceptin/orphanin FQ (N/OFQ), the endogenous ligand of the opioid receptor-like receptor or nociceptin receptor (NOP), has been shown to induce feeding, locomotion, anti-stress and anxiolytic effects in rodents after central nervous system injection. In this study, the effect of intracerebroventricular (icv) injection of N/OFQ on feeding and locomotion behavior was evaluated in male broiler-type chickens. The icv injection of N/OFQ caused a moderate but significant increase in feed intake similar to the classical opioid peptides in rats. It also increased feed pecking frequency and feeding time 1 h after injection. Stepping, wing flapping and preening were not affected by N/OFQ. These results suggest that N/OFQ can act within the central nervous system of chickens to increase feed intake.  相似文献   
10.
The purpose of this investigation was to determine if a chronic Parkinson's disease mouse model will display less certainty in its gait pattern due to basal ganglia dysfunction. A chronic Parkinson's disease mouse model was induced by injecting male C57/BL mice with 10 doses of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (25 mg/kg) (MPTP) and probenecid (250 mg/kg) (P) over 5 weeks. This chronic model produces a severe and persistent loss of nigrostriatal neurons resulting in dopamine depletion and locomotor impairment. The control mice were treated with probenecid alone. Fifteen weeks after the last MPTP/P treatment, the mice were videotaped in the sagittal plane with a digital camera (60 Hz) as they ran on a motorized treadmill at a speed of 10 m/min. The indices of gait and gait variability were calculated. Stride length was significantly (p = 0.016) more variable in the chronic MPTP/P mice. Additionally, the chronic MPTP/P mice had a statistically less certain gait pattern when compared to the control mice (p = 0.02). These results suggest that variability in the gait pattern can be used to evaluate changes in neural function. Additionally, our results imply that disorder of the basal ganglia results in less certainty in modulating the descending motor command that controls the gait pattern.  相似文献   
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