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PubMed2001

Slow oscillations in blood pressure via a nonlinear feedback model.

Blood pressure is well established to contain a potential oscillation between 0.1 and 0.4 Hz, which is proposed to reflect resonant feedback in the baroreflex loop. A linear feedback model, comprising delay and lag terms for the vasculature, and a linear proportional derivative controller have been proposed to account for the 0.4-Hz oscillation in blood pressure in rats. However, although this model can produce oscillations at the required frequency, some strict relationships between the controller and vasculature parameters must be true for the oscillations to be stable. We developed a nonlinear model, containing an amplitude-limiting nonlinearity that allows for similar oscillations under a very mild set of assumptions. Models constructed from arterial pressure and sympathetic nerve activity recordings obtained from conscious rabbits under resting conditions suggest that the nonlinearity in the feedback loop is not contained within the vasculature, but rather is confined to the central nervous system. The advantage of the model is that it provides for sustained stable oscillations under a wide variety of situations even where gain at various points along the feedback loop may be altered, a situation that is not possible with a linear feedback model. Our model shows how variations in some of the nonlinearity characteristics can account for growth or decay in the oscillations and situations where the oscillations can disappear altogether. Such variations are shown to accord well with observed experimental data. Additionally, using a nonlinear feedback model, it is straightforward to show that the variation in frequency of the oscillations in blood pressure in rats (0.4 Hz), rabbits (0.3 Hz), and humans (0.1 Hz) is primarily due to scaling effects of conduction times between species.

Animals↗
PubMed2001

A construct of interactive feedback control of the GH axis in the male.

Growth hormone (GH) secretion is controlled by GH-releasing hormone (GHRH), the GH release-inhibiting hormone somatostatin (SRIF), and autofeedback connections. The ensemble network produces sexually dimorphic patterns of GH secretion. In an effort to formalize this system, we implemented a deterministically based autonomous feedback-driven construct of five principal dose-responsive regulatory interactions: GHRH drive of GH pituitary release, competitive inhibition of GH release by SRIF, GH autofeedback via SRIF with a time delay, delayed GH autonegative feedback on GHRH, and SRIF inhibition of GHRH secretion. This formulation engenders a malelike pattern of successive GH volleys due jointly to positive time-delayed feedback of GH on SRIF and negative feedback of SRIF on GH and GHRH. The multipeak volley is explicated as arising from a reciprocal interaction between GH and GHRH during periods of low SRIF secretion. The applicability of this formalism to neuroendocrine control is explored by initial parameter sensitivity analysis and is illustrated for selected feedback-dependent experimental paradigms. The present construct is not overparameterized and does not require an ad hoc pulse generator to achieve pulsatile GH output. Further evolution of interactive constructs could aid in exploring more complex feedback postulates that confer the vivid sexual dimorphism of female GH profiles.

Animals↗
PubMed1977

Feedback control of glomerular filtration rate in isolated, blood-perfused dog kidneys.

Micropuncture studies were done in isolated, blood-perfused dog kidneys to investigate the intrarenal nature of tubuloglomerular feedback regulation of nephron filtration rate. Collections were made at early proximal tubular sites during alterations in flow through the loop of Henle to elicit the feedback response. Renal blood flow in the 10 isolated kidneys averaged 4 ml/ min-g kidney after an initial vasoconstriction. Filtration rate was 0.52 +/- 0.12 ml/min-g kidney for the period 90-120 min, but progressively fell after 120 min, as did fractional sodium reabsorption and PAH extraction. The feedback regulation of nephron filtration rate was demonstrated during the first 3 hrs of perfusion even with subnormal renal function. The feedback response expressed as the percent reduction of early proximal flow rate when loop of Henle flow was elevated from 0 to 45 nl/min was 41.3 +/- 4.5 (for the first 90 min), 35.3 +/- 7.5 (90-120 min), 24.3 +/- 6.8 (120-150 min), and 26.6 +/- 7.7% (150-180 min). After 180 min, the feedback response was no longer demonstrated. These results show that feedback-induced changes in nephron filtration rate are achieved in the absence of nervous system influences.

Animals↗
PubMed1985

Tubuloglomerular feedback activity in virgin and 12-day-pregnant rats.

Tubuloglomerular feedback activity was evaluated by micropuncture and microperfusion techniques in virgin and 12-day-pregnant Munich-Wistar rats. Plasma volume increases in pregnancy, which could suppress feedback activity, thus contributing to the rise in glomerular filtration rate observed in normal midterm pregnancy. Late proximal tubules were microperfused at 0, 10, 20, and 40 nl/min and the resulting filtration rate in the same nephron was evaluated. Nephron filtration rate (SNGFR) in proximal and distal tubules of other nephrons was also measured to assess the degree of activation of the tubuloglomerular feedback system and the relation of the spontaneous (normal) late proximal flow rate and SNGFR (distal tubule collections). SNGFR decreased significantly (from the 0 nl/min perfusion value) when late proximal tubules were perfused at 20 and 40 nl/min in both virgin and 12-day-pregnant rats. Tubuloglomerular feedback activity was not suppressed in pregnancy, but the relationship between SNGFR and late proximal tubule perfusion rate was reset for a higher value for SNGFR. The difference between proximal and distal SNGFR suggests that the feedback system was more activated in the virgin than in the pregnant rat. Thus, in spite of the known increases in plasma volume that occur in pregnancy, the kidney does not sense this volume expansion as a stimulus to suppress feedback activity.

Animals↗
PubMed1988

Enhanced tubuloglomerular feedback during peritubular infusions of angiotensins I and II.

Experiments were performed in pentobarbital sodium-anesthetized rats to determine whether increases in intrarenal generation of angiotensin II (ANG II) can enhance the sensitivity of the tubuloglomerular feedback mechanism. Stop-flow pressure (SFP) feedback responses to step increases in late proximal perfusion rate were obtained during control conditions and during simultaneous peritubular capillary infusion of either angiotensin I (ANG I) or ANG II. Infusion of either 10(-7) M ANG II or 10(-5) M ANG I, at rates (18.3 +/- 0.9 and 14.8 +/- 1.5 nl/min, respectively) that did not affect resting SFP, enhanced the magnitude of SFP feedback responses both at a low proximal perfusion rate of 10 nl/min (2.9 +/- 0.9 vs. 0.3 +/- 0.2 and 4.5 +/- 1.0 vs. 0.1 +/- 0.1 mmHg, respectively) and at proximal perfusion rates (greater than 30 nl/min) that elicited a maximal feedback response (13.1 +/- 1.0 vs. 10.1 +/- 0.7 and 13.5 +/- 1.6 vs. 9.8 +/- 0.8 mmHg, respectively). With a higher ANG I infusion rate (20 nl/min), control SFP measured in the absence of distal volume delivery decreased from 39.2 +/- 0.6 to 12.0 +/- 2.8 mmHg (n = 18). These effects were blocked when the ANG II receptor antagonist, saralasin (10(-5) M, Sar), was added to the infusate. In addition, the magnitude of the maximal SFP feedback response was not altered during infusion of Sar alone or ANG I + Sar. These findings indicate that ANG II, either added or formed de novo beyond the glomerular circulation, can enhance the sensitivity of the tubuloglomerular feedback mechanism.

Angiotensin I↗
PubMed1989

Tubuloglomerular feedback activity after glomerular immune injury.

Tubuloglomerular feedback responses were examined in control euvolemic and glomerulonephritic rats 4 wk after administration of antiglomerular basement membrane antibody (AGBM). Single-nephron glomerular filtration rate (SNGFR) was reduced approximately 30% in AGBM rats. Tubuloglomerular feedback responses were also tested with both artificial and native tubular fluid. SNGFR was evaluated at 0, 10, 20, 30, and 40 nl/min. Tubuloglomerular feedback response was present in both control and AGBM rats, although there was a shift in turning point or perfusion rate down and leftward at which SNGFR decreased in the AGBM rats. No difference in tubuloglomerular feedback responses was observed between artificial and native tubular fluids. In this model of moderate glomerulonephritis, tubuloglomerular feedback activity appears to be appropriate and intact, and the composition of the fluid entering the loop of Henle does not appear to determine or to be a condition for the presence or absence of tubuloglomerular feedback activity.

Animals↗
PubMed1995

Instantaneous and steady-state gains in the tubuloglomerular feedback system.

The load of water and solute entering each nephron of the mammalian kidney is regulated by the tubuloglomerular feedback (TGF) mechanism, a negative feedback loop. Experiments in rats have shown that key variables of this feedback system may exhibit TGF-mediated oscillations. Mathematical modeling studies have shown that the open-feedback-loop gain is a crucial parameter for determining whether oscillations will emerge. However, two different formulations of this gain have been used. The first is the steady-state gain, a readily measurable quantity corresponding to the steady-state reduction in single-nephron glomerular filtration rate (SNGFR) subsequent to a sustained increased in ascending limb flow rate. The second is an instantaneous gain, a variable arising from theoretical considerations corresponding to the maximum reduction in SNGFR resulting from an instantaneous shift of the ascending limb flow column, with the assumption that the SNGFR response is also instantaneous. Here we show by an analytic argument how the steady-state and instantaneous open-feedback-loop gains for the ascending limb are related. In the case of no solute backleak into the ascending limb, the two formulations of gain are equivalent; however, in the presence of solute backleak, the instantaneous gain is larger in magnitude than the steady-state gain. With typical physiological parameters for the rat, calculations with a model previously devised by us show that the gains differ by 5-10%. Hence, experimental measurements of the steady-state gain may provide useful lower-bound estimates of the instantaneous gain of the feedback system in the normal rat. However, the gains may diverge significantly in pathophysiological states where ascending limb transport is compromised by abnormally high NaCl permeability.

Animals↗
PubMed1995

ANG II dependence of tubuloglomerular feedback responsiveness in hypertensive ren-2 transgenic rats.

The present study was performed to determine the angiotensin II (ANG II) dependence of stop-flow pressure (SFP) tubuloglomerular feedback responses in hypertensive transgenic rats [strain name: TGR(mRen2)27] harboring the mouse ren-2 renin gene. SFP feedback responses to increases in late proximal perfusion rate were assessed in pentobarbital-anesthetized male ren-2 transgenic rats during control conditions and after administration of the AT1 receptor antagonist, L-158,809 (1 mg/kg iv). During control conditions, increases in late proximal perfusion rate elicited flow-dependent decreases in SFP. The magnitude of the maximal SFP feedback response to a late proximal perfusion rate of 40 nl/min averaged 16.1 +/- 1.4 mmHg (n = 7), a value higher than that normally observed in normotensive rats. Administration of L-158,809 decreased mean arterial blood pressure (174 +/- 6 vs. 117 +/- mmHg, P < 0.01, n = 10) and attenuated the magnitude of the maximal SFP feedback response by 84 +/- 4% (16.1 +/- 1.4 vs. 2.6 +/- 0.5 mmHg, P < 0.01, n = 7). In contrast, mechanical reduction of renal arterial pressure from 179 +/- 5 to 113 +/- 1 mmHg (P < 0.01, n = 7) attenuated the magnitude of the maximal SFP feedback response by only 43 +/- 5% (14.4 +/- 1.9 vs. 7.9 +/- 0.7 mmHg, P < 0.01, n = 7), indicating that approximately one-half of the attenuation of SFP feed-back responses elicited by AT1 receptor blockade was due to removal of the stimulatory effect of ANG II on the sensitivity of the tubuloglomerular feedback mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1997

Spectral properties of the tubuloglomerular feedback system.

A simple mathematical model was used to investigate the spectral properties of the tubuloglomerular feedback (TGF) system. A perturbation, consisting of small-amplitude broad-band forcing, was applied to simulated thick ascending limb (TAL) flow, and the resulting spectral response of the TGF pathway was assessed by computing a power spectrum from resulting TGF-regulated TAL flow. Power spectra were computed for both open- and closed-feedback-loop cases. Open-feedback-loop power spectra are consistent with a mathematical analysis that predicts a nodal pattern in TAL frequency response, with nodes corresponding to frequencies where oscillatory flow has a TAL transit time that equals the steady-state fluid transit time. Closed-feedback-loop spectra are dominated by the open-loop spectral response, provided that gamma, the magnitude of feedback gain, is less than the critical value gamma c required for emergence of a sustained TGF-mediated oscillation. For gamma exceeding gamma c, closed-loop spectra have peaks corresponding to the fundamental frequency of the TGF-mediated oscillation and its harmonics. The harmonics, expressed in a nonsinusoidal waveform for tubular flow, are introduced by nonlinear elements of the TGF pathway, notably TAL transit time and the TGF response curve. The effect of transit time on the flow waveform leads to crests that are broader than troughs and to an asymmetry in the magnitudes of increasing and decreasing slopes. For feedback gain magnitude that is sufficiently large, the TGF response curve tends to give a square waveshape to the waveform. Published waveforms and power spectra of in vivo TGF oscillations have features consistent with the predictions of this analysis.

Feedback↗
PubMed1986

Inhibition of inspiratory upper airway motoneuron activity by phasic volume feedback.

The effects of phasic volume feedback on efferent hypoglossal, recurrent laryngeal and phrenic nerve activity were studied in decerebrate, paralyzed intubated cats ventilated with a phrenic-driven servo-respirator. The gain of the respirator was altered for single inspirations, and the resulting changes in neural activities were quantified by comparison with respective neural activities without phasic volume feedback. The volume thresholds for suppression of hypoglossal and recurrent laryngeal activities were time independent. Above these two thresholds and extending over a substantial range, volume feedback caused graded inhibition of upper airway motoneuron outputs. At any particular time during inspiration the relationships between hypoglossal or recurrent laryngeal inhibition and volume were concave to the volume axis. Rate of airflow appeared to exert an effect on upper airway motoneuron activity independent of volume. These results indicate that for hypoglossal and recurrent laryngeal efferent activity 1) volume feedback can cause a sustained graded inhibition throughout inspiration; 2) the volume thresholds are time independent; and 3) partial inhibition decreases susceptibility to additional inhibition. These actions of volume feedback on upper airway motoneuron output differ from those on phrenic efferent discharge and show that phasic vagal volume feedback has a marked and differential effect on upper airway motoneuron activity. The vagus, in this preparation, appears to play a critical role in the regulation of upper airway motoneuron activity and therefore maintenance of upper airway patency.

Animals↗
PubMed2005

Interaction of visual and proprioceptive feedback during adaptation of human reaching movements.

People tend to make straight and smooth hand movements when reaching for an object. These trajectory features are resistant to perturbation, and both proprioceptive as well as visual feedback may guide the adaptive updating of motor commands enforcing this regularity. How is information from the two senses combined to generate a coherent internal representation of how the arm moves? Here we show that eliminating visual feedback of hand-path deviations from the straight-line reach (constraining visual feedback of motion within a virtual, "visual channel") prevents compensation of initial direction errors induced by perturbations. Because adaptive reduction in direction errors occurred with proprioception alone, proprioceptive and visual information are not combined in this reaching task using a fixed, linear weighting scheme as reported for static tasks not requiring arm motion. A computer model can explain these findings, assuming that proprioceptive estimates of initial limb posture are used to select motor commands for a desired reach and visual feedback of hand-path errors brings proprioceptive estimates into registration with a visuocentric representation of limb position relative to its target. Simulations demonstrate that initial configuration estimation errors lead to movement direction errors as observed experimentally. Registration improves movement accuracy when veridical visual feedback is provided but is not invoked when hand-path errors are eliminated. However, the visual channel did not exclude adjustment of terminal movement features maximizing hand-path smoothness. Thus visual and proprioceptive feedback may be combined in fundamentally different ways during trajectory control and final position regulation of reaching movements.

Adaptation, Physiological↗
PubMed2005

Slow dynamics of postural sway are in the feedback loop.

Postural sway is considered to have two fundamental stochastic components, a slow nonoscillatory component and a faster damped-oscillatory component. The slow component has been shown to account for the majority of sway variance during quiet stance. Postural control is generally viewed as a feedback loop in which sway is detected by sensory systems and appropriate motor commands are generated to stabilize the body's orientation. Whereas the mechanistic source for the damped-oscillatory sway component is most likely feedback control of an inverted pendulum, the underlying basis for the slow component is less clear. We investigated whether the slow process was inside or outside the feedback loop by providing standing subjects with sum-of-sines visual motion. Linear stochastic models were fit to the experimental sway trajectories to determine the stochastic structure of sway as well as the transfer function from visual motion to sway. The results supported a fifth-order stochastic model, consisting of a slow process and two damped-oscillatory components. Importantly, the slow process was determined to be inside the feedback loop. This supports the hypothesis that the slow component is due to errors in state estimation because state estimation is inside the feedback loop rather than a moving reference point or an exploratory process outside the feedback loop.

Adult↗
PubMed1997

Excitatory amino acid receptors at a feedback pathway in the electrosensory system: implications for the searchlight hypothesis.

The electrosensory lateral line lobe (ELL) of the South American gymnotiform fish Apteronotus leptorhynchus has a laminar structure: electroreceptor afferents terminate ventrally whereas feedback input distributes to a superficial molecular layer containing the dendrites of the ELL principle (pyramidal) cells. There are two feedback pathways: a direct feedback projection that enters the ELL via a myelinated tract (stratum fibrosum, StF) and terminates in the ventral molecular layer (VML) and an indirect projection that enters as parallel fibers and terminates in the dorsal molecular layer. It has been proposed that the direct feedback pathway serves as a "searchlight" mechanism. This study characterizes StF synaptic transmission to determine whether the physiology of the direct feedback projection is consistent with this hypothesis. We used field and intracellular recordings from the ELL to investigate synaptic transmission of the StF in an in vitro slice preparation. Stimulation of the StF produced field potentials with a maximal negativity confined to a narrow band of tissue dorsal to the StF. Current source density analysis revealed two current sinks: an early sink within the StF and a later sink that corresponded to the anatomically defined VML. Field potential recordings from VML demonstrated that stimulation of the StF evoked an excitatory postsynaptic potential (EPSP) that peaked at a latency of 4-7 ms with a slow decay ( approximately 50 ms) to baseline. Intracellular recordings from pyramidal cells revealed that StF-evoked EPSPs consisted of at least two components: a fast gap junction mediated EPSP (peak 1.2-1.8 ms) and a chemical synaptic potential (peak 4-7 ms) with a slow decay phase ( approximately 50 ms). The amplitudes of the peak and decay phases of the chemical EPSP were increased by depolarizing current injection. Pharmacological studies demonstrated that the chemical EPSP was mainly due to ionotropic glutamate receptors with bothN-methyl--aspartate (NMDA) and non-NMDA components. NMDA receptors contributed substantially to both the early and late phase of the EPSP, whereas non-NMDA receptors contributed mainly to the early phase. Stimulation of the StF at physiological rates (100-200 Hz, 100 ms) produced an augmenting depolarization of the membrane potential of pyramidal cells. Temporal summation and a voltage-dependent enhancement of later EPSPs in the stimulus train permitted the compound EPSP to reach spike threshold. The nonlinear behavior of StF synaptic potentials is appropriate for the putative role of the direct feedback pathway as part of a searchlight mechanism allowing these fish to increase the electrodetectability of scanned objects.

Animals↗
PubMed2001

Feedback connections act on the early part of the responses in monkey visual cortex.

We previously showed that feedback connections from MT play a role in figure/ground segmentation. Figure/ground coding has been described at the V1 level in the late part of the neuronal responses to visual stimuli, and it has been suggested that these late modulations depend on feedback connections. In the present work we tested whether it actually takes time for this information to be fed back to lower order areas. We analyzed the extracellular responses of 169 V1, V2, and V3 neurons that we recorded in two anesthetized macaque monkeys. MT was inactivated by cooling. We studied the time course of the responses of the neurons that were significantly affected by the inactivation of MT to see whether the effects were delayed relative to the onset of the response. We first measured the time course of the feedback influences from MT on V1, V2, and V3 neurons tested with moving stimuli. For the large majority of the 51 neurons for which the response decreased, the effect was present from the beginning of the response. In the responses averaged after normalization, the decrease of response was significant in the first 10-ms bin of response. A similar result was found for six neurons for which the response significantly increased when MT was inactivated. We then looked at the time course of the responses to flashed stimuli (95 neurons). We observed 15 significant decreases of response and 14 significant increases. In both populations, the effects were significant within the first 10 ms of response. For some neurons with increased responses we even observed a shorter latency when MT was inactivated. We measured the latency of the response to the flashed stimuli. We found that even the earliest responding neurons were affected early by the feedback from MT. This was true for the response to flashed and to moving stimuli. These results show that feedback connections are recruited very early for the treatment of visual information. It further indicates that the presence or absence of feedback effects cannot be deduced from the time course of the response modulations.

Animals↗
PubMed2001

Response modulations by static texture surround in area V1 of the macaque monkey do not depend on feedback connections from V2.

We analyzed the extracellular responses of 70 V1 neurons (recorded in 3 anesthetized macaque monkeys) to a single oriented line segment (or bar) placed within the cell classical receptive field (RF), or center of the RF. These responses could be modulated when rings of bars were placed entirely outside, but around the RF (the "near" surround region), as described in previous studies. Suppression was the main effect. The response was enhanced for 12 neurons when orthogonal bars in the surround were presented instead of bars having the same orientation as the center bar. This orientation contrast property is possibly involved in the mediation of perceptual pop-out. The enhancement was delayed compared with the onset of the response by about 40 ms. We also observed a suppression originating specifically from the flanks of the surround. This "side-inhibition," significant for nine neurons, was delayed by about 20 ms. We tested whether these center/surround interactions in V1 depend on feedback connections from area V2. V2 was inactivated by GABA injections. We used devices made of six micropipettes to inactivate the convergent zone from V2 to V1. We could reliably inactivate a 2- to 4-mm-wide region of V2. Inactivation of V2 had no effect on the center/surround interactions of V1 neurons, even those that were delayed. Therefore the center/surround interactions of V1 neurons that might be involved in pop-out do not appear to depend on feedback connections from V2, at least in the anesthetized monkey. We conclude that these properties are probably shaped by long-range connections within V1 or depend on other feedback connections. The main effect of V2 inactivation was a decrease of the response to the single bar for about 10% of V1 neurons. The decrease was delayed by <20 ms after the response onset. Even the earliest neurons to respond could be affected by the feedback from V2. Together with the results on feedback connections from MT (previous paper), these findings show that feedback connections potentiate the responses to stimulation of the RF center and are recruited very early for the treatment of visual information.

Anesthesia↗
PubMed1994

Fast glucocorticoid feedback inhibition of ACTH secretion in the ovariectomized rat: effect of chronic estrogen and progesterone.

The purpose of this study was to determine whether estrogen and progesterone influence fast glucocorticoid negative feedback regulation of the ACTH and corticosterone (CORT) responses to stress. Mature rats were ovariectomized and 6 weeks later implanted with 17 beta-estradiol (E2, 0.5 mg), E2 and progesterone (P, 100 mg; E2 + P group) or placebo pellets (OVX). Seven days later rats were subjected to a single or repeated intermittent footshock stress (0.2 mA, 15 s duration, 0.5 s on). The repeated stress was of the same intensity and duration, and was applied either during the time domain of the rate-sensitive fast glucocorticoid feedback when plasma CORT levels are rising (5 min after the onset of the first stress), or at the time of peak CORT response (15 min) to the initial stress. Plasma ACTH and CORT were measured from serial samples. Estrogen replacement alone or in combination with progesterone lowered the immediate (t = 5) ACTH and CORT response to a single stress in ovariectomized animals. The second stress applied 5 min after the initial stress produced net ACTH responses similar to those obtained after a single stress in the OVX and E2 + P-replaced hormone groups, while total ACTH responses were lower in the E2-treated group. In ovariectomized animals, a facilitation of ACTH response by a prior stress is apparent in response to a footshock 15 min later, when the integrated ACTH secretion is significantly greater than the response measured after a single shock, or after a repeated shock 5 min apart. Anterior pituitary proopiomelanocortin (POMC) mRNA levels were lower in groups with E2 or E2 + P replacement compared to OVX animals. In contrast, hypothalamic corticotropin-releasing factor (CRF) mRNA levels did not increase significantly. However, hypothalamic glucocorticoid receptor (GR) mRNA levels increased after 17 beta-estradiol treatment, and this increase was reversed by progesterone. These results suggest that prior stress leads to both a fast-feedback inhibition and a facilitation of the subsequent stress response. In the absence of gonadal hormones this facilitation is balanced by fast-feedback inhibition during the glucocorticoid fast-feedback time domain, and is unmasked outside of this time domain. Estrogen suppresses POMC mRNA synthesis leading to a decrease in the availability of releasable ACTH, thereby reducing the facilitation. Progesterone may counter this effect of estrogen by decreasing the efficacy of the fast rate-sensitive glucocorticoid negative feedback.

Adrenocorticotropic Hormone↗
PubMed1994

Teleoperator performance with varying force and visual feedback.

An experimental study was conducted to determine the effects of various forms of visual and force feedback on human performance for several "peg-in-hole"-type telemanipulation tasks. Each of six human test subjects used a master/slave manipulator during two experimental sessions. In one session the subjects performed the tasks with direct vision, where subtended visual angle, force feedback, task difficulty, and the interaction of subtended visual angle and force feedback made significant differences in task completion times. During the other session the tasks were performed using a video monitor for visual feedback, and video frame rate, force feedback, task difficulty, and the interaction of frame rate and force feedback were found to make significant differences in task times. An analysis between the direct and video viewing environments showed that apart from subtended visual angle and reduced frame rate, the video medium itself did not significantly affect task times relative to direct viewing.

Artificial Intelligence↗
PubMed2005

Instruction of jump-landing technique using videotape feedback: altering lower extremity motion patterns.

BACKGROUND: Anterior cruciate ligament injury prevention programs have used videotapes of jump-landing technique as a key instructional component to improve landing performance. HYPOTHESIS: All videotape feedback model groups will increase knee flexion angles at initial contact and overall knee flexion motion and decrease peak vertical ground reaction forces and peak proximal anterior tibial shear forces to a greater extent than will a nonfeedback group. The secondary hypothesis is that the videotape feedback using the combination of the expert and self models will create the greatest change in each variable. STUDY DESIGN: Controlled laboratory study. METHODS: Knee kinematics and kinetics of college-aged recreational athletes randomly placed in 3 different videotape feedback model groups (expert only, self only, combination of expert and self) and a nonfeedback group were collected while participants performed a basketball jump-landing task on 3 testing occasions. RESULTS: All feedback groups significantly increased knee angular displacement flexion angles [F(6,70) = 8.03, P = .001] and decreased peak vertical ground reaction forces [F(6,78) = 2.68, P = .021] during performance and retention tests. The self and combination groups significantly increased knee angular displacement flexion angles more than the control group did; the expert model group did not change significantly more than the control group did. All feedback groups and the nonfeedback group significantly reduced peak vertical forces across performance and retention tests. There were no statistically significant changes in knee flexion angle at initial ground contact (P = .111) and peak proximal anterior tibial shear forces (P = .509) for both testing sessions for each group. CONCLUSION: The use of self or combination videotape feedback is most useful for increasing knee angular displacement flexion angles and reducing peak vertical forces during landing. CLINICAL RELEVANCE: The use of self or combination modeling is more effective than is expert-only modeling for the implementation of instructional programs aimed at reducing the risk of jump-landing anterior cruciate ligament injuries.

Adolescent↗