Identifying the causal mechanisms of the quiet eye.

Scientists who have examined the gaze strategies employed by athletes have determined that longer quiet eye (QE) durations (QED) are characteristic of skilled compared to less-skilled performers. However, the cognitive mechanisms of the QE and, specifically, how the QED affects performance are not yet fully understood. We review research that has examined the functional mechanism underlying QE and discuss the neural networks that may be involved. We also highlight the limitations surrounding QE measurement and its definition and propose future research directions to address these shortcomings. Investigations into the behavioural and neural mechanisms of QE will aid the understanding of the perceptual and cognitive processes underlying expert performance and the factors that change as expertise develops.

Rapid changes in corticospinal excitability during force field adaptation of human walking.

Force field adaptation of locomotor muscle activity is one way of studying the ability of the motor control networks in the brain and spinal cord to adapt in a flexible way to changes in the environment. Here, we investigate whether the corticospinal tract is involved in this adaptation. We measured changes in motor-evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) in the tibialis anterior (TA) muscle before, during, and after subjects adapted to a force field applied to the ankle joint during treadmill walking. When the force field assisted dorsiflexion during the swing phase of the step cycle, subjects adapted by decreasing TA EMG activity. In contrast, when the force field resisted dorsiflexion, they increased TA EMG activity. After the force field was removed, normal EMG activity gradually returned over the next 5 min of walking. TA MEPs elicited in the early swing phase of the step cycle were smaller during adaptation to the assistive force field and larger during adaptation to the resistive force field. When elicited 5 min after the force field was removed, MEPs returned to their original values. The changes in TA MEPs were larger than what could be explained by changes in background TA EMG activity. These effects seemed specific to walking, as similar changes in TA MEP were not seen when seated subjects were tested during static dorsiflexion. These observations suggest that the corticospinal tract contributes to the adaptation of walking to an external force field.

Afferent contribution to locomotor muscle activity during unconstrained overground human walking: an analysis of triceps surae muscle fascicles.

Plantar flexor series elasticity can be used to dissociate muscle-fascicle and muscle-tendon behavior and thus afferent feedback during human walking. We used electromyography (EMG) and high-speed ultrasonography concomitantly to monitor muscle activity and muscle fascicle behavior in 19 healthy volunteers as they walked across a platform. On random trials, the platform was dropped (8 cm, 0.9 g acceleration) or held at a small inclination (up to +/-3 degrees in the parasagittal plane) with respect to level ground. Dropping the platform in the mid and late phases of stance produced a depression in the soleus muscle activity with an onset latency of about 50 ms. The reduction in ground reaction force also unloaded the plantar flexor muscles. The soleus muscle fascicles shortened with a minimum delay of 14 ms. Small variations in platform inclination produced significant changes in triceps surae muscle activity; EMG increased when stepping on an inclined surface and decreased when stepping on a declined surface. This sensory modulation of the locomotor output was concomitant with changes in triceps surae muscle fascicle and gastrocnemius tendon length. Assuming that afferent activity correlates to these mechanical changes, our results indicate that within-step sensory feedback from the plantar flexor muscles automatically adjusts muscle activity to compensate for small ground irregularities. The delayed onset of muscle fascicle movement after dropping the platform indicates that at least the initial part of the soleus depression is more likely mediated by a decrease in force feedback than length-sensitive feedback, indicating that force feedback contributes to the locomotor activity in human walking.

Evidence for a supraspinal contribution to the human quadriceps long-latency stretch reflex.

In sitting humans a rapid unexpected lengthening of the knee extensors elicits a stretch reflex (SR) response as recorded by the electromyogram (EMG) which comprises multiple bursts. These are termed short latency responses (SLR), medium latency responses (MLR) and long latency responses (LLR). The aim of this study was to determine if a transcortical pathway contributes to any of these bursts. Flexion perturbations (amplitude =4 degrees, velocity=150 degrees/s) were imposed on the right knee joint of sitting subjects (n=11). The effect of the perturbation on the electromyographic (EMG) response of the pre-contracted quadriceps muscle to magnetic stimulation of the contralateral motor cortex was quantified. Transcranial magnetic stimulation (TMS) was applied to elicit a compound motor evoked potential (MEP) in the target muscle rectus femoris (RF), in the vastus lateralis (VL), vastus medialis (VM) and biceps femoris (BF). The MEP and SR were elicited either in combination or separately. When applied in combination the delay between the SR and the MEP varied from 0 to 150 ms in steps of 4, 5 and 10 ms. Somatosensory evoked potentials (SEPs) were recorded from four subjects during the imposed stretch to quantify the latency of the resulting afferent volley. Onset latencies of responses in RF were 25+/-2 ms for the SR and 20+/-4 ms for the MEP. The average SEP latency was 24+/-2 ms. A transcortical pathway thus has the potential to contribute to the RF SR no earlier than 54+/-6 ms (SEP + MEP + 10 ms central processing delay) following the stretch onset. The duration of the total reflex burst was 85+/-6 ms. Significant facilitation of the MEP commenced at 78 ms, coinciding with the LLR component of the stretch response. No such facilitation was observed in the synergists VL and VM, or in the antagonist BF. Our results indicate that the LLR of the RF likely involves supraspinal pathways. More importantly, of the investigated muscles, this involvement of higher centers in the shaping of the LLR is specific to the RF muscle during the investigated task.

Group II muscle afferents probably contribute to the medium latency soleus stretch reflex during walking in humans.

1. The objective of this study was to determine which afferents contribute to the medium latency response of the soleus stretch reflex resulting from an unexpected perturbation during human walking. 2. Fourteen healthy subjects walked on a treadmill at approximately 3.5 km h(-1) with the left ankle attached to a portable stretching device. The soleus stretch reflex was elicited by applying small amplitude (approximately 8 deg) dorsiflexion perturbations 200 ms after heel contact. 3. Short and medium latency responses were observed with latencies of 55 +/- 5 and 78 +/- 6 ms, respectively. The short latency response was velocity sensitive (P < 0.001), while the medium latency response was not (P = 0.725). 4. Nerve cooling increased the delay of the medium latency component to a greater extent than that of the short latency component (P < 0.005). 5. Ischaemia strongly decreased the short latency component (P = 0.004), whereas the medium latency component was unchanged (P = 0.437). 6. Two hours after the ingestion of tizanidine, an alpha(2)-adrenergic receptor agonist known to selectively depress the transmission in the group II afferent pathway, the medium latency reflex was strongly depressed (P = 0.007), whereas the short latency component was unchanged (P = 0.653). 7. An ankle block with lidocaine hydrochloride was performed to suppress the cutaneous afferents of the foot and ankle. Neither the short (P = 0.453) nor medium (P = 0.310) latency reflexes were changed. 8. Our results support the hypothesis that, during walking the medium latency component of the stretch reflex resulting from an unexpected perturbation is contributed to by group II muscle afferents.

Soleus stretch reflex during cycling.

The modulation and strength of the human soleus short latency stretch reflex was investigated by mechanically perturbing the ankle during an unconstrained pedaling task. Eight subjects pedaled at 60 rpm against a preload of 10 Nm. A torque pulse was applied to the crank at various positions during the crank cycle, producing ankle dorsiflexion perturbations of similar trajectory. The stretch reflex was greatest during the power phase of the crank cycle and was decreased to the level of background EMG during recovery. Matched perturbations were induced under static conditions at the same crank angle and background soleus EMG as recorded during the power phase of active pedaling. The magnitude of the stretch reflex was not statistically different from that during the static condition throughout the power phase of the movement. The results of this study indicate that the stretch reflex is not depressed during active cycling as has been shown with the H-reflex. This lack of depression may reflect a decreased susceptibility of the stretch reflex to inhibition, possibly originating from presynaptic mechanisms.

CPMG sequences with enhanced sensitivity to chemical exchange.

Improved relaxation-compensated Carr-Purcell-Meiboom-Gill pulse sequences are reported for studying chemical exchange of backbone 15N nuclei. In contrast to the original methods [J. P. Loria, M. Rance, and A. G. Palmer, J. Am. Chem. Soc. 121, 2331-2332 (1999)], phenomenological relaxation rate constants obtained using the new sequences do not contain contributions from 1H-1H dipole-dipole interactions. Consequently, detection and quantification of chemical exchange processes are facilitated because the relaxation rate constant in the limit of fast pulsing can be obtained independently from conventional 15N spin relaxation measurements. The advantages of the experiments are demonstrated using basic pancreatic trypsin inhibitor.

Psychosocial adjustment of latency-aged diabetics: determinants and relationship to control.

The relationship of psychosocial adjustment, family functioning, self-esteem, and diabetic control was studied in 20 latency-aged diabetic children and their parents. Moderate to severe adjustment problems were found in 11 (55%) of the patients. Child self-esteem, parental self-esteem, and family functioning, as scored by standard instruments, were all significantly greater in the group of children considered to be well-adjusted as compared to the maladjusted group (P less than .05 to .001). Of these, parental self-esteem appeared to correlate most closely with the child's adjustment. Twenty-four-hour urinary glucose excretion was two- to threefold greater in maladjusted as compared to well-adjusted patients (71 +/- 20 vs 20 +/- 5 gm, P less than .05). These data suggest that psychosocial adjustment problems frequently occur in latency-aged children with diabetes, are associated with poorer chemical control, and require a family-centered approach to intervention and management.