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1. To be detected, movements of the interphalangeal joint of the big toe must be greater than at other joints. This poor acuity may arise because the anatomy of the foot and ankle results in poor coupling between the toe and the muscles that operate it. To vary this coupling, the effect of ankle position on proprioceptive acuity at the toe was measured. 2. We measured proprioceptive acuity at the toe with the ankle in different positions and found that ankle plantarflexion did improve acuity. This implies that, with the ankle at mid-range or dorsiflexed, toe movement is inadequately transferred to muscle fascicles. 3. To determine actual changes in fascicle length of the toe extensor, movements of extensor hallucis longus near the toe and at the muscle-tendon junction were measured during surgical exposure in one subject. Ankle position greatly affected movement transfer from toe to muscle-tendon junction: no tendon movement was transferred with the ankle dorsiflexed, but all movement was transferred with the ankle plantarflexed. 4. When the relationship between joint rotation and muscle fascicle length measured in vivo was used to express the smallest detectable movements of the toe as proportional changes in muscle fascicle length, these detectable changes were similar to those at all other limb joints. This suggests that change in muscle fascicle length is of major interest to the nervous system.

1. The effects of hydrostatic changes in perfusion pressure on performance of working fatigue-resistant muscle fibres in the hand were studied in six normal subjects. 2. Supramaximal stimuli were delivered in trains of 200 ms duration, at 1 train S-1, to the ulnar nerve proximal to the wrist to produce isometric contractions of adductor pollicis. The force of contraction was measured and, after a level contraction force was achieved, the arm was passively raised or lowered. 3. Lifting the hand 45 cm above the heart produced a decline in force output from the muscle within several seconds which, after 4 min, fell by 22% below the steady-state level. Lowering the hand 45 cm below heart level produced an 8% increase in force output. Greater changes in force output occur at higher workloads. 4. It is concluded that in human subjects, muscle performance is sensitive to changes in perfusion pressure that occur across the physiological range. At moderate work levels, force output of the working muscles in the hand can vary by up to 30% over the physiological range of blood pressure. This dependence of muscular force on blood perfusion is of potential importance to motor control during normal activities.

1. The angular displacements necessary for 70% correct detection were determined in normal subjects at the hip, knee and ankle joints, and the interphalangeal joint of the big toe. Angular velocities between 0.1 and 50 deg s-1 were tested. The hip and knee joints were tested in slight flexion and the ankle and toe joints were tested in the mid-range of the normal excursion. The joints were carefully supported for testing and the muscles acting at the joints were relaxed. 2. When detection thresholds and velocities were assessed in terms of angular displacements and angular velocities, proprioceptive performances at the hip, knee and ankle joints were superior to that at the toe joint. 3. When detection levels and displacement velocities were expressed in terms of linear displacements and velocities at the tip of the extended toe for all four joints, instead of in angular terms, the ankle gave the best performance and the hip and knee the worst. 4. The detection level and velocity data were expressed also in terms of proportional changes in the fascicle lengths of muscles operating these joints. Analysis in these terms showed that performance was similar at the hip, knee and ankle joints, but that performance for the toe was much poorer than for the other joints. 5. These results for the hip, knee and ankle are similar to those previously measured for the elbow and distal interphlangeal joint of the finger, and are consistent with the theory that muscle fascicle length is the variable of significance to the central nervous system. However, the proprioceptive performance at the big toe is notably poorer than all other joints studied and analysed in terms of this variable.

1. This study investigated the sources of sensory information upon which normal subjects' ability to stand depends. 2. An 'equivalent body' was used to simulate the physical properties of each subject's body during standing. The modulation of ankle torque required to support the equivalent body in an upright position was similar to that required to support the subject's own body when standing. However, when balancing the equivalent body, vestibular inputs were excluded from directing the appropriate changes in ankle torque. Thus, stability of stance could be studied with (normal stance) and without (balancing equivalent body) modulation by vestibular inputs. Vision could be excluded by closing the eyes. Sensory input from the feet and ankles could be removed by local anaesthesia from prolonged ischaemia, induced by occluding blood flow with inflated pneumatic cuffs just above the ankles. With vestibular, visual and peripheral sensory inputs negated, standing could rely only upon remaining sensory inputs, notably those from sensory receptors in the leg muscles. 3. Unlike the human body, the equivalent body used to negate vestibular inputs is not segmented. Therefore, the effects on stability of having a segmented body were determined by splinting subjects during standing so that only ankle movement was possible. This was done in the presence and absence of visual stabilization. 4. For each experimental task, either standing or balancing the equivalent body, sway was recorded while posture was unperturbed. Root mean square values of sway amplitude and power spectra were used to compare conditions. 5. Every subject could balance the equivalent body in a stable way when the eyes were closed, and when the feet were anaesthetized.(ABSTRACT TRUNCATED AT 250 WORDS)

1. Thresholds for the perception of postural sway induced by gentle perturbations were determined for five normal standing subjects. In this context we understand 'perception' to mean 'able to give a subjective report'. The thresholds for the perception of movements that were equivalent to sway in velocity and amplitude were determined when the available sensory input was limited to only one, or a pair, of the vestibular, visual, and proprioceptive systems. To examine vestibular inputs alone, vision was excluded and the whole body was moved with the ankles in a fixed position. To examine visual inputs alone, the body was kept stationary and a 'room' was moved around the subjects to simulate the relative visual-field movement that occurs during standing. To limit the available sensory input to proprioception from the legs, subjects were held stationary and balanced a load that was equivalent to their own body using their ankles. In this situation, perturbations were applied to the 'equivalent body' and these could only be perceived from the resulting ankle movements. Thresholds for perceiving ankle movements were also determined in the same posture, but with the leg muscles bearing no load. 2. The thresholds for the perception of sway during standing were very small, typically 0.003 rad at a velocity of 0.001 rad s-1, and even smaller movements were perceived as the mean velocity of the sway increased up to 0.003 rad s-1. No difference was found between the thresholds for perceiving forward sway and backward sway. Eye closure during standing did not affect the threshold for perceiving sway. 3. When sensory input was limited to proprioception from the legs, the thresholds for the perception of passive ankle movements were equivalent to the thresholds for the perception of sway during standing with all sensory inputs available. When the leg muscles were relaxed, the thresholds for perceiving ankle movements increased approximately twofold. 4. The visual thresholds for perceiving movement were higher than the proprioceptive thresholds at slower velocities of movement, but there was no difference at higher velocities. 5. Both the proprioceptive and visual thresholds were sufficiently small to allow perception of the sway that was recorded when the subjects stood normally in a relaxed manner. In contrast, the vestibular thresholds were an order of magnitude greater than the visual or proprioceptive thresholds and above the largest sway movements that were recorded during normal standing.(ABSTRACT TRUNCATED AT 400 WORDS)

1. Galantide, a putative galanin antagonist composed of twenty amino acids, caused a significant reduction in the vagal attenuating action of galanin injection (20 micrograms/kg; 6.2 nmol/kg) in anaesthetized cats at both ten times (137 micrograms/kg; 62 nmol/kg) and twenty-five times (343 micrograms/kg: 156 nmol/kg) the molar dose of galanin. Galantide did not block the depressor action of galanin in these animals. 2. Galantide, at both doses, also significantly reduced the vagal attenuating action of a 5 min period of cardiac sympathetic stimulation at 16 Hz in anaesthetized cats. 3. In anaesthetized dogs, galantide, at the same dose used in cats (137 micrograms/kg; 62 nmol/kg) had no significant effect on the vagal attenuation evoked by cardiac sympathetic stimulation or injection of neuropeptide Y (35 micrograms/kg; 8.2 nmol/kg). 4. This study therefore demonstrates antagonist properties of galantide on the vagal inhibitory action of galanin. It supports the hypothesis that the vagal inhibitory factor released by cardiac sympathetic nerve stimulation in the cat, but not the dog, is galanin, although it does not exclude the possibility of other factors playing a more minor role. Because galantide was not shown to block the depressor action of galanin, this study also suggests that there may be more than one galanin receptor subtype.

1. Stimulation of the right cardiac sympathetic nerve for 2 min at 16 Hz in the presence of either beta- or alpha- and beta-adrenoceptor blockade evoked attenuation of cardiac vagal action in eight possums: 31.3 +/- 10.3% maximum inhibition of cardiac vagal action on prolonging pulse interval, with a time to half-recovery of 4.9 +/- 1.1 min. 2. Intravenous injection of galanin (2-3.5 nmol kg-1) evoked similar inhibition of cardiac vagal action: 41.3 +/- 4.1% maximum inhibition of cardiac vagal action on pulse interval, with a time to half-recovery of 13.4 +/- 2.3 min. 3. Intravenous injection of neuropeptide Y (NPY) at greater molar doses (6.5-10 nmol kg-1) caused no inhibition of cardiac vagal action. 4. The galanin injections caused a powerful pressor response: 57.1 +/- 4.9 mmHg increase in systolic blood pressure. NPY caused a smaller pressor response, despite administration of higher molar doses: 36.7 +/- 3.0 mmHg increase in systolic blood pressure. 5. In the possum, galanin but not NPY can mimic the effects of cardiac sympathetic nerve stimulation on vagal action. Galanin also causes large pressor effects.

1. Subjects' ability to detect movements imposed at the elbow during active flexion was measured. Movements of three different angular velocities (0.04, 0.4 and 4.4 deg/s) were applied to the arm while subjects maintained one of two force levels of active flexion. The threshold magnitudes for detection of the direction of imposed movement were found. 2. All thresholds were very small. At the lowest velocity of movement the average threshold was 0.13 deg and no subject had a threshold of greater than 0.3 deg. This contrasts with thresholds of over 2 deg measured in a previous study when the muscles about the joint were relaxed. Thresholds decreased further with increasing velocity of movement. 3. No difference was found between the two levels of contraction of the elbow flexors. However, extension (stretch of the contracting muscle) and flexion thresholds were calculated separately, and smaller extensions than flexions could be detected. 4. These findings indicate that conscious detection of imposed movements is greatly enhanced during active muscle contraction. Movements which cause unloading of the contracting agonist, as well as movements which result in stretch, are more easily detected than when the muscle is contracting. The discussion focuses on possible mechanisms for this enhancement.

1. It has been demonstrated that subjects can alter the reflex stiffness of the elbow and wrist in response to imperceptibly slow perturbations applied through a complaint coupling. We used this technique to measure ankle stiffness in standing subjects as a means of examining reflex activity. 2. During unperturbed stance, a linear relationship between ankle torque and ankle angle is expressed as a load stiffness. The load stiffness predicted from a subject's measured physical dimensions corresponds closely with the value measured by standing the subject on a force platform. 3. Slow perturbations were applied at waist level, through a spring, to standing subjects. The perturbations caused sway similar in magnitude and rate to the sway of normal stance. Ankle stiffness was measured during the period when the perturbations were unperceived. The contribution to ankle stiffness of reflexes that use visual information was assessed by eye closure. The ability of reflexes based on sensory information from the legs to maintain upright posture was assessed when subjects balanced a load equivalent to their own body, in a situation where neither visual nor vestibular information could assist. Ankle stiffness was measured while the load was perturbed. 4. The results show that a simple mechanical model of stance predicts the torque-angle relationship at the ankle. This relationship determines the minimal ankle stiffness required to stand, and reflex muscle stiffness is a necessary component of this ankle stiffness. Visual, vestibular and lower limb sensorimotor reflexes each contribute to ankle stiffness; however, the local sensory reflexes alone are sufficient to stand. For responses to unperceived perturbations, standing subjects can alter their reflex ankle stiffness according to intentional set.

1. Stimulation of the right cardiac sympathetic nerve for 3 or 5 min at 16 Hz in the presence of effective beta-adrenoceptor blockade evoked prolonged attenuation of subsequent cardiac vagal action in anaesthetized cats. Concurrent sympathetic and vagal stimulation, both at 16 Hz for the same period of time as sympathetic stimulation alone, reduced or abolished the inhibition of vagal action which followed when sympathetic stimulation was given alone. 2. A series of three successive intravenous injections of galanin all caused attenuation of vagally induced slowing of the heart, but the effect of each injection was less than that of the previous one. A fourth injection of galanin given after a 45 or 60 min rest period showed return of sensitivity. 3. Sympathetic stimulation at 16 Hz for 5 min was less efficient in causing attenuation of vagal slowing when applied following the administration of exogenous galanin. This is consistent with galanin being the mediator of vagal attenuation following sympathetic stimulation.

1. Stimulation of the right cardiac sympathetic nerve for 3 min at 16 Hz in the presence of effective beta-adrenoceptor blockade evoked prolonged attention of cardiac vagal action in the cat: 40.8 +/- 5.4% maximum inhibition of cardiac vagal action on prolonging pulse interval, with half-time to recovery of 8.3 +/- 1.4 min. 2. Intravenous injection of galanin (1.6-3.1 nmol/kg) evoked prolonged attenuation of cardiac vagal action: 40.9 +/- 8.2% maximum inhibition with a half-time to recovery of 13.6 +/- 2.6 min. This effect of galanin was not significantly different from the action of sympathetic nerve stimulation. A slight depressor response (-14.4 +/- 1.9 mmHg) was seen in nine of sixteen cats. 3. Intravenous injection of neuropeptide Y (NPY) (2.8-6.3 nmol/kg) evoked slight attenuation of cardiac vagal action: 11.9 +/- 4.5% maximum inhibition of cardiac vagal action on pulse interval, with a half-time to recovery of 4.1 +/- 1.7 min. Blood pressure increased by 68.6 +/- 5.7 mmHg. 4. Following administration of guanethidine (1 mg/kg I.V.) the inhibitory effect of sympathetic nerve stimulation on cardiac vagal action was significantly reduced (P less than 0.001). The responses to exogenous NPY and galanin on vagal action were unchanged after guanethidine. 5. The prolonged attenuation of cardiac vagal action can be mimicked by exogenous galanin in the cat but not by exogenous NPY.

1. It has been demonstrated recently that, when suitably instructed, subjects could alter the stiffness at the elbow in response to a slowly and imperceptibly changing elastic load. Although evidence was provided in favour of this occurring via changes in gain of the reflex response to stretch, changes in the degree of co-contraction could not be entirely ruled out. The major objective of the present experiments was to determine if subjects could alter stiffness at the wrist in a similar task, and then to determine whether they retained this ability when co-contraction was made impossible by anaesthetizing the nerve to the wrist extensors. A second objective was to determine if changes in stiffness could be controlled independently at the wrist and elbow. 2. Subjects, with eyes closed, initially held position constant against a constant force that loaded the flexors. For the wrist, they were instructed: (i) to keep the hand as still as possible (keep position constant) or (ii) to let the hand be moved by the perturbation (keep force constant). The perturbation was an initially imperceptible elastic load whose direction (loading or unloading) could not be predicted. Subjects were also asked to indicate when the perturbation was first perceived. 3. When asked to hold position constant or force constant at the wrist, subjects demonstrated task-dependent changes in stiffness prior to perception of the perturbation. These changes in stiffness were still achieved when the nerve to the wrist extensors was anesthetized and thus co-contraction was prevented. 4. Five subjects demonstrated the ability to control stiffness independently at the wrist and the elbow although most subjects had difficulty with the task we employed to demonstrate this. 5. The results demonstrate: (i) that for the wrist, set-dependent changes in stiffness that occur prior to perception of a slowly developing perturbation can be mediated by changes in gain of reflex responses to those perturbations, and (ii) that stiffness can be controlled independently at the wrist and elbow, presumably in part by changes in gain of stretch reflexes.

1. Stimulation of cardiac sympathetic nerves caused prolonged inhibition of vagal effects on heart rate, an effect which has been proposed on the basis of previous studies to be due to neuropeptide Y or a neuropeptide Y-like substance, released from the sympathetic nerves. 2. This prolonged vagal inhibitory effect was attenuated or abolished when the sympathetic stimulation responsible was given together with continuous vagal stimulation. 3. Continuous vagal stimulation alone did not modify the ability of administered neuropeptide Y to cause inhibition of cardiac vagal action. 4. The results are consistent with the cardiac vagal nerves releasing a transmitter (probably acetylcholine) which acts on cardiac sympathetic nerve endings, inhibiting them from releasing neuropeptide Y or a neuropeptide Y-like substance.

1. The carotid sinus nerve was electrically stimulated in dogs anaesthetized with chloralose. Stimuli (1 ms, 1-10 V, less than or equal to 1 Hz) evoked responses in single cardiac efferent fibres dissected from the cervical part of the vagus nerve. The mean latencies of these responses varied, from fibre to fibre, between 30 and 120 ms. 2. Stimuli given during the expiratory phase of the respiratory cycle evoked vagal responses with a shorter latency than similar stimuli given only during the inspiratory phase of the respiratory cycle. 3. Following the vagal response to carotid sinus nerve stimulation a period of inhibition of vagal activity, lasting 100-150 ms, occurred. Refractoriness of the responding vagal motoneurone following an action potential could not account for this post-excitatory depression. 4. The inhibitory effects of electrical stimulation of the carotid sinus nerve were further studied by applying pairs of similar electrical stimuli to the carotid sinus nerve. The second stimulus of a pair had to be given 80-100 ms after the first to evoke a second response. 5. Trains of electrical stimuli (30-100 Hz) were also studied. At low frequencies the inhibitory effect of successive stimuli on vagal responses became less marked, but at higher frequencies only the first and last stimulus of the train reliably evoked responses. For trains of stimuli at both low and high frequencies, the last stimulus of the train evoked a vagal response, which was succeeded by a period of inhibition of vagal firing: this inhibition was then followed by further excitation before vagal discharge returned to resting levels.

1. The centrally generated ;effort' or direct voluntary command to motoneurones required to lift a weight was studied using a simple weight-matching task when the muscles lifting a reference weight were weakened. This centrally generated input to motoneurones was increased when the lifting muscles were partially paralysed with curare or decamethonium as judged by the increased perceived heaviness of a reference weight lifted by the weakened muscles.2. If subjects were asked simply to make matching isometric contractions when the lifting muscles were weakened the isometric tension produced by a weakened muscle was over-estimated.3. When subjects matched weights by flexing the distal joint of the thumb the perceived heaviness of a reference weight during a control partial curarization was compared with its perceived heaviness during a similar partial curarization when the thumb was also anaesthetized. At any level of maximal strength during curarization the perceived heaviness (which reflects the motor command to lifting motoneurones) was increased when the thumb was anaesthetized.4. This increased voluntary command to lifting motoneurones may be required because automatic reflex assistance provided by apparent servo action from the long flexor of the thumb is suppressed by anaesthesia of the thumb (Marsden, Merton & Morton, 1971, 1973, 1976a; Dyhre-Poulsen & Djørup, 1976).

1. The cardiovascular responses to voluntary isometric contractions performed by human subjects are determined by the proportion of maximal tension achieved by the muscles contracting, and not by the mass of the contracting muscles, nor by the absolute tension achieved (Lind & McNicol, 1967; confirmed here). When two or more muscle groups contract simultaneously at different relative tensions, the increments in heart rate and blood pressure are the same as when the muscle group at the higher relative tension contracts alone at that tension (Lind & McNicol, 1967). It is known that there are both central and reflex stimuli to the cardiovascular system in exercise, and the present study examines whether the muscular reflex stimuli are related to the proportion of maximal tension achieved or to the mass of contracting muscle. 2. Isometric hind-limb contractions were induced in anaesthetized dogs and cats by stimulation of spinal ventral roots. Pressor responses to contraction of both hind limbs were greater than responses to contractions of either hind limb alone. No differences were observed between heart rate responses to single or combined hind-limb contractions. 3. When human subjects perform isometric contractions, a pressor response can be maintained beyond the conclusion of the exercise by occluding muscle blood flow. This response is generally attributed to a reflex set up in the muscle by the action of chemical factors on afferent nerves. When comparable pressor responses were evoked by comparable proportional efforts with either the whole hand or the little finger, it was found here that the pressor responses remaining during the period of post-exercise occlusion were greater when the greater mass of muscle had been exercised. 4. It is concluded that the muscular reflex drive in isometric exercise is related to the bulk of contracting muscle.

1. An anatomical peculiarity allows the hand to be positioned so that the terminal phalanx of the middle finger cannot be moved by voluntary effort. When positioned in this way only joint and cutaneous mechanisms subserve position sense. By altering the position of the hand the muscles are again engaged and able to move the finger. Moving the joint then also excites muscular afferents. 2. The position sense of twelve subjects was assessed with and without engagement of the muscles at the joint. Three tests were used in which either angular displacement, angular velocity or duration of displacement were held constant. 3. When muscular attachment was restored, performance in all tests was greatly enhanced. As engagement of the muscles caused little change in the 'stiffness' of the joint, it is unlikely that the improved performance resulted from increased discharges from the joint receptors. Cutaneous mechanisms are unlikely to mediate this improvement as they are likely to have been unaffected by engagement of muscles. It is concluded that intramuscular receptors are partly responsible for normal position sense. 4. In seven of the twelve subjects the test finger was anaesthetized to isolate the contribution of intramuscular receptors. This muscle sense was variable. In some subjects it provided accurate kinaesthetic information but in others the information was crude. If with the test finger anaesthetized subjects exerted voluntary tension with the muscles that move the joint the muscle sense was improved.

1. Weights were lifted by flexing the distal joints of the anaesthetized thumbs. A weight-matching task was used to determine the perceived heaviness of a reference weight during control estimates when it was freely lifted, and during experimental estimates when the weight was not lifted, but simply 'gave way' when a reference isometric tension of the same magnitude was attained. 2. Limitation of the afferent input, by anaesthesia of the digit and by replacing lifting with a sudden unloading, did not grossly impair the judgement of heaviness. The sense of heaviness increased when the muscles became fatigued. 3. These results suggest that the central nervous system can interpret the voluntary motor command as an index of heaviness even when provided with only a crude peripheral signal that the weight has been moved.

1. Action potentials were recorded in single baroreceptor fibres dissected from the carotid sinus nerves in dogs during increases in blood pressure caused by I.V. injection of angiotensin II, and by I.V. injection of phenylephrine or inflation of an aortic balloon. Action potentials were recorded in single cardiac efferent fibres dissected from the right cervical vagus nerve in other dogs during increases in blood pressure caused by angiotensin II, and by phenylephrine or by inflation of an aortic balloon. 2. There was no difference in the discharge frequency of single carotid sinus baroreceptor fibres at any blood pressure when phenylephrine, balloon inflation, or angiotensin II were used to raise the pressure. 3. Activity in single cardiac vagal efferent fibres was increased when blood pressure was increased by phenylephrine or by inflation of an aortic balloon. However, when blood pressure rose by a comparable amount in response to angiotensin II, vagal firing decreased (three fibres), was little changed from control levels (four fibres), or increased less than it did in response to phenylephrine (one fibre). 4. It is concluded that while angiotensin II has no effect on baroreceptor sensitivity, it does inhibit vagal discharge which is evoked by stimulation of arterial baroreceptors.

1. Brief stimuli were delivered to the carotid chemoreceptors or baroreceptors in dogs anaesthetized with pentobarbitone or chloralose. Chemoreceptor stimulation was achieved by rapid retrograde injections of 0-2-0-5 ml. warmed, CO2-equilibrated saline through a cannula in the external carotid artery. Baroreceptor stimulation was achieved by forceful retrograde injection of 2-5 ml. air-equilibrated saline, or of freshly drawn arterial blood, into the external carotid artery after first clamping the common carotid artery. 2. Brief baroreceptor stimuli had no noticeable effect on breathing. Brief chemoreceptor stimuli had no effect on breathing in some dogs, but in many produced a reflex increase in the depth of inspiration when delivered during inspiration. In these same dogs, brief chemoreceptor stimuli delivered in expiration either prolonged the expiratory pause or evoked an active expiratory effort. 3. Prompt decreases in heart rate were elicited by brief sudden chemoreceptor or baroreceptor stimuli when these were delivered during the expiratory phase of respiration. The stimuli did not modify the control heart rate pattern when delivered during inspiration. If the carotid sinus nerve or the vagus nerves were cut the responses were abolished. 4. Brief chemoreceptor or baroreceptor stimuli remained effective in evoking prompt decreases in heart rate during periods of apnoea in the end-inspiratory position (Hering-Breuer inflation reflex). In periods of apnoea after prolonged artificial hyperventilation the stimuli were sometimes ineffective at first, but were always effective late in the period of apnoea, again producing prompt cardiac slowing. 5. After denervation of the lungs, brief baroreceptor and chemoreceptor stimuli continued to evoke prompt falls in heart rate when given during expiration. When delivered during inspiration the same stimuli were either ineffective, or less effective.

1. Digital pressure applied to the eyes evokes reflex bradycardia in human subjects and anaesthetized dogs. The bradycardia is most pronounced when breathing stops. 2. In the dog oculo-cardiac reflex bradycardia is mediated by vegal stimulation and by sympathetic withdrawal. 3. Oculo-cardiac reflex bradycardia in the dog is reduced by central neural inspiratory activity and by the excitation of pulmonary afferents by inflation of the lungs. In human subjects it is reduced when inspiratory efforts are made against a closed glottis. 4. Nasopharyngeal stimulation with water evokes reflex bradycardia in the anaesthetized dog. This bradycardia is reduced by central neural inspiratory activity and by the excitation of pulmonary afferents by inflation of the lungs. 5. Bradycardia occurs in normal human subjects during immersion of the face in water ('diving'). This bradycardia is reduced when inspiratory efforts are made against a closed glottis. 6. Swallowing evokes transient tachycardia in human subjects. During diving or the application of ocular pressure, swallowing reduces the reflex bradycardia which these evoke.

1. Brief stimuli were delivered to the carotid baroreceptors or chemoreceptors in dogs anaesthetized with chloralose and paralysed with D-turbocurarine. Baroreceptor stimulation was achieved by forceful retrograde injection of 2-5 ml or air-equilibrated saline into the external carotid artery after first clamping the common carotid artery. Chemoreceptor stimulation was achieved by rapid retrograde injections of 0.2-0.5 ml of warmed CO2-equilibrated saline into the external carotid artery. Observations were made during periods of temporary cessation of artificial ventilation. 2. When the volume of the lungs was not changing, prompt decreases in heart rate were evoked by chemoreceptor or baroreceptor stimuli except when these were delivered during the inspiratory phase of breathing (as judged from the records of phrenic nerve activity). 3. No changes in heart rate were evoked when these stimuli were timed to occur during expansion of the lungs in response to a rapid increase in intratracheal pressure (6-10 mmHg in 1-2 sec). Decreases in heart rate were evoked when the stimuli occurred during slower inflations of the lungs. 4. Both stimuli regained their effectiveness on heart rate with time after inflations of the lung when the lungs were held inflated. Both stimuli evoked large decreases in heart rate when delivered during deflations of the lung. 5. The effects of lung inflation on the effectiveness of both cardiodepressor reflexes were abolished by surgical denervation of the lungs.

The angular displacements necessary for 70% correct detection were determined in normal subjects at the shoulder and elbow joints and at the terminal joint of the middle finger. Angular velocities of displacement between 0.125 degrees and 160 degrees/s were tested. Each joint was tested in the mid-range of its normal excursion. The joints were carefully supported for testing and the muscles acting at the joints were relaxed. When assessed in terms of angular displacements and angular velocities, proprioceptive performance at the shoulder and elbow joints was superior to that at the finger joint. Optimal performance at the finger joint was attained over the range of angular velocities from 10 degrees to 80 degrees/s. Optimal performance at both more proximal joints was optimal over a wider range (2 degrees-80 degrees/s). Active pointing movements made without vision of the moving part were performed at each joint at velocities within the range of optimal proprioceptive performance. However, when detection levels and displacement velocities were expressed in terms of linear displacements and velocities at the finger tip for all three joints, the finger joint gave the best performance and the shoulder the worst. In practical terms, therefore, displacements of a given linear extent are best detected if they move distal joints and worst if they move proximal joints. For the elbow and finger joints the detection level and velocity data were expressed also in terms of proportional changes in the lengths of muscles operating at these joints, and as proportional changes in the distance between the points of attachment of the joint capsules. Analysis in terms of proportional changes of muscle length showed remarkably similar performance levels at both joints. This suggests that intramuscular receptors are important determinants of proprioceptive performance. Analysis in terms of joint capsular displacement did not unify the data: on this form of analysis proprioceptive performance at the elbow joint was superior.

1. Brief stimuli were delivered to the carotid chemoreceptors or baroreceptors in dogs anaesthetized with chloralose. Chemoreceptor stimulation was achieved by rapid retrograde injection of 0.2-0.5 ml. CO2 equilibrated saline through a cannula in the external carotid artery. Baroreceptor stimulation was achieved by forceful retrograde injection of 2-5 ml. air-equilibrated saline into the external carotid artery after first clamping the common carotid artery. 2. prompt decreases in heart rate were elicited by brief sudden chemoreceptor or baroreceptor stimuli when these were delivered during the expiratory phase of respiration. The stimuli did not modify the control heart rate pattern when delivered in the inspiratory phase of respiration. This respiratory modulation of reflex effectiveness persisted when the animals were completely paralysed and the phase of the respiratory cycle was monitored through a phrenic electroneurogram. 3. single cardiac vagal efferent nerve fibres were dissected from the cut central end of the right cervical vagus nerve. They were classified as cardiac efferents by their cardiac and respiratory rhythmicity, and by their increased activity in response to stimulation of a carotid sinus nerve or to mechanical elevation of the systemic arterial pressure. These efferent fibres increased their activity in response to brief chemoreceptor or baroreceptor stimuli delivered in expiration, but did not respond to stimuli delivered in inspiration. This respiratory modulation of both reflexes persisted after bilateral cervical vagotomy.

1. The perception of the heaviness of lifted objects was studied using a weight-matching task when sensory inputs from parts related to the lifting task were altered.2. A weight lifted by flexing the index finger feels heavier when the thumb is anaesthetized and lighter when the thumb is electrically stimulated. A weight lifted by flexing the distal joint of the thumb feels heavier when the sensory input from the skin and joint of the thumb is abolished by anaesthesia. It also feels heavier when the index (but not the little) finger is anaesthetized, and lighter when the index (but not the little) finger is electrically stimulated.3. A weight lifted by extending the thumb feels lighter when the sensory input from the thumb is abolished.4. The perceived heaviness of a weight lifted by flexing the thumb is increased during anaesthesia of the thumb when the flexor of the thumb is the prime mover but not when it is acting simply as a postural fixator to support the weight.5. The sensation of the heaviness of lifted objects derives from the effort or centrally generated voluntary motor command employed in the lift. Our results indicate that the motor commands to either thumb or index finger flexors are facilitated by sensory inputs arising from a wide sensory field usually involved in co-operative motor performances carried out by both muscle groups together.

1. It was shown by Gandevia & McCloskey (1977) that anaesthesia of the thumb causes weights lifted by thumb flexion to feel heavier, and weights lifted by thumb extension to feel lighter. This was confirmed by Marsden, Rothwell & Traub (1979). Gandevia & McCloskey explained the effects in terms of altered motor command (and so, altered 'sense of muscular force, or heaviness') required when sources of peripheral reflex facilitation or inhibition were removed by anaesthesia. Marsden et al. proposed, instead, that co-contraction of antagonists altered in anaesthesia. They said that increases in heaviness occurred for flexion because anaesthesia was associated with increased activity in the thumb extensor and, similarly, that decreases in heaviness occurred for extension because anaesthesia reduced activity in the thumb flexor. 2. The apparent heaviness of weights lifted by flexion of the thumb is not systematically altered by paralysis of the extensor of the thumb (radial nerve block at the elbow). Heaviness is increased by local anaesthetization of the thumb (digital nerve block). If paralysis of the thumb extensor is induced after digital nerve block, no further alteration in apparent heaviness occurs. 3. If extensor co-contraction is encouraged for stabilization of the wrist, as by having subjects perform an isometric contraction with the index-finger while lifting weights by thumb flexion, the apparent heaviness of the weights is increased. If co-contraction of the extensors is prevented by radial nerve block the manoeuvre of simultaneous contraction of the index finger then fails to alter the heaviness of weights lifted by thumb flexion. 4. The middle finger can be postured in such a way that active extension but not active flexion of its distal joint is impossible. When co-contraction of the extensor cannot act at the distal joint, anaesthetization of the middle finger causes an increase in apparent heaviness of weights lifted by flexion of this joint. 5. The effects of digital anaesthesia on the apparent heaviness of objects lifted by digital flexion are not caused by co-contraction of the extensors of the digits, as proposed by Marsden et al. Where extensor co-contraction occurs unrelated to the digital flexion task, as in stabilization of the wrist during simultaneous flexion of more than one digit, it may affect the apparent heaviness of objects borne by individual digits.

Long-latency (40-80 ms) electromyographic (e.m.g.) responses of the contracting flexor pollicis longus to stretches applied at the thumb-tip, were studied in normal human subjects. Stretches were applied during four classes of contraction: (i) isometric 'hold', in which the subject held a steady isometric contraction; (ii) isometric tracking, in which the subject tracked a steadily rising force target; (iii) isotonic tracking, in which the subject flexed against a constant torque to track a position target; (iv) weight-lifting, in which the subject lifted a weight hung at one end of a lever by pressing the thumb-tip on the other end of the lever. The effects on the responses of prior instructions to 'resist' or to 'let go', and of local anaesthesia of the thumb, were studied. The ability to modify the size of the long-latency e.m.g. response in accordance with prior instruction was variable. All subjects tested could do so during isometric holding contractions, but many could not do so during the other forms of contraction. Local anaesthesia of the thumb significantly reduced the long-latency e.m.g. response in only some subjects, and abolished it in none. The reduction was most reliably seen for isometric force tracking contractions. During thumb anaesthesia in different subjects, there was a significant correlation between the proportional increase in apparent heaviness of an object lifted by thumb flexion and the proportional reduction in the size of the long-latency e.m.g. response to muscle stretch.

This paper extends previous work (Gandevia & McCloskey, 1976) on proprioception in the terminal joint of the middle finger. By positioning the finger in appropriate ways proprioceptive acuity at the joint can be assessed when no muscular afferents could contribute, or when afferents in the flexor but not the extensor could contribute, or when afferents from both muscles could contribute. Digital nerve block anaesthetizes joint and cutaneous receptors and so was used to study the contributions from muscle afferents in isolation. Displacements (10 degrees) at various angular velocities were better detected when muscle afferents from both flexor and extensor muscles could contribute. This was so whether joint and cutaneous receptors were also available, or after digital anaesthesia. Performance when only muscle afferents are available is, however, inferior to that when all sensory mechanisms are intact. It is concluded that muscle afferents contribute to kinaesthesia, and that a full complement of such receptors from agonist and antagonist muscles gives superior acuity to that achieved when only the receptors of one of the muscle groups is available. The angular displacements necessary for 70% correct detection were determined at angular velocities between 0.25 degrees and 160 degrees/s. Proprioceptive performance was optimal with all proprioceptive mechanisms intact over the range of angular velocities 10 degrees -80 degrees/s: 70% correct detection of displacements of 0.8 degrees-1.2 degrees occurred in this range. Performance deteriorated slightly at higher velocities of displacement. Performance was significantly poorer when only joint and cutaneous receptors could contribute (in the absence of intramuscular receptors), and when only intramuscular receptors could contribute (in the absence of joint and cutaneous receptors). Full proprioceptive acuity depends upon the availability of receptors in muscles and in skin and/or joints.

1. Normal subjects, with closed eyes, attempted to keep constant either the force exerted at the wrist or the position of the wrist against an elastic load. The load was attached to the wrist 275 mm from the axis of rotation of the elbow joint. During recording, the far end of the elastic load was displaced slowly enough that it was not immediately perceived but far enough for perception to occur before its completion. 2. The over-all relation between wrist force and position for the two conditions was approximately linear and could be described in terms of effective stiffness. The effective stiffness for the constant-position task averaged 2.8 N/mm (210 N m/rad), while for the constant-force task the mean effective stiffness was -0.028 N/mm (-2.1 N m/rad), indicative of slight over-compensation. 3. Averaging the performance at the onset of the imposed disturbance indicated that the subjects' behaviour consisted of two parts: an initial, small-range response followed by a second phase over the remainder of the displacement. The transition corresponded to the subjects' threshold for detection of the disturbance. 4. The stiffness measured for the response prior to perception was taken as a measure which included the tonic stretch reflex. The stiffness was altered appropriately for the two tasks, being lower when the subjects tried to maintain the force exerted constant (average 1.1 N/mm, 83 N m/rad) than when they attempted to keep the position constant (average 2.3 N/mm, 170 N m/rad). A small degree of co-contraction occurred but could be dissociated from the stiffness changes. 5. Scaling the results allowed comparison of the initial stiffness with values for the decerebrate cat. When analysed in this way, the values recorded in man during the constant-position task were similar to those reported for short-range stiffness in the decerebrate cat. 6. The thresholds for detection of the disturbance were much lower than those reported for subjects with relaxed muscles. 7. The stretch reflex in man has a direct role in compensating for small disturbances during motor tasks. It may also function to improve detection of applied disturbances by magnifying the corresponding force change. Once the stimulus is perceived and voluntary intervention is possible, a greater contrast is seen between the subjects' performance of the two tasks.

1. Kinaesthetic acuity was tested at the distal interphalangeal joint of the middle finger when the hand was postured so that the joint was effectively disengaged from its muscular attachments. Subjects were required to detect the direction of 5 deg movements applied at different angular velocities from a mid-position under control conditions, after intra-articular injection of a plasma expander and after intra-articular injection of a local anaesthetic. 2. Kinaesthetic performance was enhanced after the injection of a plasma expander and deteriorated after injection of local anaesthetic. This deterioration could not be explained by spread of the local anaesthesic from the injection site on the dorsum of the joint. 3. The results suggest that the discharge of joint receptors can produce perceived signals of joint movement. Under normal conditions these receptors may duplicate the kinaesthetic input from muscle spindle endings.

1. Surface electromyographic recordings were made in eight normal subjects from the isometrically contracting elbow flexors before and during forcible extension of the elbow through 7 degrees in 50-150 msec. 2. Weh the subjects were instructed prior (2-5 sec) to a forthcoming stretch to 'resist' or to 'let go', they could reliably enhance or suppress e.m.g. activity occurring between 40 and 70 msec from commencement of the stretch. Such e.m.g. activity represents a 'long-latency' (or 'M2') reflex response: it occurs with a latency longer than the spinal segmental monosynaptic reflex, but shorter than a voluntary reaction time. When the subjects were given their instructions (by means of a light) at the moment the stretch commenced, however, none of them could adjust the long-latency reflex appropriately. 3. It is concluded that central, evaluative processes commencing at the time of a perturbation cannot influence long-latency reflex responses to that perturbation.

1. Brief stimuli were delivered to the carotid body chemoreceptors or the carotid sinus baroreceptors at different phases of the respiratory cycle in anaesthetized dogs. Chemoreceptor stimulation was achieved by injecting small volumes (0.2-0.5 ml.) of warmed saline equilibrated with CO(2) near to the carotid bodies on both sides. Baroreceptor stimulation was achieved by injecting larger volumes (2-5 ml.) of saline equilibrated with air into the region of the carotid bifurcation on both sides, after first clamping the common carotid arteries.2. When the vagus nerves were intact, but sympathetic nervous effects on heart rate were blocked by administration of propranolol, there was a prompt and pronounced bradycardia evoked when either baroreceptor or chemoreceptor stimuli were given in expiration, but little or no change in heart rate when they were given in inspiration.3. When the vagus nerves were cut, but sympathetic nervous function was intact, respiratory modulation of both baroreceptor and chemoreceptor reflex effects on heart rate could still be demonstrated. The bradycardia evoked by either stimulus was more marked for stimuli given in expiration than for stimuli given in inspiration. A complementary response pattern for brief decreases in baroreceptor stimulation (carotid occlusions) was demonstrated: the tachycardia evoked by occlusions timed during inspiration was greater than that evoked by occlusions timed during expiration. All the reflex effects were mediated by the sympathetic system because they were abolished by administration of propranolol.4. Typically, the sympathetic reflex effects were slight in comparison with the vagal reflexes evoked by either chemoreceptor or baroreceptor stimuli.

1. In anaesthetized and decerebrate cats isometric exercise of the hind limb muscles was elicited by stimulating the spinal ventral roots L7-S1. This caused a rise in arterial blood pressure, with small increases in heart rate and pulmonary ventilation. These changes were abolished by cutting the dorsal roots receiving afferents from the exercising muscle.2. When the triceps surae muscle was made to exercise by ventral root stimulation, occlusion of the femoral artery and vein through and beyond the period of exercise caused the blood pressure to remain raised until the occlusion was removed. The ventilatory and heart rate responses were not markedly altered or prolonged by such circulatory occlusion.3. Injection of small volumes of 5% NaCl or isotonic KCl into the arterial blood supplying hind limb muscles gave cardiovascular and respiratory responses similar to those evoked by exercise. Like the responses to exercise, these responses were abolished by dorsal root section.4. Direct current anodal block of the dorsal roots receiving afferents from the exercising muscle was used to block preferentially large myelinated fibres: this form of block did not abolish the evoked cardiovascular and respiratory responses. Local anaesthetic block of the dorsal roots was used to block preferentially unmyelinated and small myelinated fibres: this form of block abolished the cardiovascular and respiratory responses. It is concluded that the reflex responses are mediated by fibres within groups III and IV (small myelinated fibres and unmyelinated fibres).

1. Experiments were designed to show whether elements of the command descending from higher centres to exercising muscles provide an input for cardiovascular and respiratory control. Vibration, known to be a powerful stimulus to the primary afferents from muscle spindles, was applied to the biceps tendon of human subjects performing sustained isometric contractions with the biceps or the triceps muscle. When the biceps was contracting this activation of muscle spindle primary afferents in it provided an element of reflex excitation, so that less central command was required to achieve a given tension. When triceps was contracting, the activation of muscle spindle primary afferents in its antagonist, biceps, contributed an element of reflex inhibition, so that more central command than normally was required to achieve a given tension. The cardiovascular and respiratory responses to an isometric effort could thus be investigated at any tension when the central command was normal, decreased, or increased.2. Blood pressure, heart rate, and pulmonary ventilation all increase in an isometric effort. The increase in each is less when the central command is reduced. The increase in each is greater when the central command is increased.3. It is concluded that there is irradiation of cardiovascular and respiratory control centres by the descending central command during voluntary muscular contractions in man.