Can all residual force enhancement be explained by sarcomere non-uniformities?
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Biomedical subjects
Publications and source records attributed to Uwe Proske.
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The role of afferent inflow and efferent outflow (or command) signals in judgements of limb position has been debated for over a century. One way to assess this is to check for changes during complete paralysis, with the current view being that perceived movements or position changes do not usually accompany attempts to contract paralysed muscles. To re-examine this, we asked six naïve subjects to carry out a simple position-matching task at the wrist. In the absence of vision, subjects accurately perceived the position to which their right wrist had been moved by the experimenter by matching it with their left hand. There was no significant change in perception when position was matched during sustained flexion or extension efforts. Then we paralysed and anaesthetized the right arm with ischaemia in order to produce a 'phantom' hand. The perceived position of the wrist changed by more than 20 deg when subjects attempted to flex or extend their hand when it was paralysed and anaesthetized. Further studies showed that this illusion was not dependent on the way in which the paralysis was produced and that the size of the position illusion increased when the level of effort during paralysis increased. These results establish for the first time a definitive role for 'outflow' signals in position sense.
The kinesthetic sense, the sense of position and movement of our limbs, has been the subject of speculation for more than 400 years. The present-day view is that it is signaled principally by muscle spindles, with a subsidiary role played by skin and joint receptors. The problem with muscle spindles as position sensors is that they are able to generate impulses in response to muscle length changes as well as from fusimotor activity. The central nervous system must be able to distinguish between activity from the two sources. Recent observations on position sense after fatigue and during load-bearing suggest that an additional source of kinesthetic information comes from a centrally generated sensation, the sense of effort. This has consequences for kinesthesia in the presence of the force of gravity. A contribution from central feedback mechanisms to the sense of effort is relevant to certain clinical conditions.
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The role of muscle afferents is discussed in terms of their contribution to kinesthesia, the senses of position and movement of the limbs. It is argued that muscle spindles are not well suited as position sensors, on several grounds. Yet we know from muscle vibration experiments that they do contribute to kinesthesia. A number of recent experiments have shown that positional information is of particular significance to the central nervous system. In other experiments it has been demonstrated that a disturbance to kinesthesia follows fatigue from exercise. Fatigue of elbow flexor muscles led subjects to make significant positional errors in a forearm matching task. The size of the errors correlated with the fall in force from fatigue. These data suggest that we derive a positional cue from the effort required to hold a limb against the force of gravity. A challenge for the future will be to reveal how the centrally derived sense of effort and peripherally derived afferent information interact to give us our kinesthetic sense.
Evidence is provided for a mechanical event as the first step in the process leading to muscle damage after a series of eccentric contractions. Aspects discussed include the decline in active tension, increase in passive tension, shift in length-tension relation, soreness, swelling, and disturbed proprioception.
PURPOSE: A commonly used method for warm-up before exercise is to stretch muscles. How this benefits performance remains uncertain. After a period of eccentric exercise, there is muscle damage accompanied by an increase in passive tension, perceived as a sensation of increased stiffness in the exercised muscles. We have tested the idea that warm-up stretches might reduce levels of passive tension to reduce sensations of stiffness and soreness after eccentric exercise. METHODS: Subjects eccentrically exercised elbow flexors of one arm on an isokinetic dynamometer. The other arm acted as a control. After the exercise, measurements were made of resting elbow angle, as an indication of passive tension levels, before and after one or five large, passive arm extensions. Additional measurements made at 24 h included soreness levels in response to muscle stretch or vibration. RESULTS: After the exercise, the relaxed elbow adopted a more flexed posture than normal, an effect that slowly subsided over the next 4 d. Five rapid arm extensions returned arm posture back to near control levels. The flexed posture then gradually re-developed over the next hour. At 24 h postexercise, extending the arm produced some soreness as did muscle vibration. The pain from arm extension and vibration was reduced after a series of arm extensions. CONCLUSIONS: The flexed posture at the elbow is due to an increase in passive tension in elbow flexors as a result of muscle damage from the eccentric exercise. Stretch reduces passive tension. Benefits from the lower tension are reduced sensations of stiffness and soreness. This represents a new proposal for the mechanism for passive stretches as a warm-up strategy.
1. Exercise that involves stretching a muscle while active cause microscopic areas of damage, delayed onset muscle soreness and adaptation to withstand subsequent similar exercise. 2. Longer muscle lengths are associated with greater damage and recent animal experiments show that it is the length relative to optimum that determines the damage. 3. In humans, walking down stairs, taking two at a time, increases the length of the muscle during the lengthening and increases the delayed onset muscle soreness. 4. The observed pattern of damage is consistent with explanations based on sarcomere length instabilities. 5. The pattern of adaptation is consistent with the number of sarcomeres in series in a muscle being modulated by exercise, especially the range of muscle lengths over which eccentric exercise regularly occurs.
INTRODUCTION: Eccentric exercise, where the contracting muscle is lengthened, produces microscopic damage in muscle fibers, and sensations of stiffness and soreness, the next day. These normally resolve within a week. A more major sports injury is the muscle strain. Because strain injuries are known to occur during eccentric contractions, it is hypothesized that the microscopic damage from eccentric exercise can, at times, progress to a muscle strain. As the amount of microscopic damage depends on the muscle's optimum length for active tension, it is further proposed that optimum length is a measure of susceptibility for muscle strains. The athletes most at risk of a hamstring strain are those with a previous history of such injuries. Here the prediction is tested that optimum lengths of previously injured hamstrings are shorter and therefore more prone to eccentric damage than uninjured muscles. METHODS: Mean optimum angle for peak torque in a previously injured muscle of nine athletes with a history of unilateral hamstring strains was compared with the uninjured muscle of the other leg and with muscles of 18 uninjured athletes. Optimum angle was determined with isokinetic dynamometry. RESULTS: In previously injured muscles, torque peaked at significantly shorter lengths than for uninjured muscles. Peak torque and quadriceps:hamstrings torque ratios were not significantly different. CONCLUSIONS: The shorter optimum of previously injured muscles makes them more prone to damage from eccentric exercise than uninjured muscles and this may account for the high reinjury rate. The shorter optimum may reflect the muscle's preinjury state or be a consequence of the healing process. To reduce the incidence of strain injuries, it is recommended that a combined program of eccentric exercise and muscle testing be carried out.
In the platypus, electroreceptors are located in rostro-caudal rows in skin of the bill, while mechanoreceptors are uniformly distributed across the bill. The electrosensory area of the cerebral cortex is contained within the tactile somatosensory area, and some cortical cells receive input from both electroreceptors and mechanoreceptors, suggesting a close association between the tactile and electric senses. Platypus can determine the direction of an electric source, perhaps by comparing differences in signal strength across the sheet of electroreceptors as the animal characteristically moves its head from side to side while hunting. The cortical convergence of electrosensory and tactile inputs suggests a mechanism for determining the distance of prey items which, when they move, emit both electrical signals and mechanical pressure pulses. Distance could be computed from the difference in time of arrival of the two signals. Much of the platypus' feeding is done by digging in the bottom of streams with the bill. Perhaps the electroreceptors could also be used to distinguish animate and inanimate objects in this situation where the mechanoreceptors would be continuously stimulated. Much of this is speculation, and there is still much to be learned about electroreception in the platypus and its fellow monotreme, the echidna.
To test the possible role of ATP in transducing or modulating touch sensation, an isolated skin-nerve preparation from the toad, Bufo marinus, perfused on the inner side, was used to examine the effects of ATP on slowly adapting (SA) and rapidly adapting (RA) mechanoreceptors, identified by ramp and hold indentation of the skin. ATP (1-50 mM) did not generate impulse activity in either SA or RA mechanoreceptors nor increase their responses to mechanical stimulation. Instead, ATP (> or =5 mM) reversibly and selectively suppressed impulse discharge from SA mechanoreceptors. Our results indicate that while ATP may modulate the responses of specific touch receptors, it is not involved in transducing touch into nerve impulses.
Some important issues for muscle receptors remain unresolved. For muscle spindles it is uncertain how responses to combined static and dynamic fusimotor stimulation may summate. Such summation may occur during certain phases of locomotion. Two mechanisms considered here include electrotonic spread of generator current between sources of impulse activity and mechanical interactions between contracting intrafusal fibres. For tendon organs, it remains uncertain what aspects of muscle tension they signal. Here they were tested for their ability to respond to rises in whole-muscle passive tension after eccentric contractions. It was found that only when motor units were contracted which had a direct action on a tendon organ did it signal the rise in tension. The finding raises questions about the role of tendon organs as monitors of muscle tension.