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J Appl Physiol 98: 1487-1494, 2005. First published November 12, 2004; doi:10.1152/japplphysiol.01032.2004
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Conduction velocity of low-threshold motor units during ischemic contractions performed with surface EMG feedback

Dario Farina,1 Marco Gazzoni,2 and Federico Camelia2

1Center for Sensory-Motor Interaction (SMI), Department of Health Science and Technology, Aalborg University, Aalborg, Denmark; and 2Laboratorio di Ingegneria del Sistema Neuromusculare, Dipartmento di Elettronica, Politecnico di Torino, Torino, Italy

Submitted 17 September 2004 ; accepted in final form 10 November 2004


   ABSTRACT
TOP
 ABSTRACT
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
The aim of this study was to analyze the effect of ischemia on low-threshold motor unit conduction velocity. Nine subjects were trained to isolate the activity of a single motor unit (target motor unit) in the abductor pollicis brevis muscle with feedback on surface EMG signals recorded with a 16-electrode linear array. After training, the subjects activated the target motor unit at ~8 pulses per second (pps) for five 3-min-long contractions. During the third and fourth contractions, a cuff inflated at 180 mmHg around the forearm induced ischemia of the hand. The exerted force (mean ± SE, 4.6 ± 2.1% of the maximal voluntary contraction force), discharge rate (8.6 ± 0.4 pps), interpulse interval variability (34.8 ± 2.5%), and peak-to-peak amplitude of the target motor unit action potentials (176.6 ± 18.2 µV) were not different among the five contractions. Conduction velocity, mean power spectral frequency, and action potential duration were the same in the beginning of the five contractions (2.8 ± 0.2 m/s, 195.2 ± 10.5 Hz, and 5.4 ± 0.3 ms, respectively) and changed over the 3 min of sustained activation only during the fourth contraction. Conduction velocity and mean power spectral frequency decreased (10.05 ± 1.8% and 8.50 ± 2.18% during the 3 min, respectively) and action potential duration increased (8.2 ± 4.6% in the 3 min) during the fourth contraction. In conclusion, 1) subjects were able to isolate the activity of a single motor unit with surface EMG visual feedback in ischemic conditions maintained for 16 min, and 2) the activation-induced decrease in single motor unit conduction velocity was significantly larger with ischemia than with normal circulation, probably due to the alteration of mechanisms of ion exchange across the fiber membrane.

electromyogram; electrode array

THE ANALYSIS OF MOTOR UNIT properties is of interest for the investigation of motor control and adaptations of control strategies due to changes in muscle properties. The detection of single motor unit activities may be achieved with intramuscular electromyographic (EMG) recordings (3, 4). However, these recordings do not allow an easy assessment of muscle fiber membrane properties, such as the velocity of propagation of the motor unit action potentials (conduction velocity). In contrast, multichannel surface EMG signals allow conduction velocity estimation (5, 7), but their poor spatial selectivity makes it difficult to identify the contributions of single motor units (6). The analysis of single motor unit conduction velocity from surface EMG requires signal decomposition, which is a difficult task due to poor spatial selectivity (29). Increase in selectivity by spatial filtering (13, 35, 36) may allow, in specific conditions, the identification of single motor unit action potentials but not the detection of the entire motor unit discharge pattern.

A method for detecting the activity of single motor units consists of providing feedback from intramuscular EMG recordings and requiring the subject to control a target motor unit (2, 15, 38). Following this concept, we recently proposed the use of surface EMG signals as visual feedback, instead of intramuscular recordings (7). The poor selectivity of the surface recording was counteracted by increasing the number of recording systems to enhance the feedback to the subject. After ~20 min of training, the subjects were able to control and continuously activate low-threshold motor units for up to 5 min of sustained activation with feedback from the surface EMG (7). With this method, we could measure conduction velocity for each discharge of the target motor unit, which thus allowed the assessment of fiber membrane properties at each activation of the motor unit (8).

Muscle fiber conduction velocity is influenced by the concentration of ions in the extracellular environment (20). During fiber activation, there is a net loss of potassium from the cell (9, 10). This results in an increased extracellular potassium concentration, which decreases conduction velocity (20) by altering the resting membrane potential (22). Even at contraction levels as low as 3–4% of the maximal voluntary force, a decrease in conduction velocity is detectable in single motor units (7). Changes in conduction velocity depend on many mechanisms involved in the regulation of ion concentrations across the fiber membrane. These mechanisms are altered in the absence of oxygen; thus ischemia is expected to have an effect on conduction velocity and its changes with sustained activation.

Several previous studies (e.g., 26, 30, 37, 40, 41) have shown that ischemia reduces average conduction velocity (an indication of the mean conduction velocity of all active motor units). These results can be interpreted as due to the accumulation of metabolic byproducts in the muscle due to the activity of muscle fibers (26). However, average conduction velocity is affected by motor unit recruitment-derecruitment (1, 17) and by the distribution of discharge rates (32); thus these studies do not provide a direct indication of the modifications of fiber membrane properties in single motor units with ischemia.

A way to measure conduction velocity from single motor units in ischemic conditions is to control motor units with feedback from the surface EMG, as has been done in conditions of normal blood circulation (7). The aim of the study was thus to investigate the effect of ischemia on conduction velocity of low-threshold motor units, activated with surface EMG visual feedback.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects.   Nine healthy male subjects [age (mean ± SD): 26.5 ± 1.7 yr, height: 1.77 ± 0.07 m, body mass: 73.1 ± 7.5 kg] participated in the study after signing an informed consent form. The study was approved by the local ethics committee.

Surface EMG recording.   Surface EMG signals were detected using a linear array of 16 silver electrodes (point electrodes, 1-mm diameter, 2.5-mm interelectrode distance) (24, 28) (Fig. 1B) from the abductor pollicis brevis muscle of the dominant hand. The signals were amplified by a multichannel surface EMG amplifier (EMG 16, LISiN-Prima Biomedical and Sport, Treviso, Italy), band-pass filtered (–3-dB bandwidth, 10–500 Hz), sampled at 2,048 samples/s, and converted to digital data by a 12-bit analog-to-digital converter board. The acquisition software allowed the real-time display of the 15 bipolar surface EMG signals.



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  		Fig. 1. A: fixation of the hand to the brace for force measurement. Cuff for blocking blood flow is also shown. B: linear electrode array used in this study to record surface EMG signals. Array is made of 16 point electrodes located along a line at the fixed distance of 2.5 mm between each other. From the 16 electrodes, 15 bipolar recordings are obtained from the differences between signals detected by consecutive electrodes. C: schematic sequence of the contractions in the experimental protocol. Five contractions, C1-C5, are with surface EMG feedback on single motor unit. C3 and C4 are in ischemic conditions. C3 begins after 5 min of ischemia, C4 after 13 min of ischemia.

 
To obtain an optimal electrode placement, EMG signals were recorded in a few test contractions during which the electrode array was moved over the skin to detect the location of the main innervation zone(s) and tendon regions, as described previously (24). The array was then located between the innervation zone and the distal tendon (28), following the direction of the muscle fibers. The orientation of the array was selected on the basis of visual signal analysis, choosing the angle of inclination that led to the most similar potentials traveling along the array from the innervation zone to the distal tendon. Because the semi-fiber length was shorter than the length of the array, some of the electrodes covered the innervation zone(s) and the proximal semi-fiber. The region of the skin where the array was located was slightly abraded with abrasive paste (Meditec-Every, Parma, Italy). The array was fixed to the skin surface by adhesive tape, and a reference electrode was placed at the wrist.

General procedures.   The hand of the subject was fixed in a brace (Fig. 1A). The first phalanx of the thumb touched a force sensor (load cell 8523–50N, Burster, Gernsbach, Germany). The force signal was amplified (force amplifier, MISO-II, LISiN) and recorded at a sampling frequency of 2,048 Hz.

The subject performed three maximal voluntary contractions (MVCs) of 3–4 s each, separated by 2-min rest (Fig. 1C). The maximum of the three force measures was considered the reference MVC. Five minutes of rest followed the last maximum force contraction. The surface electrode array was then located as described above. In a training phase, the multichannel surface EMG signals were real-time displayed on a computer screen, and the subject was instructed to vary the abduction force to isolate the electrical activity of a single motor unit from the surface EMG traces (Fig. 2). Once a motor unit was identified (target motor unit), the subject trained the modulation of its discharge rate. Repositioning of the array was necessary in a few cases when the subject could not identify a clear single motor unit with the initial electrode location. The training phase lasted ~20 min. A thermometer was attached to the skin surface next to the array to monitor skin temperature.



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  		Fig. 2. Portions (500 ms) of multichannel surface EMG signals recorded during a contraction with feedback on the target motor unit. Bipolar recordings are shown, as they were provided as feedback to the subject. {bullet}, Occurrences of action potentials of the target motor unit. Action potentials are recorded by the 15 bipolar systems of the array. Distance between 2 consecutive bipolar recordings over the muscle is 2.5 mm (interelectrode distance of the array). A: contraction with normal blood flow (C2 in Fig. 1C). B: contraction during ischemia applied for 13 min (C4 in Fig. 1C). Note the possibility of isolating single motor unit activities in both conditions. Potentials originate at the innervation zone and propagate toward the tendons. The 2 vertical arrows indicate the directions of propagation. Propagation in the distal direction is from the innervation zone to the tendon, whereas in the proximal direction, only a part of the semi-fiber length is covered by the array. Velocity of propagation (conduction velocity) is estimated from the delay between potentials detected at adjacent recording locations (5). IPI, interpulse interval; IZ, innervation zone.

 
A total of five 3-min-long contractions was performed by the subject after a 5-min rest after the training phase (Fig. 1C). In each contraction, the subject was asked to activate the target motor unit at the minimum stable discharge rate (~8 pps). The first two contractions (C1 and C2) were performed with intact blood flow. Five minutes of rest was given to the subject between these two contractions. After 5 min following the second contraction, a cuff was inflated around the distal half of the forearm at a pressure of ~180 mmHg (Fig. 1A). The blocking of blood flow was confirmed by the absence of a palpable peripheral pulse. After 5 min of blood occlusion, the subject performed two contractions (C3 and C4) identical to the first two and separated by 5-min rest. Immediately after the fourth contraction, the cuff was released and, 5 min later, the last contraction (C5) was performed. In all contractions the subject was asked to activate the same target motor unit with the surface EMG feedback.

Signal analysis.   The recorded signals were offline decomposed into the constituent motor unit action potentials by a surface EMG decomposition algorithm previously described (12). Instantaneous discharge rate was computed as the inverse of the time interval between subsequent detected discharges of the target motor unit.

Conduction velocity was computed from each action potential of the target motor unit with a multichannel maximum likelihood estimation method (5). The method estimates the delay that best aligns the set of propagating signals, according to a mean square error measure of shape similarity derived in the frequency domain. The analysis in the frequency domain avoids limitations in the resolution with which the delay is estimated (25). Double differential signals were obtained by subtraction of consecutive bipolar recordings and were used for estimating conduction velocity (7). The signals used for the estimation were the same for the five contractions of the same subject and were selected among the channels distal to the innervation zone, with the condition of minor shape changes during propagation (7).

Mean power spectral frequency, peak-to-peak amplitude, and duration [area divided by the peak-to-peak amplitude (31)] were also computed from each detected action potential of the target motor unit. Mean power spectral frequency was computed from the periodogram spectral estimation with zero padding to 2,048 samples (frequency resolution of 1 Hz).

Conduction velocity, mean power spectral frequency, and duration of the action potentials of the target motor unit exhibited a linear trend over the 3 min and were fitted by a regression line. The intercept of the regression line was assumed as the initial value of the variable, the slope indicated its rate of change over time. The percent change of conduction velocity, mean power spectral frequency, and duration was defined as the difference between final (at the end of the contraction) and initial value of the regression line, divided by the initial value and expressed as a percentage.

Global muscle activity was assessed by computing the average rectified value from the central surface EMG signal among those used for conduction velocity estimation. The signal was divided in consecutive, nonoverlapping portions of 1 s, from which the average rectified value was computed. Its mean value over the 180 signal portions in each contraction was assumed as representative of the intensity of muscle activity during the contraction.

Statistical analysis.   Data are reported as means ± SE. One- and two-way repeated-measures ANOVA was used to analyze the data. The post hoc Student-Newman-Keuls (SNK) test for multiple comparisons was applied when necessary. Statistical significance was set to P < 0.05.


   RESULTS
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 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
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 REFERENCES
 
The activation of the same motor unit in the five contractions was verified a posteriori by comparing the shape and amplitude of the average template of the detected multichannel action potentials. All subjects were able to activate the same target motor unit in the five contractions, as representatively shown in Fig. 3.



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  		Fig. 3. Signals detected in the 5 contractions (3rd and 4th are in ischemic conditions). Signals are shown as double differential derivations (i.e., as the subtraction of consecutive bipolar signals), as they were used for conduction velocity estimation. Top: 500-ms signal portions in the 5 contractions. Spikes (4 for each signal portion in this case) correspond to the activity of the target motor unit that was controlled by the subject. Bottom: action potentials belonging to the target motor unit (MUAP), as identified by offline surface EMG signal decomposition, are shown superimposed to each other. Note that the potentials propagate in 2 directions from the innervation zone. Channels used in this case for conduction velocity estimation are indicated.

 
Skin temperature tended to decrease in the ischemic condition, but its variation was in all cases <2°C during the whole experimental session.

Force, surface EMG amplitude, and discharge rate.   Exerted force, surface EMG average rectified value, average discharge rate, and interpulse interval variability of the target motor unit were not different among the five contractions (Table 1; 1-way ANOVA).


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  		Table 1. Exerted force and properties of the discharge pattern and action potentials of the target motor unit in the 5 contractions

 
Properties of the target motor unit action potential.   The number of double differential signals used for conduction velocity estimation, selected according to the criterion introduced above, was 4.9 ± 0.3 (average over the 5 contractions). The standard deviation of conduction velocity estimation with respect to the regression line was 0.14 ± 0.05 m/s (average over the 5 contractions).

Initial conduction velocity, mean power spectral frequency, potential duration, and peak-to-peak amplitude were not different among the five contractions (Table 1; 1-way ANOVA). The percent change in conduction velocity, mean power spectral frequency, and potential duration in the 3 min were not significantly different from zero for all contractions except the fourth one (C4; Fig. 1C). Thus the percent change of conduction velocity, mean power spectral frequency, and potential duration depended on the contraction (Table 1 and Fig. 4; 1-way ANOVA: F > 6.9, P < 0.001). The SNK test revealed that the fourth contraction resulted in a larger decrease in conduction velocity and mean power spectral frequency and an increase in potential duration, with respect to all other contractions (Table 1; P < 0.01). The percent changes in conduction velocity, mean power spectral frequency, and potential duration were not significantly different in absolute value (2-way ANOVA with factors the contraction and the variable). Moreover, there was a significant correlation between the percent change of conduction velocity and mean power spectral frequency (R = 0.79, P < 0.001) and that of conduction velocity and potential duration (R = –0.74, P < 0.001).



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  		Fig. 4. Conduction velocity (CV), mean power spectral frequency (MNF), and instantaneous discharge rate (IDR) computed for each detected action potential of the target motor unit of 1 subject in the 5 3-min-long contractions. The 3rd and 4th contractions are in ischemic conditions. Note the large decrease of conduction velocity and mean power spectral frequency with sustained activation observed only after 13 min of ischemia (contraction C4).

 

   DISCUSSION
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Low-threshold motor units of the abductor pollicis brevis were activated with surface EMG visual feedback in conditions of normal blood flow and during ischemia (up to 16 min). The subjects could activate the target motor unit and recall it during ischemia. The interpulse interval variability of the target motor unit was not altered by ischemia. Moreover, conduction velocity was not affected by ischemia per se, at least for ischemic periods up to 13 min. The rate of decline of conduction velocity due to sustained activation was significantly affected by ischemia only after 13 min in ischemic conditions.

Control of single motor units by surface EMG visual feedback.   Intramuscular recordings have been used to provide feedback for controlling single motor units for more than 40 years (2, 15). Surface recordings are less selective than intramuscular ones; thus discrimination of single motor units is usually not possible. Nevertheless, we recently showed that multichannel surface EMG signals provide sufficient feedback for controlling single motor units (7). This result was confirmed in the two preischemic contractions of this study. Surface EMG feedback has advantages over intramuscular recordings, because it is possible to estimate motor unit conduction velocity for each potential generated by the target motor unit. In this study we provided surface EMG feedback to control motor units in ischemic conditions to verify if the ability to control a motor unit with feedback was altered by changes in afferent inputs.

Simard et al. (38) observed that it was very difficult to maintain and recall motor unit activity with feedback during ischemia (up to 10 min). They explained this observation by noting that ischemia suppresses the innate proprioceptive feedback mechanism. However, with complete absence of muscle afferent feedback, subjects can voluntarily recruit motor neurons, grade their discharge rate, and sustain a constant level of activity (11, 23). Thus the otherwise-intact nervous system can perform some simple motor tasks (such as the activation of a single motor unit) with no proprioceptive input other than the knowledge of the motor commands (11).

The results of this study are in agreement with these observations and indicate that altered afferent feedback due to ischemia does not preclude the control of single motor units when visual feedback on their action potentials is provided. Because the selectivity of EMG recordings depended on factors different for each subject, such as the thickness of the subcutaneous layer, the force at which the target motor unit was identified by the nine subjects varied in a rather large range with respect to the mean value (Table 1). However, because the same motor unit was tracked by the subjects in the five conditions analyzed, this variability was not an issue for the conclusions presented.

The beginning of the first contraction and the end of the last contraction with feedback from the surface EMG were separated by 40 min (Fig. 1C). The subjects could recall the same motor unit throughout this time period with rest intervals up to 10 min (between contractions C2 and C3) and with ischemia during 16 of 40 min. The inherent variability of the interpulse interval was not altered by ischemia (Table 1); thus ischemia did not affect the stability of the discharge rate. The ability to activate and recall the motor unit was overall unaltered by ischemia.

Effect of ischemia on single motor unit conduction velocity.   Ischemia by itself did not alter conduction velocity if the motor unit was not activated. The initial value of conduction velocity in the five contractions was indeed the same (Table 1). Because temperature influences conduction velocity (14), the finding of no change in initial values of conduction velocity in the five contractions indicates that the change in intramuscular temperature due to ischemia was rather small. The maximum skin temperature variation over the entire duration of the experiment was <2°C in the worst case, and the intramuscular temperature (not measured) probably varied much less. Merletti et al. (26) reported a change in intramuscular temperature due to prolonged ischemia of <1°C in the first dorsal interosseous muscle.

During sustained activation, conduction velocity, mean power spectral frequency, and action potential duration did not significantly change, except for the fourth contraction (C4, Fig. 1C). The generation of an action potential is associated with an outward flux of K+, which thus determines a net loss of K+ from the cell (9). The increase in interstitial potassium concentration reduces the resting membrane potential and results in a reduced facilitation of propagation of the action potential (19). The loss of K+ is counteracted by the Na+-K+ pump. However, even in conditions of intact blood flow, the Na+-K+ pump does not keep pace with the K+ efflux (39), and the conduction velocity of single motor units decreases even during activation at the minimum discharge rate (7).

The modification of interstitial K+ concentration is due to a number of phenomena. The delayed rectifier K+ channels open during the repolarization phase of the action potential, with an associated K+ efflux. In addition, ATP- and Ca+-sensitive K+ channels may be also involved in K+ efflux from the cell (18, 34). These mechanisms and the activity of the Na+-K+ pump may be altered by ischemia, with an effect on the resting membrane potential and propagation velocity of the action potential. However, after 5 min of ischemia (contraction C3, Fig. 1C) there were no changes in the initial value of conduction velocity or in its variations over time with sustained activation (Table 1). Thus a short ischemic period did not significantly alter membrane properties of the muscle fibers. In previous studies, at medium-high contraction levels, similar periods of ischemia determined a clear decrease of global conduction velocity or mean power spectral frequency in the surface EMG signal (e.g., Refs. 26, 30). However, this was due to the simultaneous activation of many motor units. In the present study, the contractions involved few low-threshold motor units (with usually only 1 visible in the surface recordings); thus we could exclude masking effects due to the activation of a large number of motor units.

Conduction velocity was not altered even after 13 min in ischemic conditions (beginning of contraction C4; Table 1). Even in quiescent muscle fibers, Na+-K+ pumping is necessary to compensate for the inward flux of Na+ and associated loss of K+. This basic function was thus probably unaltered with ischemia. However, the relative change in conduction velocity with sustained activation during C4 was almost 15 times faster than that observed by Farina et al. (7) in normal blood supply conditions.

The significant change in the trend of conduction velocity with sustained activation in contraction C4 with respect to C3 may have been due to the activation of more motor units after 13 min than after 5 min of ischemia, due to modifications in the afferent inputs. If more motor units were active, the activation-induced accumulation of interstitial potassium would be faster. This possibility cannot be completely ruled out. However, additional motor units were not observed in the surface EMG decomposition, and the average rectified value of the EMG signal was not different in the five contractions (Table 1). This indicates that motor units with thresholds higher than that of the target unit were probably not recruited with ischemia. Most likely, altered mechanisms at the level of the single fiber membrane were thus responsible for the observed results. The alteration of these mechanisms should be strictly related to the activation of the target motor unit, that is to the propagation of the action potential along the fiber membrane, because, without activation, no effect of ischemia on conduction velocity was observed (initial values of conduction velocity in C3 and C4; Table 1).

Occlusion of blood flow precludes removal of the interstitial potassium, which thus accumulates at a faster rate than in conditions of normal circulation. Blood flow has indeed a main role in the maintenance of maximal force (33). In addition to this phenomenon, changes in the mechanisms of regulation of ion concentration across the membrane may have occurred. With the generation of the action potential, the Na+-K+ pumping should increase with respect to the resting conditions to counteract the increased outward flux of potassium associated with the passage of the action potential (16). The mechanisms responsible for the regulation of potassium concentration in the extracellular environment may have been altered by ischemia with an activation-induced rapid modification of the fiber membrane properties (Fig. 4 and Table 1). A decreased efficiency of the Na+-K+ pump or an increase in the outward efflux of K+ associated with the action potential are potential reasons for the observed conduction velocity changes. The delayed effect of ischemia on the modifications of membrane muscle fiber properties was probably due to the time needed to deplete the supply of oxygen in the abductor pollicis brevis.

The significant effect of prolonged ischemia on the rate of decline in conduction velocity underlines that ischemia may be one of the main factors altering muscle fiber membrane properties during sustained contractions at high force levels when the intramuscular pressure becomes larger than the systolic pressure. In these conditions, oxygen depletion is probably much faster than in the present experiment due to the larger number of active fibers.

Changes in surface action potential properties with ischemia.   The main change observed in the surface action potentials with sustained activation in contraction C4 was a decrease in conduction velocity. A decrease in conduction velocity determines the same relative increase in potential duration and decrease in mean power spectral frequency (21, 27). This was confirmed by the correlation between changes in conduction velocity, mean power spectral frequency, and duration found in this study at the level of single motor units. Because the relative changes in conduction velocity, mean power spectral frequency, and duration were not significantly different, conduction velocity was the main factor affecting EMG power spectrum and action potential duration. Moreover, peak-to-peak amplitude of the surface potentials did not vary with ischemia. Thus modifications in the shape of the intracellular action potential did not have a major role in the properties of the surface-detected potentials. These results confirm that a change in conduction velocity is the main membrane phenomenon responsible for the observed modifications in surface EMG spectral variables during sustained contractions (27).

In conclusion, this study analyzed low-threshold motor units of the abductor pollicis brevis muscle. The main conclusions are 1) single motor units can be identified by surface EMG visual feedback in ischemic conditions, 2) without activation, motor unit conduction velocity is not affected by ischemia per se (for up to 13 min), and 3) the decrease in conduction velocity with sustained activation is significantly enhanced by prolonged ischemia with respect to the condition of normal blood circulation.


   GRANTS
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 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 GRANTS
ACKNOWLEDGMENTS
 REFERENCES
 
This work was partially supported by the European Shared Cost Project "Neuromuscular Assessment in the Elderly Worker" (NEW) (QLRT-2000–00139).


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
REFERENCES
 
The authors are sincerely grateful to Kevin G. Keenan of the Department of Integrative Physiology, University of Colorado, for the careful review of the first version of the manuscript.


   FOOTNOTES
 

Address for reprint requests and other correspondence: D. Farina, Center for Sensory-Motor Interaction (SMI), Dept. of Health Science and Technology, Aalborg Univ., Fredrik Bajers Vej 7 D-3, DK-9220 Aalborg, Denmark (E-mail: df{at}hst.aau.dk)

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.


   REFERENCES
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 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 

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