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1 Division of Sports and Work Physiology, Hannover Medical School, Carl-Neuberg Strasse 1, D-30625, Hanover, Germany
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(Received 31 October 2006;
accepted after revision 10 April 2007; first published online 13 April 2007)
Corresponding author V. Shushakov: Hannover Medical School, Carl-Neuberg-Strasse 1, D-30625, Hanover, Germany. Email: chouchakov.vladimir{at}mh-hannover.de
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Introduction |
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To assess changes in muscle membrane excitability, the evoked compound muscle action potential (M-wave) is used most often. In vitro it has been shown that elevated [K+]o causes a reduction of the M-wave amplitude or area parallel to reduction in force (Overgaard et al. 1999; Pedersen et al. 2003). Besides the amplitude, the propagation velocity of the muscle action potential also became slower during incubation at high [K+]o (Juel, 1988; Kossler et al. 1989). Similar effects were found in vitro for repeated electrical stimulation, which induced a significant decrease in the M-wave area and a decline in muscle force (Harrison & Flatman, 1999; Clausen et al. 2004).
However, the significance of the extracellular potassium elevation, caused by muscle activity, in fatigue is not unambiguous. First, it has been shown that an increase in [K+]o to 9 mM or less may potentiate force development (Holmberg & Waldeck, 1980; Renaud & Light, 1992). Second, a decrease of muscle excitability is not an inevitable consequence of muscle activity. In vitro and in vivo experiments have demonstrated an increase of M-wave in response to exercise (Hicks & McComas, 1989; Cupido et al. 1996), even when [K+]o increased (West et al. 1996). It has been suggested that this effect is caused by the activation of the Na+–K+-ATPase. In vitro studies have shown that activation of the Na+–K+-ATPase with salbutamol can restore the M-wave area simultaneously with the tetanic force in rat soleus muscle depressed by high [K+]o and low [Na+]o (Overgaard et al. 1999). Third, the effect of elevated [K+]o on the M-wave area is highly temperature dependent (Pedersen et al. 2003).
Therefore, the role of exercise-induced potassium shifts in muscle excitability and fatigue should be tested under conditions of voluntary muscle activity. Surprisingly, there are only a few studies in which venous potassium and M-wave have been measured simultaneously during voluntary exercise (West et al. 1996; Unsworth et al. 1998; Jammes et al. 2005). In these studies, no relationship was found between venous potassium and M-wave parameters. This discrepancy with in vitro results may be attributed to the combined action of several effects, such as ion shifts and changes of Na+–K+-ATPase activity and temperature on the muscle excitability.
Since changes in sarcolemmal excitability influence the amplitude and propagation velocity of the muscle action potential (AP), they should influence the amplitude and spectral characteristics of the myoelectrical signal during voluntary contraction (EMG). It has been claimed that the reduction of the average propagation velocity of muscle AP is the major factor causing the shifts of the EMG spectrum towards lower values during sustained contraction (Lindstrom et al. 1970, 1977; Stulen & De Luca, 1982; Hagg, 1992). This effect has been proposed as an indication of localized muscle fatigue (Lindstrom et al. 1977). However, there are no data showing that potassium shifts impair evoked or voluntary muscle electrical activity during voluntary exercise.
The purpose of the present study was to evaluate the relationship between extracellular potassium and myoelectrical activity during voluntary exercise. We hypothesized that, similar to in vitro data, an increase in extracellular potassium owing to voluntary activity depolarizes the muscle membrane and thereby may decrease its excitability, leading to decreases in the amplitude and the propagation velocity of muscle action potentials. Therefore, we investigated the relationship between [K+]o and variables of evoked and voluntary EMG signals. Since reduced sarcolemmal excitability is assumed to be a cause of fatigue, we compared the effects in the EMG with changes in muscle performance. The experiments were performed on a small muscle group in humans. Studies on a small muscle group have the advantage that most changes in electrolytes and the acid–base state are localized within the active muscles (Maassen, 1996; Pedersen et al. 1999). Since the ion concentrations depend on muscle blood flow, which is different between dynamic and static exercise, both types of exercise were performed. The degree of [K+]o increase was varied through changes of the exercise intensity. In order to distinguish between short-term potassium shifts and comparatively slower changes of other variables (e.g. temperature, blood flow and pH), the exercise intensity was varied randomly.
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Methods |
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Eighteen healthy male subjects (age 29.1 ± 6.5 years, height 184.2 ± 5.8 cm and weight 80.3 ± 3.7 kg) volunteered for the study, which consisted of two parts with different protocols. Prior to any testing, the subjects were informed of the risks and discomforts of the experiment and gave their written consent. The study was performed according to the Declaration of Helsinki. The procedures were approved by the ethics committee at Hanover Medical School.
Exercise protocol
Ten subjects participated in the experiment with the exercise protocol P1, and nine subjects participated in protocol P2 (one individual participated in both experiments). Figure 1 shows the experimental set-up. In both experiments the subjects performed handgrip exercises with a hand-ergometer. Sitting subjects had to lift a basket (weight 1.2 kg) hanging over a pulley with different weights using exclusively the flexor muscles of the forearm. The arm was in a horizontal position with support under the elbow and hand. The elbow angle was kept at 170 deg to restrict muscle activity in upper arm and shoulder regions.
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The P2 protocol included a 15 min warm-up phase, a 4 min resting phase, and the test phase consisting of 12 exercise periods [6 dynamic (DE) and 6 static (SE)] of 1 min separated by 4 min of passive rest (Fig. 2A). Before and after the warm-up phase, the subjects had to lift the basket with the weight of 30 kg as fast as possible to obtain the maximal EMG amplitude for EMG normalization. During the warm-up phase, the subjects lifted the weight of 7.5 kg dynamically with a contraction frequency of 0.4 Hz, which was set by a PC-based acoustic generator.
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Blood sampling
A cubital vein was catheterized percutaneously with a Teflon catheter (Introcan 18 gauge, B. Braun Melsungen AG, Melsungen, Germany). Patency of the catheter was maintained with isotonic saline (0.9% NaCl, B. Braun Melsungen AG). The blood sampling took place before the exercise, after the warm-up phase, close to the beginning and at the end of each exercise bout. Blood samples at the end of the exercise bouts were taken under conditions of restricted blood flow. After 55 s of exercise, the blood flow in the exercising arm was occluded for 15–20 s by inflating a cuff, placed on the upper arm, to a pressure of 240 mmHg. The occlusion should prevent the blood in the muscle from admixture with fresh blood as well as from washing out. Control experiments showed that this procedure does not alter the plasma [K+], [Na+] and pH, or M-wave variables under resting conditions. Blood sampling was completed mostly during the exercise and the first 5 s after the exercise. For eight blood samples the time of sampling was too long, so they were excluded from the final analysis. Each blood sample (approximately 4.0 ml) was collected in a 5 ml plastic syringe (Luer, B. Braun Melsungen AG), prepared with 10 µl sodium heparin (Liquemin N 2500, Hoffmann La Roche, Grenzbach-Wyhlen, Germany).
Analysis of plasma ion concentrations
About 20 µl of blood was injected into a blood gas and electrolyte analyser (ABL 505, Radiometer, Copenhagen, Denmark) to determine plasma [K+] ([K+]v), [Na+] (values given in mmol l–1) and pH. The ion concentrations were measured with ion-selective electrodes. A lactate analyser (Biosen 5130, EKF, Barleben, Germany) was used for the polarographic measurement of blood lactate concentration ([La–]) (values are given in mmol l–1).
Stimulating and recording
The M-wave recordings took place before the exercise (control), after the warm-up phase, close to the beginning of each exercise bout and immediately after each exercise bout. Three M-waves were recorded at each measurement point with a rate of one stimulus per second. The duration of the M-wave recordings was 4–5 s. To stimulate the muscle, a metal electrode of 1 cm diameter was applied on the main motor point of the m. flexor digitorum superficialis while the metal reference electrode (12.5 cm2) was attached to the opposite foot. Rectangular current pulses were delivered from a constant current unit (CCU1), connected via a stimulus isolation unit (SIU5) to the high-voltage stimulator (S48; all devices from Grass Instrument Division of Astro-Medical, Inc., West Warwick, RI, USA). The stimuli were of supramaximal amplitude and duration (1.1–1.3 ms). Both stimulating electrodes were coated with conducting gel (Spectra 360, Parker Laboratories, Inc., Fairfield, NJ, USA).
Electromyogram and M-waves were recorded in a bipolar configuration in two positions using six disposable silver–silver chloride monitoring electrodes (ClearTrace 1700, ConMed Corporation, Utica, NY, USA). The recording electrodes were placed between the stimulating electrode and the wrist, parallel to the muscle fibres (Lieber et al. 1992), with an interelectrode distance of about 20 mm. One group of recording electrodes was placed close to the stimulating electrode and the second group was placed more distally.
The EMG signals were amplified and stored using an EMG system (BIOPAC Systems, Inc., Santa Barbara, CA, USA) connected to an IBM-PC-compatible computer. The EMG signals were amplified 500 times and sampled at 1000 Hz; the M-waves were sampled at 6878 Hz. The M-wave recordings were synchronized with the stimulation.
Electromyogram analysis
Epochs of EMG recordings from 4 to 14 s and from 45 to 55 s of each exercise bout were analysed. The root-mean-square amplitude of the EMG signal (RMS) and the median frequency of power spectrum (MFEMG) were calculated for these epochs. The integrated EMG (IEMG) was measured over the entire exercise bout. For the dynamic exercise, the durations of EMG bursts were measured. Before the processing, the raw EMG was filtered from 10 to 500 Hz. The power density spectrum of the EMG was obtained after Hamming windowing, using the fast Fourier transform (FFT). The RMS and MFEMG were computed from the raw EMG off-line, using AcqKnowledge data analysis software (BIOPAC Systems, Inc.). To normalize the IEMG, the ratio between each IEMG and the maximal RMS amplitude obtained for this subject over the entire test was calculated. The RMS and MFEMG measured at the end of each exercise bout were normalized to values at the beginning of the bout. Since there was no significant difference between all three M-waves from the same recording session, they were averaged. The M-waves were analysed for the area of the negative phase and for the duration from stimulus artifact to the positive peak (Tmax) (Fig. 2B), using custom-made software. The area of the negative phase of M-wave was chosen for computer analysis, because the area under the positive phase of the M-wave is sensitive to baseline shifts and to moving artifacts, especially when recording close to the tendon. Manual measurements of the M-wave area showed a high positive correlation between changes of negative and positive area of M-waves (r
= 0.93, P < 0.001). For the same reasons, the duration of the M-wave was measured only to the positive peak. Additionally, changes in the propagation velocity of muscle AP were estimated by changes of the time difference between negative M-wave peaks at distal and proximal recording positions (
T). For the weights of 25 and 30 kg, the changes of the median frequency of the M-wave power spectrum (MFMW) were calculated. The M-wave variables were normalized either to control values (the values before the first exercise activity) or to pre-exercise values (the values before the exercise bouts). Recording conditions were monitored by calibration with constant current pulses during the entire experiment.
Mechanical parameters
Displacement of the basket was registered with a linear variable differential transformer (LVDT Type 1000 DC-D, Schaevitz Eng., Pennsauken, NJ, USA), digitalized at 1000 Hz and stored. The maximal displacement was 4 cm. Changes in the displacement velocity during dynamic exercise reflected changes of muscle power. During static exercise bouts, lowering of the basket indicated the development of fatigue. The contraction velocity and displacement at the end of exercise bouts were normalized to the values at the beginning of the corresponding exercise bouts.
Statistical analysis
Analyses were made using SPSS for Windows (version 12.0, SPSS, Chicago, IL, USA). Significant differences between values were tested either by Student's t test for paired values or by analysis of variance for repeated measurements (ANOVA) followed by Bonferroni's procedure for multiple comparisons (comparison between the control values and the values before the exercise bouts in the time course). The critical value for statistical significance was set at P < 0.05. Pearson correlation coefficients were used to measure the associations between variables of interest in the manner of Bland & Altman (1995). All values in the text are presented as means ± S.D. unless stated otherwise.
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Results |
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The P1 experiments were performed without a warm-up procedure. During the first 20 min of these experiments we observed marked changes of pre-exercise values of [K+]v and of the M-wave area. During this time, the pre-exercise [K+]v continuously declined from the control value of 4.1 ± 0.3 to 3.8 ± 0.3 mmol l–1 (P < 0.001) before the fourth exercise bout and remained at this level thereafter. Simultaneously with the decrease of [K+]v, there was an increase of the pre-exercise M-wave area to 117.5 ± 15.4% of the control value (P < 0.005). The detailed time courses of [K+]v and the M-wave area after exercise were recorded during the recovery phase, after the last exercise bout (Fig. 3A and B). The [K+]v declined during the first 2 min of recovery to 3.8 ± 0.2 mmol l–1 and remained at this level for the following 3 min. The M-wave area reached 118.3 ± 21% of the control value in the second minute of recovery and thereafter remained stable as well. In order to distinguish between the effects of the [K+]o shifts during the exercise bout and these prolonged effects, the P2 experiments were performed with a warm-up phase. The further description of the results and discussion will refer to the P2 experiments if not specified otherwise.
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Venous pH and [La–] changed during the warm-up phase as well. The pH decreased from the control value of 7.36 ± 0.01 to 7.31 ± 0.04 before the first exercise bout (P < 0.005). During this time, [La–] increased from 1.0 ± 0.3 to 2.5 ± 0.6 mmol l–1 (P < 0.01). Throughout the test phase, the pre-exercise pH value stabilized at a level of 7.29 ± 0.04 after the fourth exercise bout. The [La–] also stabilized after the fourth exercise bout, after rising to 3.5 ± 1.3 mmol l–1.
The [K+]v, [Na+]v, pH and exercise intensity
The pre- and postexercise values of [K+]v, [Na+]v and venous pH are shown in Table 1. The [K+]v rose during the exercise in accordance with the increase in workload in both dynamic and static bouts, though the increase was higher during the static exercise, reaching 6.1 ± 0.4 versus 5.2 ± 0.3 mmol l–1 at the maximal weight. Nevertheless, the [K+]v after the exercise with the maximal weight was not significantly different from the value after the bout with 25 kg. Venous sodium also increased in a weight-dependent manner after exercise bouts. Venous pH increased during the dynamic exercise bouts; during the static exercise, there was an increase of pH at weights lower than 20 kg and a decrease of pH at 25 and 30 kg.
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There were clear signs of fatigue during the exercise bouts. A reduction in the height of the basket from its initial level during the static exercise and a decrease in contraction velocity during the dynamic exercise indicated development of fatigue. These effects were more pronounced as the weight increased (Fig. 5). The decrease in contraction velocity correlated with the increase of the [K+]v (r = –0.76, P < 0.001).
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M-wave
During both the dynamic and static exercises, the increment of the weight was accompanied by a proportionally greater decrease in the M-wave area (Table 2). As shown in Fig. 7, the changes of the M-wave area during the exercise bouts correlated with the changes of the [K+]v in both exercise modes.
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T. After the exercise periods, both time parameters were slightly decreased (on average to 97.2 ± 3.8% for T and to 96.4 ± 5.2% for Tmax; P < 0.001), independent of the weight.
During the static exercise, changes of Tmax and T correlated with the weight increment (r
= 0.56 and r
= 0.52, respectively, P < 0.001). The Tmax decreased at weights less than 20 kg and increased at higher weights, compared with the pre-exercise value. The range of the Tmax changes was from –6.5 ± 7.2% at 5 kg to 3.9 ± 3.6% at 30 kg, and the range of the T was from –1.7 ± 6.1% at 5 kg to 1.6 ± 4.8% at 30 kg. Neither time parameter correlated with changes in venous pH.
Besides the measurement of Tmax and T, the effect of exercise on the muscle AP propagation velocity was tested by the calculation of MFMW for the weight steps of 25 and 30 kg. Significant changes of the MFMW were not found for either static or dynamic exercise. The MFMW was 65.0 ± 14.4 Hz after the dynamic exercise versus 62.6 ± 13.8 Hz before it, and the corresponding values were 59.7 ± 10.4 and 61.1 ± 12.9 Hz for the static exercise.
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Discussion |
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Potassium, Na+–K+-ATPase and M-wave
There exists considerable variation in observations concerning changes of the M-wave amplitude or area during muscle activity. A decrease of M-waves during sustained activity has been found in vivo (Stephens & Taylor, 1972; Milner-Brown & Miller, 1986; Bellemare & Garzaniti, 1988) and in vitro (Harrison & Flatman, 1999; Overgaard et al. 1999). Other studies have reported that the M-wave does not decrease during a 60 s maximal voluntary contraction (Bigland-Ritchie et al. 1983b; Thomas et al. 1989). An increase of the M-wave after electrical stimulation or voluntary exercise has also been observed (Hicks & McComas, 1989; Cupido et al. 1996; West et al. 1996). The most probable cause of these discrepancies may be an exercise-induced activation of the Na+–K+-ATPase, which could counteract the depolarizing effect of the extracellular potassium elevation. In our study, the simultaneously observed increase in the M-wave area and decrease in the [K+]v after the warm-up phase should result from an activation of the Na+–K+-ATPase (Hicks & McComas, 1989; Medbo & Sejersted, 1990). Nevertheless, after this initial course, the pre-exercise M-wave area and [K+]v became stable and showed no relationship either to experimental duration or to weight in the previous exercise bout.
Against this background, we found an intensity-dependent reduction in the M-wave area after 60 s of voluntary exercise, whereas the reduction of the M-wave area correlated with the elevation of [K+]v. At first sight, our results contradict those of West et al. (1996), who found a tendency for the M-wave area to be potentiated after 3 min exercise with 25–30% MVC, despite a significant rise of [K+]v. Nevertheless, this effect was observed by West and co-workers shortly after the beginning of exercise, when the effects of exercise-related activation of the Na+–K+-ATPase should still be developing.
Besides the hyperpolarizing effect of the Na+–K+-ATPase activation, the intracellular acidosis may also be able to protect the muscle excitability (Pedersen et al. 2004, 2005). Since the major changes in pH occurred during the warm-up phase, the influence of changes in muscle acidification would not have played an important role during the exercise bouts. A stable ratio of [K+]v to M-wave area over the time course of the experiment indicates that there were no additional effects that could influence the relationship between these variables.
Potassium and IEMG
Muscle electrical activity induces an increase in the extracellular potassium concentration in an intensity-dependent manner, since the rate of exercise-induced K+ efflux from the muscle fibre should be determined by the number of action potentials (Hallen et al. 1994; Vollestad et al. 1994). However, the relationship between extracellular potassium and exercise intensity can be very different depending on the site of the measurement of [K+] (in interstitium, in arterial blood or in venous blood), on the type of exercise (dynamic or static, performed using a small or a large muscle group) and on the duration of exercise (Tibes et al. 1976; Juel et al. 1990; Vollestad et al. 1994; Hallen, 1996; Green et al. 2000; Zoladz et al. 2002; Mohr et al. 2004).
In the present study, we found a linear dependency between the [K+]v and the IEMG during both static and dynamic exercises, which occurred despite the different causes of the IEMG changes. If this cause during the static exercise was the recruitment of additional motor units, as is indicated by the weight-proportional increase of RMS, then the increase of the IEMG during dynamic exercise depended not only on this effect, but also on the prolongation of periods of electrical activity during each contraction. The correlation between changes of the [K+]v and the IEMG in our experiment shows that the [K+]v increase during the activity of a small muscle group depends linearly on the total amount of the electrical activity of these muscles. It is noteworthy, though, that this relationship was observed after the warm-up period, when the pre-exercise values of the [K+]v and the M-wave area reached a steady state.
Relationship of changes in M-wave and EMG variables to muscle performance
In our study, an increase of the [K+]v was accompanied by a shift of the MFEMG towards lower frequencies, a reduction in the M-wave area and development of fatigue. The question that arises is whether the changes in the myoelectrical signal and the fatigue were due to an impaired excitability of muscle fibres. In vitro experiments have shown a very close correlation of changes of the M-wave area with the alterations of muscle force (Harrison & Flatman, 1999; Overgaard et al. 1999). It has been suggested that a cause for this relationship is a decrease of sarcolemmal excitability as a result of depolarization-induced slow inactivation of sodium channels (Ruff et al. 1988). Indeed, a depolarization of the resting membrane potential to a range between –60 and –55 mV might lead to a complete inactivation of sarcolemma (Yonemura, 1967; Juel, 1988; Hicks & McComas, 1989). The influence of the elevated [K+]o on the M-wave area can be realized through different mechanisms and stages: (1) the decrease of the potential difference across the sarcolemma, i.e. the depolarization per se; (2) the slow inactivation of the sodium channels due to this depolarization, leading to a decrease in the transmembrane current density; and (3) the decrease of the number of excitable muscle fibres due to this slow inactivation. There are a few reasons to consider the sarcolemmal depolarization per se rather than decreased excitability as the main cause of the M-wave area decrease in our study. First, the Na+–K+-ATPase activation during the warm-up phase should cause a significant hyperpolarization of the sarcolemma. The major part of the 20–25% increase in M-wave area after the warm-up phase should reflect corresponding hyperpolarization of the sarcolemma, since most Na+ channels are excitable at the resting potential (Ruff, 1999). Therefore, a stronger depolarization would be required to reach the inactivation threshold after the warming-up. Second, the development of slow inactivation of sodium channels may require several minutes (Almers et al. 1983). The duration of the exercise bouts in our experiments was only 1 min, so it is unlikely that this time was sufficient to develop a marked slow inactivation, especially with respect to the fact that the extracellular potassium increases gradually during activity. Third, the changes of time parameters of M-waves often indicated an acceleration of the AP propagation after the exercise.
It is noteworthy that in our study the changes in the M-wave time parameters during the exercise bouts were not related to MFEMG shifts. A shift of the EMG power spectrum towards lower frequencies has been proposed as an index of localized muscle fatigue (Lindstrom et al. 1977). It has been assumed that the alterations of the EMG spectrum that are usually observed during sustained muscle contraction are associated mostly with a slowing of the propagation velocity of muscle AP (Lindstrom et al. 1970; Eberstein & Beattie, 1985; Arendt-Nielsen & Mills, 1988). The possible causes of the propagation velocity slowing that have been discussed are the altered metabolic state in muscle (Mortimer et al. 1970; Kranz et al. 1983; De Luca, 1984; Masuda et al. 1999), more precisely, the decrease of muscle pH and particularly pHi (Juel, 1988; Brody et al. 1991), and the increase in the [K+]o (Juel, 1988; Kossler et al. 1989). In the present study, the negative effect of pH on the propagation velocity was minimized by the experimental design and therefore did not play the key role in the observed decrease of the MFEMG during the bouts. The main pH decrease occurred during the warm-up phase. Furthermore, it is known that during intermittent, high-intensity exercise the pHi, after an initial decrease, does not change further or even increase during 15 or 30 s exercise periods (Schneider et al. 1994; Bangsbo, 1994). This seems true also in our study, where increased venous pH after all periods of dynamic activity and after static exercise with 5, 10 or 15 kg weights appears to reflect this situation. Occasionally, the increase of venous pH appeared simultaneously with the decrease of the MFEMG.
Thus, changes in the AP propagation velocity were not the main cause of the MFEMG shifts. More probably, this cause could be changes in the recruitment of different types of motor units. A systematic decline in discharge rate during prolonged effort, the phenomenon named ‘muscle wisdom’ (Marsden et al. 1983), has been shown for muscles with a high proportion of fast-twitch motor units (Bigland-Ritchie et al. 1983a; Peters & Fuglevand, 1999) but not for predominantly slow muscle (Macefield et al. 2000). A decrease in the ratio between active fast-twitch and slow-twitch motor units will be reflected in a shift of the MFEMG towards lower frequencies.
Thus, despite the significant rise of the extracellular potassium and the M-wave decrease, a moderate reduction in the excitability can be assumed only after the maximal static exercise, because of the decreased AP propagation. It is even possible that under the conditions of this study an increase in [K+]o can play a beneficial role. As has been shown in frogs (Renaud & Light, 1992) and guinea-pigs (Holmberg & Waldeck, 1980), an increase in extracellular potassium below 9 mM potentiates twitch and submaximal tetanic force. In our study, the maximal increase in interstitial potassium should be in the same range, even if we take into account the possible gradients between interstitium and plasma amounting to 2–3 mmol l–1 (Hirche et al. 1980).
Conclusion
In conclusion, this study shows, for the first time, a relationship between the decrease in the M-wave area and the increase in plasma potassium during voluntary exercise. A significant, intensity-dependent reduction of the M-wave area was found after exercise, but the decrease in the M-wave area was not accompanied by a corresponding decrease in the propagation velocity and thus was probably not due to impaired excitability. Since the significant MFEMG decrease also showed little relationship to the M-wave time parameters, the alteration of the EMG spectrum and the decrease in muscle performance were probably caused mainly by central adaptation. Further investigation is needed to determine whether the effects of elevated extracellular potassium can play a role as a signal for the regulation of the motoneuronal activity. Furthermore, our results point out the practical aspect that, for the estimation of excitability, the measurement of the M-wave area should be enhanced with the measurement of the AP propagation velocity. The control of the propagation velocity is also important if the MFEMG decrease is used as an index for localized fatigue.
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