Slower conduction velocity and motor unit discharge frequency are associated with muscle fatigue during isometric exercise in type 1 diabetes mellitus.

Type 1 diabetes mellitus (T1DM) is associated with a peripheral neuropathy that reduces nerve conduction velocity. This may impair high motor-unit discharge frequencies (MUDF), decrease muscle activation, and curtail the ability to sustain repetitive contractile tasks. We examined (1) whether MUDF, the contractile properties of the knee extensors, and the conduction velocity of persons with T1DM differed from controls; (2) whether persons with T1DM can maintain adequate MUDF during a fatigue protocol; and (3) the relationship between these parameters and impaired glycemic control. We studied male and female subjects with T1DM and controls matched for age, height, weight, and gender. Single motor unit recordings were made from vastus lateralis during maximal and submaximal contractions and during a fatigue protocol. Glycemic control was assessed from blood glucose concentration and glycosylated hemoglobin (HbA1c). Control femoral conduction velocities were comparable to literature values and those of the T1DM subjects were slower. These values correlated with plasma glucose and HbA1c. T1DM subjects fatigued 45% sooner than controls, and time to fatigue and conduction velocity were correlated (r = 0.54, P < 0.05). Discharge frequencies tended to be slower during 50% maximal voluntary contractile force in the T1DM subjects at task failure. Persons with T1DM had slower conduction velocities and lower MUDF than their controls, which apparently leads to impaired activation of muscle and decreased endurance during isometric fatigue.

Adaptations in the activation of human skeletal muscle induced by short-term isometric resistance training.

This study employed longitudinal measures of evoked spinal reflex responses (Hoffman reflex, V wave) to investigate changes in the activation of muscle and to determine if there are "linked" neural adaptations in the motor pathway following isometric resistance training. Twenty healthy, sedentary males were randomly assigned to either the trained (n = 10) or control group (n = 10). The training protocol consisted of 12 sessions of isometric resistance training of the plantar flexor muscles over a 4-wk period. All subjects were tested prior to and after the 4-wk period. To estimate changes in spinal excitability, soleus Hoffman (H) reflex and M wave recruitment curves were produced at rest and during submaximal contractions. Recruitment curves were analyzed using the slope method (Hslp/Mslp). Modulation of efferent neural drive was assessed through evoked V wave responses (V/Mmax) at 50, 75, and 100% maximal voluntary contraction (MVC). After 4 weeks, MVC torque increased 20.0 +/- 13.9% (mean +/- SD) in the trained group. The increase in MVC was accompanied by significant increases in the rate of torque development (42.5 +/- 13.3%), the soleus surface electromyogram (60.7 +/- 30.8%), voluntary activation (2.8 +/- 0.1%), and the rate of activation (48.7 +/- 24.3%). Hslp/Mslp was not altered by training; however, V/Mmax increased 57.3 +/- 34.2% during MVC. These results suggest that increases in MVC observed in the first few days of isometric resistance training can be accounted for by an increase in the rate of activation at the onset of muscle contraction. Augmentation of muscle activation may be due to increased volitional drive from supraspinal centers.

Reflex gain of muscle spindle pathways during fatigue.

There are conflicting observations of the effects of fatigue on the sensitivity of large diameter Ia afferents. Our goal was to characterize any fatigue-related changes in the spinal reflex pathways during fatigue. Manipulation of the Ia afferent response by vibration and tendon tap, in which the motor neuron pool is modulated by both short- and long-loop activation from muscle spindles, were elicited before and after a fatigue task. The fatigue task consisted of intermittent submaximal and maximal voluntary contractions (MVCs). Percent voluntary activation fell from 98.75% MVC to 80.92% MVC following the fatigue task as measured by the twitch interpolation technique. Voluntary contractions of the same force profile as the force produced by 30 s of vibration were produced by having participants (n = 10) follow the trajectory on a computer monitor, before and after the fatigue task. Recruitment thresholds (RTs) of voluntarily activated units showed no change during fatigue; however, units activated via the reflex pathway were recruited approximately 30% sooner during fatigue (P < 0.05). The ratio of the electrical-to-mechanical response of the tendon tap increased significantly with fatigue. Our findings of decreased RTs in response to vibration and increased EMG activity during the tendon tap following the fatigue task indicate that Ia afferent input to the motoneuron pool was increased. The decrease in MVC force indicates that during this time the descending drive was compromised. These results provide evidence that the gain of the gamma loop is increased during fatigue, indicating possible peripheral neural compensation to the motor neuron pool in order to preserve force output.

Transcranial magnetic stimulation during resistance training of the tibialis anterior muscle.

During the first few weeks of resistance training, maximal voluntary contraction (MVC) force increases at a faster rate than can be accounted for by increases in protein synthesis. This early increase in MVC force has been attributed to neural mechanisms but the sources have not been identified. The purpose of this study was to measure changes in cortical excitability with transcranial magnetic stimulation during 4 weeks of resistance training of the tibialis anterior muscle. Ten individuals performed 6 sets of 10 MVCs 3 times per week for 4 weeks and ten participated as a control group. There were no changes in any parameters tested in the control group over the 4 weeks. In the training group, TA muscle strength increased significantly by 10% at week 2 and by 18% at week 4. As hypothesized, cortical excitability during resistance training also increased. The amplitude of the TA surface EMG motor evoked potential elicited by TMS during a low-level contraction increased by 32% after training with no change in the M-wave. These data indicate that there may be an increase in cortical excitability during the first few weeks of resistance training of the TA muscle.

Increased spinal excitability does not offset central activation failure.

We hypothesized that if reduced spinal excitability contributes to central activation failure, then a caffeine-induced increase in spinal excitability would enhance postfatigue maximal voluntary activation and maximal voluntary contraction (MVC). Ten male volunteer subjects attended two laboratory sessions separated by at least 1 week. Contractile and electrical properties were assessed before, and 1 h after oral administration of caffeine (6 mg/kg) or placebo (all-purpose flour), and again following a fatigue protocol. The slope of the H reflex recruitment curve, normalized to that of the M wave (H(slp)/M(slp)), was used to estimate spinal excitability. Maximal voluntary activation was assessed using maximal EMG (EMG(max)) and twitch interpolation. Postfatigue, MVC torque declined (P<0.05) to 75.2+/-12.7 and 70.2+/-9.3% of the prefatigue values in the placebo (PL) and caffeine (CF) trials, respectively, and remained depressed throughout the recovery period. This was accompanied by a decline in % activation (P<0.05) from 99.6+/-0.3% (PL) and 99.8+/-0.3% (CF) to 94.8+/-3.5% (PL) and 95.3+/-5.0% (CF), indicating the presence of central activation failure. Caffeine offset the decline in H(slp)/M(slp )observed in the placebo trial (P<0.05), but it did not prevent the decline in maximal voluntary activation or MVC torque. Furthermore, although the decline in spinal excitability was correlated to the decline in EMG(max) (r=0.55, P<0.05) it was not correlated with the decline in % activation or MVC torque. Thus a fatigue-induced decline in spinal excitability did not limit maximal activation.

Central excitability does not limit postfatigue voluntary activation of quadriceps femoris.

After fatigue, motor evoked potentials (MEP) elicited by transcranial magnetic stimulation and cervicomedullary evoked potentials elicited by stimulation of the corticospinal tract are depressed. These reductions in corticomotor excitability and corticospinal transmission are accompanied by voluntary activation failure, but this may not reflect a causal relationship. Our purpose was to determine whether a decline in central excitability contributes to central fatigue. We hypothesized that, if central excitability limits voluntary activation, then a caffeine-induced increase in central excitability should offset voluntary activation failure. In this repeated-measures study, eight men each attended two sessions. Baseline measures of knee extension torque, maximal voluntary activation, peripheral transmission, contractile properties, and central excitability were made before administration of caffeine (6 mg/kg) or placebo. The amplitude of vastus lateralis MEPs elicited during minimal muscle activation provided a measure of central excitability. After a 1-h rest, baseline measures were repeated before, during, and after a fatigue protocol that ended when maximal voluntary torque declined by 35% (Tlim). Increased prefatigue MEP amplitude (P=0.055) and cortically evoked twitch (P<0.05) in the caffeine trial indicate that the drug increased central excitability. In the caffeine trial, increased MEP amplitude was correlated with time to task failure (r=0.74, P<0.05). Caffeine potentiated the MEP early in the fatigue protocol (P<0.05) and offset the 40% decline in placebo MEP (P<0.05) at Tlim. However, this was not associated with enhanced maximal voluntary activation during fatigue or recovery, demonstrating that voluntary activation is not limited by central excitability.

Maximal motor unit firing rates during isometric resistance training in men.

This study measured changes in maximal voluntary contraction (MVC) force, percentage maximal activation, maximal surface EMG, M-wave amplitude and average motor unit firing rates during the initial 3 weeks of isometric resistance training of the quadriceps muscle. Ten men participated in a resistance training programme three times a week for 3 weeks and 10 men participated as a control group. In the training group, MVC increased by 35% (from 761 +/- 77 to 1031 +/- 78 N) by the end of the 3 weeks. There were no changes in mean motor unit firing rates during submaximal or maximal voluntary contractions of 50 (15.51 +/- 1.48 Hz), 75 (20.23 +/- 1.85 Hz) or 100% MVC (42.25 +/- 2.72 Hz) with isometric resistance training. There was also no change in maximal surface EMG relative to the M-wave amplitude. However, there was a small increase in maximal activation (from 95.7 +/- 1.83 to 98.44 +/- 0.66%) as measured by the twitch interpolation technique. There were no changes in any of the parameters measured in the control group. It is suggested that mechanisms other than increases in average motor unit firing rates contributed to the increase in maximal force output with resistance training. Such mechanisms may include a combination of increased motor unit recruitment, enhanced protein synthesis, and changes in motor unit synchronization and muscle activation patterns across the quadriceps synergy.

Caffeine increases time to fatigue by maintaining force and not by altering firing rates during submaximal isometric contractions.

Caffeine increases time to fatigue [limit of endurance (T(lim))] during submaximal isometric contractions without altering whole muscle activation or neuromuscular junction transmission. We used 10 male volunteers in a randomized, double-blind, repeated-measures experiment to examine single motor unit firing rates during intermittent submaximal contractions and to determine whether administering caffeine increased T(lim) by maintaining higher firing rates. On 2 separate days, subjects performed intermittent 50% maximal voluntary contractions of the quadriceps to T(lim), 1 h after ingesting a caffeine (6 mg/kg) or placebo capsule. Average motor unit firing rates recorded with tungsten microelectrodes were constant for the duration of contractions. Caffeine increased average T(lim) by 20.5 +/- 8.1% (P < 0.05) compared with placebo conditions. This increase was due to seven subjects, termed responders, who increased T(lim) significantly. Two other subjects showed no response, and a third had a shorter T(lim). Neither the increased T(lim) nor the responders' performance could be explained by alterations in firing rates or other neuromuscular variables. However, the amplitude of the evoked twitch and its maximal instantaneous rate of relaxation did not decline to the same degree in the caffeine trial of the responders; this resulted in values 20 and 30% higher at the time point matching the end of the placebo trial (P < 0.05). The amplitude of the evoked twitch and the maximal instantaneous rate of relaxation were linearly correlated (caffeine r = 0.72, placebo r = 0.80, both P < 0.001), suggesting that the increase in T(lim) may be partially explained by caffeine's effects on calcium reuptake and twitch force.

Caffeine: a valuable tool to study central fatigue in humans?

This review focuses on caffeine's effects on the central modulation of muscle activation in humans. The drug's effects on voluntary muscle activation, the Hoffman reflex, motor-evoked potentials, self-sustained firing, pain, and sensation are discussed, and the possibility that caffeine maybe useful in the study of central fatigue is explored.

Central fatigue and transcranial magnetic stimulation: effect of caffeine and the confound of peripheral transmission failure.

In this experiment, we attempt to replicate the fatigue-induced decline in voluntary surface electromyography (EMG) and motor evoked potentials (MEPs) observed in previous studies and determine: (1) if this decline can be attributed to central failure, and (2) whether this failure is offset by caffeine. Seven subjects each attended two sessions (caffeine and placebo). Central excitability was estimated using transcranial magnetic stimulation (TMS), and surface EMG and twitch interpolation were used to estimate voluntary activation before, during and after fatigue of the first dorsal interosseous (FDI). Mass action potentials (M waves) were evoked to assess peripheral transmission throughout the experiment. We observed an increase in post-activation potentiation of the motor evoked potential in the caffeine trial and a fatigue-induced decline in the MEP and maximal EMG in both the placebo and caffeine trials. However, there was also a fatigue-induced decline in peripheral transmission, and estimates of central failure were considerably reduced when normalized to the M wave. A review of central fatigue literature revealed many studies that attribute the decline in voluntary EMG or MEPs wholly to central failure and fail to consider peripheral transmission. Thus, we conclude by stressing the importance of reporting peripheral transmission when surface recordings are used to estimate central mechanisms.

Caffeine increases spinal excitability in humans.

The Hoffman reflex (H reflex) has long been established as a measure of spinal excitability. Caffeine is one of the most widely consumed drugs in the world. Because it is known to increase excitatory neurotransmission, we hypothesized that caffeine would increase spinal excitability and thus alter the H reflex by increasing its amplitude. Seven subjects each attended the laboratory on 2 days. Caffeine (6 mg/kg) was administered on one day and a placebo was administered on the other. The tibial nerve was stimulated at incremental intensities to create an H-reflex recruitment curve prior to capsule administration (pretest) and 1 h later (posttest) on each day. The slope of H-reflex recruitment curve normalized to that of the M wave (H(slp)/M(slp)) was compared (pretest to posttest). Caffeine increased spinal excitability 43 +/- 17% (P < 0.05). Thus, caffeine may be used to safely increase spinal excitability in electrophysiological studies of the human neuromuscular system. Our results also suggest that caffeine intake should be controlled when the H reflex is used in diagnostic and experimental situations.

Ia Afferent input alters the recruitment thresholds and firing rates of single human motor units.

Vibration of the patellar tendon recruits motor units in the knee extensors via excitation of muscle spindles and subsequent Ia afferent input to the alpha-motoneuron pool. Our first purpose was to determine if the recruitment threshold and firing rate of the same motor unit differed when recruited involuntarily via reflex or voluntarily via descending spinal pathways. Although Ia input is excitatory to the alpha-motoneuron pool, it has also been shown paradoxically to inhibit itself. Our second purpose was to determine if vibration of the patellar tendon during a voluntary knee extension causes a change in the firing rate of already recruited motor units. In the first protocol, 10 subjects voluntarily reproduced the same isometric force profile of the knee extensors that was elicited by vibration of the patellar tendon. Single motor unit recordings from the vastus lateralis (VL) were obtained with tungsten microelectrodes and unitary behaviour was examined during both reflex and voluntary knee extensions. Recordings from 135 single motor units showed that both recruitment thresholds and firing rates were lower during reflex contractions. In the second protocol, 7 subjects maintained a voluntary knee extension at 30 N for approximately 40-45 s. Three bursts of patellar tendon vibration were superimposed at regular intervals throughout the contraction and changes in the firing rate of already recruited motor units were examined. A total of 35 motor units were recorded and each burst of superimposed vibration caused a momentary reduction in the firing rates and recruitment of additional units. Our data provide evidence that Ia input modulates the recruitment thresholds and firing rates of motor units providing more flexibility within the neuromuscular system to grade force at low levels of force production.

Effect of caffeine on self-sustained firing in human motor units.

This study examined the effect of caffeine on self-sustained firing (SSF) of human motor units. At physiological doses, caffeine acts as a competitive antagonist to the inhibitory effects of adenosine. This antagonism has many possible effects on the central nervous system. One of these effects is to increase the release of the excitatory neurotransmitters serotonin and noradrenaline. In addition, caffeine increases serotonin concentration in brainstem regions that have excitatory projections to spinal motor neurons. Since plateau potentials, which are responsible for SSF, are facilitated by these neurotransmitters, we hypothesized that caffeine would increase the frequency at which SSF occurs. A double-blind, repeated-measures design using either drug (6 mg kg(-1) caffeine) or placebo (flour) was carried out on seven male subjects who reported ingesting less than 200 mg week(-1) caffeine. We investigated the occurrence of SSF in tibialis anterior motor units (214 trials) and found a significant (P < 0.05) increase in the occurrence of SSF in the caffeine trial (87.0 +/- 5.8 %) compared to the placebo (64.6 +/- 9.7 %). These data further verify the presence of SSF in the tibialis anterior motor units of young men and provide indirect evidence of the facilitation of plateau potentials by monoamines in the human neuromuscular system.

Caffeine increases endurance and attenuates force sensation during submaximal isometric contractions.

Caffeine has known ergogenic effects, some of which have been observed during submaximal isometric contractions. We used 15 subjects in a randomized, double-blind, repeated-measures experiment to determine caffeine's ergogenic effects on neuromuscular variables that would contribute to increased endurance capacity. Subjects performed repeated submaximal (50% maximal voluntary contraction) isometric contractions of the right quadriceps to the limit of endurance (T(lim)) 1 h after oral caffeine administration (6 mg/kg). Time to reach T(lim) increased by 17 +/- 5.25% (P < 0.02) after caffeine administration compared with the placebo trial. The changes in contractile properties, motor unit activation, and M-wave amplitude that occurred as the quadriceps reached T(lim) could not account for the prolonged performance after caffeine ingestion. In a separate experiment with the same subjects, we used a constant-sensation technique to determine whether caffeine influenced force sensation during 100 s of an isometric contraction of the quadriceps. The results of this experiment showed that caffeine reduced force sensation during the first 10-20 s of the contraction. The rapidity of this effect suggests that caffeine exerts its effects neurally. Based on these data, the caffeine-induced increase in T(lim) may have been caused by a willingness to maintain near-maximal activation longer because of alterations in muscle sensory processes.

Obtaining force-frequency curves with a single 3-second train of stimuli.

We devised a method to assess the force-frequency relationship (FFR) in human skeletal muscle that involved delivery of a single 2.8-s train of shocks directly to the femoral nerve. This increasing-frequency train (IFT) was based on a power function, with a range of stimulation frequencies beginning at 5 Hz and rising to 100 Hz. We compared the IFT to a standard series of constant-frequency trains (CFT) under two conditions. Force-frequency curves were examined, first in response to altered muscle length and second, following fatigue. There was no leftward shift in the curve when the knee extensors were shortened, although maximal force increased. In contrast, we observed a rightward shift in the curve after fatigue with both protocols; the frequency required to develop 50% of maximal force increased by 48% (P <.01) with CFT and 58% (P <.001) with an IFT. The CFT produced an irregular pattern of low-frequency fatigue recovery. In the IFT, low-frequency fatigue was greatest at the onset of recovery and decreased linearly until 120 s. These experiments show that the IFT protocol reveals alterations in muscle performance similar to the more traditional CFT. However, it requires only 2.8 s to administer and was judged more tolerable by 70% of our subjects. This suggests that the IFT may be an effective alternative for determining the FFR in human muscle for clinical and experimental purposes.

Submaximal motor unit firing rates after 8 wk of isometric resistance training.

PURPOSE: The purpose of this study was to test the hypothesis that average motor unit firing rates change in parallel with the contractile properties of vastus lateralis following 8 wk of isometric resistance training. METHODS: The firing rates from more than 400 motor units of vastus lateralis were obtained during voluntary isometric contractions of 50% MVC, before and again after training in male subjects (N = 10) and their untrained controls (N = 10). Single motor unit spike trains were recorded with tungsten microelectrodes. RESULTS: Training resulted in a 36% (P < 0.05) increase in MVC. We also found significant increases (P < 0.05) in maximal twitch amplitude (+17%), time to peak tension (+9%) and the maximal instantaneous rate of contraction (+20%) in the trained leg of the experimental group. Neither the maximal integrated EMG nor the rate of increase of integrated EMG was different after training. There were no significant changes in any of these measures from the untrained leg or the control group. Average firing rates were not different after training despite the increase in twitch contractile speed. CONCLUSION: These findings suggest that the control properties of the nervous system are not altered despite sizable changes in the contractile properties of muscle following 8 wk of resistance training.

Effects of caffeine on neuromuscular function.

This double-blind, repeated-measures study examined the effects of caffeine on neuromuscular function. Eleven male volunteers [22.3 +/- 2.4 (SD) yr] came to the laboratory for control, placebo, and caffeine (6 mg/kg dose) trials. Each trial consisted of 10 x 1-ms stimulation of the tibial nerve to elicit maximal H reflexes of the soleus, four attempts at a maximal voluntary contraction (MVC) of the right knee extensors, six brief submaximal contractions, and a 50% MVC held to fatigue. Isometric force and surface electromyographic signals were recorded continuously. The degree of maximal voluntary activation was assessed with the twitch-interpolation technique. Single-unit recordings were made with tungsten microelectrodes during the submaximal contractions. Voluntary activation at MVC increased by 3.50 +/- 1.01 (SE) % (P < 0. 01), but there was no change in H-reflex amplitude, suggesting that caffeine increases maximal voluntary activation at a supraspinal level. Neither the force-EMG relationship nor motor unit firing rates were altered by caffeine. Subjects were able to hold a 50% MVC for an average of 66.1 s in the absence of caffeine. Time to fatigue (T(lim)) increased by 25.80 +/- 16.06% after caffeine administration (P < 0.05). There was no significant change in T(lim) from pretest to posttest in the control or placebo trials. The increase in T(lim) was associated with an attenuated decline in twitch amplitude, which would suggest that the mechanism is, at least in part, peripheral.

The mixed nerve silent period is prolonged during a submaximal contraction sustained to failure.

The purpose of this study was to determine the effect of a sustained contraction of vastus lateralis on the silent period (SP) in the surface electromyogram (EMG) following direct neural stimulation. Five men and 5 women performed isometric knee extension at 30% maximal voluntary contraction (MVC) to the limit of endurance. During the contraction, EMG increased, and superimposed twitch amplitude and time to peak tension decreased, but the SP duration did not change. After 10 min of recovery, MVC had returned to its initial value, and the potentiated twitch amplitude was 70% of initial value, but the SP was now 11% shorter. Based on these results, we hypothesize that during a sustained contraction of 30% MVC, the increase in central drive may have been offset by inhibitory input from the periphery, but after 10 min of recovery the SP was shortened because of increased central drive. This aspect of the SP's behavior should be taken into account whenever it is employed as a diagnostic tool.

Probabilities associated with counting average motor unit firing rates in active human muscle.

Motor unit firing rates in human muscle can be determined from recordings made with small-diameter microelectrodes inserted directly into the muscle during voluntary contraction. Frequently, these counts are pooled to give an average motor unit firing rate under a given set of conditions. Since the fibers of one motor unit are dispersed among the cells of several others, it is conceivable that discharge rates can be measured in more than one cell from the same unit. If this occurred frequently, the distribution of firing rates could be influenced by those from units counted more than once. Based on literature values, we made the following assumptions: vastus lateralis contains approximately 300 motor units, with an average innervation ratio of 1500. Muscle cell diameter is about 50 to 100 microns and cells are randomly distributed over a motor unit territory of 10 microns diameter. The recording range of a microelectrode is about 600 microns. Given the distribution of cells normally found in whole human muscle, the probability of recording from two or more cells of the same motor unit at 50% MVC follows a Poisson distribution with a mean of 0.44. This model suggests that although there is a low probability of some duplication in this technique, the extent to which it influences the distribution of average motor unit firing rates is minimal over the entire range of forces produced by vastus lateralis.

Neuromuscular drive and force production are not altered during bilateral contractions.

Several investigators have studied the deficit in maximal voluntary force that is said to occur when bilateral muscle groups contract simultaneously. A true bilateral deficit (BLD) would suggest a significant limitation of neuromuscular control; however, some of the data from studies in the literature are equivocal. Our purpose was to determine whether there is a BLD in the knee extensors of untrained young male subjects during isometric contractions and whether this deficit is associated with a decreased activation of the quadriceps, increased activation of the antagonist muscle, or an alteration in motor unit firing rates. Twenty subjects performed unilateral (UL) and bilateral (BL) isometric knee extensions at 25, 50, 75, and 100% maximal voluntary contraction. Total UL and BL force (delta 3%) and maximal rate of force generation (delta 2.5%) were not significantly different. Total UL and BL maximal vastus lateralis electromyographic activity (EMG; 2.7 +/- 0.28 vs. 2.6 +/- 0.24 mV) and coactivation (0.17 +/- 0.02 vs. 0.20 +/- 0.02 mV) were also not different. Similarly, the ratio of force to EMG during submaximal UL and BL contractions was not different. Analysis of force production by each leg in UL and BL conditions showed no differences in force, rate of force generation, EMG, motor unit firing rates, and coactivation. Finally, assessment of quadriceps activity with the twitch interpolation technique indicated no differences in the degree of voluntary muscle activation (UL: 93.6 +/- 2.51 Hz, BL: 90.1 +/- 2.43 Hz). These results provide no evidence of a significant limitation in neuromuscular control between BL and UL isometric contractions of the knee extensor muscles in young male subjects.