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Fatigue characteristics following ankle fractures


Medicine & Science in Sports & Exercise: September 1997 - Volume 29 - Issue 9 - pp 1115-1123
Clinical Sciences: Clinical Investigations

The purpose of the study was to examine the effects of surgical and nonsurgical treatment of previously immobilized ankle fractures on voluntary and evoked contractile properties before and following fatigue. Twelve control and 12 previously immobilized (4-14 wk postfracture) internally fixated and nonfixated ankles were investigated before and following an isometric, intermittent, submaximal, fatigue protocol of the plantar flexors. Before fatigue, fracture groups had significantly lower force output (42.7 vs 78.8 Nm) and muscle activation (78.3 vs 98.7%) than controls. Decreased activation may be attributed to the inhibitory effects of injured muscle and swelling. All groups had similar force and muscle activation decreases (7-10%) following fatigue; however, the internally fixated group performed significantly fewer contractions during the fatigue test (19) than the nonfixated (71) and controls (61). In contrast to the other groups, internally fixated subjects experienced increased (13%) rather than decreased EMG activity (controls: 10.9%, nonfixated: 21.1%). M-waves and twitch torques potentiated to a similar extent in the fracture groups (4.5 and 5.7%) but decreased significantly in the control group (24.2 and 9.8%). The similar fatigue durations of nonfixated subjects compared with controls may be attributed to a lack of impairment in nonfixated neuromuscular propagation and contractile kinetics, while the increased fatigability of fixated subjects with a similar lack of evoked contractile property impairments suggested a greater intrinsic fatigability.

School of Physical and Occupational Therapy, McGill University, Montreal, Quebec, H3G 1Y5 CANADA

Submitted for publication September 1996.

Accepted for publication May 1997.

Address for correspondence: David Behm, School of Physical Education and Athletics, Memorial University of Newfoundland, St. John's, Newfoundland, Canada A1C 5S7; e-mail:

Immobilization for joint fractures can have dramatic consequences upon muscle function. Deficits due to immobilization in humans include muscle atrophy (19,26), decreases in dynamic(26) and static strength (46), and increases in the duration of twitch contractile properties(16,46). Indices of muscle activation such as electromyographic (EMG) activity (24), reflex potentiation (40), and maximum motor unit firing rates(17) have been reported to decrease with immobilization. Surprisingly, fatigue is not affected to the same extent as the immobilized-induced deficits in muscle strength, size, and activation. Animal immobilization studies have reported no change(39,47), improvements (35), and increases (39) in fatigability using maximal evoked stimulation. A lack of significant changes in fatigability have been reported in human immobilization studies (18,26), which predominantly used voluntary contractions. However, the activation levels of the voluntary contractions were not strictly controlled in these studies. Immobilization studies of healthy (46) and patient(16,30) populations have demonstrated greater deficits with maximum voluntary contractions (MVC) than tetanic force, suggesting immobilization had affected the ability to fully activate the muscle. It would be difficult to compare or measure the extent of fatigue between individuals with varying degrees of muscle activation. A preliminary assessment of muscle activation with the interpolated twitch technique (ITT) could predict an individual's true MVC ensuring that individuals were working at similar intensities. One of the purposes of the study was to investigate the effects of immobilization following ankle fractures on muscle fatigue and recovery following similar intensities of fatiguing contractions.

In addition to immobilization, surgery or the severity of the fracture may affect the extent of muscle recovery. Edwards et al. (20) demonstrated the repercussions of surgery with the significant decrements in lower extremity isometric strength and isokinetic endurance following abdominal surgery. Thus, the effects on voluntary and evoked contractile properties of previously immobilized internally fixated (surgery) and nonfixated ankle fractures were compared with healthy control plantar flexors.

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Experimental Design and Methodology

Subjects. Twelve control subjects (mean age, 26.2 ± 8.2 yr(SD)) were recruited from the McGill University staff and student population. Twelve previously immobilized ankle fracture patients (37.6 ± 12.4 yr(SD)) from three Montreal area hospitals (Jewish General, Queen Elizabeth, and Royal Victoria) were selected with the help of physiotherapy staff(Table 1). All patients followed conventional physiotherapy treatment for reduction of swelling and pain, improvements in range of motion, strength, and proprioception. Physiotherapists identified and informed prospective patients and requested their permission to be contacted. The investigators contacted the patients by phone to inform them of the study and seek their cooperation. Ten of the 12 subjects were fully weight bearing within the first week postimmobilization. Two subjects who were nonweight bearing for a longer duration (3-4 wk following immobilization) were able to bear weight for 2-3 wk before testing. Furthermore, two patients in the nonfixated group were fully weight bearing during the final week of immobilization. Thus, all patients were fully weight bearing at the time of testing.

Patients were not tested immediately following immobilization since our previous research with the ITT (8) had indicated that nonweight bearing patients could not exert sufficient force to provide reliable muscle activation data. Superimposed twitches that exceeded the potentiated twitches were found with low force outputs providing inaccurate estimations of muscle activation. In addition, the availability of patients for testing determined the testing date. However, both nonfixated and fixated groups were tested at similar times following their fractures (nonfixated: 9.1 wk ± 3.9, fixated: 9.6 wk ± 2.6). Previously immobilized patients met the following criteria:

1. The subject's ankle was immobilized for an ankle fracture in either a rigid (plaster) or removable casts (air splint, back slab). Both internally fixated (surgery) and nonfixated ankle fractures were included since the duration of immobilization and long-term clinical recovery has been reported to be similar (5). Subjects however were stratified into internally fixated and nonfixated groups, since surgery has been reported to influence the degree of atrophy, muscle weakness (26), and isokinetic endurance (20) following immobilization. The casted ankle was set at a neutral position (90° ± 5°) for all subjects.

2. Presence of a sound contralateral leg as well as no other major joint problems of either limb that would interfere with the subject's ability to participate in the study.

All subjects read and signed a consent form before experimentation. All appropriate McGill University and hospital ethics committee approval was obtained.

Testing protocol. Evaluations were conducted at the Sports Medicine laboratory of McGill University's School of Physical and Occupational Therapy. Patients were given a pain analog scale before, during, and following fatigue testing to measure the possible influence of pain. In addition, both limbs were immersed separately in a specially designed cylinder filled with water. Percent differences in water displacement between limbs was measured as an indicator of lower limb swelling (13). Previously immobilized patients had both the affected and contralateral limbs pretested. Fatigue testing was conducted only on the affected limb because of possible contralateral fatigue effects in a single testing session and the subjects' time constraints. Healthy subjects served as controls for voluntary and evoked fatigue testing.

Experimental set-up. Subjects were seated in a straight back chair with hips and knees at 90°. The leg was secured in a modified boot apparatus with the ankle at 90° (9). All voluntary and evoked torques were detected by a force transducer (custom design), amplified(recording amplifier NL107, and AC-DC differential amplifiers NL106 from Neurolog Systems-Model NL900A), and monitored on an oscilloscope (Tektronix Model 2220). All data were stored on computer (Seanix ASI 9000 486 DX) after being directed through an analog-digital board (Lab Master)(2000 Hz). Data were recorded and analyzed with a commercially designed software program(Actran; Distributions Physiomonitor Ltd.).

Bipolar surface stimulating electrodes were secured to the proximal and distal aspects of the triceps surae muscle group. Surface EMG recording electrodes (Medi-Trace) were placed 3-5 cm apart over the tibialis anterior(TA) and distal portion of the soleus. A ground electrode was secured superficially to the head of the tibia. Thorough skin preparation for all electrodes included sanding of the skin around the designated areas followed by cleansing with an isopropyl alcohol swab. Agonist and antagonist EMG activity were amplified (Isolated Head-Stage 830 Isolation amplifier, Biomedical Amplifier 830 CWE, Ardmore, PA), filtered (10-1000 Hz), monitored on oscilloscope and stored on computer at a sampling rate of 2000 Hz. For analysis the EMG signal was rectified and integrated (IEMG) over a 500-ms period during a MVC.

Pre- and postfatigue measurements. Peak twitches were evoked with electrodes connected to a high voltage stimulator (Digitimer Stimulator; Model DS7H+). The amperage (10 mA-1A) of a 100 V rectangular pulse (50 μs) was progressively increased until a maximum peak twitch torque was achieved. In two of the 12 previously immobilized patients, maximum twitch torques were not achieved due to patient discomfort. The average of three trials was used to measure twitch amplitude, time to peak twitch torque (TPT) and half relaxation time (0.5 RT) and muscle action compound (M-wave) amplitude.

The ITT was administered with a series of 3-s duration submaximal (20, 40, 60, and 80% of MVC) and three maximal contractions. Three doublets (two twitches with a 10-ms interval) interspersed at 900-ms intervals were evoked and superimposed on the voluntary contractions to obtain an average response. Superimposed doublets were utilized in an attempt to ensure a large signal to noise ratio. Two potentiated doublets were also recorded at 1-s intervals following the voluntary contractions. Torque signals were sent through both a low and high gain amplifier. The resident software program offset the gained(10×) superimposed signal, 100 ms before each stimulation to improve resolution. An interpolated twitch (IT) ratio was calculated comparing the amplitudes of the superimposed doublets with the potentiated doublet to estimate the extent of inactivation during a voluntary contraction. Since the potentiated doublet represents full muscle activation, the superimposed torque using the same intensity of stimulation would activate those fibers left inactivated by the voluntary contraction. An index of muscle activation(percentage) was derived by subtracting the IT ratio from a value of 1 and multiplying by 100. Previous work from our laboratory has demonstrated that the use of a second order polynomial equation to predict a fully activated MVC was more accurate than the analysis of single IT ratios. Thus, before fatigue, an interpolated twitch ratio-force relationship was derived from the indices of muscle activation of submaximal and maximal contractions and analyzed with a second order polynomial equation. Submaximal contractions were not included during recovery to limit the number of possibly fatiguing contractions.

Fatigue. After voluntary and evoked testing, the subjects proceeded with the fatigue test. The fatigue protocol had the subject gradually increase the contraction intensity for 3 s until 50% of the predicted MVC (calculated from the index of muscle activation) was attained. This intensity was maintained for 10 s, followed by a 3-s gradual decrease to a resting state. The sequence was resumed after a 4-s rest period. The contraction cycles (work: rest ratio of 16 s: 4 s) continued until the effects of fatigue disrupted the subject's ability to maintain the desired force for the 10 s period. Voluntary and evoked properties were monitored at 30 s, 1, 2, 5, and 10 min of recovery.

Statistical analyses. This study was analyzed using a two-way ANOVA with repeated measures on the second factor. The two factors (3 × 6) included subject groups (internally fixated, nonfixated, and controls) and testing period. F-ratios were considered significant at P< 0.05. If significant interactions were present, a Tukeypost-hoc test was conducted. Correlation coefficients were used to compare pain analog scores and the extent of swelling with the index of muscle activation. Descriptive statistics include means ± SD. Data in the figures are presented as mean ± SE. The statistical power of these tests when analyzing controls and previously immobilized groups was high(>0.95) with groups of N = 12 each.

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Prefatigue. There were no significant differences prefatigue, between internally fixated, and nonfixated groups in MVC, muscle activation, twitch torque, TPT, 0.5 RT (Table 2), swelling, or pain. A poor linear regression (r = 0.13) indicated there was no relation between the duration of immobilization and the percentage deficit in MVC between healthy and affected legs.

The control group MVC (78.8 Nm) significantly (P < 0.0001) exceeded the previously immobilized (40.4 Nm) groups. The mean index of muscle activation for controls (98.7%) exceeded (P < 0.01) the previously immobilized groups (78.3%). Since the IT ratio force-relationship was best described by a shallow hyperbolic curve, a second order polynomial equation was derived. The polynomial equation also demonstrated a significantly (P = 0.04) lower muscle activation in previously immobilized subjects (83.4% ± 15.1) than controls (94.5% ± 4.1). In addition, IT ratios derived from MVC (index of muscle activation) were not significantly different from the inactivation predicted from second order polynomial equations, suggesting that the index of muscle activation would be a valid indicator both pre- and postfatigue. The contralateral limb MVC and index of muscle activation of the previously immobilized groups were not significantly different from the control group, indicating control and patient groups were similar when unaffected by injury (Table 2).

To determine the factors contributing to the greater inactivation of the previously immobilized groups, coefficient correlations comparing the index of muscle activation with either a pain analog scale or the extent of swelling were analyzed. There were nonsignificant correlations (r = 0.49) between swelling and muscle activation as well as for pain and activation (r = 0.1)(Fig. 1).

Fatigue and recovery. A lack of difference between groups in the voluntary force decrement following fatigue (mean: 29% ± 4.5) contrasted with the significantly (P < 0.01) fewer number of contractions to fatigue of the internally fixated group(Table 3). There were no significant differences between the controls and nonfixated groups in the number of contractions until the onset of fatigue (Table 3).

Index of muscle activation. Although the number of contractions to fatigue was significantly less in the internally fixated group(Table 3), this greater fatigability could not be explained by differences in muscle activation between groups(Fig. 2). Whereas the absolute amount of muscle activation differed between groups, the pattern of fatigue-induced muscle inactivation(7-10% decrease from prefatigue over entire recovery period) was similar. In addition, the index of muscle activation was not significantly different between individuals immobilized for 5 wk or less compared to those immobilized for more than 6 wk.

IEMG. The agonist and antagonist IEMG responses of the internally fixated group following fatigue contrasted with the other groups. Both the control (10.9%) and nonfixated (21.1%) groups experienced declines in agonist maximal IEMG activity following fatigue. In contrast, despite the decline in voluntary force following fatigue, internally fixated individuals had significant increases (13%) in agonist IEMG activity at 30 s and 1, 5, and 10 min of recovery (Fig. 3, top).

Similarly, the internally fixated group also showed significant(P < 0.01) overall increases (8.5%) in antagonist IEMG activity following fatigue. The control group experienced significantly (P< 0.01) greater decreases (26.1%) in antagonist IEMG activity than the nonfixated (14.1%) group before the 10 min recovery testing period(Fig. 3, bottom).

M-wave amplitude. There were no significant differences in M-wave amplitude between internally fixated and nonfixated groups. The overall 24.2% decline of the control M-wave amplitude contrasted with a lack of significant change in previously immobilized individuals (Fig. 4A).

Evoked twitch contractile properties. There were no significant differences in twitch torque between the internally fixated and nonfixated groups. The twitch torque potentiation of previously immobilized groups conflicted with the twitch torque depression of the control group. The previously immobilized groups had significant (P < 0.01) potentiation of the twitch torque until 5 min of recovery(Fig. 4B). The control group experienced a significant(P < 0.0001) decline in twitch torque until 2 min of recovery. After 5 min of recovery, there was again significant (P < 0.01) differences between the control and previously immobilized groups as the patient groups lost their twitch torque potentiation and the control group began to experience a late potentiation.

Although there was little change in the TPT during the recovery period, the internally fixated group had a significant (P = 0.02) prolongation of TPT at 30 s of recovery (Fig. 4C). At the same time nonfixated and control groups experienced a significant (P < 0.05) decrease in TPT. The control group also demonstrated a significantly(P < 0.01) longer prolongation of TPT than the other groups at 5 min of recovery.

There were no significant differences between groups in 0.5 RT. Overall, 0.5 RT was significantly (P < 0.0001) shortened 13.9%(±13.4) over the entire recovery period.

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This is the first study to use the ITT to assess the effects of disuse on muscle activation, pre- and postfatigue. Previously immobilized subjects could not activate to the same extent as controls before fatigue. Therefore, to investigate the effects of disuse on fatigue, it was important to measure muscle activation while controlling for differences in the relative intensity of the contractions.

Effects of disuse on muscle activation. The significant prefatigue decrease in the index of muscle activation of previously immobilized subjects (78.3%) could arise from reflex inhibition of either or both the joint capsule and muscle afferents. McComas et al.(32) demonstrated greater inactivation in patients with joint pathology. Sabbahi et al. (38) desensitized healthy ankle joint receptors with xylocaine and then observed motoneuron excitability by monitoring H-reflex activity. They found no significant changes in H-reflex activity, suggesting the joint receptors have minimal inhibitory effects on the excitability of the motoneurons. Fatigues studies have illustrated fatigue-induced inhibition of motoneurons may be derived from muscle afferents(25,31). Thus, the reflex inhibition of motoneurons with immobilization might be attributed more to disruptions of the muscle than the joint capsule.

Other factors related to musculoskeletal injury such as swelling may affect muscle activation as well. A number of studies have documented decreases in muscle force, EMG activity (15,48), and H-reflex amplitude (43) with knee joint effusion in humans. Decreases in EMG activity and H-reflex amplitude would indicate a decline in motoneuron excitability resulting from a swelling induced reflex inhibition. In the present study we showed a correlation coefficient of 0.49 between the index of muscle activation and the extent of swelling (Fig. 1). This indicates that approximately 25% of the muscle inactivation could be related to the extent of swelling.

In contrast to swelling, a statistical treatment of the pain analog data revealed a correlation coefficient (pain analog and index of muscle activation) of only 0.1, indicating that pain may only be related to about 1% of the muscle inactivation (Fig. 1). Rutherford et al.(37) reported extensive quadriceps inactivation with muscle pain. However, both deAndrade et al. (15) and Wood et al. (48) reported that swelling-induced reflex inhibition of the quadriceps was independent of pain. Stokes and Young(44) infiltrated human knee joints with bupivacaine to block the pain of postsurgery meniscectomies and reported no change in the severity of inhibition. Thus, the major factors affecting muscle inactivation would be inhibitory afferents arising from swelling and muscle with minor contributions from pain and possibly joint capsule afferents.

Cross-education or cross-transfer effects have been observed in the untrained contralateral limb following unilateral training of the ipsilateral limb. This has been demonstrated in a number of studies and attributed to central or neural adaptations (29). It might be logical to assume that if training effects are transferable, then detraining or injury effects may be transferred as well. The uninjured leg of arthroscopic patients in the Hurley et al. (28) study experienced greater inactivation (18.6%) than what has been reported in the literature on quadriceps activation in healthy individuals(36,37). Long-term testing of previously immobilized patients (1-5 yr) showed full activation of both the affected and contralateral limbs (37). The 1.7% inactivation of the contralateral plantar flexors was similar to the 1.3% inactivation of healthy controls in this study. Thus cross-education injury effects were not evident in the present study.

Effects of disuse on fatigue. Previous human studies investigating the impact of immobilization on muscle fatigue have not controlled for interindividual differences in the ability to maximally activate (18). The similar fatigue characteristics reported between controls and previously immobilized subjects could be attributed to a comparison of maximal and submaximal voluntary efforts. The major finding in this study was that greater muscle fatigability was observed in the previously immobilized internally fixated subjects in comparison to controls and nonfixated subjects, when subjects were working at the same relative intensity. One of the puzzling findings, however, was the mechanism underlying the greater fatigability of fixated subjects in view of the fact that both fixated and nonfixated subjects were characterized by similar changes in muscle activation, M-wave, and twitch contractile properties.

Mechanisms of fatigue with internally fixated previously immobilized subjects. The increased fatigability of the internally fixated subjects could not be attributed to a greater degree of inactivation postfatigue. Indeed, muscle inactivation increased to a similar extent in all groups following fatigue and during the recovery period (7-10%). McKenzie and Gandevia (33) indicated that their subjects failed to activate 4-10% of their elbow flexors with intermittent maximal contractions. In a previous study with healthy subjects, we determined that the extent of muscle inactivation postfatigue was related to the duration of the fatigue protocol (7). However, in this study, internally fixated subjects experienced similar levels of inactivation with a shorter fatigue duration than nonfixated subjects, suggesting that the time to fatigue does not influence the degree of inactivation postfatigue in previously immobilized muscles.

The changes observed in maximum agonist EMG activity postfatigue were also unexpected. Both control and nonfixated ankles were characterized by a decrease in maximal agonist EMG activity, whereas significant increases were observed in the internally fixated ankles. Typically in submaximal fatigue protocols, EMG activity initially increases to maintain the same tension output by recruiting additional motor units(12,34). Subsequently EMG activity starts to decrease when the target torque can no longer be maintained in the muscle(12). Increases in maximal EMG postfatigue are usually indicative of failure to reach the point of true fatigue. However, the percent drop in MVC and muscle activation was the same in all groups. Therefore, the efficiency of the muscle contraction (EMG/muscle torque) may actually be less in the internally fixated group. This greater inefficiency combined with a shorter time to fatigue could suggest a greater intrinsic fatigability in the internally fixated subjects.

The efficiency of the muscle contraction could be affected by changes in fiber type, muscle enzymatic activity, or circulation. A number of studies have reported a preferential atrophy of Type I fibers (6) or a decrease in Type I fiber number (14) with immobilization. The loss of fatigue-resistant Type I fibers would contribute to a greater fatigability. However, unless surgery had a specific effect upon Type I fibers, the greater endurance of the nonfixated subjects would suggest that it was unlikely that the two immobilized groups had separate fiber type adaptations. Similarly, it is doubtful that disuse-induced decreases in oxidative enzymes such as succinic dehydrogenase, citrate synthase, and cytochrome c (3,6) would specifically target fixated muscle. This was evident in a study by Halkjaer-Kristensen and Ingemann-Hansen(26), who reported no significant difference between nonsurgical and surgical repair of knee ligaments in the extent of aerobic enzymatic changes. Muscles fixed in a shortened position generally experience greater atrophy and greater decreases in tension generating capacity and metabolism (6). However, fixated subjects were not immobilized with their muscles in a shortened position in comparison to the nonfixated group suggesting the position or angle of immobilization was not a pivotal factor. Alternatively, research has demonstrated an impaired blood flow due to a decrease in the absolute number of capillaries of disused muscle(3). Conceivably the combined disruptive effects of both surgery and immobilization could impair circulation affecting substrate and oxygen transport.

Alterations in antagonist activity must also be considered. The fact that antagonist EMG activity significantly increased by 8.5% in the internally fixated group postfatigue suggests an increase in cocontractions, which would overestimate to some extent the fatigue-induced drop in MVC. The decrease in antagonist EMG activity of the nonfixated (14.1%) and control (26.1%) groups would suggest, on the other hand, a decrease in cocontractions, which would tend to underestimate the observed drop in MVC postfatigue. Whereas antagonist cocontractions provide protection from the inertial forces of the agonist(4,47), increases in the antagonist EMG activity of the internally fixated group could represent a strategy of greater joint protection for the more severely fractured subjects. Although force output was maintained at the same relative intensity for all groups during fatigue, internally fixated subjects may have been working at a greater intensity due to greater antagonist activity. However, greater antagonist activity probably does not fully explain the significantly fewer internally fixated contractions. Since neuromuscular propagation (M-wave amplitude) and excitation-contraction coupling (twitch torque) were not impaired postfatigue, the greater fatigability of internally fixated muscle may be associated with a deficiency of the contractile proteins to maintain repeated submaximal contractions.

Mechanisms of fatigue with nonfixated previously immobilized subjects. The similar fatigability of previously immobilized nonfixated subjects and controls in this and other studies while experiencing impaired force production (18,35,47) and decreased oxidative capacity (47) may be due to a number of reasons. The similar fatigability of nonfixated and control subjects could not be attributed to differences in the extent of fatigue-induced neural or central inhibition since decreases in muscle activation were comparable(7-10%). However, the fatigue-induced impairments in neuromuscular propagation and contractile kinetics evident in controls were not present in previously immobilized groups. Control subjects experienced a 24.2% decrease in M-wave amplitude in contrast to the lack of change in internally fixated and nonfixated groups. Decline in M-wave amplitude has been reported in the abductor pollicis of healthy subjects, after 90-100 s of fatiguing MVC(10). Fuglevand et al. (22) also illustrated declines in M-wave amplitude of healthy subjects with fatigue, concluding that when force is sustained at a submaximal value, impairment in muscle membrane propagation may occur. A reduction in M-wave amplitude or area may signify an impairment in neuromuscular transmission or muscle membrane excitability (11). Conversely, human paralyzed soleus muscle exhibited minimal changes in M-wave amplitude compared with significant fatigue-induced decreases in torque, suggesting that the source of fatigue was within the contractile mechanism and not attributable to neuromuscular transmission compromise (41). The maintenance of previously immobilized M-wave amplitudes in the present study may be related to the lower maximum firing frequencies of motoneurons in immobilized subjects(17), resulting in a decrease in the frequency and total quantity of stimuli reaching the muscle membrane. Thus, the mechanisms underlying fatigue in immobilized muscle could not be related to impairments of neuromuscular propagation or muscle membrane excitability.

The decrease in the control subjects' twitch torque (9.8%) contrasted with the potentiation of the other groups. Other studies have found both decreases(2) and no change (1) in twitch torque following prolonged intermittent maximal fatigue protocols with healthy subjects. Conversely, potentiation (27) of twitch torque has been demonstrated following a short-term maximal fatigue protocol in healthy subjects. Although Fuglevand et al. (23) showed twitch potentiation in nonfatigued short-term immobilized human hand muscle, they found the twitch torque to be depressed in the same subjects following a submaximal (35% MVC) fatigue protocol. Detraining or atrophic effects on the myofibrillar component with immobilization or disuse are not accompanied by the same relative decreases in sarcoplasmic reticulum (SR) activity(42). A relatively more expansive SR within an atrophied muscle fiber may augment Ca2+ delivery, providing greater concentrations of Ca2+ to the myofibrils. Twitch torque potentiation would preclude excitation-contraction coupling as a mechanism underlying fatigue in previously immobilized muscle.

The similar fatigue characteristics of control and nonfixated subjects may be a function of alterations in energy requirements or diffusion. Witzmann et al. (47) suggested that a lower force output in immobilized muscle is a result of a lower number of active cross-bridges, resulting in lower energy expenditure and thus greater than expected endurance. Turcotte et al. (45) reported lower levels of myosin ATPase with disused muscle, which would slow cross-bridge cycling reducing energy demand. St.-Pierre and Gardiner (39) suggested that the atrophic changes in the muscle would result in a smaller surface area contributing to improved diffusion. This study suggests that even with similar contraction intensities, changes in muscle energetics may be responsible for the similar fatigability of nonfixated previously immobilized and control subjects.

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Before fatigue, previously immobilized subjects experienced greater muscle inactivation than controls, which could be attributed to the inhibitory effects of injured muscle and swelling. Nonfixated and control subjects performed a comparable number of similar intensity contractions when subjected to a submaximal intermittent fatigue protocol. Although there were no differences in the fatigue-induced decreases in muscle activation between groups, a lack of impairment to the previously immobilized groups' M-wave amplitude (neuromuscular propagation) and twitch torque (contractile kinetics) illustrated differences between the groups in the underlying mechanisms of fatigue. The shorter duration of internally fixated fatigue was associated with increases rather than decreases in agonist and antagonist IEMG. Since internally fixated muscle did not experience greater impairments in muscle activation, membrane excitability, or contractile kinetics than the other groups, the more severe ankles fractures may contribute to an intrinsically more fatigable muscle than normal or less severely injured muscles.

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