Neutrophil accumulation following passive stretches contributes to adaptations that reduce contraction-induced skeletal muscle injury in mice.

Skeletal muscles can be injured by their own contractions, especially when the muscle is stretched during a lengthening contraction. Exposing a muscle to a conditioning protocol of stretches without activation (passive stretches) before lengthening contractions reduces contraction-induced injury. Although passive stretching does not damage muscle fibers, neutrophils are elevated in the muscle after passive stretches. Our purpose was to investigate the relationship between neutrophil accumulation following passive stretches and the protection from subsequent contraction-induced injury provided by the passive stretches. Our hypothesis was that passive stretch conditioning would not provide protection from subsequent lengthening contraction-induced injury under circumstances when the increase in muscle neutrophils in response to the conditioning was prevented. Extensor digitorum longus muscles of mice were conditioned with passive stretches 14 days before exposure to a protocol of damaging lengthening contractions. Mice were either untreated or treated with an antibody (RB6-8C5) that reduced the level of circulating neutrophils by over 95% before administration of passive stretches. Neutrophil levels recovered in treated mice by the time lengthening contractions were performed. Lengthening contractions were also administered to muscles with no prior exposure to passive stretches. Maximum isometric force, number of damaged fibers, and muscle neutrophil concentration were measured 3 days after lengthening contractions. Compared with nonconditioned control muscles, the severity of contraction-induced injury was not reduced by prior passive stretch conditioning when mice were treated with RB6-8C5 before conditioning. We conclude that neutrophils contribute to adaptations that protect muscles from injury.     

Lengthening contractions are not required to induce protection from contraction-induced muscle injury

We tested the hypothesis that lengthening contractions and subsequent muscle fiber degeneration and/or regeneration are required to induce exercise-associated protection from lengthening contraction-induced muscle injury. Extensor digitorum longus muscles in anesthetized mice were exposed in situ to repeated lengthening contractions, isometric contractions, or passive stretches. Three days after lengthening contractions, maximum isometric force production was decreased by 55%, and muscle cross sections contained a significant percentage (18%) of injured fibers. Neither isometric contractions nor passive stretches induced a deficit in maximum isometric force or a significant number of injured fibers at 3 days. Two weeks after an initial bout of lengthening contractions, a second identical bout produced a force deficit (19%) and a percentage of injured fibers (5%) that was smaller than those for the initial bout. Isometric contractions and passive stretches also provided protection from lengthening contraction-induced injury 2 wk later (force deficits = 35 and 36%, percentage of injured fibers = 12 and 10%, respectively), although the protection was less than that provided by lengthening contractions. These data indicate that lengthening contractions and fiber degeneration and/or regeneration are not required to induce protection from lengthening contraction-induced injury.     

Characteristics of lengthening contractions associated with injury to skeletal muscle fibers

Lengthening (eccentric) contractions result in injury to skeletal muscle fibers. Two hypotheses were tested through lengthening contractions of an in situ muscle preparation: the extent of injury increases with increases in the duration; and the extent of injury increases with increases in the peak force. Mice were anesthetized, and distal tendons of the extensor digitorum longus muscles were attached to a servomotor. Muscles were stimulated at 150 Hz and lengthened 20% of fiber length (Lf). Lengthening contractions were performed at 0.2, 0.5, or 1.0 Lf/s with durations of 0.5-15 min. Peak force during lengthening contractions at 1.0 Lf/s was decreased by inducing fatigue with isometric contractions, stimulating at 70-100 Hz, or 3) lengthening 10% of Lf. Injury was assessed 3 days after lengthening contractions by histological appearance and maximum force (Po) development. Injury increased with duration up to 5 min. After 5 min, fatigue appeared to prevent further injury. Results for 0.2 and 0.5 Lf/s were similar to those for 1.0 Lf/s but with less injury. A high correlation was observed between histological appearance of injury and the decrease in Po. The extent of injury was related to the peak force developed during the lengthening contractions.     

Rises in whole muscle passive tension of mammalian muscle after eccentric contractions at different lengths.

This is a report of experiments carried out on the medial gastrocnemius muscle of the anesthetized cat, investigating the effects of eccentric contractions carried out at different muscle lengths on the passive and active length-tension relationships. In one series of experiments, the motor supply to the muscle was divided into three approximately equal parts; in the other, whole muscles were used. Fifty eccentric contractions were carried out over different regions of the active length-tension curve for each partial or whole muscle. Active and passive length-tension curves were measured before and after the eccentric contractions. When eccentric contractions were carried out at longer lengths, there was a larger shift of the optimum length for active tension in the direction of longer muscle lengths and a larger fall in peak isometric tension. Passive tension was higher immediately after the eccentric contractions, and if the muscle was left undisturbed for 40 min, it increased further to higher values, particularly after contractions at longer lengths. A series of 20 passive stretches of the same speed and amplitude and covering the same length range as the active stretches, reduced the passive tension which redeveloped over a subsequent 40-min period. It is hypothesized that there are two factors influencing the level of passive tension in a muscle after a series of eccentric contractions. One is injury contractures in damaged muscle fibers tending to raise passive tension; the other is the presence of disrupted sarcomeres in series with still-functioning sarcomeres tending to reduce it.     

Voluntary activation level and muscle fiber recruitment of human quadriceps during lengthening contractions.

Voluntary activation levels during lengthening, isometric, and shortening contractions (angular velocity 60 degrees/s) were investigated by using electrical stimulation of the femoral nerve (triplet, 300 Hz) superimposed on maximal efforts. Recruitment of fiber populations was investigated by using the phosphocreatine-to-creatine ratio (PCr/Cr) of single characterized muscle fibers obtained from needle biopsies at rest and immediately after a series of 10 lengthening, isometric, and shortening contractions (1 s on/1 s off). Maximal voluntary torque was significantly higher during lengthening (270 +/- 55 N.m) compared with shortening contractions (199 +/- 47 N.m, P < 0.05) but was not different from isometric contractions (252 +/- 47 N.m). Isometric torque was higher than torque during shortening (P < 0.05). Voluntary activation level during maximal attempted lengthening contractions (79 +/- 8%) was significantly lower compared with isometric (93 +/- 5%) and shortening contractions (92 +/- 3%, P < 0.05). Mean PCr/Cr values of all fibers from all subjects at rest were 2.5 +/- 0.6, 2.0 +/- 0.7, and 2.0 +/- 0.7, respectively, for type I, IIa, and IIax fibers. After 10 contractions, the mean PCr/Cr values for grouped fiber populations (regardless of fiber type) were all significantly different from rest (1.3 +/- 0.2, 0.7 +/- 0.3, and 0.8 +/- 0.6 for lengthening, isometric, and shortening contractions, respectively; P < 0.05). The cumulative distributions of individual fiber populations after either contraction mode were significantly different from rest (P < 0.05). Curves after lengthening contractions were less shifted compared with curves from isometric and shortening contractions (P < 0.05), with a smaller shift for the type IIax compared with type I fibers in the lengthening contractions. The results indicate a reduced voluntary drive during lengthening contractions. PCr/Cr values of single fibers indicated a hierarchical order of recruitment of all fiber populations during maximal attempted lengthening contractions.     

Inflammatory cells in rat skeletal muscle are elevated after electrically stimulated contractions.

We determined the effect of muscle contractions resulting from high-frequency electrical stimulation (HFES) on inflammatory cells in rat tibialis anterior (TA), plantaris (Pln), and soleus (Sol) muscles at 6, 24, and 72 h post-HFES. A minimum of four and a maximum of seven rats were analyzed at each time point. HFES, applied to the sciatic nerve, caused the Sol and Pln to contract concentrically and the TA to contract eccentrically. Neutrophils were higher (P < 0.05) at 6 and 24 h after HFES in the Sol, Pln, and TA muscles relative to control muscles. ED1(+) macrophages in the Pln were elevated at 6 and 24 h after HFES and were also elevated in the Sol and TA after HFES relative to controls. ED2(+) macrophages in the Sol and TA were elevated at 24 and 72 h after HFES, respectively, and were also elevated in the Pln after HFES relative to controls. In contrast to the TA muscles, the Pln and Sol muscles showed no gross histological abnormalities. Collectively, these data indicate that both eccentric and concentric contractions can increase inflammatory cells in muscle, regardless of whether overt histological signs of injury are apparent.     

Dihydropyridine and ryanodine receptor binding after eccentric contractions in mouse skeletal muscle.

The purpose of this study was to determine whether there are alterations in the dihydropyridine and/or ryanodine receptors that might explain the excitation-contraction uncoupling associated with eccentric contraction-induced skeletal muscle injury. The left anterior crural muscles (i.e., tibialis anterior, extensor digitorum longus, and extensor hallucis longus) of mice were injured in vivo by 150 eccentric contractions. Peak isometric tetanic torque of the anterior crural muscles was reduced approximately 45% immediately and 3 days after the eccentric contractions. Partial restoration of peak isometric tetanic and subtetanic forces of injured extensor digitorum longus muscles by 10 mM caffeine indicated the presence of excitation-contraction uncoupling. Scatchard analysis of [3H]ryanodine binding indicated that the number of ryanodine receptor binding sites was not altered immediately postinjury but decreased 16% 3 days later. Dihydropyridine receptor binding sites increased approximately 20% immediately after and were elevated to the same extent 3 days after the injury protocol. Muscle injury did not alter the sensitivity of either receptor. These data suggest that a loss or altered sensitivity of the dihydropyridine and ryanodine receptors does not contribute to the excitation-contraction uncoupling immediately after contraction-induced muscle injury. We also concluded that the loss in ryanodine receptors 3 days after injury is not the primary cause of excitation-contraction uncoupling at that time.     

Modulation of passive force in single skeletal muscle fibres

In this study, we investigated the effects of activation and stretch on the passive force-sarcomere length relationship in skeletal muscle. Single fibres from the lumbrical muscle of frogs were placed at varying sarcomere lengths on the descending limb of the force-sarcomere length relationship, and tetanic contractions, active stretches and passive stretches (amplitudes of ca 10% of fibre length at a speed of 40% fibre length/s) were performed. The passive forces following stretch of an activated fibre were higher than the forces measured after isometric contractions or after stretches of a passive fibre at the corresponding sarcomere length. This effect was more pronounced at increased sarcomere lengths, and the passive force-sarcomere length relationship following active stretch was shifted upwards on the force axis compared with the corresponding relationship obtained following isometric contractions or passive stretches. These results provide strong evidence for an increase in passive force that is mediated by a length-dependent combination of stretch and activation, while activation or stretch alone does not produce this effect. Based on these results and recently published findings of the effects of Ca2+ on titin stiffness, we propose that the observed increase in passive force is caused by the molecular spring titin.     

Strength training improves the steadiness of slow lengthening contractions performed by old adults.

When old adults participate in a strength-training program with heavy loads, they experience an increase in muscle strength and an improvement in the steadiness of submaximal isometric contractions. The purpose of this study was to determine the effect of light- and heavy-load strength training on the ability of old adults to perform steady submaximal isometric and anisometric contractions. Thirty-two old adults (60-91 yr) participated in a 4-wk training program of a hand muscle. Both the light- and heavy-load groups increased one-repetition maximum and maximal voluntary contraction (MVC) strength and experienced similar improvements in the steadiness of the isometric and shortening and lengthening contractions. The increase in MVC strength was greater for the heavy-load group and could not be explained by changes in muscle activation. Before training, the lengthening contractions were less steady than the shortening contractions with the lightest loads (10% MVC). After training, there was no difference in steadiness between the shortening and lengthening contractions, except with the lightest load. These improvements were associated with a reduced level of muscle activation, especially during the lengthening contractions.     

Impaired neuromuscular function during isometric, shortening, and lengthening contractions after exercise-induced damage to elbow flexor muscles

The purpose of this study was to examine the effect of exercise-induced damage of the elbow flexor muscles on steady motor performance during isometric, shortening, and lengthening contractions. Ten healthy individuals (age 22+/-4 yr) performed four tasks with the elbow flexor muscles: a maximum voluntary contraction, a one repetition maximum (1 RM), an isometric task at three joint angles (short, intermediate, and long muscle lengths), and a constant-load task during slow (approximately 7 degrees/s) shortening and lengthening contractions. Task performance was quantified as the fluctuations in wrist acceleration (steadiness), and electromyography was obtained from the biceps and triceps brachii muscles at loads of 10, 20, and 40% of 1 RM. Tasks were performed before, immediately after, and 24 h after eccentric exercise that resulted in indicators of muscle damage. Maximum voluntary contraction force and 1-RM load declined by approximately 45% immediately after exercise and remained lower at 24 h ( approximately 30% decrease). Eccentric exercise resulted in reduced steadiness and increased biceps and triceps brachii electromyography for all tasks. For the isometric task, steadiness was impaired at the short compared with the long muscle length immediately after exercise (P<0.01). Furthermore, despite no differences before exercise, there was reduced steadiness for the shortening compared with the lengthening contractions after exercise (P=0.01), and steadiness remained impaired for shortening contractions 24 h later (P=0.01). These findings suggest that there are profound effects for the performance of these types of fine motor tasks when recovering from a bout of eccentric exercise.     

Attenuation of force deficit after lengthening contractions in soleus muscle from trained rats.

The purposes of this study were 1) to determine the extent to which endurance training reduces the functional deficit induced by lengthening contractions in the soleus (Sol) muscle and 2) to determine whether young and old rats training at a comparable relative exercise intensity would demonstrate a similar protective effect from lengthening-contraction-induced injury. Young (3-mo-old) and old (23-mo-old) male Fischer 344 rats were randomly assigned to either a control or exercise training group [young control (YC), old control (OC), young trained (YT), old trained (OT)]. Exercise training consisted of 10 wk of treadmill running (15% grade, 45 min/day, and 5 days/wk) such that by the end of training the young and old rats were exercising at 27 and 15 m/min, respectively. After training, contractile properties of the Sol muscle were measured in vitro at 26 degrees C. The percent decrease in maximal isometric specific force (P(o)) was determined after a series of 20 lengthening contractions (20% strain from optimal muscle length, 1 contraction every 5 s). After the lengthening-contraction protocol, Sol muscle P(o) was decreased by approximately 26% (19.6 vs. 14.6 N/cm(2)) and 28% (14.8 vs. 9.6 N/cm(2)) in the YC and OC rats, respectively. After exercise training, the reduction in P(o) was significantly (P < 0.05) attenuated to a similar degree ( approximately 13%) in both YT rats (18.7 vs. 16.2 N/cm(2)) and OT rats (15.8 vs. 13.7 N/cm(2)). It is concluded that exercise training attenuates the force deficit after repeated lengthening contractions to a comparable extent in young and old rats training at a similar exercise intensity.     

Tumor necrosis factor-alpha promotes the accumulation of neutrophils and macrophages in skeletal muscle.

Tumor necrosis factor-alpha (TNF-alpha) has been associated with cachexia and is known to regulate multiple inflammatory cell (neutrophil and macrophage) responses. We tested the hypothesis that neutrophils and macrophages accumulate in the extensor digitorum longus (EDL) and soleus muscles of mice after chronic TNF-alpha administration. Murine recombinant TNF-alpha (approximately 100 microg x kg(-1) x day(-1)) in vehicle solution or vehicle solution alone (sham) was administered to C57BL/6 mice for 7 days via osmotic minipumps. In EDL muscles from TNF-alpha-treated mice, neutrophil and macrophage concentrations were elevated seven- and threefold, respectively, compared with sham mice. Neutrophil and macrophage concentrations were also elevated five- and twofold, respectively, in solei of TNF-alpha- relative to sham-treated mice. Treatment with TNF-alpha elevated ubiquitin content by approximately 25% relative to sham values for both the EDL and soleus muscles; however, these elevations were not statistically significant. No differences were observed between TNF-alpha- and sham-treated mice in body weight, food consumption, muscle mass, myofiber cross-sectional area, carbonyl groups, total protein content, or relative abundance of myosin heavy chain protein. Furthermore, no overt signs of muscle injury or regeneration were observed in muscles from TNF-alpha-treated mice in either the EDL or soleus muscles. These observations suggest that 7 days of TNF-alpha administration promote muscle inflammation as indicated by the accumulation of neutrophils and macrophages without overt signs of atrophy, injury, or regeneration.     

Residual force enhancement during submaximal and maximal effort contractions of the plantar flexors across knee angle

Following active muscle lengthening, steady-state isometric force is elevated compared with an isometric contraction without prior lengthening for the same muscle length and activation level. This property of muscle contraction is known as residual force enhancement (RFE). Here, we aimed to determine whether neural factors may mask some of the mechanical benefits of RFE on plantar flexion torque production. Inherent to lengthening contractions is an increase in cortical and spinal-mediated inhibition, while knee flexion places the medial gastrocnemius at a neuromechanical disadvantage. Neuromuscular properties of the plantar flexors were investigated with a Humac Norm dynamometer in 10 males (∼27 years) with a flexed (90°) and extended (180°) knee and with or without calcaneal tendon vibration (frequency range: 80–110 Hz). There was no effect for vibration (p > 0.05), but there was an effect for knee angle (p < 0.05) such that there was a 2 fold increase in RFE with the knee flexed compared with extended. During submaximal torque matching, following active lengthening there was an activation reduction (electromyography; EMG) of 7.2 and 4.7% with the knee flexed and extended, respectively for soleus as compared with the reference isometric contraction, but no difference for the medial gastrocnemius. Despite attempting to excite Ia input onto the plantar flexor motor neuron pool, vibration had no influence on RFE. Surprisingly, RFE was elevated more for the knee flexed than extended, which was possibly owing to the activation differences across the disparate muscles of the triceps surae during the plantar flexion task.     

Macrophages,not neutrophils,infiltrate skeletal muscle in mice deficient in P/E selectins after mechanical reloading

Our objective was to test the hypothesis that endothelial selectins, P and E selectins, are necessary for leukocyte migration after muscle injury from unloading/reloading. Mice hindlimbs were suspended for 10 days followed by reloading periods of 6 or 24 h after which the soleus muscle was dissected. Light microscopic observations showed that macrophages, but not neutrophils, were able to invade soleus muscles in mice deficient in P/E selectins (P/E-/-) during reloading periods. The recruitment efficiency of neutrophils after 6 and 24 h of reloading was minimal in P/E-/- mice relative to unloaded animals. The recruitment of macrophages in the soleus muscle was preserved in P/E-/- mice. The concentration of macrophages increased by 8.1-fold compared with unloaded muscles in double-mutant mice after 24 h of reloading. The accumulation of macrophages in reloaded muscles did not lead to fiber necrosis. Together, these findings indicate that macrophages can invade skeletal muscle through cellular mechanisms that do not involve P/E selectins during skeletal muscle reloading.     

Adjustment of muscle mechanics model parameters to simulate dynamic contractions in older adults

The generation of muscle-actuated simulations that accurately represent the movement of old adults requires a model that accounts for changes in muscle properties that occur with aging. An objective of this study was to adjust the parameters of Hill-type musculo-tendon models to reflect nominal age-related changes in muscle mechanics that have been reported in the literature. A second objective was to determine whether using the parametric adjustments resulted in simulated dynamic ankle torque behavior similar to that seen in healthy old adults. The primary parameter adjustment involved decreasing maximum isometric muscle forces to account for the loss of muscle mass and specific strength with age. A review of the literature suggested the need for other modest adjustments that account for prolonged muscular deactivation, a reduction in maximum contraction velocity, greater passive muscle stiffness and increased normalized force capacity during lengthening contractions. With age-related changes incorporated, a musculo-tendon model was used to simulate isometric and isokinetic contractions of ankle plantarflexor and dorsiflexor muscles. The model predicted that ankle plantarflexion power output during 120 deg/s shortening contractions would be over 40% lower in old adults compared to healthy young adults. These power losses with age exceed the 30% loss in isometric strength assumed in the model but are comparable to 39-44% reductions in ankle power outputs measured in healthy old adults of approximately 70 years of age. Thus, accounting for age-related changes in muscle properties, other than decreased maximum isometric force, may be particularly important when simulating movements that require substantial power development.     

A mechanism accounting for independence on starting length of tension increase in ramp stretches of active skeletal muscle at short half-sarcomere lengths

Based on previous experimental results of independence on starting length of the tension gradient in constant-velocity stretches of active skeletal muscle at muscle lengths including the ascending limb and the plateau of the tension-length relation, a possible physiological mechanism determining the tension increase in lengthening active muscle is discussed. Considering the sliding filament theory, it is suggested that the tension-length relation of a half-sarcomere in lengthening contractions is different from that in isometric contractions. The assumed mechanism predicts, among others, that the thick filament retains its shortened length in lengthening contractions starting from a half-sarcomere length where this filament is compressed. An example model is implemented and checked with simulations.     

Midkine is involved in neutrophil infiltration into the tubulointerstitium in ischemic renal injury.

Midkine (MK) is a multifunctional heparin-binding protein and promotes migration of neutrophils, macrophages, and neurons. In the normal mouse kidney, MK is expressed in the proximal tubules. After renal ischemic reperfusion injury, its expression in proximal tubules was increased. Immediate increase of MK expression was found when renal proximal tubular epithelial cells in culture were exposed to 5 mM H(2)O(2). Histologically defined tubulointerstitial damage was less severe in MK-deficient (Mdk(-/-)) than in wild-type (Mdk(+/+)) mice at 2 and 7 days after ischemic reperfusion injury. Within 2 days after ischemic injury, inflammatory leukocytes, of which neutrophils were the major population, were recruited to the tubulointerstitium. The numbers of infiltrating neutrophils and also macrophages were lower in Mdk(-/-) than in Mdk(+/+) mice. Induction of macrophage inflammatory protein-2 and macrophage chemotactic protein-1, chemokines for neutrophils and macrophages, respectively, were also suppressed in Mdk(-/-) mice. Furthermore, renal tubular epithelial cells in culture expressed macrophage inflammatory protein-2 in response to exogenous MK administration. These results suggested that MK enhances migration of inflammatory cells upon ischemic injury of the kidney directly and also through induction of chemokines, and contributes to the augmentation of ischemic tissue damage.     

Rapid muscle-specific gene expression changes after a single bout of eccentric contractions in the mouse

Eccentric contractions (ECs), in which a muscle is forced to lengthen while activated, result in muscle injury and, eventually, muscle strengthening and prevention of further injury. Although the mechanical basis of EC-induced injury has been studied in detail, the biological response of muscle is less well characterized. This study presents the development of a minimally invasive model of EC injury in the mouse, follows the time course of torque recovery after an injurious bout of ECs, and uses Affymetrix microarrays to compare the gene expression profile 48 h after ECs to both isometrically stimulated muscles and contralateral muscles. Torque dropped by 55% immediately after the exercise bout and recovered to initial levels 7 days later. Thirty-six known genes were upregulated after ECs compared with contralateral and isometrically stimulated muscles, including five muscle-specific genes: muscle LIM protein (MLP), muscle ankyrin repeat proteins (MARP1 and -2; also known as cardiac ankyrin repeat protein and Arpp/Ankrd2, respectively), Xin, and myosin binding protein H. The time courses of MLP and MARP expression after the injury bout (determined by quantitative real-time polymerase chain reaction) indicate that these genes are rapidly induced, reaching a peak expression level of 6–11 times contralateral values 12–24 h after the EC bout and returning to baseline within 72 h. Very little gene induction was seen after either isometric activation or passive stretch, indicating that the MLP and MARP genes may play an important and specific role in the biological response of muscle to EC-induced injury. muscle LIM protein; cardiac ankyrin repeat protein; muscle ankyrin repeat protein; microarray     

Length-force characteristics of aponeurosis in passive muscle and during isometric and slow dynamic contractions of rat gastrocnemius muscle

Length-force characteristics of aponeurosis of rat gastrocnemius medialis muscle and achilles tendon were studied for passive and active muscle. Active muscle performed isometric as well as slow concentric and eccentric contractions at low velocity. For isometric conditions, different aponeurosis and tendon length-force characteristics were found between passive and active muscle: At comparable low levels of force longer aponeuroses were encountered in passive than in active muscle. Similar results were found for achilles tendon, but the magnitude of the length change involved was smaller than for aponeurosis. For active muscle, no differences of aponeurosis length- force characteristics could be distinguished between the isometric contractions and a slow concentric contraction. Indications that such differences of aponeurosis length-force characteristics may exist between slow concentric and eccentric contractions were found. It is concluded that, for gastrocnemius medialis muscle, aponeurosis and tendon length - force characteristics may be quite variable depending on recent history of muscle length and activity.     

Ia-afferent input to motoneurons during shortening and lengthening muscle contractions in humans.

The central nervous system employs different strategies to execute specific motor tasks. Because afferent feedback during shortening and lengthening muscle contractions differs, the neural strategy underlying these tasks may be quite distinct. Cortical drive may be adjusted or afferent input regulated. The exact mechanisms are not clear. Here, we examine the control of synaptic transmission across the Ia synapse during shortening and lengthening muscle contractions. Subjects were instructed to maintain isolated activity in a single tibialis anterior (TA) motor unit while muscle length was varied from flexion to extension and back. At a fixed interval after a firing of the active motor unit, a single electrical stimulus was applied to the common peroneal nerve to activate Ia afferents from the TA muscle. We investigated the stimulus-induced change in firing probability of 19 individual low-threshold TA motor units during shortening and lengthening contractions. Any change in firing probability depends on both pre- and postsynaptic mechanisms. In this experiment, motoneuron firing rate was similar during both contraction types. There was no difference in the firing probability between shortening and lengthening contractions (0.23 +/- 0.03 and 0.20 +/- 0.02, respectively). We suggest that there is no contraction type-specific control of Ia input to the motoneurons during shortening and lengthening muscle contractions. Cortical adjustments may have occurred.