Soleus Activity Research Articles

Muscular compensation and lesion of the anterior cruciate ligament: Contribution of the soleus muscle during recovery from a forward fall

Knee stability following an anterior cruciate ligament lesion has been widely studied. Only recent studies focused on the contribution of the soleus muscle. Our purpose was to characterize the dynamic and muscular activity of balance recovery in healthy subjects and patients with an anterior cruciate ligament rupture. The role of the soleus was investigated in the ipsilateral compensation developed to stabilize the knee and in the contralateral compensation to recover balance. Twelve anterior cruciate ligament deficient patients, ten anterior cruciate ligament repaired patients and 14 control subjects were recorded during a forward fall involving stepping to recover balance. The dynamic of the centre of gravity remained normal when compared to the control group regardless of the treatment, suggesting an adapted compensation to knee instability in this situation. A bilateral increase in soleus activity was related to an increased duration in the balance recovery process in all patients. Patients used one of two strategies to recover balance regardless of the treatment: reducing the step length, involving an early recruitment of the soleus before heel contact, or anticipating braking with a similar step length requiring a predominant activity of the hamstrings. These results suggest that bilateral activity of the soleus is involved to compensate for instability and highlight the contribution of the soleus to rehabilitation after an anterior cruciate ligament lesion, not only as a compensatory muscle acting at the knee level but also at a higher level in the bilateral control of stance.

The Effect of Endurance Exercise Training on Skeletal Muscle Apoptosis Induced by Mitochondrion

PURPOSE: To investigate the influence of exercise training on skeletal muscle apoptosis induced by mitochondrial pathway. METHODS: Animals, male Wistar rats, were randomly assigned to either a control group or an exercise group. Exercise group were trained 5 days weekly for 12 weeks on treadmill. An exhausted exercise test was performed after a rest period of 7 days after 12 weeks exercise training. Rats were sacrificed at pre-exercise (PRE), post-exercise 0 hour (PE0) and post-exercise 48 hour (PE48), respectively. The soleus and gastrocnemius were dissected out and frozen in liquid nitrogen rapidly. Muscle samples were stored at −80°C until subsequent analysis RESULTS: The citrate synthesis activity of soleus of trained was significantly higher than untrained at PRE, PE0 and PE48 (p <.05), respectively. The gastrocnemius weight-to-body weight ratio and soleus weight-to-body weight ratio of trained were significantly higher than untrained (p <.05), respectively. In gastrocnemius, the apoptosis index of trained at PE48 was significantly higher than PRE (p <.05); the untrained at PE48 was significantly higher than PRE and PE0 (p <.05), respectively. The apoptosis index of gastrocnemius and soleus of trained were significantly lower than untrained after PE48 (p <.05), respectively. CONCLUSIONS These finding suggest that skeletal muscle may modulate their apoptotic signals expression and the oxidative activity of mitochondria after exercise training, lead to attenuating the time of skeletal muscle apoptosis or inhibiting the apoptotic signals expression, and then the probability of hypertrophy occurred.

Afferent-mediated modulation of the soleus muscle activity during the stance phase of human walking

The aim of this study was to investigate the contribution of proprioceptive feedback to the amplitude modulation of the soleus muscle activity during human walking. We have previously shown that slow-velocity, small-amplitude ankle dorsiflexion enhancements and reductions applied during the stance phase of the step cycle generate, respectively, increments and decrements on the ongoing soleus activity. We have also shown that the increments in soleus activity are at least partially mediated by feedback from group Ia fibres. In the present study, we further investigated the afferent-mediated contribution from muscle group II afferents, cutaneous and proprioceptive afferents from the foot, and load-sensitive afferents to the soleus EMG. Slow-velocity, small-amplitude ankle trajectory modifications were combined with the pharmaceutical depression of group II polysynaptic pathways with tizanidine hydrochloride, anaesthetic blocking of sensory information from the foot with injections of lidocaine hydrochloride, and modulation of load feedback by increasing and decreasing the body load. The depression of the group II afferents significantly reduced the soleus response to the ankle trajectory modifications. Blocking sensory feedback from the foot did not have an effect on the soleus muscle activity. Changes in body load affected the ongoing soleus activity level; however, it did not affect the amplitude of the soleus EMG responses to the ankle trajectory modifications. These results suggest that the feedback from group II afferents, and possibly from load-sensitive afferents, contribute to the amplitude modulation of the soleus muscle activity during the stance phase of the step cycle. However, feedback from cutaneous afferents and instrinsic proprioceptive afferents from the foot does not seem to contribute to this muscle activation.

Postfatigue potentiation of the paralyzed soleus muscle: evidence for adaptation with long-term electrical stimulation training

Understanding the torque output behavior of paralyzed muscle has important implications for the use of functional neuromuscular electrical stimulation systems. Postfatigue potentiation is an augmentation of peak muscle torque during repetitive activation after a fatigue protocol. The purposes of this study were 1) to quantify postfatigue potentiation in the acutely and chronically paralyzed soleus and 2) to determine the effect of long-term soleus electrical stimulation training on the potentiation characteristics of recently paralyzed soleus muscle. Five subjects with chronic paralysis (>2 yr) demonstrated significant postfatigue potentiation during a repetitive soleus activation protocol that induced low-frequency fatigue. Ten subjects with acute paralysis (<6 mo) demonstrated no torque potentiation in response to repetitive stimulation. Seven of these acute subjects completed 2 yr of home-based isometric soleus electrical stimulation training of one limb (compliance = 83%; 8,300 contractions/wk). With the early implementation of electrically stimulated training, potentiation characteristics of trained soleus muscles were preserved as in the acute postinjury state. In contrast, untrained limbs showed marked postfatigue potentiation at 2 yr after spinal cord injury (SCI). A single acute SCI subject who was followed longitudinally developed potentiation characteristics very similar to the untrained limbs of the training subjects. The results of the present investigation support that postfatigue potentiation is a characteristic of fast-fatigable muscle and can be prevented by timely neuromuscular electrical stimulation training. Potentiation is an important consideration in the design of functional electrical stimulation control systems for people with SCI.

Adaptations of walking pattern on a compliant surface to regulate dynamic stability

Dynamic stability can be threatened by various travel surface changes that humans encounter on a daily basis. The central nervous system (CNS) must acquire appropriate information about upcoming surface changes and provide necessary proactive and reactive changes to maintain stability. The purpose of this study was to examine stability control by characterizing adaptations in step patterns, center of mass (COM) trajectory, and lower limb muscle activity when stepping onto and walking on a compliant surface. Eight young adults walked under two conditions: baseline ground walking and while walking on a large foam mat (compliant surface). Optotrak system was used to collect 3D-full body kinematics and electromyography was collected for the rectus femoris, biceps femoris, tibialis anterior, medial gastrocnemius, and soleus bilaterally. Vertical COM decreased on the compliant surface while medio-lateral COM was not affected. This lowering of the vertical COM peak would provide a more stable posture when walking on the surface. Toe trajectory during the swing phase was elevated to avoid tripping on the deformable compliant surface. Step width and length increased on the compliant surface which would increase base of support and provide better control of COM. Increases in gastrocnemius and soleus activity during push-off accounted for increases in step length seen on the compliant surface. Dynamic stability margin in the anterior-posterior direction demonstrated a constant overcompensation and subsequent correction in COM control. These proactive and reactive changes in motor patterns show how the CNS actively coordinates all body segments while traveling on a compliant surface in order to maximize stability.

561. Novel Tissue-Specific Regulatory Cassettes Direct High-Level Transgene Expression in Skeletal and Cardiac Muscle

Top of pageAbstract Systemic delivery of rAAV6 vectors can achieve efficient transduction of the entire striated musculature, making this an attractive strategy for gene therapy of Duchenne Muscular Dystrophy. However, this delivery method also transduces cells in many non-muscle tissues, which may cause therapeutic problems including toxicity and a transgene-directed immune response. These problems could be avoided by limiting transgene expression through the use of muscle-specific promoters. Unfortunately, the expression levels of such promoters following systemic delivery of rAAV vectors are lower than viral promoters in most skeletal muscles and negligible in cardiac muscle. The goal of this project is to design regulatory cassettes that drive high levels of skeletal and cardiac muscle-specific transgene expression while also being sufficiently short (<800bp) to fit into rAAV vectors containing microdystrophin cDNA (3.8-kb). Our lab has developed a series of muscle-specific regulatory cassettes based on the enhancer and promoter of the murine muscle creatine kinase (MCK) gene. The CK6 cassette, previously thought to be the strongest modification, has higher activity than the wild type cassette in skeletal muscle, but very low activity in cardiac and diaphragm muscle. We have designed new cassettes to increase expression, and their activities have been evaluated in various muscles and non-muscle tissues following systemic delivery of rAAV6 vectors expressing a human placental alkaline phosphatase reporter gene. First, we designed a 570-bp MCK-based cassette, CK7, which exhibited activity levels similar to CK6 in quadriceps, a predominantly fast-twitch muscle, but had significantly higher activity in cardiac muscle, diaphragm, and soleus, a predominantly slow-twitch muscle. To further improve expression, especially in cardiac muscle, we added a 190-bp enhancer from the murine alpha-myosin heavy chain gene (|[alpha]|MHC) to the CK7 cassette to produce MHCK7, a 770-bp cassette that has the highest overall activity. When compared to CK6, the activity of MHCK7 was about 400-fold higher in cardiac muscle and 10-fold higher in soleus, which was equivalent to the activity of the CMV promoter. Staining for AP activity in cross-sections of both muscles revealed strong expression in virtually all fibers. The activity in diaphragm was about 40-fold higher, but was still considerably lower than the CMV promoter, with only about 20% of the fibers staining positive. Finally, the activity in quadriceps muscle was equivalent to CK6. The activity of MHCK7 in kidney, aorta, brain, testes, and intestine was at background levels, while a very slight increase in activity, about 50|[ndash]|200-fold lower than in muscle, was detected in liver, spleen, and lung. Based on these results, the MHCK7 cassette is currently being tested with respect to its capacity for driving microdystrophin expression in mdx mice following intramuscular and systemic injections of rAAV6 vectors.

NO-1886 (ibrolipim), a lipoprotein lipase activator, increases the expression of uncoupling protein 3 in skeletal muscle and suppresses fat accumulation in high-fat diet–induced obesity in rats

Although the lipoprotein lipase (LPL) activator NO-1886 shows antiobesity effects in high-fat–induced obese animals, the mechanism remains unclear. To clarify the mechanism, we studied the effects of NO-1886 on the expression of uncoupling protein (UCP) 1, UCP2, and UCP3 in rats. NO-1886 was mixed with a high-fat chow to supply a dose of 100 mg/kg to 8-month-old male Sprague-Dawley rats. The animals were fed the high-fat chow for 8 weeks. At the end of the administration period, brown adipose tissue (BAT), mesenteric fat, and soleus muscle were collected and levels of UCP1, UCP2, and UCP3 messenger RNA (mRNA) were determined. NO-1886 suppressed the body weight increase seen in the high-fat control group after the 8-week administration (585 ± 39 vs 657 ± 66 g, P < .05). NO-1886 also suppressed fat accumulation in visceral (46.9 ± 10.4 vs 73.7 ± 14.5 g, P < .01) and subcutaneous (43.1 ± 18.1 vs 68.9 ± 18.8 g, P < .05) tissues and increased the levels of plasma total cholesterol and high-density lipoprotein cholesterol in comparison to the high-fat control group. In contrast, NO-1886 decreased the levels of plasma triglycerides, nonesterified free fatty acid, glucose, and insulin. NO-1886 increased LPL activity in soleus muscle (0.082 ± 0.013 vs 0.061 ± 0.016 μmol of free fatty acid per minute per gram of tissue, P < .05). NO-1886 increased the expression of UCP3 mRNA in soleus muscle 3.14-fold ( P < .01) compared with the high-fat control group without affecting the levels of UCP3 in mesenteric adipose tissue and BAT. In addition, NO-1886 did not affect the expression of UCP1 and UCP2 in BAT, mesenteric adipose tissue, and soleus muscle. In conclusion, NO-1886 increased the expression of UCP3 mRNA and LPL activity only in skeletal muscle. Therefore, a possible mechanism for NO-1886's antiobesity effects in rats may be the enhancement of LPL activity in skeletal muscle and the accompanying increase in UCP3 expression.

Ankle Muscle Activation During Functional Reach in Hemiparetic and Healthy Subjects

To compare the differences of reaching ability and electromyography of ankle muscles between healthy and hemiparetic subjects. This is a cross-sectional control trial. A total of 31 subjects with hemiparesis and 31 age-matched healthy adults meeting our selection criteria participated in this study. Subjects performed forward reach and lateral reach, in random sequence, in a sitting position. The average reaching velocity, reaching distance, and onset time and mean muscle activity of bilateral tibialis anterior and soleus were recorded. Subjects with hemiparesis had slower movement velocity and less reaching distance than that of healthy subjects (P < 0.05). The distance for the lateral reach was shorter than that of the forward reach (P < 0.05). The high correlations between contralateral tibialis anterior and soleus were noted in forward (r = 0.66, P < 0.01) and lateral (r = 0.68, P < 0.01) reaching in healthy subjects, but such correlations were not established in subjects with hemiparesis. Except for the ipsilateral soleus, normalized electromyographic activities (percentage of maximal voluntary isometric contraction) during forward and lateral reach were higher for the hemiparetic subjects than that for the healthy subjects (P < 0.05). The functional reach abilities and the ankle electromyographic activity patterns in hemiparetic subjects were significantly different from those of healthy subjects. The muscles in the affected ankle cannot be recruited timely and efficiently for the reaching task, even with relative recovery.

Motor Strategies Responsible for Maintaining Standing Posture After Deafferentation of the Unilateral Leg

Imai S, Hase K, Imanaka K, Suzuki E, Tanaka N, Liu M. Motor strategies responsible for maintaining standing posture after deafferentation of the unilateral leg. Objective To identify the motor strategies responsible for maintaining standing posture after deafferentation of the unilateral leg. Design Pretest-posttest, repeated-measures design. Setting A Japanese university hospital rehabilitation facility. Participants Nine healthy subjects aged 25 to 32 years. Intervention Two separate sessions that consisted of prolonged standing (control task) and standing until the H-reflex disappeared through the application of an inflated pneumatic cuff above the right knee. Main Outcome Measures Center of pressure (COP), hip and ankle joint positions, and electromyographic activities. Results In the control task, no time-related change during prolonged standing was found in any of the measured parameters. After deafferentation, the right soleus activity decreased significantly ( P<.01), so the mean velocities of the COP in the anteroposterior and mediolateral directions were greater and the average COP position under the right foot shifted backward compared with those in the previous periods ( P<.01). Also, the left tibialis anterior and soleus were activated, as was the bilateral gluteus medius. Conclusions The unilateral loss of leg and foot sensory information necessitated additional regulatory activities to stabilize the standing posture. The newly organized posture appeared to partly simulate the standing posture in patients with sensory disturbance of a unilateral leg.

Neuromechanical adaptation to hopping with an elastic ankle-foot orthosis

When humans hop or run on different surfaces, they adjust their effective leg stiffness to offset changes in surface stiffness. As a result, the overall stiffness of the leg-surface series combination remains independent of surface stiffness. The purpose of this study was to determine whether humans make a similar adjustment when springs are placed in parallel with the leg via a lower limb orthosis. We studied seven human subjects hopping in place on one leg while wearing an ankle-foot orthosis. We used an ankle-foot orthosis because the ankle joint is primarily responsible for leg stiffness during hopping. A spring was added to the ankle-foot orthosis so that it increased orthosis stiffness by providing plantar flexor torque during ankle dorsiflexion. We hypothesized that subjects would decrease their biological ankle stiffness when the spring was added to the orthosis, keeping total ankle stiffness constant. We collected kinematic, kinetic, and electromyographic data during hopping with and without the spring on the orthosis. We found that total ankle stiffness and leg stiffness did not change across the two orthosis conditions (ANOVA, P > 0.05). This was possible because subjects decreased their biological ankle stiffness to offset the orthosis spring stiffness (P < 0.0001). The reduction in biological ankle stiffness was accompanied by decreases in soleus, medial gastrocnemius, and lateral gastrocnemius muscle activation (P < 0.0002). These results suggest that an elastic exoskeleton might improve human running performance by reducing muscle recruitment.

Effects of dietary curcumin or N-acetylcysteine on NF-κB activity and contractile performance in ambulatory and unloaded murine soleus

BackgroundUnloading of skeletal muscle causes atrophy and loss of contractile function. In part, this response is believed to be mediated by the transcription factor nuclear factor-kappa B (NF-κB). Both curcumin, a component of the spice turmeric, and N-acetylcysteine (NAC), an antioxidant, inhibit activation of NF-κB by inflammatory stimuli, albeit by different mechanisms. In the present study, we tested the hypothesis that dietary curcumin or NAC supplementation would inhibit unloading-induced NF-κB activity in skeletal muscle and thereby protect muscles against loss of mass and function caused by prolonged unloading.MethodsWe used hindlimb suspension to unload the hindlimb muscles of adult mice. Animals had free access to drinking water or drinking water supplemented with 1% NAC and to standard laboratory diet or diet supplemented with 1% curcumin. For 11 days, half the animals in each dietary group were suspended by the tail (unloaded) and half were allowed to ambulate freely.ResultsUnloading caused a 51–53% loss of soleus muscle weight and cross-sectional area relative to freely-ambulating controls. Unloading also decreased total force and force per cross-sectional area developed by soleus. Curcumin supplementation decreased NF-κB activity measured in peripheral tissues of ambulatory mice by gel shift analysis. In unloaded animals, curcumin supplementation did not inhibit NF-κB activity or blunt the loss of muscle mass in soleus. In contrast, NAC prevented the increase in NF-κB activity induced by unloading but did not prevent losses of muscle mass or function.ConclusionIn conclusion, neither dietary curcumin nor dietary NAC prevents unloading-induced skeletal muscle dysfunction and atrophy, although dietary NAC does prevent unloading induced NF-κB activation.

An index of spindle efficacy obtained by measuring electroneurographic activity and passive tension in the rat soleus muscle

While muscle spindle afferent discharges are known to change with altered muscle use, the way in which the changes in spindle discharge are affected by modifications to the elastic properties of the muscle–tendon unit remains to analyze. This paper describes a methodology to define, in the rat, a spindle efficacy index. This index relates the spindle afferent discharges recorded from electroneurograms (ENG) due to muscle stretch to the passive elastic properties of the muscle–tendon unit quantified during the stretch imposed for the ENGs recordings. The stretches were applied to the rat soleus muscle after the Achilles tendon was severed. The spindle afferent discharges were characterized from the root mean square (RMS) values of electroneurograms (ENGs) recorded from the soleus nerve. The first step of the study was to validate the definition of dynamic and static indices (DI and SI) of spindle discharges from RMS-ENG as classically done when isolated afferents are studied. The slopes of the DI-stretch velocity or SI-stretch amplitude relationships gave the indices of spindle sensitivity under dynamic and static conditions, respectively. Incremental stiffness was calculated to describe the passive elastic properties during the dynamic and static phases of ramp and hold stretches applied at different amplitudes and velocities. The spindle efficacy index (SEI) is the ratio between the indices of spindle sensitivity and incremental stiffness values. Both spindle discharges and incremental stiffness increased with stretch amplitude under dynamic and static conditions. The corresponding SEI values were constant whatever the stretch amplitude. This result validates the relationship between spindle discharges and passive incremental stiffness. This method can be proposed to study, in the rat, the spindle function when the muscles are suspected to present changes in their neuromechanical properties.

Mechanisms underlying increases in rat soleus Na+-K+-ATPase activity by induced contractions

Acute regulation of the Na(+)-K(+)-ATPase activity in rat soleus muscle was investigated in response to 15 and 90 min of electrically induced contractile activity (500-ms trains at 30 Hz every 1.5 s). Kinetic measurements of Na(+)-K(+)-ATPase activity, assessed by the 3-O-methylfluorescein K(+)-stimulated phosphatase assay (3-O-MFP), were performed on crude homogenates (Hom) and on tissue separated into two membrane fractions, the sarcolemmal/particulate (SLP) and endosomal (En), in both stimulated (Stim) and contralateral control (Con) muscles. Maximal 3-O-MFP activity (V(max), nmol.mg protein(-1).h(-1)) was elevated (P < 0.05) in Stim by 40% and by 53% in Hom and by 37 and 40% in SLP at 15 and 90 min, respectively. The 38% increase (P < 0.05) in the alpha(2)-isoform subunit distribution in SLP at 15 min, as assessed by quantitative immunoblotting, persisted at 90 min, whereas for En a 42% decrease (P < 0.05) was observed only at 15 min. For the alpha(1)-subunit at 15 min, a 27% decrease (P < 0.05) was observed in En, whereas the 13% increase observed in SLP was not significant (P = 0.08). At 90 min, alpha(1) was increased (P < 0.05) by 14% in SLP and by 29% in En. No changes were observed in beta(1)-subunit distribution in En and SLP regardless of time of stimulation. Immunoprecipitation with antiphosphotyrosine antibody and quantitative immunoblotting with alpha(1)- and alpha(2)-antibodies indicated increases (P < 0.05) in tyrosine phosphorylation of 51% in alpha(2) at 15 min only. These results suggest that the increases in V(max) during contractile activity are mediated both by increased phosphorylation and by translocation of the enzyme to the plasma membrane.

Glucocorticoid-induced insulin resistance in skeletal muscles: defects in insulin signalling and the effects of a selective glycogen synthase kinase-3 inhibitor

Treatment with glucocorticoids, especially at high doses, induces insulin resistance. The aims of the present study were to identify the potential defects in insulin signalling that contribute to dexamethasone-induced insulin resistance in skeletal muscles, and to investigate whether the glycogen synthase-3 (GSK-3) inhibitor CHIR-637 could restore insulin-stimulated glucose metabolism. Skeletal muscles were made insulin-resistant by treating male Wistar rats with dexamethasone, a glucocorticoid analogue, for 12 days. Insulin-stimulated glucose uptake, glycogen synthesis and insulin signalling were studied in skeletal muscles in vitro. Dexamethasone treatment decreased the ability of insulin to stimulate glucose uptake, glycogen synthesis and glycogen synthase fractional activity. In addition, the dephosphorylation of glycogen synthase by insulin was blocked. These defects were paralleled by reduced insulin-stimulated protein kinase B (PKB) and GSK-3 phosphorylation. While expression of PKB, GSK-3 and glycogen synthase was not reduced by dexamethasone treatment, expression of the p85alpha subunit of phosphatidylinositol 3-kinase (PI 3-kinase) was increased. Inhibition of GSK-3 by CHIR-637 increased glycogen synthase fractional activity in soleus muscle from normal and dexamethasone-treated rats, although the effect was more pronounced in control rats. CHIR-637 did not improve insulin-stimulated glucose uptake in muscles from dexamethasone-treated rats. We demonstrated that chronic dexamethasone treatment impairs insulin-stimulated PKB and GSK-3 phosphorylation, which may contribute to insulin resistance in skeletal muscles. Acute pharmacological inhibition of GSK-3 activated glycogen synthase in muscles from dexamethasone-treated rats, but GSK-3 inhibition did not restore insulin-stimulated glucose uptake.

Effect of different ankle- and knee-joint positions on gastrocnemius medialis fascicle length and EMG activity during isometric plantar flexion

The purpose of this study was to provide evidence on the fact that the observed decrease in EMG activity of the gastrocnemius medialis (GM) at pronounced knee flexed positions is not only due to GM insufficiency, by examining muscle fascicle lengths during maximal voluntary contractions at different positions. Twenty-two male long distance runners (body mass: 78.5±6.7 kg, height: 183±6 cm) participated in the study. The subjects performed isometric maximal voluntary plantar flexion contractions (MVC) of their left leg at six ankle–knee angle combinations. To examine the resultant ankle joint moments the kinematics of the left leg were recorded using a Vicon 624 system with 8 cameras operating at 120 Hz. The EMG activity of GM, gastrocnemius lateralis (GL), soleus (SOL) and tibialis anterior (TA) were measured using surface electromyography. Synchronously, fascicle length and pennation angle values of the GM were obtained at rest and at the plateau of the maximal plantar flexion using ultrasonography. The main findings were: (a) identifiable differences in fascicle length of the GM at rest do not necessarily imply that these differences would also exist during a maximal isometric plantar flexion contraction and (b) the EMG activity of the biarticular GM during the MVC decreased at a pronounced flexed knee-joint position (up to 110°) despite of no differences in GM fascicle length. It is suggested that the decrease in EMG activity of the GM at pronounced knee flexed positions is due to a critical force–length potential of all three muscles of the triceps surae.

Inhibition from the plantar nerve to soleus muscle during the stance phase of walking

The purpose of this study is to investigate the effect and the circuit from the branch of tibial (plantar) nerve to soleus muscle and its modulation during walking in humans. Stimulation of the plantar nerve produced short latency inhibition of soleus EMG activity and the H-reflex in humans. The threshold of afferent fibers was lower than that of motor fibers. This inhibition did not converge to disynaptic reciprocal Ia inhibition nor did inhibition from the cutaneous nerve of the big toe, but to Ib inhibition from the medial gastrocnemius nerve. The inhibitory pathway from the plantar nerve therefore is considered to include Ib inhibitory interneurones. Modulation of the inhibition was investigated during walking. Less EMG depression after plantar nerve stimulation occurred in the stance phase of walking than for tonic or dynamic plantar flexion at similar background EMG activity level. The inhibition of the soleus H-reflex after plantar nerve stimulation was also decreased during the stance phase. For investigating the influence of load on the inhibition from the plantar nerve, more EMG depression occurred in the stance phase with body unloading. Similar findings were observed in Ib inhibition from the medial gastrocnemius nerve, but not in disynaptic reciprocal Ia inhibition to soleus muscle. It is concluded that transmission of inhibition from the plantar nerve to soleus muscle is modulated during walking. It would minimize this inhibition during the stance phase of walking and might enhance soleus muscle activity via this reflex pathway for the support of weight.

Can Muscle Sarcoplasmic Reticulum Ca2+-ATPase Defects Be Implicated In Exercise Intolerance In Chronic Heart Failure?

PURPOSE The purpose of this study was to determine the effects of experimental chronic heart failure (CHF) on maximal sarcoplasmic reticulum Ca2+-ATPase activity (Vmax) and Hill co-efficient (nH) in soleus (SOL), red gastrocnemius (RG) and white gastrocnemius (WG) and left ventricle (LV). METHODS Experimental CHF following ligation of the left main coronary artery in adult rats was confirmed by elevations (p < 0.05) in left-ventricle to body wt ratios (0.168±0.04 vs 0.186±0.07 g/g.100) in CHF compared to controls (CON). RESULTS Comparisons between CHF (n = 8) and CON (n = 8) indicated reduced (p < 0.05) Vmax (μmol.g protein−1·min−1) in SOL (197±22 vs 152±20), RG (399±8.2 vs 314±25) and WG (584±47 vs 449±59) in CHF. The nH was not different between CHF and CON for any of the muscles examined. The lower Vmax was accompanied by increases (p < 0.05) in SERCA 2 (% standard) in RG (38.7±10 vs 56.1±7.6) and WG (19.4±3.0 vs 27.0±2.2) only. No changes were observed in SERCA 1, as measured by Western blotting techniques. Reductions in Vmax were observed for LV (207±22 vs 162±14) in the absence of change in SERCA 2. CONCLUSION These results suggest that altered protein levels cannot explain the reduced Vmax observed in CHF. The results also suggest that defects in Ca2+-cycling may be involved in weakness and fatigue in CHF. Supported by Heart and Stroke Foundation (Ontario)

Endurance training increases lactate transport in male Zucker fa/ fa rats

The purpose of this study was to investigate the effect of endurance training (10 weeks) on previously reported alterations of lactate exchange in obese Zucker fa/ fa rats. We used sarcolemmal vesicles to measure lactate transport capacity in control sedentary rats, Zucker ( fa/ fa), and endurance trained Zucker ( fa/ fa) rats. Monocarboxylate transporter (MCT) 1 and 4 content was measured in sarcolemmal vesicles and skeletal muscle. Training increased citrate synthase activity in soleus and in red tibialis anterior, and improved insulin sensitivity measured by intraperitoneal glucose tolerance test. Endurance training increased lactate influx in sarcolemmal vesicles at 1 mM of external lactate concentration and increased MCT1 expression on sarcolemmal vesicles. Furthermore, muscular lactate level was significantly decreased after training in red tibialis anterior and extensor digitorum longus. This study shows that endurance training improves impairment of lactate transport capacity that is found in insulin resistance state like obesity and type 2 diabetes.

Hyperbaric exposure with high oxygen concentration enhances oxidative capacity of neuromuscular units

The effects of hyperbaric exposure with high oxygen concentration on spinal motoneurons and the skeletal muscle fibers that they innervate were investigated. Five-week-old male rats were exposed to a hyperbaric (1.25 atmospheric pressure) environment with a high oxygen concentration (35.0%) for 6 h daily. The number, cell body size, and oxidative enzyme activity of motoneurons innervating the soleus and plantaris muscles were examined after 8 weeks of hyperbaric exposure. In addition, the fiber type distribution, cell size, and oxidative enzyme activity of the slow soleus and fast plantaris muscles were examined. The oxidative enzyme activity of alpha motoneurons innervating the soleus and plantaris muscles increased after hyperbaric exposure, irrespective of their cell body sizes. The percentage of high-oxidative fibers in the soleus and plantaris muscles increased after hyperbaric exposure. The oxidative enzyme activity of all types of fibers in the soleus and plantaris muscles increased after hyperbaric exposure. It is concluded that hyperbaric exposure with high oxygen concentration enhances the oxidative capacity of neuromuscular units.

Voluntary exercise training enhances glucose transport but not insulin signaling capacity in muscle of hypertensive TG(mREN2)27 rats

Male heterozygous TG(mREN2)27 rats (TGR) overexpress a murine renin transgene, display marked hypertension, and have insulin resistance of skeletal muscle glucose transport and insulin signaling. We have shown previously that voluntary exercise training by TGR improves insulin-mediated skeletal muscle glucose transport (Kinnick TR, Youngblood EB, O'Keefe MP, Saengsirisuwan V, Teachey MK, and Henriksen EJ. J Appl Physiol 93: 805-812, 2002). The present study evaluated whether this training-induced enhancement of muscle glucose transport is associated with upregulation of critical insulin signaling elements, including insulin receptor substrate-1 (IRS-1), phosphatidylinositol 3-kinase, Akt, and glycogen synthase kinase-3. TGR remained sedentary or ran spontaneously in activity wheels for 6 wk, averaging 7.1 +/- 0.8 km/day by the end of week 3 and 4.3 +/- 0.5 km/day over the final week of training. Exercise training reduced total abdominal fat by 20% (P < 0.05) in TGR runners (2.64 +/- 0.01% of body weight) compared with sedentary TGR controls (3.28 +/- 0.01%). Insulin-stimulated (2 mU/ml) glucose transport activity in soleus muscle was 36% greater in TGR runners compared with sedentary TGR controls. However, the protein expression and functionality of tyrosine phosphorylation of insulin receptor and IRS-1, IRS-1 associated with the p85 regulatory subunit of phosphatidylinositol 3-kinase, and Ser473 phosphorylation of Akt were not altered by exercise training. Only insulin-stimulated glycogen synthase kinase-3beta Ser9 phosphorylation was increased (22%) by exercise training. These results indicate that voluntary exercise training in TGR can enhance insulin-mediated glucose transport in skeletal muscle, as well as reduce total abdominal fat mass. However, this adaptive response in muscle occurs independently of modifications in the proximal elements of the insulin signaling cascade.