Effects of two types of neuromuscular electrical stimulation training on vertical jump performance

This study examined the effects of different types of neuromuscular electrical stimulation (NMES) programs on vertical jump performance. Twenty seven healthy trained male students in sports-sciences were recruited and randomized into three groups. The control group (C group, n = 8) did not perform NMES training. Two other groups underwent 3 training sessions a week over 5 weeks on the quadriceps femoris muscle [F group (n = 9): stimulation with an 80 Hz current for 15 min for improving muscle strength; E group (n = 10): stimulation with a 25 Hz current for 60 min for improving muscle endurance]. The height of the vertical jump was measured before NMES training (test 1), one week (test 2) and five weeks (test 3) after the end of the programs. The results showed that the height of the vertical jump significantly increased in both the F and E groups between tests 1 and 2 (5 cm and 3 cm respectively). Results of test 3 showed that both groups preserved their gains. A NMES training program destined to improve muscle endurance does not interfere on vertical jump performance. It can even durably enhance it in the same way as a NMES training program destined to improve muscle strength. Thus, to improve muscle endurance without deteriorating muscle power, sportsmen can use electrical stimulation.     

Effect of hypoxia exposure on the recovery of skeletal muscle phenotype during regeneration

Hypoxia impairs the muscle fibre-type shift from fast-to-slow during post-natal development; however, this adaptation could be a consequence of the reduced voluntary physical activity associated with hypoxia exposure rather than the result of hypoxia per se. Moreover, muscle oxidative capacity could be reduced in hypoxia, particularly when hypoxia is combined with additional stress. Here, we used a model of muscle regeneration to mimic the fast-to-slow fibre-type conversion observed during post-natal development. We hypothesised that hypoxia would impair the recovery of the myosin heavy chain (MHC) profile and oxidative capacity during muscle regeneration. To test this hypothesis, the soleus muscle of female rats was injured by notexin and allowed to recover for 3, 7, 14 and 28 days under normoxia or hypobaric hypoxia (5,500 m altitude) conditions. Ambient hypoxia did not impair the recovery of the slow MHC profile during muscle regeneration. However, hypoxia moderately decreased the oxidative capacity (assessed from the activity of citrate synthase) of intact muscle and delayed its recovery in regenerated muscle. Hypoxia transiently increased in both regenerated and intact muscles the content of phosphorylated AMPK and Pgc-1α mRNA, two regulators involved in mitochondrial biogenesis, while it transiently increased in intact muscle the mRNA level of the mitophagic factor BNIP3. In conclusion, hypoxia does not act to impair the fast-to-slow MHC isoform transition during regeneration. Hypoxia alters the oxidative capacity of intact muscle and delays its recovery in regenerated muscle; however, this adaptation to hypoxia was independent of the studied regulators of mitochondrial turn-over.     

Effect of thyroid hormone on the myosin heavy chain isoforms in slow and fast muscles of the rat

The myosin heavy chain (MHC) was studied by biochemical methods in the slow-twitch (soleus) and two fast-twitch leg muscles of the triiodothyronine treated (hyperthyroid), thyroidectomized (hypothyroid) and euthyroid (control) rats. The changes in the contents of individual MHC isoforms(MHC-1, MHC-2A, MHC-2B and MHC-2X) were evaluated in relation to the muscle mass and the total MHC content. The MHC-1 content decreased in hyperthyreosis, while it increased in hypothyreosis in the soleus and in the fast muscles. The MHC-2A content increased in hyperthyreosis and it decreased in hypothyreosis in the soleus muscle. In the fast muscles hyperthyreosis did not affect the MHC-2A content, whereas hypothyreosis caused an increase in this MHC isoform content. The MHC-2X, present only in traces or undetected in the control soleus muscle, was synthesised in considerable amount in hyperthyreosis; in hypothyreosis the MHC-2X was not detected in the soleus. In the fast muscles the content of MHC-2X was not affected by any changes in the thyroid hormone level. The MHC-2B seemed to be not influenced by hyperthyreosis in the fast muscles, whereas the hypothyreosis caused a decrease of its content. In the soleus muscle the MHC-2B was not detected in any groups of rats. The results suggest that the amount of each of the four MHC isoforms expressed in the mature rat leg muscles is influenced by the thyroid hormone in a different way. The MHC-2A and the MHC-2X are differently regulated in the soleus and in the fast muscles; thyroid hormone seems to be necessary for expression of those isoforms in the soleus muscle.     

Myosin heavy chain isoform composition in striated muscle after denervation and self-reinnervation

The total content of myosin heavy chains (MHC) and their isoform pattern were studied by biochemical methods in the slow-twitch (soleus) and fast-twitch (extensor digitorum longus) muscles of adult rat during atrophy after denervation and recovery after self-reinnervation. The pattern of fibre types, in terms of ultrastructure, was studied in parallel. After denervation, total MHC content decreased sooner in the slow-twitch muscle than in the fast-twitch. The ratio of MHC-1 and the MHC-2B isoforms to the MHC-2A isoform decreased in the slow and the fast denervated muscles, respectively. After reinnervation of the slow muscle, the normal pattern of MHC recovered within 10 days and the type 1 isoform increased above the normal. In the reinnervated fast muscle, the 2B/2A isoform ratio continued to decrease. Traces of the embryonic MHC isoform, identified by immunochemistry, were found in both denervated and reinnervated slow and fast muscles. A shift in fibre types was similar to that found in the MHC isoforms. Within 2 months of recovery a tendency to normalization was observed. The results show that (a) MHC-2B isoform and the morphological characteristics of the 2B-type muscle fibres are susceptible to lack of innervation, similar to those of type 1, (b) during muscle recovery induced by reinnervation the MHC isoforms and muscle fibres shift transiently to type 1 in the soleus and to type 2A in the extensor digitorum longus muscles, and (c) the embryonic isoform of MHC may appear in the adult skeletal muscles if innervation is disturbed.     

Effects of T3 treatment on HSP72 and calcineurin content of functionally overloaded rat plantaris muscle

The content of both heat shock protein 72 (HSP72) and calcineurin (CaN) in skeletal muscle fibers have been reported to be associated with the slow phenotype. The purpose of the present study was to determine the adaptations/contributions of HSP72 and CaN to experimental conditions producing dramatic shifts in fiber phenotype. Two weeks of functional overload (FO) of the rat plantaris by cutting the tendons of its major synergists resulted in a shift towards a slower MHC profile. Two weeks of thyroid hormone (T3) administration (150 microg/kg/day, i.p.) resulted in a shift towards a faster MHC profile in control rats and an attenuation of the shift towards a slower profile in FO rats. HSP72 and CaN-A content were 63% and 47% higher, respectively, in the plantaris of FO than age-matched control rats. These increases were significantly attenuated by T3 treatment in FO rats. CaN-B levels were approximately 50% higher in FO and FO plus T3-treated than control rats. T3 treatment alone had no effect on the levels of HSP72, CaN-A or -B in control rats. Therefore, chronic overload of a muscle results in an increase in the percentage of slow fibers/MHC and enhances the levels of HSP72 and CaN. In turn, these FO-induced adaptations are attenuated by T3 treatment. Combined, these results indicate that muscle HSP72 and CaN protein levels are modulated by mechanical stress and that their levels appear to be related to changes in fiber type/MHC composition, at least in chronically overloaded muscles.     

Parallel and divergent adaptations of rat soleus and plantaris to chronic exercise and hypergravity

It has been demonstrated that endurance exercise and chronic acceleration, i.e., hypergravity, produce comparable adaptations in a variety of physiological systems, including decreased adiposity, increased energy metabolism, and altered intermediary metabolism. Similar adaptations have not been demonstrated for skeletal muscle per se. To further differentiate between these general responses with respect to gravity and exercise, this study tested the hypothesis that chronic exercise (voluntary wheel running) and chronic acceleration (2 G via centrifugation) will induce similar changes in muscle myosin heavy chain (MHC) isoform expression in rat plantaris, a fast extensor, and in rat soleus, a slow "antigravity" extensor. The experimental design involved four groups of mature male rats (n = 8/group): 1 G and 2 G with running wheels, and 1 G and 2 G controls without running wheels. The primary observations from the study were as follows: 1) 8 wk of 2 G are an adequate stimulus for MHC compositional changes in rat plantaris and soleus muscle; 2) both exercise and +G caused an increase in the slow MHC1 isoform in soleus muscle, suggesting that loading is a primary stimulus for this shift; and 3) 2 G and exercise appeared to have differential effects on the plantaris muscle MHC isoforms, with 2 G causing an increase in MHC2b, and exercise causing a decrease in MHC2b with a concomitant increase in MHC1, suggesting that factors other than enhanced loading, possibly locomotor activity levels, are the primary stimulus for this shift.     

Stretching prior to resistance training promotes adaptations on the postsynaptic region in different myofiber types

The morphology of the neuromuscular junction adapts according to changes in its pattern of use, especially at the postsynaptic region according to the myofibrillar type and physical exercise. This investigation revealed the morphological adaptations of the postsynaptic region after static stretching, resistance training, and their association in adult male Wistar rats. We processed the soleus and plantaris muscles for histochemical (muscle fibers) and postsynaptic region imaging techniques. We observed muscle hypertrophy in both groups submitted to resistance training, even though the cross-section area is larger when there is no previous static stretching. The soleus postsynaptic region revealed higher compactness and fragmentation index in the combined exercise. The resistance training promoted higher adaptations in the postsynaptic area of plantaris; moreover, the previous static stretching decreased this area. In conclusion, the neuromuscular system’s components responded according to the myofiber type even though it is the same physical exercise. Besides, static stretching (isolated or combined) plays a crucial role in neuromuscular adaptations.Key words: Neuromuscular junction, motor endplate, muscle hypertrophy, static stretching, resistance training     

Myosin isoform expression and MAFbx mRNA levels in hibernating golden-mantled ground squirrels (Spermophilus lateralis)

Hibernating mammals present many unexplored opportunities for the study of muscle biology. The hindlimb muscles of a small rodent hibernator (Spermophilus lateralis) atrophy slightly during months of torpor, representing a reduction in the disuse atrophy commonly seen in other mammalian models. How torpor affects contractile protein expression is unclear; therefore, we examined the myosin heavy-chain (MHC) isoform profile of ground squirrel skeletal muscle before and after hibernation. Immunoblotting was performed first to identify the MHC isoforms expressed in this species. Relative percentages of MHC isoforms in individual muscles were then measured using SDS-PAGE (sodium dodecyl sulfate-polyacrylamide gel electrophoresis). The soleus and diaphragm did not display differences in isoforms following hibernation, but we found minor fast-to-slow isoform shifts in MHC protein in the gastrocnemius and plantaris. These subtle changes are contrary to those predicted by other models of inactivity but may reflect the requirement for shivering thermogenesis during arousals from torpor. We also measured mRNA expression of the Muscle Atrophy F-box (MAFbx), a ubiquitin ligase important in proteasome-mediated proteolysis. Expression was elevated in the hibernating gastrocnemius and the plantaris but was not associated with atrophy. Skeletal muscle from hibernators displays unusual plasticity, which may be a combined result of the intense activity during arousals and the reduction of metabolism during torpor.     

The effects of electromechanical wrist robot assistive system with neuromuscular electrical stimulation for stroke rehabilitation

An electromyography (EMG)-driven electromechanical robot system integrated with neuromuscular electrical stimulation (NMES) was developed for wrist training after stroke. The performance of the system in assisting wrist flexion/extension tracking was evaluated on five chronic stroke subjects, when the system provided five different schemes with or without NMES and robot assistance. The tracking performances were measured by range of motion (ROM) of the wrist and root mean squared error (RMSE). The performance is better when both NMES and robot assisted in the tracking than those with either NMES or robot only (P<0.05). The muscle co-contractions in the upper limb measured by EMG were reduced when NMES provided assistance (P<0.05). All subjects also attended a 20-session wrist training for evaluating the training effects (3-5 times/week). The results showed improvements on the voluntary motor functions in the hand, wrist and elbow functions after the training, as indicated by the clinical scores of Fugl-Meyer Assessment, Action Research Arm Test, Wolf Motor Function Test; and also showed reduced spasticity in the wrist and the elbow as measured by the Modified Ashworth Score of each subject. After the training, the co-contractions were reduced between the flexor carpi radialis and extensor carpi radialis, and between the biceps brachii and triceps brachii. Assistance from the robot helped improve the movement accuracy; and the NMES helped increase the muscle activation for the wrist joint and suppress the excessive muscular activities from the elbow joint. The NMES-robot assisted wrist training could improve the hand, wrist, and elbow functions.     

Fiber type conversion alters inactivation of voltage-dependent sodium currents in murine C2C12 skeletal muscle cells

Each skeletal muscle of the body contains a unique composition of "fast" and "slow" muscle fibers, each of which is specialized for certain challenges. This composition is not static, and the muscle fibers are capable of adapting their molecular composition by altered gene expression (i.e., fiber type conversion). Whereas changes in the expression of contractile proteins and metabolic enzymes in the course of fiber type conversion are well described, little is known about possible adaptations in the electrophysiological properties of skeletal muscle cells. Such adaptations may involve changes in the expression and/or function of ion channels. In this study, we investigated the effects of fast-to-slow fiber type conversion on currents via voltage-gated Na⁺ channels in the C₂C₁₂ murine skeletal muscle cell line. Prolonged treatment of cells with 25 nM of the Ca²⁺ ionophore A-23187 caused a significant shift in myosin heavy chain isoform expression from the fast toward the slow isoform, indicating fast-to-slow fiber type conversion. Moreover, Na⁺ current inactivation was significantly altered. Slow inactivation less strongly inhibited the Na⁺ currents of fast-to-slow fiber type-converted cells. Compared with control cells, the Na⁺ currents of converted cells were more resistant to block by tetrodotoxin, suggesting enhanced relative expression of the cardiac Na⁺ channel isoform Na_v1.5 compared with the skeletal muscle isoform Na_v1.4. These results imply that fast-to-slow fiber type conversion of skeletal muscle cells involves functional adaptation of their electrophysiological properties. muscle plasticity; myosin heavy chain expression; sodium channel expression     

Slow myosin heavy chain expression in the absence of muscle activity

Innervation has been generally accepted to be a major factor involved in both triggering and maintaining the expression of slow myosin heavy chain (MHC-1) in skeletal muscle. However, previous findings from our laboratory have suggested that, in the mouse, this is not always the case (30). Based on these results, we hypothesized that neurotomy would not markedly reduced the expression of MHC-1 protein in the mouse soleus muscles. In addition, other cellular, biochemical, and functional parameters were also studied in these denervated soleus muscles to complete our study. Our results show that denervation reduced neither the relative amount of MHC-1 protein, nor the percentage of muscle fibers expressing MHC-1 protein (P > 0.05). The fact that MHC-1 protein did not respond to muscle inactivity was confirmed in three different mouse strains (129/SV, C57BL/6, and CD1). In contrast, all of the other histological, biochemical, and functional muscle parameters were markedly altered by denervation. Cross-sectional area (CSA) of muscle fibers, maximal tetanic isometric force, maximal velocity of shortening, maximal power, and citrate synthase activity were all reduced in denervated muscles compared with innervated muscles (P < 0.05). Contraction and one-half relaxation times of the twitch were also increased by denervation (P < 0.05). Addition of tenotomy to denervation had no further effect on the relative expression of MHC-1 protein (P > 0.05), despite a greater reduction in CSA and citrate synthase activity (P < 0.05). In conclusion, a deficit in neural input leads to marked atrophy and reduction in performance in mouse soleus muscles. However, the maintenance of the relative expression of slow MHC protein is independent of neuromuscular activity in mice.     

Functional adaptations of rat skeletal muscle arterioles to aerobic exercise training.

This study tested the hypothesis that both structural and functional adaptations of arterioles occur within the skeletal muscle of rats aerobically trained for 8-10 wk with treadmill exercise. The training regimen used has been shown to elicit a 37% increase in plantaris citrate synthase activity but did not result in an elevation in citrate synthase activity in the spinotrapezius or gracilis muscles of rats used in this study. In the in vivo resting spinotrapezius muscle, arteriole diameters were similar in sedentary (SED) and trained (TR) rats. However, large- (1A) and intermediate- (2A) sized arterioles dilated proportionately more in TR than in SED rats during 1- to 8-Hz muscle contractions, even though the passive mechanical properties (circumference-passive wall tension relationships) were similar between groups. Vascular casts demonstrated a trend for an increase in the number of small (3A) arterioles and an approximately 20% increase in the passive diameter of 1A and 2A arterioles in the spinotrapezius muscle of TR rats. In contrast, in the gracilis muscle, arteriole diameters and density were identical in SED and TR rats, but the capillary-to-muscle fiber ratio was approximately 15% higher in TR rats. The results suggest that aerobic exercise training can greatly increase functional vasodilation and induce a slight increase in vascular density in skeletal muscle tissues, even if the oxidative capacity of these tissues is not increased by the training regimen.     

Effects of strength, endurance, and concurrent training on aerobic power and dynamic neuromuscular economy in elderly men

The aim of this study was to investigate the effects of concurrent training on endurance capacity and dynamic neuromuscular economy in elderly men. Twenty-three healthy men (65 ± 4 years) were divided into 3 groups: concurrent (CG, n = 8), strength (SG, n = 8), and aerobic training group (EG, n = 7). Each group trained 3 times a week for 12 weeks, strength training, aerobic training, or both types of training in the same session. The maximum aerobic workload (Wmax) and peak oxygen uptake (VO2peak) of the subjects were evaluated on a cycle ergometer before and after the training period. Moreover, during the maximal test, muscle activation was measured at each intensity by means of electromyographic signals from the vastus lateralis (VL), rectus femoris (RF), biceps femoris long head, and gastrocnemius lateralis to determine the dynamic neuromuscular economy. After training, significant increases in VO2peak and Wmax were only found in the CG and EG (p < 0.05), with no difference between groups. Moreover, there was a significant decrease in myoelectric activity of the RF muscle at 50 (EG), 75 and 100 W (EG and CG) and in the VL for the 3 groups at 100 W (p < 0.05). No change was seen in the electrical signal from the lateral gastrocnemius muscle and biceps femoris. The results suggest specificity in adaptations investigated in elderly subjects, because the most marked changes in the neuromuscular economy occurred in the aerobically trained groups.     

Regenerated rat fast muscle transplanted to the slow muscle bed and innervated by the slow nerve,exhibits an identical myosin heavy chain repertoire to that of the slow muscle

 The hypothesis that the limited adaptive range observed in fast rat muscles in regard to expression of the slow myosin is due to intrinsic properties of their myogenic stem cells was tested by examining myosin heavy chain (MHC) expression in regenerated rat extensor digitorum longus (EDL) and soleus (SOL) muscles. The muscles were injured by bupivacaine, transplanted to the SOL muscle bed and innervated by the SOL nerve. Three months later, muscle fibre types were determined. MHC expression in muscle fibres was demonstrated immunohistochemically and analysed by SDS-glycerol gel electrophoresis. Regenerated EDL transplants became very similar to the control SOL muscles and indistinguishable from the SOL transplants. Slow type 1 fibres predominated and the slow MHC-1 isoform was present in more than 90% of all muscle fibres. It contributed more than 80% of total MHC content in the EDL transplants. About 7% of fibres exhibited MHC-2a and about 7% of fibres coexpressed MHC-1 and MHC-2a. MHC-2x/d contributed about 5–10% of the whole MHCs in regenerated EDL and SOL transplants. The restricted adaptive range of adult rat EDL muscle in regard to the synthesis of MHC-1 is not rooted in muscle progenitor cells; it is probably due to an irreversible maturation-related change switching off the gene for the slow MHC isoform. Accepted: 11 June 1996     

Effects of isometric training on skeletal myosin heavy chain expression

This studytested the hypothesis that an isometric resistance-training programinduces upregulation of slow myosin heavy chain (MHC) expression in afast-twitch skeletal muscle. Thus we studied the effects of tworesistance-training programs on rodent medial gastrocnemius (MG) musclethat were designed to elicit repetitive isometric contractions(10-12 per set; 4 sets per session) of different duration (8 vs. 5 s) and activation frequency (100 vs. 60 Hz) per contraction during eachtraining session (total of 6 and 12 sessions). Results showed that bothtraining paradigms produced significant increases in muscle weight(~11-13%) after completion of training(P < 0.05). Significanttransformations in MHC expression occurred and involved specifically adecrease in the relative expression of the fast type IIb MHC andconcomitant increased expression of the fast type IIx MHC.These adaptations were observed in both the "white" and"red" regions of the MG, and they occurred at both the mRNA andprotein levels. These adaptations were detected after onlysix training sessions. Neither of the training programs produced anychange in the relative expression of either the slow type I MHC or themoderately fast type IIa MHC, which can be upregulated in the red MG bychronic functional overload. These findings show that theisometric protocols used in this investigation were not sufficient toinduce the hypothesized changes in the myosin heavy chain isoformexpression in rodent skeletal muscle.

     

Neuromuscular Electrical Stimulation as a Method to Maximize the Beneficial Effects of Muscle Stem Cells Transplanted into Dystrophic Skeletal Muscle

Cellular therapy is a potential approach to improve the regenerative capacity of damaged or diseased skeletal muscle. However, its clinical use has often been limited by impaired donor cell survival, proliferation and differentiation following transplantation. Additionally, functional improvements after transplantation are all-too-often negligible. Because the host microenvironment plays an important role in the fate of transplanted cells, methods to modulate the microenvironment and guide donor cell behavior are warranted. The purpose of this study was to investigate whether the use of neuromuscular electrical stimulation (NMES) for 1 or 4 weeks following muscle-derived stem cell (MDSC) transplantation into dystrophic skeletal muscle can modulate the fate of donor cells and enhance their contribution to muscle regeneration and functional improvements. Animals submitted to 4 weeks of NMES after transplantation demonstrated a 2-fold increase in the number of dystrophin+ myofibers as compared to control transplanted muscles. These findings were concomitant with an increased vascularity in the MDSC+NMES group when compared to non-stimulated counterparts. Additionally, animals subjected to NMES (with or without MDSC transplantation) presented an increased maximal specific tetanic force when compared to controls. Although cell transplantation and/or the use of NMES resulted in no changes in fatigue resistance, the combination of both MDSC transplantation and NMES resulted in a faster recovery from fatigue, when compared to non-injected and non-stimulated counterparts. We conclude that NMES is a viable method to improve MDSC engraftment, enhance dystrophic muscle strength, and, in combination with MDSC transplantation, improve recovery from fatigue. These findings suggest that NMES may be a clinically-relevant adjunct approach for cell transplantation into skeletal muscle.     

Modulation of the rate of force development in hip abductor muscles by neuromuscular electrical stimulation during gait

Abstract

Purpose/aim of the study: An increase of hip abductor muscle strength contributes to the increase in gait speed. It is known that the rate of force development (RFD), an indicator of muscle strength, is increased by the combined use of low-intensity neuromuscular electrical stimulation (NMES) to the glutaeus medius (GM) and low-load resistance training (RT). However, it is unclear whether low-intensity neuromuscular electrical stimulation of the glutaeus medius during walking also increases the rate of force development. The aim of this study was to clarify whether NMES to the GM during gait modulates the RFD of the hip abductor muscles in healthy adults.

Materials and methods: Twenty-two healthy adults randomly received both gait with sub-motor threshold NMES and gait with sham NMES conditions. The RFD was assessed at pre- and post-intervention. A two-way repeated measures analysis of variance was used to analyse the effects of time and intervention.

Results: Gait with sub-motor threshold NMES condition significantly increased the RFD in shorter time interval (0–50 and 0–100?ms) compared to gait with sham NMES condition.

Conclusions: These findings suggest that the adding low-intensity NMES of the GM to gait is effective in increasing the RFD of the hip abductor muscles.     

Motor unit recruitment when neuromuscular electrical stimulation is applied over a nerve trunk compared with a muscle belly: quadriceps femoris

Neuromuscular electrical stimulation (NMES) can be delivered over a nerve trunk or muscle belly and both can generate contractions through peripheral and central pathways. Generating contractions through peripheral pathways is associated with a nonphysiological motor unit recruitment order, which may limit the efficacy of NMES rehabilitation. Presently, we compared recruitment through peripheral and central pathways for contractions of the knee extensors evoked by NMES applied over the femoral nerve vs. the quadriceps muscle. NMES was delivered to evoke 10 and 20% of maximum voluntary isometric contraction torque 2-3 s into the NMES (time(1)) in two patterns: 1) constant frequency (15 Hz for 8 s); and 2) step frequency (15-100-15 Hz and 25-100-25 Hz for 3-2-3 s, respectively). Torque and electromyographic activity recorded from vastus lateralis and medialis were quantified at the beginning (time(1)) and end (time(2); 6-7 s into the NMES) of each pattern. M-waves (peripheral pathway), H-reflexes, and asynchronous activity (central pathways) during NMES were quantified. Torque did not differ regardless of NMES location, pattern, or time. For both muscles, M-waves were ～7-10 times smaller and H-reflexes ～8-9 times larger during NMES over the nerve compared with over the muscle. However, unlike muscles studied previously, neither torque nor activity through central pathways were augmented following 100 Hz NMES, nor was any asynchronous activity evoked during NMES at either location. The coefficient of variation was also quantified at time(2) to determine the consistency of each dependent measure between three consecutive contractions. Torque, M-waves, and H-reflexes were most variable during NMES over the nerve. In summary, NMES over the nerve produced contractions with the greatest recruitment through central pathways; however, considering some of the limitations of NMES over the femoral nerve, it may be considered a good complement to, as opposed to a replacement for, NMES over the quadriceps muscle for maintaining muscle quality and reducing contraction fatigue during NMES rehabilitation.     

Diaphragm contractile dysfunction in MyoD gene-inactivated mice

MyoD is one of four myogenic regulatory factors found exclusively in skeletal muscle. In an effort to better understand the role that MyoD plays in determining muscle contractile properties, we examined the effects of MyoD deletion on both diaphragmatic contractile properties and myosin heavy chain (MHC) phenotype. Regions of the costal diaphragm from wild-type and MyoD knockout [MyoD (-/-)] adult male BALB/c mice (n = 8/group) were removed, and in vitro diaphragmatic contractile properties were measured. Diaphragmatic contractile measurements revealed that MyoD (-/-) animals exhibited a significant (P < 0.05) downward shift in the force-frequency relationship, a decrement in maximal specific tension (P(o); -33%), a decline in maximal shortening velocity (V(max); -37%), and concomitant decrease in peak power output (-47%). Determination of MHC isoforms in the diaphragm via gel electrophoresis revealed that MyoD elimination resulted in a fast-to-slow shift (P < 0.05) in the MHC phenotype toward MHC types IIA and IIX in MyoD (-/-) animals. These data indicate that MyoD deletion results in a decrease in diaphragmatic submaximal force generation and P(o), along with decrements in both V(max) and peak power output. Hence, MyoD plays an important role in determining diaphragmatic contractile properties.