Extensor motoneurone properties are altered immediately before and during fictive locomotion in the adult decerebrate rat.

This study examined motoneurone properties during fictive locomotion in the adult rat for the first time. Fictive locomotion was induced via electrical stimulation of the mesencephalic locomotor region in decerebrate adult rats under neuromuscular blockade to compare basic and rhythmic motoneurone properties in antidromically identified extensor motoneurones during: (1) quiescence, before and after fictive locomotion; (2) the 'tonic' period immediately preceding locomotor-like activity, whereby the amplitude of peripheral flexor (peroneal) and extensor (tibial) nerves are increased but alternation has not yet occurred; and (3) locomotor-like episodes. Locomotion was identified by alternating flexor-extensor nerve activity, where the motoneurone either produced membrane oscillations consistent with a locomotor drive potential (LDP) or did not display membrane oscillation during alternating nerve activity. Cells producing LDPs were referred to as such, while those that did not were referred to as 'idle' motoneurones. LDP and idle motoneurones during locomotion had hyperpolarized spike threshold (Vth ; LDP: 3.8 mV; idle: 5.8 mV), decreased rheobase and an increased discharge rate (LDP: 64%; idle: 41%) during triangular ramp current injection even though the frequency-current slope was reduced by 70% and 55%, respectively. Modulation began in the tonic period immediately preceding locomotion, with a hyperpolarized Vth and reduced rheobase. Spike frequency adaptation did not occur in spiking LDPs or firing generated from sinusoidal current injection, but occurred during a sustained current pulse during locomotion. Input conductance showed no change. Results suggest motoneurone modulation occurs across the pool and is not restricted to motoneurones engaged in locomotion.

Adaptations of motoneuron properties to chronic compensatory muscle overload.

The aim of the study was to determine whether chronic muscle overload has measurable effect on electrophysiological properties of motoneurons (MNs), and whether duration of this overload influences intensity of adaptations. The compensatory overload was induced in the rat medial gastrocnemius (MG) by bilateral tenotomy of its synergists (lateral gastrocnemius, soleus, and plantaris); as a result, only the MG was able to evoke the foot plantar flexion. To assure regular activation of the MG muscle, rats were placed in wheel-equipped cages and subjected to a low-level treadmill exercise. The intracellular recordings from MG motoneurons were made after 5 or 12 wk of the overload, and in a control group of intact rats. Some of the passive and threshold membrane properties as well as rhythmic firing properties were considerably modified in fast-type MNs, while remaining unaltered in slow-type MNs. The significant changes included a shortening of the spike duration and the spike rise time, an increase of the afterhyperpolarization amplitude, an increase of the input resistance, a decrease of the rheobase, and a decrease of the minimum current necessary to evoke steady-state firing. The data suggest higher excitability of fast-type MNs innervating the overloaded muscle, and a shift towards electrophysiological properties of slow-type MNs. All of the adaptations could be observed after 5 wk of the compensatory overload with no further changes occurring after 12 wk. This indicates that the response to an increased level of chronic activation of MNs is relatively quick and stable.

Transcriptional changes in rat α-motoneurons resulting from increased physical activity.

Electrophysiological properties of lumbar α-motoneurons change after chronic increases and decreases in hindlimb neuromuscular activity. Although modeling of these changes suggests that motoneurons probably alter gene expression in these situations, there is no evidence that this is the case. In this study, we measured the content of several mRNAs in lumbar motoneurons, harvested using laser capture microdissection, from rats previously subjected to normal cage activity, voluntary wheel exercise for 16weeks, and forced treadmill training for 7days and 16weeks. As a result of the prolonged daily treadmill training, but not the voluntary wheel training, significant increases occurred in muscle peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (PGC-1α) mRNA, and in muscle PGC-1α and cytochrome oxidase proteins, in soleus and plantaris muscles. Significant changes in mRNA contents (decreases) were evident for the receptors 5-hydroxytryptamine (serotonin) receptor 1A (5HT1a), GABA A receptor, subunit alpha 2 (GABAAα2), and for the potassium conductance calcium-activated channel protein (SK2) in the motoneurons from 16-week-trained rats, and for glutamate receptor, metabotropic 1 (mGluR1) in the voluntary wheel-trained rats. Motoneurons from 16-week treadmill-trained rats also did not demonstrate the decreases in several mRNAs that were evident after 7days of treadmill exercise, suggesting an adaptation of motoneurons to acute stress. The mRNA changes following prolonged daily treadmill training are consistent with a reduction in inhibitory influences onto motoneurons, and a transition toward motoneurons that innervate slower contracting muscle fibers. These results demonstrate that the previously reported physiological changes in motoneurons with altered activity are accompanied by changes in gene expression.

Plasticity of rat motoneuron rhythmic firing properties with varying levels of afferent and descending inputs.

Hindlimb motoneuron excitability was compared among exercise-trained (E), sedentary (S), and spinal cord transected (T) Sprague-Dawley rats by examining the slope of the frequency-current (F/I) relationship with standard intracellular recording techniques in rats anesthetized with ketamine-xylazine. The T group included spinal transected and spinal isolated rats; the E animals were either spontaneously active (exercise wheel) or treadmill trained; and rats in the S group were housed in pairs. An analysis of motoneuron initial [1st interspike interval (ISI)], early (mean of 1st three ISIs), and steady-state (mean of last 3 ISIs) discharge rate slopes resulting from increasing and decreasing 500-ms injected square-wave depolarizing current pulses was used to describe rhythmic motoneuron properties. The steepest slope occurred in the S group (55.3 ± 22.2 Hz/nA), followed by the T group (35.5 ± 15.3 Hz/nA), while the flattest slope was found in the E group (25.4 ± 10.9 Hz/nA). The steepest steady-state slope occurred in the S group but was found to be similar between the T and E groups. Furthermore, a spike-frequency adaptation (SFA) index revealed a slower adaptation in motoneurons of the E animals only (∼40% lower). Finally, evidence for a secondary range of firing existed more frequently in the T group (41%) compared with the S (12%) and E (31%) groups. The lower F/I slope and lower SFA index of motoneurons for E rats may be a result of an increase in Na(+) conductance at the initial segment. The results show that motoneuronal rhythmic firing behavior is plastic, depending on the volume of daily activation and on intact descending pathways.

Insight into skeletal muscle mechanotransduction: MAPK activation is quantitatively related to tension.

The mechanism by which mechanical forces acting through skeletal muscle cells generate intracellular signaling, known as mechanotransduction, and the details of how gene expression and cell size are regulated by this signaling are poorly understood. Mitogen-activated protein kinases (MAPKs) are known to be involved in mechanically induced signaling in various cell types, including skeletal muscle where MAPK activation has been reported in response to contraction and passive stretch. Therefore, the investigation of MAPK activation in response to mechanical stress in skeletal muscle may yield important information about the mechanotransduction process. With the use of a rat plantaris in situ preparation, a wide range of peak tensions was generated through passive stretch and concentric, isometric, and eccentric contractile protocols, and the resulting phosphorylation of c-Jun NH(2)-terminal kinase (JNK), extracellular regulated kinase (ERK), and p38 MAPKs was assessed. Isoforms of JNK and ERK MAPKs were found to be phosphorylated in a tension-dependent manner, such that eccentric > isometric > concentric > passive stretch. Peak tension was found to be a better predictor of MAPK phosphorylation than time-tension integral or rate of tension development. Differences in maximal response amplitude and sensitivity between JNK and ERK MAPKs suggest different roles for these two kinase families in mechanically induced signaling. A strong linear relationship between p54 JNK phosphorylation and peak tension over a 15-fold range in tension (r(2) = 0.89, n = 32) was observed, supporting the fact that contraction-type differences can be explained in terms of tension and demonstrating that MAPK activation is a quantitative reflection of the magnitude of mechanical stress applied to muscle. Thus the measurement of MAPK activation, as an assay of skeletal muscle mechanotransduction, may help elucidate mechanically induced hypertrophy.

Habitual exercise enhances neuromuscular transmission efficacy of rat soleus muscle in situ.

Rat motor nerve terminals and the endplates they interact with exhibit changes to varying patterns of use, as when exposed to increased activation in the form of endurance exercise training. The extent to which these changes affect neuromuscular transmission efficacy is uncertain. In this study, the effects of habitual exercise on the electrophysiological properties of neuromuscular transmission in rat soleus muscle were investigated using a novel in situ approach. Consistent with previous reports, miniature endplate potential frequency was enhanced by habitual exercise. Other passive properties, such as resting membrane potential, miniature endplate potential amplitude, and "giant" miniature endplate potential characteristics were unaltered by the training program. Full-size endplate potentials were obtained by blocking soleus muscle action potentials with mu-conotoxin GIIIb. Quantal content values were 91.5 and 119.9 for control and active groups, respectively (P < 0.01). We also measured the rate and extent of endplate potential amplitude rundown during 3-s trains of continuous stimulation at 25, 50, and 75 Hz; at 50 and 75 Hz, we found both the rate and extent of rundown to be significantly attenuated (10--20%) in a specific population of cells from active rats (P < 0.05). The results establish the degree of activity-dependent plasticity as it pertains to neuromuscular transmission in a mammalian slow-twitch muscle.

Changes in electrophysiological properties of tibial motoneurones in the rat following 4 weeks of tetrodotoxin-induced paralysis.

In this study, we test the hypothesis that 4 weeks tetrodotoxin (TTX) paralysis altered the passive membrane properties of rat tibial motoneurones. Impulse activity along the sciatic nerve was blocked for 4 weeks using TTX delivered by an osmotic minipump to a Silastic cuff placed around the nerve. That portion of the sample exhibiting the 20% slowest After-hyperpolarization (AHP) decay time (AHPd), and which therefore included presumptive type S motoneurons, demonstrated responses (reduced AHPd, increased rheobase and rheobase voltage), which were not evident in the rest of the sample (presumptive fast motoneurons), in which an increased AHPd, in fact, was found. The results thus support the hypothesis that retrograde signals from inactive slow and fast muscle fibers have different effects on their innervating motoneurones.

Myosin heavy chains in fibers of TTX-paralyzed rat soleus and medial gastrocnemius muscles.

The expression of five myosin heavy chain (MHC) isoforms was analyzed in the rat soleus (Sol) and the deep and superficial medial gastrocnemius (dGM, sGM) muscle after 2 and 4 wk of TTX paralysis by using immunohistochemical techniques. In Sol, after 4 wk of paralysis, fibers containing type I MHC were either pure type I (14%) or also contained developmental (D; 76%), IIa (26%), or IIx (18%) MHC. Values for corresponding fibers in dGM were 8.5, 65, 38, and 22%. Also, by 4 wk an increase was seen in the proportions of fibers expressing IIa MHC in Sol (from 16 to 38%) and dGM (from 24 to 74%). In a region of sGM in control muscles containing pure IIb fibers, a major proportion (86%) remained pure after 4 wk of paralysis, with the remainder coexpressing IIb and IIx. The results indicate that TTX-induced muscle paralysis results in an increase in fibers containing multiple MHC isoforms and that the D isoform appears in a major proportion of these hybrid fibers.

Salbutamol effect in spinal cord injured individuals undergoing functional electrical stimulation training.

OBJECTIVE: Preliminary study to investigate possible changes in skeletal muscle morphology and function, as well as hormonal and metabolic effects, after treatment with a selective beta2-adrenergic receptor agonist. DESIGN: Double-blind, placebo-controlled trial. PARTICIPANTS: Three individuals with spinal cord injury (SCI). INTERVENTION: Two-week treatment with salbutamol (2mg) or placebo (ascorbic acid, 50mg) twice a day. Program of functional electronic stimulation (FES) cycling for 30 minutes twice a week. MAIN OUTCOME MEASURES: Body weight, three measures of leg circumference (gluteal furrow, one third of subischial height up from tibial-femoral joint space, and minimum circumference above the knee), muscle fiber area, and total work output per session. RESULTS: There were increases in body weight (2.30 +/- .70kg), leg circumferences (gluteal furrow 1.70 +/- .27cm, one third subischial height 1.53 +/- 1.65cm, minimum circumference above the knee .43 +/- .04cm), and muscle (vastus lateralis) cross-sectional area (1,374 +/- 493 to 2,446 +/- 1,177microm2) after salbutamol treatment, whereas quadriceps muscle contractile function was not modified. Total work output during FES cycling sessions was increased more during salbutamol treatment (64%) compared with training alone (27%). Salbutamol treatment was associated with a large decrease in skeletal muscle beta-adrenergic receptor density. CONCLUSION: Although some side effects were noted, these results suggest that a short treatment with the beta2-adrenergic receptor agonist salbutamol during a training program with FES cycling could be beneficial in patients with SCI.

Fatigability of rat hindlimb muscles after acute irreversible acetylcholinesterase inhibition.

The purpose of this study was to investigate the functional impact of acute irreversible inhibition of acetylcholinesterase (AChE) on the fatigability of medial gastrocnemius and plantaris muscles of Sprague-Dawley rats. After treatment with methanesulfonyl fluoride (a lipid-soluble anticholinesterase), which reduced their AChE activity by >90%, these muscles were subjected to an in situ indirect stimulation protocol, including a series of isolated twitch and tetanic contractions preceding a 3-min fatigue regimen (100-ms trains at 75 Hz applied every 1.5 s). During the first minute of the fatigue regimen, the effects of AChE inhibition were already near maximal, including marked reductions in peak tension and the force-time integral (area), as well as a decrement of compound muscle action potential amplitudes within a stimulus train. Neuromuscular transmission failure was the major contributor of the force decreases in the AChE-inhibited muscles. However, despite this neuromuscular transmission failure, muscles of which all AChE molecular forms were nearly completely inhibited were still able to function, although abnormally, during 3 min of intermittent high-frequency nerve stimulation.

Nifedipine does not impede clenbuterol-stimulated muscle hypertrophy.

The mechanism(s) responsible for beta2-adrenergic receptor-mediated skeletal muscle and cardiac hypertrophy remains undefined. This study examined whether calcium influx through L-type calcium channels contributed to the development of cardiac and skeletal muscle (plantaris; gastrocnemius; soleus) hypertrophy during an 8-day treatment with the beta2-adrenergic receptor agonist clenbuterol. Concurrent blockade of L-type calcium channels with nifedipine did not reverse the hypertrophic action of clenbuterol. Moreover, nifedipine treatment alone resulted in both cardiac and soleus muscle hypertrophy (6% and 7%, respectively), and this effect was additive to the clenbuterol-mediated hypertrophy in the heart and soleus muscles. The hypertrophic effects of nifedipine were not associated with increases in total beta-adrenergic receptor density, nor did nifedipine reverse clenbuterol-mediated beta-adrenergic receptor downregulation in either the left ventricle or soleus muscle. Both nifedipine and clenbuterol-induced hypertrophy increased total protein content of the soleus and left ventricle, with no change in protein concentration. In conclusion, our results support the hypothesis that beta2-adrenergic receptor agonist-induced muscle hypertrophy is mediated by mechanisms other than calcium influx through L-type calcium channels.

Endurance training increases acetylcholine receptor quantity at neuromuscular junctions of adult rat skeletal muscle.

The aim of the study was to test the hypothesis that a 16 week endurance training program would alter the abundance of endplate-associated nicotinic acetylcholine receptors (nAChR) in various rat skeletal muscles. We found a 20% increase in endplate-specific [125I]alpha-bungarotoxin binding in several muscles of trained rats, accompanied by equal susceptibility of toxin binding to the inhibitory effect of D-tubocurarine in sedentary and trained muscles. We conclude that the neuromuscular junction adaptations that occur with increased chronic activation include an increase in nAChR number. Results of experiments designed to determine nAChR turnover also suggest that this effect is mediated by an alteration in the receptor's metabolic state. The potential implications and mechanisms of this adaptation are discussed.

The case for adaptability of the neuromuscular junction to endurance exercise training.

Although the adaptability of the neuromuscular junction (NMJ) has been demonstrated using the models of denervation/reinnervation, electrical stimulation, development, aging, and pathological states, relatively little is known about the effects of increased chronic voluntary use on the morphology and physiological function of the NMJ. A review of findings relating to adaptations in the various pre- and postsynaptic components of the NMJ with exercise training is presented. These findings are discussed as they pertain to NMJ function during exercise. Other physiological modulators of the NMJ, such as trophic factors released by nerve terminals and muscles, and circulating substances are discussed in terms of possible roles they may play in training-induced adaptations.

Chronic beta-blockade increases skeletal muscle beta-adrenergic-receptor density and enhances contractile force.

The effects of a chronic 14-day administration of a selective beta2-adrenergic-receptor antagonist (ICI-118551) on skeletal muscle were evaluated in female Sprague-Dawley rats. Chronic ICI-118551 treatment did not modify muscle mass, oxidative potential, or protein concentration of the medial gastrocnemius muscle, suggesting that maintenance of these skeletal muscle characteristics is not dependent on beta2-adrenergic-receptor stimulation. However, the drug treatment increased beta-adrenergic-receptor density of the lateral gastrocnemius (42%) and caused an increase in specific (g/g) isometric in situ contractile forces of the medial gastrocnemius [twitch, 56%; tetanic (200 Hz), 28%]. The elevated contractile forces observed after a chronic treatment with ICI-118551 were completely abolished when the beta2-adrenergic antagonist was also administered acutely before measurement of contractile forces, suggesting that this response is beta2-adrenergic-receptor dependent. Possible mechanisms for the increased forces were studied. Caffeine administration potentiated twitch forces but had little effect on tetanic force in control animals. Administration of dibutyryl adenosine 3',5'-cyclic monophosphate in control animals also resulted in small increases of twitch force but did not modify tetanic forces. We conclude that increases in beta-adrenergic-receptor density and the stimulation of the receptors by endogenous catecholamines appear to be responsible for increased contractile forces but that the mechanism remains to be demonstrated.

The effects of tetrodotoxin-induced muscle paralysis on the physiological properties of muscle units and their innervating motoneurons in rat.

1. Although the inactivity of a slow muscle (cat soleus) induced via nerve impulse blockade has been demonstrated to have some axotomy-like effects (decreased after-hyperpolarization (AHP) duration) on its innervating motoneurons, the reported effects of inactivity on motoneurons which innervate fast muscles containing mixtures of motor unit types are equivocal. This study was designed to determine the effect of a period (2 weeks) of complete hindlimb muscle paralysis, via tetrodotoxin (TTX) blockade of sciatic nerve impulses, on the contractile (muscle units) and electrophysiological (motoneurons) properties of motor units in the rat gastrocnemius. Motoneuron properties were also compared with those of rats subjected to sciatic nerve axotomy 2 weeks earlier. 2. At the time of the terminal experiment (24 h after the removal of the TTX delivery system) in anaesthetized animals, properties of tibial motoneurons (i.e. rheobase current, input resistance, time course of after-potentials) were determined using conventional microelectrode techniques. For those tibial motoneurons innervating the gastrocnemius, muscle unit responses (i.e. twitch force and time course, maximum tetanic tension, fatigability) were also recorded in response to current injection. 3. Consistent with previously reported whole-muscle responses to TTX-induced disuse, the TTX-treated gastrocnemius muscle units showed weaker tetanic forces, prolonged twitches and elevated twitch/tetanic ratios. These effects were similar for motor units classified as small, medium and large according to their tetanic tension-generating capacities. Muscle unit fatigue resistances appeared to be unchanged. 4. The mean values, distributions and ranges of tibial motoneuron properties were similar between control and TTX-treated groups for rheobase, input resistance and AHP half-decay time. In the case of the latter, the proportion of motoneurons possessing "slow' AHP half-decay times (> 20 ms) was not significantly different in control (17%) and TTX-treated groups (11%). 5. Motoneurons axotomized 2 weeks earlier had a significantly higher (42-69%) mean input resistance and a longer (34-42%) mean AHP half-decay time when compared with the control and TTX-treated groups. 6. It appears that, for fast muscles containing several different motor unit types, TTX-induced axon blockade does not produce similar effects on motoneuron intrinsic properties to those evoked by axotomy. This lack of effect on the distribution and range of these properties of tibial motoneurons indicates that none of the motoneurons which innervate muscles of mixed fibre type are particularly susceptible to the decreased activity and the atrophy-associated muscle changes produced by this condition. Thus, the apparent 'retrograde signalling' of muscle on motoneuron properties reported previously for the cat soleus may be specific to this particular muscle or species.

The effect of diazepan and exercise training on selected biochemical and histochemical properties of rat skeletal muscle.

The effects of chronic diazepam (D) treatment and exercise training on total body mass (TBM), microsomal protein yield (MPY), calcium uptake by fragmented sarcoplasmic reticulum (SR), muscle fibre cross-sectional area, and both PFK and SDH activities were investigated in the tibialis anterior (TA), soleus (Sol), and plantaris (Plt) muscles of 50 male albino Sprague-Dawley rats. Rats were assigned randomly to control (C), sprint-trained (S), or endurance-trained (E) groups. Training was of 12 weeks duration. One-half of each group received daily intraperitoneally D doses of 5 mg kg-1 of TBM. Exercise reduced TBM (p < 0.05); increased the relative BM of the TA (E = 2.02 +/- 0.02, p < 0.01) and Plt (E = 1.15 +/- 0.02, p < 0.01; S = 1.13 +/- 0.03, p < 0.01), as well as the Ca++ uptake of the Sol SR (C = 0.08 +/- 0.02, E = 0.16 +/- 01, p < 0.05). MPY was elevated in S-Sol (C = 1.12 +/- 0.6, S = 1.52 +/- 0.1, p < 0.01). D elevated Sol MPY as well as TA PFK. S-trained animals had lower mean fibre areas than the E-trained (D-treated and untreated) animals. The elevated relative masses of TA and Plt are explained by a decreased TBM with exercise. The increased Ca++ uptake of the Sol indicates that E enhances this function, and the increased MPY probably implies an increased SR. The D could be responsible for the D-elevated Sol MPY as well as the TA PFK. El D did not reduce neuromuscular activity to a level adversely affecting oxidative enzyme activity, but in the case of PFK activity in the TA muscle, such a reduction was evident.

The effect of diazepan and exercise training on selected biochemical and histochemical properties of rat skeletal muscle

The effects of chronic diazepan (D) treatment and exercise training on total body mass (TBM), microsomal protein yield (MPY), calcium uptake by fragmented sarcoplasmic reticulum (SR), muscle fibre cross-sectional area, and both PFK and SDH activities were investigated in the tibialis anterior (TA), soleus (Sol), and plantaris (Plt) muscles of 50 male albino Sprague-Dawley rats. Rats were assigned randomly to control (C), sprint-trained (S), or endurance-trained (E) groups. Training was of 12 weeks duration. One-half of each group received daily intraperitoneally D doses of 5 mg kg(-1) of TBM. Exercise reduced TBM (p<0.05); increased the relative BM of the TA (E=2.02+0.02, p<0.01) and Plt (E=1.15+0.02, p<0.01; S=1.13+0.03, p<0.01), as well as the Ca++ uptake of the Sol SR (C=0.08+0.02, E=0.16+01, p<0.05). MPY was elevated in S-Sol (C=1.12+0.6, S=1.52+0.1, p<0.01). Delevated Sol MPY as well as TA PFK. S-trained animals had lower mean fibre areas than the E-trained (D-treated and untreated) animals. The elevated relative masses of TA and Plt are explained by a decreased TBM with exercise. The increased Ca++ uptake of the Sol indicates that E enhances this function, and the increased MPY probably implies an increased SR. The D could be responsible for the D-elevated Sol MPY as well as the TA PFK. El D did not reduce neuromuscular activity to a level adversely affecting oxidative enzyme activity, but in the case of PFK activity in the TA muscle, such a reduction was evident. (AU)

The effect of diazepan and exercise training on selected biochemical and histochemical properties of rat skeletal muscle

The effects of chronic diazepan (D) treatment and exercise training on total body mass (TBM), microsomal protein yield (MPY), calcium uptake by fragmented sarcoplasmic reticulum (SR), muscle fibre cross-sectional area, and both PFK and SDH activities were investigated in the tibialis anterior (TA), soleus (Sol), and plantaris (Plt) muscles of 50 male albino Sprague-Dawley rats. Rats were assigned randomly to control (C), sprint-trained (S), or endurance-trained (E) groups. Training was of 12 weeks duration. One-half of each group received daily intraperitoneally D doses of 5 mg kg(-1) of TBM. Exercise reduced TBM (p<0.05); increased the relative BM of the TA (E=2.02+0.02, p<0.01) and Plt (E=1.15+0.02, p<0.01; S=1.13+0.03, p<0.01), as well as the Ca++ uptake of the Sol SR (C=0.08+0.02, E=0.16+01, p<0.05). MPY was elevated in S-Sol (C=1.12+0.6, S=1.52+0.1, p<0.01). Delevated Sol MPY as well as TA PFK. S-trained animals had lower mean fibre areas than the E-trained (D-treated and untreated) animals. The elevated relative masses of TA and Plt are explained by a decreased TBM with exercise. The increased Ca++ uptake of the Sol indicates that E enhances this function, and the increased MPY probably implies an increased SR. The D could be responsible for the D-elevated Sol MPY as well as the TA PFK. El D did not reduce neuromuscular activity to a level adversely affecting oxidative enzyme activity, but in the case of PFK activity in the TA muscle, such a reduction was evident.

Properties of sprouted rat motor units: effects of period of enlargement and activity level.

The effects of short and prolonged partial denervation of lateral gastrocnemius muscles in sedentary and active rats (running) were examined. In PD muscles of sedentary animals the mean motor unit (MU) tetanic force after 30 days was not different than that measured after 90 days. Increased locomotor activity over the same period (voluntary running, approximately equal to 6 km/day) resulted in an increase in mean MU tetanic force of enlarged MUs (28%). The absence of a significant increase in mean muscle fiber area suggested an activity-related enhancement of motoneuron sprouting. However, the small magnitude of this increase, relative to the potential for further sprouting, indicates the activity effect is not strong and may be partly due to fiber area changes not evident with whole muscle analysis. Nonetheless, these data demonstrate that daily locomotor activity can enhance the tension-generating capacity of chronically enlarged MUs.

Similar age-related changes in two regions of muscle with different properties.

Two regions of the medial gastrocnemius (MG) muscle, with different contractile properties and innervated by different nerve branches, were investigated in male Sprague-Dawley rats at three ages: 2-3 months, 6-7 months and 24-25 months (i.e., the '50% survival age and beyond': a recommended definition of aged rodents derived from lifespan data on a given colony). At the 50% survival age, both regions of the MG showed decreased mass, slowed contraction times and a decreased number of fast-twitch, but not slow-twitch, muscle fibres. The 40% loss of fast-twitch muscle fibres was not reflected in the loss of motoneurones, suggesting that muscle degeneration precedes motoneurone loss at the 50% survival age in the rat.