Metabolic cost of lengthening, isometric and shortening contractions in maximally stimulated rat skeletal muscle.

AIM: The present study investigated the energy cost of lengthening, isometric and shortening contractions in rat muscle (n = 19). METHODS: With electrical stimulation the rat medial gastrocnemius muscle was maximally stimulated to perform 10 lengthening, isometric and shortening contractions (velocity 25 mm s(-1)) under experimental conditions (e.g. temperature, movement velocity) that resemble conditions in human movement. RESULTS: Mean +/- SD force-time-integral of the first contraction was significantly different between the three protocols, 2.4 +/- 0.2, 1.7 +/- 0.2 and 1.0 +/- 0.2 N s, respectively (P < 0.05). High-energy phosphate consumption was not significantly different between the three modes of exercise but a trend could be observed from lengthening (7.7 +/- 2.7 micromol approximately P muscle(-1)) to isometric (8.9 +/- 2.2 micromol approximately P muscle(-1)) to shortening contractions (10.4 +/- 1.6 micromol approximately P muscle(-1)). The ratio of high-energy phosphate consumption to force-time-integral was significantly lower for lengthening [0.3 +/- 0.1 micromol approximately P (N s)(-1)] and isometric [0.6 +/- 0.2 micromol approximately P (N s)(-1)] contractions compared with shortening [1.2 +/- 0.2 micromol approximately P (N s)(-1)] contractions (P < 0.05). CONCLUSION: The present results of maximally stimulated muscles are comparable with data in the literature for voluntary human exercise showing that the energy cost of force production during lengthening exercise is approximately 30% of that in shortening exercise. The present study suggests that this finding in humans probably does reflect intrinsic muscle properties rather than effects of differential recruitment and/or coactivation.

Changes in characteristics of rat skeletal muscle after experimental allergic encephalomyelitis.

Experimental allergic encephalomyelitis (EAE) serves as an animal model for certain neuroinflammatory diseases of the central nervous system, in particular multiple sclerosis (MS). EAE is accompanied by transient weakness or paralysis of hind limbs. We have investigated the effect of partial and transient conduction failure in the central nervous system on skeletal muscle function. At approximately 2.5 days after development of maximal clinical signs, body and medial gastrocnemius muscle mass were lower (by approximately 21 and 33%, respectively; P < 0.05) in EAE rats compared with controls. Fiber cross-sectional area was lower by 40-50% in all fiber types. Maximal force and power were substantially lower (by 58% and 73%) in EAE rats, as was the force normalized for muscle mass (35%). However, no such weakness was found when lower stimulation frequencies were used. Generation of similar submaximal forces was attributable to a slower relaxation in EAE muscles. This advantage for the EAE muscles was lost during repeated exercise. While fatigability was similar, the difference in relaxation rate between EAE and control disappeared in fatigue. Our data suggest that, as a result of central neuroinflammatory diseases, maximal performance of skeletal muscle is impaired but submaximal performance is relatively well maintained.

Rat medial gastrocnemius muscles produce maximal power at a length lower than the isometric optimum length.

The interaction of relative muscle length and force-velocity characteristics was investigated in the fully activated rat medial gastrocnemius muscle in situ. Average maximal isometric force (as a percentage of the of the maximal isometric force at L(o,iso)) at relative lengths measured below isometric optimum (L(o,iso)) was 96% at L(o,iso)-2 mm, 88% at L(o,iso)-4 mm and 58% at L(o,iso)-6 mm. Force-velocity curves were obtained at the four relative muscle lengths. There were no significant differences in maximal shortening velocity (approximately 280 mm x s(-1)) between the different muscle lengths. The highest power output (P<0.05) was found at L(o,iso)-2 mm (mean+/-SEM 435+/-19 mW). Peak power values at L(o,iso) (390+/-10 mW) and L(o,iso)-4 mm (395+/-12 mW) were not significantly different, whereas peak power was lowest (P<0.05) at L(o,iso)-6 mm. There was a significant (P<0.01) shift of approximately 1.5 mm in optimum muscle length for force generation during shortening contractions compared with isometric contractions. Shortening velocity had only a minor influence on optimum muscle length for force generation. It is concluded that fully activated muscles produce their maximal power at a length lower than L(o,iso). The difference in optimum length between isometric and dynamic contractions may be related to length-dependent variations in sarcomere length in series during shortening.

Skeletal muscle of mice with a mutation in slow alpha-tropomyosin is weaker at lower lengths.

Skeletal muscle function was measured in anaesthetised transgenic mice having a mutation in the TPM3 gene (slow alpha-tropomyosin), a similar mutation as found in some patients with nemaline myopathy, and was compared with control muscles. Measurements of isometric and dynamic muscle performance were done with electrical nerve stimulation at physiological temperatures. No muscle weakness was found in the transgenic muscles when performance was measured at muscle optimum length. This was true not only with full activation but also at lower activation levels, indicating that calcium sensitivity was not affected at this length. Also, fatigability was not affected in these conditions. However, isometric force of the muscles with the mutation in TPM3 was lower at lengths below optimum, with more impairment at decreasing length. As the muscles are active over a large range of different muscle lengths during daily activities, this finding may explain, at least in part, the muscle weakness experienced by patients with nemaline myopathy.