Roland R. Roy

The architectural features of the major knee extensors and flexors and ankle plantar flexors and dorsiflexors were determined in three human cadavers. There was marked uniformity of fiber length throughout a given muscle and a trend toward similar fiber lengths within muscles of a synergistic group. Muscle length/fiber length ratios were remarkably similar for all three limbs. Angles of fiber pinnation were relatively small (0 degree-15 degrees) and generally consistent throughout the muscle. From these architectural data, the performance of a muscle was studied with respect to its tension production and velocity of shortening potentials. The tension is a function of the number of sarcomeres in parallel, and the velocity of shortening is a function of the number of sarcomeres in series. Muscles were grouped according to whether they showed a predilection for tension or velocity of shortening.

We have investigated potential mechanisms by which exercise can promote changes in neuronal plasticity via modulation of neurotrophins. Rodents were exposed to voluntary wheel running for 3 or 7 days, and their lumbar spinal cord and soleus muscle were assessed for changes in brain-derived neurotrophic factor (BDNF), its signal transduction receptor (trkB), and downstream effectors for the action of BDNF on synaptic plasticity. Exercise increased the expression of BDNF and its receptor, synapsin I (mRNA and phosphorylated protein), growth-associated protein (GAP-43) mRNA, and cyclic AMP response element-binding (CREB) mRNA in the lumbar spinal cord. Synapsin I, a synaptic mediator for the action of BDNF on neurotransmitter release, increased in proportion to GAP-43 and trkB mRNA levels. CREB mRNA levels increased in proportion to BDNF mRNA levels. In separate experiments, the soleus muscle was paralyzed unilaterally via intramuscular botulinum toxin type A (BTX-A) injection to determine the effects of reducing the neuromechanical output of a single muscle on the neurotrophin response to motor activity. In sedentary BTX-A-treated rats, BDNF and synapsin I mRNAs were reduced below control levels in the spinal cord and soleus muscle. Exercise did not change the BDNF mRNA levels in the spinal cord of BTX-A-treated rats but further reduced the BDNF mRNA levels in the paralyzed soleus relative to the levels in sedentary BTX-A-treated rats. Exercise also restored synapsin I to near control levels in the spinal cord. These results indicate that basal levels of neuromuscular activity are required to maintain normal levels of BDNF in the neuromuscular system and the potential for neuroplasticity.

Force, velocity, and displacement properties of a muscle are determined in large part by its architectural design. The relative effect of muscle architecture on these physiological variables was studied by determining muscle weight, fiber length, average sarcomere length, and approximate angle of pinnation of 24 cat hind limb muscles. Muscle lengths ranged from 28.3 to 144 mm, whereas fiber lengths ranged from 8.4 to 105.5 mm. Generally, fiber to muscle length ratios were similar throughout a muscle. Estimated angles of pinnation of muscle fibers varied from 0 to 21 degrees with most having an angle of less than 10 degrees. The cross-sectional area of the knee extensors was similar to the knee flexors (16.43 vs. 16.83 cm2) whereas the cross-sectional area of the ankle extensors was more than six times greater than the ankle flexors (18.59 vs. 2.83 cm2). There was a 6.7-fold difference in the maximal force between muscles, when normalized to a constant weight, that could be attributed to architectural features. Ratios of wet weight to predicted maximal tetanic tension for each muscle and muscle group were calculated to compare the relative priority of muscle force versus muscle length-velocity for a given mass of muscle. These ratios varied from 0.4 to 4.84. The ratios suggest that velocity and/or displacement is a priority for the hamstrings, whereas force is a priority for the quadriceps and lower leg muscles. As much as a 12.6-fold difference in maximal velocity between muscles can be attributed to differences in fiber lengths. This can be compared to approximately a 2.5-fold difference in maximal velocity reported to occur as a result of biochemical (intrinsic) differences.