Degree Name

Doctor of Philosophy


Department of Biomedical Science


Lengthening muscle actions differ in many aspects from shortening and isometric actions. Although a great deal of research has examined mechanical and, to a lesser extent, the neural characteristics of dynamic muscle actions, still little is known about the regulation of muscle force during lengthening and shortening actions. Therefore, this thesis examined the mechanical and neural aspects of lengthening and shortening actions of the plantar flexors, and more specifically the triceps surae. All experiments were conducted on the triceps surae using a custom built ankle torque motor to accurately control angular displacement, velocity and acceleration during lengthening, shortening and isometric muscle actions.

Study I investigated the influence of the type and intensity of muscle activation on tension regulation during isometric and controlled lengthening and shortening actions of the soleus muscle (SOL). The resultant joint torque-angular velocity relationship was examined across three angular velocities (±5, ±15, and ±30o·s-1) und~r three activation conditions: (i) Maximal Voluntary Activation (MVA); (ii) Submaximal Voluntary Activation (SVA; equivalent to 30% of maximal voluntary isometric effort); and (iii) Submaximal Electrical Activation (SEA; equivalent to 30% of maximal voluntary isometric effort). Normalised joint torques recorded during lengthening muscle actions at each angular velocity in both the voluntary activation conditions (MV A and SV A) were not significantly different from the isometric plantar flexion torque. The lengthening torques produced during the SEA condition, however, were greater than isometric and increased at faster angular velocities. For shortening muscle actions, plantar flexion torques during MV A were significantly less than the isometric torque,

but did not decrease with increasing angular velocity, as would be expected based on the traditional force-velocity relationship. The plantar flexion torque produced during both SV A and SEA were significantly less than the isometric torque and decreased at faster angular velocities. These data indicate that the regulation of tension during lengthening actions was predominantly influenced by the type of activation, that is, voluntary activation versus electrical stimulation, whereas, during shortening muscle actions, it was the intensity of activation, that is, maximal versus submaximal that had the greatest influence on tension regulation. The discrepancies in lengthening plantar flexion torque produced under voluntary activation and that produced by electrical stimulation of the muscle may indicate a neural basis for the regulation of tension during lengthening muscle actions. However, unusually high levels of antagonist activation were recorded during the SV A condition and may account for the inhibition of lengthening torque in the submaximal voluntary condition.

Therefore, Study II was designed to investigate the influence of co-activation of the antagonist, tibialis anterior (TA), on torque production during submaximal voluntary activation of SOL. These experiments were perfonned using the same set-up as III Study I, however, in this study, joint torque-angular velocity relationships were generated before and after the blocking of TA activation by applying a local anaesthetic (Lidocain) to the common peroneal nerve (CPN). There was no significant difference in nonnalised plantar flexion torque between pre-and post-block conditions indicating that co-activation of TAwas not a limiting factor to force production during lengthening muscle actions. Surprisingly, the absolute plantar flexion torque decreased significantly after blocking activation of the antagonist muscle. It is possible that the anaesthetic block of the CPN disrupted the 'normal' neural processes associated with antagonist and

synergist muscle function during voluntary muscle activation. Although this study did not quantify the antagonist contribution to plantar flexion torque, it did allude to the complex neural interactions between antagonist muscles.

Study III used the H-reflex technique to investigate the neural aspects associated with lengthening and shortening actions of the triceps surae. H-reflexes and M-wave responses were recorded from SOL and medial gastrocnemius (MG) during isometric and passive lengthening and shortening muscle actions at three angular velocities (±2, ±5, and ± 15°·s-1). Reflex responses were recorded at two stimulation intensities; (i) 50% of the maximum H-reflex amplitude (50% Hmax); and (ii) 50% of the maximum M-wave amplitude (50% Mmax), where the M-wave is sensitive to small changes in effective stimulus intensity. The consistency of M-wave amplitudes at 50% Mmax indicated that modulations in the H-reflex amplitude were not likely to be due to alterations in the spatial relationship between the stimulating electrode and the nerve.

At both stimulation intensities, H-reflex amplitudes were significantly depressed during passive lengthening actions and slightly facilitated when the muscle was shortening. There was evidence of velocity specific modulation of the reflex response as H-reflex amplitudes at the slowest angular velocity was significantly greater than those at the faster angular velocities during both lengthening and shortening muscle actions. Part of this modulation can be attributed to spinal mechanisms, as the H-reflex amplitude was significantly inhibited within a latency of 57 ms from the onset of movement.

These findings extend the current knowledge pertaining to the disparities between lengthening and shortening muscle actions and allude to unique mechanical and neural characteristics associated with these muscle actions.