Date of Award


Degree Type


Degree Name

Bachelor of Science Honours


Faculty of Communications, Health and Science

First Advisor

Dr Paul Sacco

Second Advisor

Carmel Nottle


A reduction in capacity of the neuromuscular system associated with exercise can occur from a wide range of physiological and psychological factors. Many researchers have investigated neural activation during exercise, or the effects of muscle damage associated with eccentric exercise, but few have studied the prolonged effects of a bout of eccentric exercise on strength and motorneuron excitability. Eleven male and female subjects (aged 20-43 years) were tested to determine the effects of a fatiguing bout of eccentric exercise upon maximal isometric plantarflexion strength, motorneuron excitability, and neural activation of the soleus (SOL) and medial gastrocnemius (MG). The exercise consisted of two hours on a calf raise machine, the only the right leg performing eccentric repetitions, with three sets of 60 repetitions at 60% of the concentric one repetition maximum (1RM). Hoffman reflex (H-reflex), evoked responses, maximum voluntary contraction (MVC) torque, voluntary root mean squared electromyography (nnsEMG), Creatine Kinase (CK), and the Achilles tendon reflex (T -reflex) were tested immediately prior to, immediately post, and l, 24, 48 and 72 hours post exercise. Results indicated that there were significant (R < 0.05) decreases of 18% and 23% in MVC torque and SOL rmsEMG respectively following the fatiguing protocol. There were also significant declines of 31% in the SOL H-reflex, 25% in the SOL HMAX:MMAX (the ratio of the maximum H-reflex to the maximum M-response ), as well as a 21% decline in the amplitude of the evoked twitch. There were no significant decreases in the M-response or T-reflex, or in any of the variables of the control leg, following the exercise bout. The reduced voluntary torque and EMG suggests that the force loss was due to a decreased neural drive. The decline in the H-reflex following exercise indicates a reduction in the excitability of the α-motorneuron pool (since altered M-waves suggest no impairment in neuromuscular propagation). The change in strength may in part be due to alterations in spinal excitability, but other factors must also contribute since the correlation between the two (although significant) is relatively weak (r2 = 0.2). The lack of change in the T-reflex may suggest that, with the combined effect of a decrease in spinal excitability and increase in spindle responsiveness and/or muscle compliance, which in part compensate for the decline in α-motorneuron excitability, the resultant net change was zero. Result suggests that alterations in motor drive associated with fatiguing eccentric exercise probably represent a combination of the modulatory effects of a number of inputs (both excitatory and inhibitory) to the α-motorneuron.