Date of Award


Degree Type


Degree Name

Doctor of Philosophy


School of Exercise and Health Sciences


Health, Engineering and Science

First Advisor

Associate Professor Anthony Blazevich

Second Advisor

Dr Greg Haff


The present research was designed to: 1) determine whether the voluntary PAP effects commonly observed after conditioning activity (CA; i.e. muscular contraction prior to a ‘test’ contraction) are a consequence of acute neuromuscular alterations relating to the CA itself, or whether they simply reflect warm-up and/or familiarisation effects; 2) clarify the influence of the contraction velocity, duration and total work characteristics of the CA on voluntary PAP; 3) determine the factors allowing stronger individuals to express higher level of voluntary PAP; and 4) determine the peripheral and central mechanisms of voluntary PAP in human skeletal muscle. In Study 1, the effects of different contraction velocity, duration and total work characteristics on PAP were examined after a complete warm-up. The contributions of peripheral and central mechanisms to PAP were also examined. Voluntary and electrically-evoked torques and electromyogram (EMG) data were captured before and after five different dynamic (isokinetic) CAs, after the participants had completed an extensive warm-up including extensive task-specific practice to the point where maximal voluntary contractile capacity was achieved. Vastus lateralis (VL) EMG amplitude normalised to the muscle compound action potentiation (M-wave) amplitude (EMG:M), was taken as a measure of central drive whereas twitch peak torque and M-wave amplitude were recorded to assess peripheral function. Even after a plateau in voluntary contractile capacity was achieved after the complete warm-up, the imposition of CAs elicited significant increases in both voluntary and twitch torques (i.e., PAP). CAs with longer total contraction duration (6s) and a minimum total work of ~750-900 J produced PAP, regardless of the velocity of the CA. No changes in EMG:M were detected after any CA suggesting that central drive was not a major factor influencing PAP under the present experimental conditions. However, the increases in twitch peak torques with lack of change in Mwave amplitude suggest that peripheral function, possibly including changes in myosin regulatory light chain (RLC) phosphorylation and increased intracellular Ca2+ release and sensitivity may have contributed to the observed PAP.

It is clear from the literature and the results of Study 1 that there is a significant inter-individual variability in the PAP phenomenon. Typically, stronger individuals are able to express higher levels of PAP but it is unclear why this occurs. Therefore, in Study 2 peak knee extensor torque at 60o·s-1, quadriceps and VL crosssectional area (CSA) and volume, and the type II myosin heavy chain (MHC) isoform percentage (VL) were measured to determine their relative contribution to PAP elicited under voluntary conditions. There were large to very large correlations between PAP magnitude and peak knee extensor torque at 60o·s-1 (r=0.62), quadriceps (r=0.68) and VL (r=0.62) CSA, and quadriceps (r=0.63) and VL (r=0.65) volume. Nonetheless, these correlations were not statistically significant after adjusting for the influence of type II MHC percentage (using partial correlation analysis). By contrast, the strongest correlation was observed for type II MHC percentage (r=0.77), and this correlation remained significant (r=0.56-0.66) after adjusting for other variables. This finding suggests that PAP magnitude is most clearly associated with the type II MHC isoform percentage in the human quadriceps femoris. This might be explained by the fact that myosin RLC phosphorylation, one proposed mechanism responsible for PAP, has been shown to be greater in type II MHC isoforms. The results of Study 1 and Study 2 suggest that changes at the peripheral level, possibly including changes in myosin RLC phosphorylation (and increased intracellular Ca2+ release and sensitivity) may be a primary candidate mechanism of PAP induced by a voluntary CA, although more direct measurements are required to test this assumption.

Therefore, tetanic stimulations and maximal isokinetic knee extensions at 180o·s-1 were used in Study 3 to provide a more detailed investigation of the role of changes in the excitation-contraction (E-C) coupling process (i.e. changes in myosin RLC phosphorylation or increased intracellular Ca2+ release and sensitivity) to the PAP response induced by a voluntary CA. Torques produced during voluntary knee extensions, 20 Hz and catch-inducing (20-Hz train preceded by a double pulse with 5-ms interval) stimulation trains, the 20- vs. 80-Hz torque ratio (20:80) as well as the force-augmenting effect of the catch-inducing train were recorded before and after a voluntary CA or a control condition (no CA, rest). Statistically significant increases in voluntary torque, torques elicited by 20-Hz and catch-inducing trains, and 20:80 were observed 1, 4 and 7 min after the CA. Moreover, the force-augmenting effects of the catch-inducing train diminished as the magnitude of PAP increased and then increased as the magnitude of PAP diminished. Statistically significant correlations (r=0.50-0.81) were also found between the changes in voluntary torque production (i.e. PAP) and the changes in these variables. These results suggest that increases in PAP following a voluntary CA are strongly associated with changes in peripheral function, most probably changes in the E-C coupling efficiency..