Passive muscle stretching reduces estimates of persistent inward current strength in soleus motor units.

Prolonged (≥60 s) passive muscle stretching acutely reduces maximal force production at least partly through a suppression of efferent neural drive. The origin of this neural suppression has not been determined; however, some evidence suggests that reductions in the amplitude of persistent inward currents (PICs) in the motoneurons may be important. The aim of the present study was to determine whether acute passive (static) muscle stretching affects PIC strength in gastrocnemius medialis (GM) and soleus (SOL) motor units. We calculated the difference in instantaneous discharge rates at recruitment and de-recruitment (ΔF) for pairs of motor units in GM and SOL during triangular isometric plantar flexor contractions (20% maximum) both before and immediately after a 5 min control period and immediately after five 1 min passive plantar flexor stretches. After stretching, there was a significant reduction in SOL ΔF (-25.6%; 95% confidence interval, CI=-45.1% to -9.1%, P=0.002) but not GM ΔF These data suggest passive muscle stretching can reduce the intrinsic excitability, via PICs, of SOL motor units. These findings (1) suggest that PIC strength might be reduced after passive stretching, (2) are consistent with previously established post-stretch decreases in SOL but not GM EMG amplitude during contraction, and (3) indicate that reductions in PIC strength could underpin the stretch-induced force loss.

New Methods for Processing and Quantifying VO2 Kinetics to Steady State: VO2 Onset Kinetics.

Current methods of oxygen uptake (VO2) kinetics data handling may be too simplistic for the complex physiology involved in the underlying physiological processes. Therefore, the aim of this study was to quantify the VO2 kinetics to steady state across the full range of sub-ventilatory threshold work rates, with a particular focus on the VO2 onset kinetics. Ten healthy, moderately trained males participated in five bouts of cycling. Each bout involved 10 min at a percentage of the subject's ventilation threshold (30, 45, 60, 75, 90%) from unloaded cycling. The VO2 kinetics was quantified using the conventional mono-exponential time constant (tau, τ), as well as the new methods for VO2 onset kinetics. Compared to linear modeling, non-linear modeling caused a deterioration of goodness of fit (main effect, p < 0.001) across all exercise intensities. Remainder kinetics were also improved using a modified application of the mono-exponential model (main effect, p < 0.001). Interestingly, the slope from the linear regression of the onset kinetics data is similar across all subjects and absolute exercise intensities, and thereby independent of subject fitness and τ. This could indicate that there are no functional limitations between subjects during this onset phase, with limitations occurring for the latter transition to steady state. Finally, the continuing use of mono-exponential modeling could mask important underlying physiology of more instantaneous VO2 responses to steady state. Consequently, further research should be conducted on this new approach to VO2 onset kinetics.