2002). Rongen et al. (2002) showed that the EMG amplitude increased whereas the muscle fiber conduction velocity decreased during sustained isometric contractions under ischemic conditions. During high-frequency NMES, muscle metabolism is highly utilized (Shenton et al. 1986) and the muscle pH decreased (Vanderthommen et al. 2003). For that reason, it is possible that changes of the muscle fiber conduction velocity can occur, but only in the stimulated GL. That does not explain the increased activity in SOL. Our results indicated different activation strategies in synergistic muscles (SOL,

GM). According Inhibitors,research,lifescience,medical to the results of Akima et al. (2002) and de Ruiter et al. (2008), it was hypothesized that EMG activity of both synergistic muscles would increase. On the other hand, Sacco et al. (1997) reported decreased EMG activity in GM after NMES of GL. However, this decline in EMG activity is attributed to the ischemia

conditions in their study. In our study, it is assumed that EMG activity of GM was affected by the NMES of the neighboring Inhibitors,research,lifescience,medical GL Inhibitors,research,lifescience,medical (Adams et al. 1993). This might induce an unaltered EMG activity in GM (P = 1.00) during NMES. Furthermore, in recovery, EMG activity of GM increased slightly compared with the baseline. The high correlations (r = 0.847, P < 0.01) between GM and GL during recovery support this assumption. During recovery, the activation of the GL goes back to baseline values. The muscle activation of GM is unaltered and muscle activation of SOL is still increased. Inhibitors,research,lifescience,medical Therefore, one would expect significant increase of force. In fact, force does not increase significantly. This might be due to metabolic fatigue in the stimulated GL (Shenton et al. 1986; Vanderthommen et al. 2003). In fact, EMG activity in the SOL increased after

NMES of the GL at high frequencies, but not EMG activity of GM. Further Inhibitors,research,lifescience,medical studies are needed to clarify whether EMG activity of the synergistic muscles results from peripheral changes or improved central activations. In conclusion, a progressive fatigue protocol of the GL by means of NMES resulted in (a) unaltered force during maximal voluntary isometric plantar flexions, (b) increased synergistic muscle activity of the SOL. It is suggested that isothipendyl these compensatory effects are caused by central contributions induced by NMES. The results provide new insights in neuromuscular control of synergist muscles. Acknowledgments No sources of funding were used to assist this study. Conflict of Interest The authors have no GPCR Compound Library supplier conflicts of interest that are directly relevant to the content of this study.
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