## 4 Discussion
### Possible Mechanisms for the Non-Linear Increases in EMG Amplitude  
Most studies on cycling performance attribute the occurrence of breakpoints in the linearity of the EMG curve to the recruitment of additional motor units and/or to the change in the type of motor units recruited [5]. However, to date, the mechanisms underlying the abrupt increases in EMG amplitude during an incremental test are not entirely clear, and could involve both local and central (global) factors.  
At the local (muscle) level, it has been shown that as fatigue develops, there is a progressive accumulation of metabolic byproducts of muscular contraction (i.e., lactate, hydrogen ions, potassium, and inorganic phosphate), which could result in impairment of excitation-contraction coupling [23; 24]. To counteract this deficit in the contractile apparatus, muscle power output during an incremental test might be increased by (1) recruiting more motor units; and (2) recruiting type IIa and type IIb motor units to obtain energy through anaerobic glycolysis. Based on this reasoning, it has been hypothesized that the first breakpoint would correspond to the moment when a large number of type IIa (fast twitch oxidative-glycolytic) motor units come into play, whereas the second threshold would occur when a large population of type IIb (fast twitch glycolytic) motor units are recruited [6]. These hypotheses, however, have not been experimentally verified, and thus remain speculative. Indeed, EMG amplitude could increase due to factors other than the number and type of active motor units, such as broadening of the trans-membrane action potential [25], crosstalk [4], and even signal cancellation [4]. Thus, motor unit recruitment is not the only peripheral factor that can account for the non-linear increases in EMG amplitude.  
Central (and not only local) factors could also explain the occurrence of abrupt increases in EMG amplitude. Indeed, impairment of the contractile machinery during the course of an incremental test could be compensated by an enhancement of motor unit rate coding. Specifically, it might be speculated that one or two of the EMG thresholds could be related to increases in motor unit discharge rate and/or synchronization [4]. The possible involvement of neural mechanisms in the EMG breakpoints is further supported by the experiments of [PERSON] et al. [26], who demonstrated that, during an incremental cycling test, both working and non-working muscles showed a shift in EMG at the same load. [PERSON]'s observations are suggestive of a global change in the neural activation of muscles. It is therefore plausible that the abrupt increases in EMG activity may be initiated not only by impairment of excitation-contraction coupling, but also by increases/adjustments in the  
\begin{table}
\begin{tabular}{c c c c c} \hline \hline
**Muscle** & **Threshold** & **First Test** & **Second Test** & **ICC** \\ \hline \multirow{2}{*}{Vastus lateralis} & EMGT1 (W) & 289.2 \(\pm\) 50.4 & 294.3 \(\pm\) 47.8 & 0.85 \\  & EMGT2 (W) & 375.2 \(\pm\) 27.2 & 380.4 \(\pm\) 31.6 & 0.87 \\ \hline \multirow{2}{*}{Vastus medialis} & EMGT1 (W) & 291.2 \(\pm\) 27.0 & 295.4 \(\pm\) 31.5 & 0.93 \\  & EMGT2 (W) & 370.2 \(\pm\) 25.9 & 374.4 \(\pm\) 30.1 & 0.89 \\ \hline \multirow{2}{*}{Biceps femoris} & EMGT1 (W) & 293.2 \(\pm\) 27.7 & 297.4 \(\pm\) 31.5 & 0.93 \\  & EMGT2 (W) & 371.2 \(\pm\) 29.9 & 376.4 \(\pm\) 28.1 & 0.86 \\ \hline \multirow{2}{*}{Gluteus maximus} & EMGT1 (W) & 298.2 \(\pm\) 27.9 & 302.4 \(\pm\) 31.2 & 0.96 \\  & EMGT2 (W) & 377.2 \(\pm\) 28.3 & 381.4 \(\pm\) 27.7 & 0.91 \\ \hline \hline \end{tabular}
\end{table}
Table 5: Reliability of measurements of the electromyographic thresholds EMGT1 and EMGT2.  
neural activity [26]. We conclude by stating that, because multiple factors influence EMG amplitude, the assumption that EMG breakpoints are caused by changes in motor unit recruitment should be treated with caution, as it remains empirically unsupported.