During environment from the muscle to the central nervous

During isometric contractions (Gandevia, Allen et al. 1996; Taylor et al. 1996) and high-intensity
cycling (Amann et al. 2008b; Amann, Blain et al. 2011) it has been shown
that the activation of group III/IV afferents, pain receptors (relays changes
in metabolic environment from the muscle to the central nervous system (Almeida et al. 2004), and acts at both a supraspinal and spinal
level to influence motor unit firing (Martin et al. 2008b)), will increase to inhibit the cortex and
in turn reduce the central motor drive. Furthermore, studies that partially
block muscle afferents in an exercising human have implied that these afferent
groups will restrain central motor drive to ensure critical threshold is not
met (Amann and Dempsey 2008a; Amann et al. 2009; Gagnon et al. 2012). If these muscle
afferent groups are completely blocked it has shown that the potentiated twitch
force in the quadriceps would continue to decrease, meaning excessive increase
of peripheral fatigue at exercise termination (Amann, Proctor et al. 2009; Gagnon, Bussieres et al. 2012).


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In the upper body, researchers have shown
that by firing the type III/IV group afferents in the triceps brachii
(antagonist) and in the first dorsal interosseous muscle, resulted in a lower
VA of the elbow flexors (Kennedy et al. 2013; Kennedy et al. 2014). A decrease in
supraspinal and an increase in spinal excitability can be induced by increasing
group III/IV afferent feedback to the supraspinal and spinal regions during a
weak isometric elbow flexor contraction (Martin, Weerakkody et al. 2008b). Pearcey,
Bradbury-Squires et al. (2016) found an increase
in CMEP amplitude after the sprinting protocol. It is possible that the
excitability of the motoneurone pool may be enhanced as motor output intensity
increased. Leading to increased activity of serotonergic neurons (~3-5 fold)
during a central pattern generator driven motor output (Fornal et al. 1996), which upper body
cycling has been shown to be involved in the operation of a spinal central
pattern generator (Zehr et al. 2004). However, it could also be possible that
various other factors can change motoneuron excitability such as a lowered
voltage threshold and decreased spike time for action potential initiation (Beaumont et al. 2003; Power et al. 2010), persistent inward
currents activating (Lee et al. 1998; Button et al. 2006; Heckman et al. 2008) (shown in human
bicep brachii motor units (Wilson et al. 2015)), and triggering
of monoaminergic system throughout exercise, which possibly alters the
persistent currents (Heckman 2003; Gardiner et al. 2006). Evidently, all
these factors could play a role in altering spinal excitability. Researchers
have shown in both leg-cycling (Girard, Bishop et al. 2013b) and running sprints (Goodall, Charlton et al. 2015) no changes in MEP
amplitudes following sprints, with one researcher showing a TMS reduced VA
exhibiting that central fatigue did in fact occur. Additionally, it has been
questioned whether sprinting had any influence on the responsiveness of the
neurons involved in motor cortical output. However, these previous studies did
not involve testing of the spinal excitability, so it may be possible that an
increase in spinal excitability had masked the decrease in the supraspinal
excitability. Pearcey,
Bradbury-Squires et al. (2016) showed this
occurrence by creating a ratio of MEP amplitude over the CMEP amplitude, in order
to isolate any changes that occurred in supraspinal excitability (Gandevia, Petersen et al. 1999). They showed a decrease in supraspinal
excitability after the 5th and 10th sprint compared to
the pre-sprint. Like speculated, the spinal excitability seemed to increase to
adjust for the decrease in supraspinal excitability, unfortunately the
mechanism for this change is unknown and more research needs to be completed in
this area. Interestingly, it has been shown that during an elbow extensor
fatiguing task group III/IV afferents will inhibit triceps brachii spinal
motoneuron excitability, while simultaneously enhancing the biceps brachii
spinal motoneuron excitability (Martin et al. 2006). During an upper
body sprint, the triceps may fatigue; hence the possibility of the spinal
excitability of the biceps brachii being increased through afferent or
reflexive feedback.