Microcontexto

The contributions of the CNS to improvements in strength are well documented (Duchateau and Enoka, 2002; Folland and Williams, 2007; Duchateau et al., 2006). However, the mechanisms underlying these improvements are less understood, particularly in the M1 and corticospinal pathway. Whilst evidence for the muscle morphological changes that occur with strength training are clearly demonstrated through hypertrophy (Folland and Williams, 2007), the neural adaptations induced by strength training may be comprised of more subtle changes (Datta and Stephens, 1990) in many areas including supraspinal centres (Carroll et al., 2002; Farmer et al., 1993b), descending neural tracts (Aagaard et al., 2002a; Fimland et al., 2009a), spinal circuitry (Cannon and Cafarelli, 1987; Garry et al., 2004; Del Balso and Cafarelli, 2007), and the motor end plate connections between motoneurons and muscle fibers (Staron et al., 1994). Several investigations have reported maximal force increases of up to 15% within days following an exercise session (Berg, 1997; Vandenborne et al., 1998; Schneck and Forward, 1965; Rogers and Evans, 1993), and up to 200% increase after eight weeks, with no changes in the cross-sectional area of muscle (Folland and Williams, 2007). These results imply that the early stages of strength development may be due to some form of neural adaptation. Although there is a general consensus that the CNS mediates this increase in strength following a period of strength training, there is considerable debate concerning the extent and nature of involvement of specific sites within the CNS. Recently, a number of studies have used TMS to determine whether the M1 and corticospinal pathway contributes to strength development, providing a potential site for neural adaptations to strength training (Carroll et al., 2002; Griffin and Cafarelli, 2007; Jensen et al., 2005; Hortobágyi et al., 2009). Given that the M1 is heavily populated with corticospinal cells that descend onto motoneurons located within

103 the spinal cord (Porter, 1985), the use of TMS enables the assessment of corticospinal excitability and inhibition following specific training interventions. For example, Carroll et al. (2002) examined the effect of moderate to heavy load (70 to 85% of MVC) isometric strength training on corticospinal excitability following four-weeks of strength training the FDI muscle. Although strength training resulted in a 33% increase in strength, the strength training program did not modify the size of the TMS produced MEPs. Carroll et al. (2002) also used TES to stimulate subcortical structures and concluded that strength training does not affect the organisation of the M1, suggesting that adaptations are confined to the spinal cord. Similarly, Jensen et al. (2005) had participants perform heavy load (80% of MVC) dynamic strength training (five sets of six to ten repetitions) of the BB three times per week for four-weeks. MEP amplitude at 5% of MVC and stimulus-response curves were constructed prior to and after the four- week training intervention. Following training, muscle strength increased by 31%, however maximal MEP amplitude produced by TMS at rest was reduced, suggesting a minimal role for the M1 and corticospinal pathway in strength development. In contrast to these findings, Beck et al. (2007) demonstrated increased MEP amplitude produced by TMS following four-weeks of ballistic strength training in the soleus muscle, whilst Griffen and Cafarelli (2007) found a 32% increase in MEP amplitude with no change in peripheral nerve excitability, suggesting that strength training leads to a task specific adaptation within the corticospinal pathway. Therefore, strength training studies using TMS show either increased (Griffin and Cafarelli, 2007; Beck et al., 2007), reduced (Jensen et al., 2005), unchanged (Carroll et al., 2002) or task specific modulation of corticospinal excitability (Beck et al., 2007).

Although the above mentioned TMS studies have tried to determine the effects of strength training on corticospinal excitability (by measuring MEP amplitude

104 produced by TMS), changes in cortical inhibition may also be an important neural adaptation that contributes to strength development. Cortical inhibition refers to the neural mechanisms by which output from M1 is attenuated by inhibitory γ-aminobutryic acid (GABA) receptor mediated interneuron transmission (McCormick, 1989). Inhibitory neurons located in the M1 use GABA as their neurotransmitter and the activity of these neurons can be investigated with paired pulse or single pulse TMS (Kujirai et al., 1993; Jones, 1993; Inghilleri et al., 1993). The paired pulse technique measures SICI that is mediated by GABAA receptors (Kujirai et al., 1993), whereas the single pulse technique measures inhibition mediated by GABAB (Siebner et al., 1998). Using the paired pulse technique, SICI can be measured and may be important for shaping the output from the M1 (Chen, 2004). For example, SICI is reduced during voluntary muscle contractions and has been proposed to improve corticospinal drive during intended movement by releasing corticospinal cells from inhibition, therefore improving subsequent excitatory drive to produce the desired movement (Floeter and Rothwell, 1999). Using single pulse TMS, it has been demonstrated that there is a reduction in the duration of the silent period (SP) during both slow and fast finger movements, illustrating a task dependant change in corticospinal inhibition mediated by GABAB interneuronal transmission (Pearce and Kidgell, 2009; Pearce and Kidgell, 2010). Currently, no studies have examined the effect of strength training on corticospinal inhibition, although adjustments in inhibition may be important in force production. Studies have demonstrated in M1 that prior to and during movement, there is not only an increase in corticospinal excitability, but there is also a reduction in corticospinal inhibition (Reynolds and Ashby, 1999; Chen et al., 1998; Ridding et al., 1995b). Furthermore, the change in inhibition is specific to the intended agonist muscle, as MEPs in antagonist muscle remain unchanged (Reynolds and Ashby, 1999;

105 Ridding et al., 1995a). Therefore, changes in inhibition seem to be selective and act to focus the output from the MI by improving excitatory drive onto corticospinal cells that produce the intended movement (Ridding et al., 1995a). In light of this, previous strength training studies that have used TMS have not included the analysis of SP duration, despite several investigations demonstrating changes in inhibition prior to and during movement (Reynolds and Ashby, 1999; Ridding et al., 1995b). The novel aspect of the present study was the investigation of whether strength training of the FDI induces changes in corticospinal inhibition (SP duration) as previous TMS strength training studies have not addressed this issue.

The purpose of the present investigation was to extend upon previous work (Jensen et al., 2005; Carroll et al., 2002) by investigating the corticospinal responses following isometric strength training of an intrinsic hand muscle. The specific aim of the investigation was to determine whether isometric strength training of the FDI altered corticospinal excitability and inhibition during moderate muscle activation. In order to investigate whether strength training causes adaptations along the corticospinal pathway, this study determined the effect of isometric strength training on the magnitude of MEPs and the duration of the cortical SP produced by TMS. It was hypothesised that strength training would alter the amplitude of the MEP, reflecting changes in corticospinal excitability and the duration of the SP, reflecting a change in corticospinal inhibition and this would result in an increase in MVC force following training.

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