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Chronic Adaptations to Eccentric Training | Bodybuilding


“(i.e. the addition of sarcomeres in series). There appears to be a preferential increase in the size of type II muscle fibres and the potential to exert a unique effect upon fibre type transitions.”

CONCLUSIONS: Eccentric training is a potent stimulus for enhancements in muscle mechanical function, and muscle-tendon unit (MTU) morphological and architectural adaptations. The inclusion of eccentric loads not constrained by concentric strength appears to be superior to traditional resistance training in improving variables associated with strength, power and speed performance.

Skeletal Muscle Remodeling in Response to Eccentric vs. Concentric Loading: Morphological, Molecular, and Metabolic Adaptations


Exercise-induced muscle damage (EIMD)

Some research suggests that EIMD may play an important role in mediating muscle growth, speculating that the associated inflammatory response and protein turnover could be critical for increase in muscle size (Evans and Cannon, 1991). As EIMD is found predominantly after ECC exercise bouts, but not CON (Fridén et al., 1986; Faulkner and Brooks, 1993), this has prompted researchers to postulate that ECC RT could lead to higher hypertrophic responses: nevertheless, as showed in Section The Contribution of Chronic Concentric vs. Eccentric Loading to Muscle Hypertrophy of the present review, even at high training intensities, many studies cannot clearly affirm which training mode results in greater long-term hypertrophy. Moreover, it is widely known that EIMD decreases since after the first exercise bout (McHugh, 2003; i.e., the repeated bout effect phenomenon) because of several factors, including neural adaptations and structural remodeling of the extra-cellular matrix (ECM; Hyldahl et al., 2017). Thus, the real contribution of EIMD in distinct long-term hypertrophic adaptations to ECC vs. CON RT remains to be determined.

Satellite cells activity after acute and chronic concentric vs. eccentric loading

If MPS and EIMD do not fully explain the contraction-specific skeletal muscle remodeling patterns, further answers may be found in the satellite cells activity in response to ECC vs. CON RT.

During muscle repair following EIMD and during subsequent hypertrophic adaptations, the role of satellite cells is central for muscle growth (Fry et al., 2017). Satellite cells are stem cell situated between the basal lamina and the sarcolemma of skeletal muscle fibers (Mauro, 1961), which, upon activation, can proliferate, and ultimately fuse with existing fibers, thus leading to an increase in muscle fibers size (Harridge, 2007). It is noteworthy to mention that greater satellite cells activity has been observed after a single bout of ECC exercise (with consequent EIMD showed) compared to load-intensity matched CON (with no damage; Hyldahl et al., 2014). When we consider RT programs overtime, chronic CON RT only has lead to an increase in satellite cells pool, compared to chronic ECC RT (Farup et al., 2014). Thus, these data suggest that distinct contractions can differently modulate satellite cells activity over RT periods.

A recent study highlighted the very close relationship between myogenic progenitor cells (MPCs) and the ECM that surrounds muscle fibers in response to hypertrophic stimuli (Fry et al., 2017). Fry and colleagues showed that when MPCs are activated by mechanical overload, they proliferate and will release exosomes containing different micro RNAs (miRNA) into the ECM-niche. Such cross talk leads to a reduction of collagen mRNA expression in the fibrogenic cell, and thus appears to regulate ECM deposition during muscle structural remodeling. Conversely, the absence of activated satellite cells results in excessive ECM deposition and attenuated myofibre growth (Fry et al., 2017). Furthermore, in a recent investigation, a reduced cohort of satellite cells did not prevent serial sarcomeres addition after chronic stretch in mice soleus, but resulted in significantly altered muscle morphology (reduced fiber CSA with concomitant fibrosis and ECM hypertrophy; Kinney et al., 2017). This proves that satellite cells play a crucial role in controlling ECM and muscle structural remodeling.
Myofiber-specific TEAD1 overexpression drives satellite cell hyperplasia and counters pathological effects of dystrophin deficiency

Super-numeral SCs attain a ‘normal’ quiescent state, accelerate regeneration, and maintain regenerative capacity over several injury-induced regeneration bouts. 
However, upon injury, the stem cells become activated, divide to increase in number and then develop into new muscle fibers to replace those that were damaged.

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