Mechanisms behind the Repeated Bout Effect
In my last blog I introduced the RBE and explained that it is currently unknown by which mechanism this effect works. To date there are four possible theories for the adaptations involved in the RBE that lead the way: neural, connective tissue, cellular tissue and a blunted inflammatory response.
Connective Tissue Adaptation
When a sarcomere is ‘popped’ the tension is then supported by passive structures. Street’s (1983) research on frogs implies that the aponeurosis, a passive structure, can provide a link to bypass damaged areas of the muscle, allowing maintenance of serial force production. However this highlights that the repeated stress placed on the passive structures will result in damage. Therefore it was proposed that an adaptation of increasing the quantity of connective tissue to dissipate myofibrillar stresses could be a mechanism for the RBE (Friden et al., 1983b; Lapier et al., 1995). It should be noted that this theory is based on research from over thirty years ago.
Cellular Tissue Adaptation
‘Popped’ sarcomeres often have a damaged sarcolemma, which results in a loss in calcium homeostasis, leading to the impairment of calcium excitation-contraction (E-C) coupling or cellular necrosis (Warren et al., 1993). ‘Popped’ sarcomeres can also cause an increase in muscle length and a shift to the right in the length-tension relationship (Saxton & Donnelly, 1996). Clarkson & Tremblay (1988) suggested if the sarcolemma or the sarcoplasmic reticulum were strengthened, they might become more damage resistant. This would prevent the impairment of the E-C coupling and the calcium influx (averting cellular necrosis). Alternatively, Morgan (1990) proposed that a longitudinal addition of sarcomeres would reduce strain, and in turn reduce ‘popping’ and cellular damage in a repeated bout of exercise. Lynne & Morgan’s (1994) work using rats, strongly supports this proposal as it has provided data confirming that downhill running increases the number of sarcomeres in series.
Neural adaptation
Nardone et al., (1989) proposed that high threshold motor units are specifically recruited for eccentric actions. Additionally research has shown these specifically chosen high threshold motor units can be recruited in relatively small numbers (Adams et al., 1992; Potvin, 1997). This implies an eccentric action would only activate a relatively small number of type II fibres, possibly resulting in these fibres receiving excessive amounts of work. This infers type II fibres are more susceptible, than type I fibres, to damage from eccentric actions, a hypothesis supported by previous research (Friden et al., 1983a; Lieber et al., 1991). Type II fibres may also be predisposed to damage because their structure consists of narrow Z-lines which reflect a lower thick and thin filament attachment. Therefore there is a weaker connection between sarcomeres (Tricoli, 2010).
Using previous research, Nosaka & Clarkson (1995) suggested that a neural adaptation to EIMD would better distribute the workload among fibres, thus reducing the stress placed on fibres in a repeated bout. This proposal is strongly supported by the work of Hortobagyi et al., (1996) who’s research highlighted that a strength increase from eccentric training came hand in hand with a decrease in the force : integrated electromyography ratio, suggesting eccentric strength training causes a decrease in force per motor unit activation.
Blunted inflammatory response
Pizza et al., (1996) found a decrease in neutrophil and monocyte activation after a repeated bout of eccentric actions. This decreased inflammatory response may reduce any secondary damage caused by inflammation. However it is hard to state with confidence whether the blunted inflammatory response is an individual adaptation or a reflection of less muscle damage due to other adaptations.
Summary
I conducted my own research as an undergraduate into this topic and the results suggested that the neural adaption is the most prominent adaptation. However I would like to highlight that my undergraduate work was exactly that, the work of an undergraduate and was never published. As with most items in the sports science world nothing is ever simple and it is likely that all of the mechanisms proposed have an influence on the RBE. To what degree each mechanism works we do not (and may never) know.