An Introduction to the Repeated Bout Effect

What is the Repeated Bout Effect?

The repeated bout effect (RBE), first described by Highman & Altland (1963), is an adaptation that occurs following a bout of exercise, which significantly reduces the symptoms of exercise-induced muscle damage (EIMD) experienced following a repeated bout. For the purpose of this blog EIMD has been defined as damage received by muscles as a result of exercise, which can impair muscle performance. It is often expressed through a loss of strength, delayed onset of muscle soreness (DOMS), inflammation, reduced

mobility and an increase in muscle proteins found in the blood.

How EIMD effects the muscle?

Friden et al., (1981) were one of the first to utilise muscle biopsies when investigating EIMD and concluded that muscle damage can be characterised by Z band streaming. Research has also provided data showing muscle damage measured by a rise in blood creatine kinase (CK) levels. Myofibrillar disturbances where also identified when assessed by an MRI (Mair et al., 1992; Nosaka & Clarkson 1996).

When EIMD occurs, the blood membrane of muscle cells can be disrupted, potentially leading to soluble proteins (such as CK) leaking from the cytoplasm and cell necrosis (Nosaka & Cowan, 2010). Additionally EIMD can cause a loss of force producing ability however there is little previous research on this performance measure and the influence of EIMD and/or the RBE.

Probably the most noted result of EIMD is DOMS. It is believed that the cause of DOMS is the inflammation caused by EIMD increases intramuscular pressure (Crenshaw et al., 1994), which may stimulate nociceptors in the muscle creating the sensation of pain (I will do a blog on DOMS and recovery practices at a later date).

How does the RBE work?

Currently the exact mechanism or mechanisms to explain how EIMD alters the muscle and how the RBE functions has not been identified. At present four possible theories for the adaptations involved in the RBE have been proposed: neural, connective tissue, cellular tissue and a blunted inflammatory response (these theories will be explained in more detail in a later blog).

Two of these theories involve the ‘popping-sarcomere’ hypothesis suggested by Morgan (1990). The hypothesis states that when tension is applied suddenly or is a consequence of high force, sarcomeres stretch in a non-uniform manner. Consequently some sarcomeres are stretched to a length beyond the filament overlap and so they ‘pop’. Some of these ‘popped’ sarcomeres will remain over-extended and will not be able to contract again to produce force until repaired or replaced.

What does all this have to do with your training?

In summary the first time you significantly increase your training intensity or try a new exercise you are likely to experience EIMD which will reduce your performance and more than likely be painful during the following days. This reduced performance and pain is nothing to be concerned about (as long as it is not excessive) and should only occur the first few times you train. To date we are not entirely sure exactly how the body adapts to reduce the pain and loss of performance. In short, with the present research this should not change your training and I’m hoping further research into this area will help identify exact mechanisms as I believe this information could then be used to optimise training.