Mechanical stress is thought to be a major cause of damage to myofibrils during eccentric contractions (Allen, 2001, Clarkson and Sayers, 1999, Howatson and Van Someren, 2008, Morgan and Allen, 1999, Proske and Morgan, 2001). The loading profile of eccentric contractions (high force with low fibre recruitment) (Figure 2.5) places a higher mechanical stress on muscle fibres than concentric contractions therefore causing a higher degree of damage (Enoka, 1996). The mechanism of force generation during eccentric actions also differs, whereby the cross-bridges are detached mechanically and with greater force rather than undergoing detachment involving ATP splitting, as with concentric actions (Eston et al., 2003). The degree of muscle damage experienced increases with an increasing number of eccentric
contractions as well as the degree of stretch occurring (Allen, 2001, Lieber and Friden, 1999, Morgan and Allen, 1999).
Figure 2.5: Difference between concentric and eccentric contractions in required muscle activation (electromyography) to achieve a given muscle force (Enoka, 1996).
Within a myofibril, some sarcomeres are stronger than others and it is hypothesized that when the myofibrils are stretched during an eccentric contraction, the weaker sarcomeres absorb more of the stretch (Morgan and Allen, 1999, Proske and Allen, 2005, Proske and Morgan, 2001). Consequently, these sarcomeres become progressively weaker and when they reach their yield point, they lengthen uncontrollably and rapidly to the point of little or no overlap (Clarkson and Sayers, 1999, Peake et al., 2005b, Proske and Morgan, 2001). During repeated contractions, first the weaker, then the stronger sarcomeres are over-stretched and this process can happen repeatedly as the next weakest structures are placed under increased tension (Peake et al., 2005b, Proske and Allen, 2005). During muscle relaxation, most of these overstretched sarcomeres re-integrate and resume normal function, however a few may fail and become disrupted (Clarkson and Sayers, 1999, Allen, 2001, Proske and Allen, 2005, Proske and Morgan, 2001). This disruption can lead to damage of nearby elements of the muscle such as the sarcoplasmic reticulum, transverse tubules or muscle membrane (Proske and Morgan, 2001). This can lead to a loss of membrane integrity therefore allowing intramuscular proteins such as creatine kinase (CK) and myoglobin (Mb) to leak out (Allen, 2001, Clarkson and Sayers, 1999).
As a result of muscle fibre damage, disruption of excitation-contraction coupling may occur and Ca2+moves freely into the sarcoplasm stimulating proteolytic pathways related to fibre degradation and repair (Peake et al., 2005b, Proske and Allen, 2005). This appears to create some of the symptoms related to muscle damage such as soreness and loss of muscle function, as well as an amplification of circulating muscle proteins which represents damage to the plasma membrane (Peake et al., 2005b, Proske and Morgan, 2001).
2.4.1.1 Muscle damage leads to swelling and inflammation
An inflammatory response occurs after muscle damage or injury in order to clear waste from the injured area in preparation for healing (Clarkson and Sayers, 1999, Clarkson and Hubal, 2002).This response is characterised by increased fluid transfer to the area of damage as well as an infiltration of plasma proteins (Clarkson and Hubal, 2002, Clarkson and Sayers, 1999). Along with the infiltration of blood, the products of muscle breakdown can attract water causing an increase to the interstitial fluid surrounding the damaged muscle known as swelling or oedema (Clarkson and Sayers, 1999, Vander et al., 1994, Clarkson and Hubal, 2002). Infiltration inflammatory cells (macrophages and phagocytes) enter the site of damage during the inflammatory response (Clarkson and Sayers, 1999, Vander et al., 1994). The proliferation of these cells is thought to amplify the initial muscle damage through an increased release of proteases and reactive oxygen species (Clarkson and Hubal, 2002). Reactive oxygen species play a role in removing damaged skeletal muscle cells but when present in large numbers have also been implicated in secondary muscle damage(Aoi et al., 2004, Basu et al., 1999, Close et al., 2005, Kon et al., 2007).
2.4.1.2 Muscle damage causes a delayed onset muscle soreness
Muscle damage and the resultant post-exercise swelling can contribute to the sensation of delayed onset muscle soreness (DOMS) (Chleboun et al., 1998, Nosaka et al., 2002). This typically presents as a sensation of muscular discomfort, a dull ache and/or pain that usually
begins 12 h post exercise (Close et al., 2005, Friden and Lieber, 2001). Depending on the amount of damage, DOMS can progress from mild to severe or even debilitating soreness (Close et al., 2005) and usually peaks between 48-72 h post-exercise before diminishing with pain typically ending after 5-7 days. Soreness aside, the result of this damage can manifest in a number of ways. Swelling can increase in a muscle or group of muscles (Chleboun et al., 1998, Vaile et al., 2007) and can be accompanied by increased stiffness (Chleboun et al., 1998), tenderness and a loss of function (Byrne et al., 2004, Close et al., 2004, MacIntyre et al., 1996, Vaile et al., 2007, Peake et al., 2005b, Proske and Morgan, 2001).
The severity of DOMS is generally associated with the degree of muscle and/or connective tissue damage and subsequent inflammation/swelling (Nosaka et al., 2002). Muscle damage and soreness are often placed in the same category and generally it is considered that the greater the amount of muscle damage, the larger the DOMS experienced (Nosaka et al., 2002). Although both DOMS and changes in indirect markers of muscle damage (such as blood increases in muscle proteins, muscle swelling and loss of strength) are induced by eccentric damage it is possible that they are not closely related. Poor correlations exist between DOMS and other indicators of muscle damage while DOMS has been considered as a poor reflector of eccentric EIMD (Nosaka et al., 2002). Therefore the amount of DOMS experienced should not be confused with the amount of muscle damage.
2.4.1.3 Eccentric exercise increases exercise induced muscle damage
The amount of EIMD experienced depends on the length and type of the exercise bout as well as the intensity of muscle contraction (Clarkson and Sayers, 1999, Close et al., 2004, Friden and Lieber, 2001, Kon et al., 2007). Muscle damage is evident following eccentric contractions (Clarkson and Sayers, 1999, Close et al., 2004, Friden and Lieber, 2001, Kon et al., 2007) and that damage increases with the number of contractions and with the length of stretch (Allen, 2001). In comparison to concentric contractions, eccentric contractions recruit fewer motor units meaning that a smaller cross-sectional area of the muscle is activated to handle the
imposed load (Enoka, 1996). In exercise where the eccentric component is unaccustomed, substantial or repeated, such as that experienced in competition by many team sport athletes, the pain, tenderness, swelling and stiffness develop more slowly and are most prominent over the days subsequent to the causative exercise (Allen, 2001).
A sequence of active eccentric action followed by active concentric action is known as a stretch shortening cycle (SSC) (Komi, 2000). This occurs when body segments are subjected to stretch, and takes place in most sporting activities (Eston et al., 2003). It is not surprising therefore that muscle damage is a common occurrence during prolonged or intense team sport activity exercise involving repeated SSC’s such as jumping, sprinting or changing direction. Additional symptoms of EIMD include DOMS, swelling, decreased range of motion, increased blood proteins and impaired neuromuscular control (Byrne et al., 2004). Athletes may be able to tolerate some soreness while a diminished range may not adversely impact performance, but of greatest consequence to an athlete is the negative influence that muscle damage may have on muscle function and any implications for athletic performance.
2.4.1.4 The repeated bout effect
It is clear that unaccustomed and eccentric exercise can induce muscle damage. Following recovery from this exercise, a repeated bout of the same exercise results in minimal symptoms of muscle damage and this has been referred to as the repeated bout effect (Nosaka and Clarkson, 1995). This repeat bout effect has a protective effect against excessive muscle damage following the initial damaging bout and may be of importance in running based activities such as AF. Two weeks after completing 100 maximal eccentric activations of the knee extensors, male subjects performed 5 x 8 min bouts of downhill treadmill running (Eston et al., 1996). Following the running bouts, muscle tenderness was lower (55%), peak creatine kinase activity was lower (50%) and both concentric (25%) and eccentric (30%) maximal torque were reduced when compared to a control group who did not perform any prior eccentric knee extensor movements. A group of male subjects (7) performed 2 downhill runs
(30 min, -10% gradient at 40% peak V.O2max) separated by 2 weeks (Westerlind et al., 1992). Creatine kinase increased more following bout 1 (61%) than after bout 2 (11%), while soreness ratings were 400% lower following bout 2 compared to bout 1. These results indicatethat muscle damage had been reduced during bout 2. The repeated bout effect has also been demonstrated following 8 weeks of downhill walking (Balnave and Thompson, 1993). Participants walked on a treadmill at 6.4 km/h once a week for 8 weeks. Peak serum myoglobin and creatine kinase were much lower in week 8 than in week 1 (-25% and -250%), while maximal voluntary contraction of the quadriceps was reduced by a much smaller magnitude after week 8 (-11%) compared to week 1 (-26%).
These results may be of benefit in athletes such as AF players where training and competition occurs at high intensities. The repeat bout effect may reduce the severity of symptoms following eccentric movements and also reduce the degree of loss in physical function which will only be of benefit to athletes during ensuing exercise bouts.