It is widely accepted that unaccustomed high muscle tension results in muscle damage, associated with a release of muscle damage markers into the extracellular space. Tiny membrane clefts that are easily resealed are thought to provide the basis for the altered membrane permeability. However, when the same loading is applied again within a certain period of time, there is only a blunted response of muscle damage markers on the one side and fewer muscle damage symptoms on the other. The underlying mechanisms of this phenomenon, denoted as the repeated bout effect (RBE), still remain unclear. Therefore, the aim of this project was investigate some of the potential mechanisms. Further, we searched for alternatives of the frequently applied muscle damage markers and developed a novel hypothesis for an alternative pathway to release the muscle damage markers from the sarcoplasm.
Following two bouts of high intensity eccentric contractions (100 drop-to-vertical jumps) that were separated by 3 w we assessed the perceived muscle pain and measured the activity and concentration of creatine kinase (CK) in the blood. Further we measured the response of novel muscle damage markers such as polyamines and collagen amino acids. Finally we assessed if increasing the metabolic stress during eccentric contractions by applying blood flow restriction (BFR) during a downhill-running protocol results in an aggravation of the induced muscle damage.
The results of this project revealed that the frequently observed blunted CK response after a second bout of eccentric contractions can partially be explained by the fact that CK is usually measured by its activity. That is, following the second bout there is an increased enzyme inactivation that masks the actual amount of muscle damage. Further, it turned out that none of the novel muscle damage markers, assessed in the present project, provides a meaningful alternative to those commonly measured. When BFR was applied during downhill-running, the response of muscle damage markers increased. This indicates that metabolic stress can aggravate the mechanically induced muscle damage. Based on our own observations and data from the literature, we developed a novel hypothesis on the exercise induced muscle damage. According to this hypothesis, certain molecules are released via membrane blebbing from the sarcoplasm to protect the muscle cell from a complete energy depletion during exhausting exercises.
|Short title||Muscle damage|
|Effective start/end date||01.01.13 → 31.12.15|