Primary & Secondary Damage Responses
Information about the exact contribution of each potential mechanism is still inconclusive. The proposed responses are currently regarded as either Primary (occurring during exercise) or Secondary (associated with inflammation). Damage is thought to be a necessary part of adaptive remodelling, despite the limiting effects on subsequent training sessions.
Primary damage.
– Mechanical. Sarcomere lengthening within the muscle is irregular during eccentric contractions. In some cases overstretching of the muscle can lead to “sarcomere popping”. This is where repeated eccentric contractions surpass the limit of myofibrils and stretch beyond the point of overlap; resulting in lesser ability to contract and produce force.
– Metabolic. It has been proposed (but not proved!)that ischemia (restricted blood supply) and hypoxia (reduced oxygen supply) can cause damage to the muscle cells. The change in ion concentrations creates metabolic waste products in the blood similar to those seen with EIMD. However, there is not much research to support this as a major contributing factor.
Secondary damage.
This can be seen as the trigger to the subsequent phases of DOMS and EIMD adaptations. The muscle damage causes disruption of signalling factors and intracellular Calcium (Ca2+) homeostasis. The increase in Ca2+ ions concentrations can cause cell degradation, oxygen shortage and fibre necrosis. The loss of membrane integrity allows leakage of intramuscular proteins such as creatine kinase (CK) and myoglobin (Mb).
Primary damage.
– Mechanical. Sarcomere lengthening within the muscle is irregular during eccentric contractions. In some cases overstretching of the muscle can lead to “sarcomere popping”. This is where repeated eccentric contractions surpass the limit of myofibrils and stretch beyond the point of overlap; resulting in lesser ability to contract and produce force.
– Metabolic. It has been proposed (but not proved!)that ischemia (restricted blood supply) and hypoxia (reduced oxygen supply) can cause damage to the muscle cells. The change in ion concentrations creates metabolic waste products in the blood similar to those seen with EIMD. However, there is not much research to support this as a major contributing factor.
Secondary damage.
This can be seen as the trigger to the subsequent phases of DOMS and EIMD adaptations. The muscle damage causes disruption of signalling factors and intracellular Calcium (Ca2+) homeostasis. The increase in Ca2+ ions concentrations can cause cell degradation, oxygen shortage and fibre necrosis. The loss of membrane integrity allows leakage of intramuscular proteins such as creatine kinase (CK) and myoglobin (Mb).