Exercise Induced Muscle Damage

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What is Exercise Induced Muscle Damage? (EIMD)

EIMD arises when muscles become damaged after exercise. This often occurs when an athlete participates in a new or unfamiliar exercise, when learning new techniques, or experiences an increase in the volume or intensity of exercise. This can lead to short term performance decrements due to changes in the make-up of the muscles. These performance decrements are commonly caused by an increase in resting energy expenditure and metabolic demand, a decrease in the strength and power output the muscles can produce, and the athletes perception of the muscle soreness. The main effects of EIMD commonly arise 24-48 hours after muscle damage occurs.

Mechanism

EIMD has been a topic of intense focus in exercise and sports science research for more than 30 yr. It is a condition characterised by transient ultrastructural myofibrillar disruption, loss of muscle strength and power, delayed onset muscle soreness (DOMS), swelling, reduced range of motion of the affected limb, systemic efflux of myocellular enzymes and proteins [e.g., creatine kinase (CK); myoglobin], or a combination of these.

It is understood that ultrastructural disruptions in muscle, decrements in muscle strength, DOMS, and efflux of muscle enzymes are greater, and the recovery of these indexes is slower after eccentric (i.e., lengthening) vs. concentric (i.e., shortening) muscle contractions. Concentric muscle contractions do not cause exercise-induced muscle damage, but exercise-induced muscle damage is evident after isometric contractions at a long muscle length and eccentric muscle contractions, even at low intensity.

Various mechanisms likely account for the loss of strength after eccentrically biased exercise, which is considered to be the best indicator of exercise-induced muscle damage. These mechanisms are outlined in the following theoretical model.

• Mechanical strain during eccentric exercise causes one-half sarcomere nonuniformity and overstretching of sarcomeres beyond filament overlap, leading to “popped sarcomeres.”
• These alterations likely directly reduce force production and overload sarcolemma and t-tubule structures. In turn, these events cause opening of stretch-activated channels, membrane disruption, and excitation-contraction coupling dysfunction.
• Ca2+ entering the cytosol through stretch-activated channels and/or permeable sections of the sarcolemma may stimulate calpain enzymes to degrade contractile proteins or excitation-contraction coupling proteins, resulting in prolonged loss of muscle strength.

Time Course of EIMD

The number of muscle fibers showing disruption of normal myofibrillar banding patterns is increased immediately after eccentric exercise. Disruption of Z disks and sarcomeres appears to peak between 1 and 3 days after exercise, but may remain elevated up to 6−8 days after exercise. There is a temporal association between the extent of loss of muscle strength after exercise and the time required to restore muscle strength back to normal.

• When muscle strength decreases by ≤20% immediately after exercise, it is usually restored within 2 days after exercise (21, 59).
• When muscle strength decreases by ∼50% immediately after exercise, especially for the initial exposure to eccentric muscle contractions, it remains below pre-exercise values at 7 days after exercise.

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Many treatments have been tested to determine whether they help to restore muscle function and reduce muscle soreness following exercise. Perhaps with the exception of massage, cold water immersion, and wearing compression garments, these treatments have not produced consistent benefits. Although evidence is lacking to support the physical benefits of some of these treatments, their perceptual effects may be important for exercise recovery. In this regard, however, a key consideration is whether by masking the perception of pain or accelerating recovery ahead of structural remodeling, some of these treatments may actually increase risk of further muscle injury.

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