Term
| How long after activity does DOMS hit its peak? |
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Definition
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Term
| What type of movement causes DOMS? |
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Definition
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Term
| Will someone experience DOMS after running on a treadmill? |
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Definition
| No. There's little eccentric control in this activity. |
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Term
| Will downhill running likely lead to DOMS? |
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Definition
| Yes. Much eccentric activity occuring during this activity. |
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Term
| Why is it that inflammation doesn't seem like a plausible cause of DOMS? |
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Definition
| Although neutrophils and monocytes are present, NSAIDS don't affect DOMS pain. If the pain was caused by inflammation, one would expect NSAIDS to decrease the pain level. |
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Term
| Describe the role substance P may play in DOMS. |
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Definition
| Substance P is released with inflammation. Although inflammation itself isn't suspected of causing DOMS, the release of substance P at this stage may be a cause. Substance P is not affected by NSAIDS, so it makes sense that NSAIDS would not affect this pain factor. |
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Term
| Are swelling and edema likely candidates for the cause of DOMS? why or why not?(3 reasons) |
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Definition
| No. The time frames don't fit. Swelling peaks at 4-5 days post activity. Pain peaks at 2-3 days. Also, with swelling, you would expect compression which would result in pain at rest. But that's not the characteristic of DOMS; DOMS occurs during activity/stretch of the involved muscle. Not only that, but muscles like the biceps have plenty of room around them, so they should be completely unaffected by swelling. |
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Term
| What is the significance of creatine kinase in the blood? |
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Definition
| CK is an enzyme within muscle tissue, that should not be free-floating in the blood. If it is detectable in the blood, we know that it has leaked out of muscle fiber as a result of muscle damage. |
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Term
| Is it likely that creatine kinase is a causal factor for DOMS? Why or why not? |
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Definition
| No, it isn't. the CK peaks at 4-6 days post activity. Pain peaks at 2-3 days. Not only that, but muscular dystrophy patients have a lot of CK in their blood as a result of destroyed muscle fibers, but experience no pain. Therefore, CK isn't likely to be the cause of pain in DOMS. |
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Term
| What happens to strength in the period of DOMS? |
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Definition
| It decreases. May be caused because of muscle damage, decreased muscle fiber shortening, or swelling. |
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Term
| Describe the Repeated Bout Effect. |
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Definition
| You are not as sore or as weak with repeated eccentric exercise. Less muscle damamge is produced by a subsequent exercise session as early as 5 days post initial exercise and up to 3-45 days post exercise. |
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Term
| What does the Popping Sarcomere Theory say happens as a result of the popped sarcomeres? |
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Definition
| Results in additional sarcomeres. |
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Term
| What effect does an antiinflammatory have on healing of muscle tissue? |
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Definition
| It alters the normal healing process and has a negative effect on force generation after eccentric exercise. It is thought that inflammation results in muscle remodelling. So without this critical phase, muscle doesn't not remodel to its full potential. |
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Term
| What happens to the Z line with eccentric exercise? |
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Definition
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Term
| What are the two theories behind Z line smearing post eccetric exercise? |
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Definition
| 1. CALPAIN theory. 2. Titin theory. |
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Term
| Describe the CALPAIN theory behind Z line smearing. |
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Definition
| CALPAIN = desmin enzyme; high force associated w/ eccentric muscle activity may increase calpain. The damage lets calcium leak out which leads to calpain disrupting of desmin, which leads to z line smearing. |
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Term
| Why is it believed that titin disruption may lead to the z line smearing seen w/ eccentric exercise. |
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Definition
| Titin holds myosin to the z line. if titin gets broken, z line smearing may occur. |
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Term
| The Sarcomere Popping Theory attempts to explain a phenomenon that occurs as a result of eccentric exercise? What is it? (it's not z line smearing) |
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Definition
| Decreased strength following eccentric exercise. |
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Term
| Explain the Sarcomere Popping Theory. |
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Definition
| At rest, some sarcomeres are shorter than others. Those that are shorter have more actin/myosin overlap than those that are longer. (short and strong vs. long and weak) As the muscle contracts, those that are short and strong maintain good actin myosin overlap. Those that are lengthened get stretched further until there is not A-M overlap. As the tension in the muscle increases, the long weak sarcomere's "pop" and the tension in them is born by passive muscle elements. At this point, the injured sarcomere no longer contributes to force generation, resulting decreased contractile strength. Nonuniformity of sarcomere length is the basis behind the popping sarcomere hypothesis. |
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