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APK3110C Ch14
| Question | Answer |
|---|---|
| what is muscular strength | max force a muscle/muscle group can generate |
| what is muscular endurance | ability to make repeated contractions against a submaximal load |
| how does percent of gains relate to initial strength | percent of gains are inversely proportional to inital strength |
| how do you increase strength | high resistance, high weight, low repetitions |
| how do you increase endurance | low resistance, low weight, high repetitions |
| how does strength training affect muscle size and strength | increases muscle size and strength |
| what causes short term gains | neural adaptations |
| what causes long term gains | increases in muscle size/hypertrophy, increase in fiber specific force, and increase in intensity |
| why is it difficult to gauge real effects of strength training | studies do often not run long enough to see effects after years |
| how are strength training effects different from endurance | strength results in muscle growth, neural adaptations are also different; strength training does not have the one arm phenomenon, it has cross education |
| what is cross education | effects of strength from one limb/group transfer to the other; this is neural and strength ONLY, not hypertrophic i.e. size |
| what is the period of time for newbie gains | first 2-8 weeks |
| what is neural drive | the magnitude of neural output from the CNS |
| why is there an increase in # of motor units recruited | LESS hinhibition from golgi tendon organs as they shift function |
| how does firing rate increase | more frequent depolarizations occur |
| what effect does an increased firing rate have | no time to relax leads to an increase in force production |
| how is neural transmission improved | size of neuromuscular junction increases, and an increase in ACh vesicles |
| what are the foour factors that cause an increase in neural drive | increased firing rate, increased motor unit synchronization, increased # of motor units, improved neural transmission |
| what happens with antagonist/agonist adaptations | agonists have increased activation, while antagonists have decreased activation to fine tune movements and reduce energy expenditure |
| why do muscle fibers adapt to exert more force per fiber | increased calcium sensitivity causes an increase in the amount of cross bridge cycling occur in a muscle, allowing them to move more |
| what are the 2 ways muscle mass increases | hypertrophy and hyperplasia |
| what is hypertrophy | increase in cross sectional area |
| how does hypertrophy cause muscle mass to increase | to increased formation of actin in myosin; increase in sarcomeres parallel to old ones |
| what type of fiber primarily increases during hypertrophy | type 2 |
| T/F hyperplasia is confirmed to happen in humans | false |
| what are the 2 main types of muscle fiber shifts | fast to slow, type IIx to IIa |
| what has more extreme adapations and fiber shifts, endurance or resistance training | endurance |
| T/F antioxidant capacity does not change with resistance traning | false |
| T/F force only affects type 1 fibers | true, small increases |
| what happens to protein synthesis following training | increases by 50-150% |
| how long does protein synthesis remain elevated | 1-4 hours after training, up to two days |
| what is the difference between trained and untrained individuals in regard to protein synthesis | untrained individuals experience longer period of elevated protein synthesis |
| what are the three factors responsible for increased protein synthesis | increased mRNA density, increased number of ribosomes, increased activation of mTOR |
| what does mTOR stand for | mechanistic target of rapamycin |
| what does mTOR do | signal for accelerated protein synthesis |
| how are muscle fiber sizes affected with resistance training | number of sizes stays the same, but parallel size of the fiber increases along with the number of myonuclei |
| what are satellite cells | stem cells between the sarcolemma and basal lamina |
| why do satellite cells become myonuclei with resistance training | they are activated to fuse with fibers to keep a constant ratui between newly synthesized proteins, which cause an increase in size; this keeps the myonuclear domain even with size increases |
| how is myonuclear domain affected | it remains constant as more cells differentiate |
| what 3 hormones increase mTOR activation | IGF-1, GH, testosterone |
| why are steroids not needed | mTOR relies on intrinsic signaling and they can help but they are not necessary for hypertrophy |
| what percent of muscle mass variability is based on genetics | 80% |
| ____-linked genes are linked to the mTOR pathway | hypertrophy |
| what activates hypertrophy genes | resistance training |
| why are there differences in the magnitude of hypertrophy | many differences in ability to activate protein sythesis genes, from highly responsive to low responsive. |
| t/f detraining causes a fast decrease in strength | false, slow |
| what do fibers get smaller | nervous system changes |
| which type of fibers reduces in size the most | type llx |
| which type of fibers reduces in size the least | type l |
| what is the mechanism behind muscle memory | increased/new myonuclei are not lost during retraining which allows for rapid protein synthesis |
| what causes muscle atrophy | inactivity such as bedrest, a cast, or fatigue |
| how much muscle is lost after 1 wk | 7-10% |
| how much muscle is lost after 1 month | 15-20% |
| how can you conserve muscle mass | synthesis rate must exceed 2x the degradation rate |
| what 2 mechanisms do free radicals use to cause atrophy | increased protein degradation and decreased protein synthesis |
| what is another word for increased free radicals | oxidative stress |
| what is the impact of both strength and endurance training | impaired strength potential |
| what are three possible causes of interference between resistance and endurance training | neural factors, overtraining, depressed protein synthesis |
| Increases in muscular strength due to short-term (2–8 weeks) resistance training are largely the result of changes in the _________________________ | nervous system |
| Gains in strength during long-term training programs (months to years) are collectively due to: (1) ___________________________; (2) ______________________________; and (3__________________________________________ | hypertrophy/increased muscle size, fiber specific tension/force, neural adaptations |
| Whether or not hyperplasia occurs in response to resistance training remains highly controversial and current evidence suggests that most of the increase in muscle mass following resistance training occurs due to muscle _______ and no _______________. | hypertrophy; hyperplasia |
| Prolonged periods of resistance training promotes a fast-to-slow shift in muscle fiber types. Most of this training-induced fiber shift is the conversion of __________ to ____________ fibers, with no increase in the number of ___________fibers. | llx; lla; l |
| Whether resistance training improves oxidative properties remains controversial. evidence reveals that __- term and ___-volume resistance training programs can improve muscle oxidative capacity & increase capillary number around the trained fibers | long; high |
| Resistance training ____________ the antioxidant capacity of the trained muscle fibers | increases |
| Resistance training __________ tendon, ligament, and bone strength. Importantly, resistance training–induced increases in muscle strength are met by equal increases in the strength of connective tissue (i.e., ligaments and tendons) | increases |
| Resistance training increases the synthesis of contractile proteins in muscle; this results in an increase in the _________________ area of the fiber (i.e., hypertrophy). | cross sectional |
| Resistance training–induced increases in protein synthesis occur via an increase in translation, which is controlled by the ________ signaling pathway. | mTOR |
| Although high circulating levels of ________, _________________, and ____can support resistance training–induced hypertrophy, increases in the circulating levels of these hormones are not required to achieve resistance training–induced hypertrophy. | IGF 1, GH, testosteron |
| Resistance training results in parallel increases in muscle fiber cross- sectional area and increased numbers of __________. | myonuclei |
| _________________are the source of additional myonuclei in muscle fibers | satellite cells |
| Although controversy exists, the addition of myonuclei to muscle fibers appears to be a requirement to achieve maximal fiber hypertrophy in response to _____________ | reisistance training |
| Approximately 80% of the differences in muscle mass between individuals can be explained by ____________ variation. | genetic |
| some individuals are genetically gifted and have high levels of hypertrophy (__ responders). some ppl have a more moderate level of hypertrophy (___ responders) or achieve limited hypertrophy following resistance exercise training (__responders). | high, moderate, low |
| Following a period of detraining, rapid strength gains occur when strength training is reinstated in previously trained individuals. This phenomenon is commonly referred to as “______________.” | muscle memory |
| Although controversial, muscle memory may be due to the large number of ______________ remaining in the trained muscle fibers | myonuclei |
| Prolonged periods of muscle inactivity (e.g., casting a limb or bedrest) results in a rapid muscle fiber atrophy due to both a decrease in muscle protein ______________ and an increase in muscle protein ______________ | synthesis, degradation |
| A key mechanism responsible for inactivity-induced muscle atrophy is an increase in __________________in the inactive fibers; this results in ______________ muscle protein synthesis and ______________ muscle protein breakdown. | free radical, decreased, increased |
| Concurrent resistance and endurance exercise bouts can theoretically impair protein _____________ following resistance exercise training | synthesis |
| At least three mechanisms can explain why concurrent training may impair strength gains. These include ____________, ____________, and ________________________ | overtraining, neural factors, depressed protein synthesis |
| Concurrent resistance and endurance exercise bouts can theoretically impair protein _____________ following resistance exercise training | synthesis |
Created by:
isabellamulet