Adaptations to Strength Training
low-resistance training
>20 reps/set. results in gains in muscular endurance, with less of a change in strength
neural factors
concurrent training impairs motor unit recruitment and therefore decreases muscle force production.
overtraining
contributes to inability to attain optimal strength gains when concurrent strength and endurance exercise training is performed.
summary
1) resistance training increases the synthesis of contractile proteins in muscle; this results in an increase in the cross-sectional area of the fiber 2) RT-induced increases in protein synthesis occur via an increase in translation, which is controlled by the IGF-1/Akt/mTOR signaling pathway 3) RT results in parallel increases in muscle fiber cross-sectional area and increased number of myonuclei 4) satellite cells are the source for additional nuclei in muscle fibers, and the supplement of myonuclei to muscle fibers is required to achieve max fiber hypertrophy in response to rt.
hypertrophy
rate of protein synthesis in muscle fibers is greater than the rate of protein breakdown. slow process because protein synthesis must exceed breakdown for several weeks to achieve significant muscle growth.
short-duration training studies
8 to 20 weeks. neural adaptations related to learning, coordination, and the baility to recruit the primary muscles play a major role in the gain in strength.
high resistance training
8-12 reps/set. results primarily in gains in muscular strength
muscular endurance
ability to make repeated contractions against a submaximal load.
myonuclei
addition of myonuclei to growing muscle fibers is a requirement to maintain the high level of translational capacity required to synthesize muscle proteins at a high rate following a strength-training session. a single myonuclus can only manage a specific volume of muscle area
aging, strength, and training
aging is associated with a decline in strength, with most occurring after fifty. due, in part, to loss of muscle mass (sarcopenia), which is related to loss of type 1 and type 2 fibers, atrophy of existing type 2 fibers, and an increase in intramuscular fat and connective tissue.
force production
amount of actin and myosin within the muscle fibers. the more myosin cross-bridges that are attached to actin and engaged in the power stroke, the more force produced.
long-term training programs
an increase in muscle size plays the major role in strength development.
hyperplasia
an increase in the total number of muscle fibers within a specific muscle. resistance training can promote an increased number of fibers in the trained muscles (still up for debate).
progressive resistance-training
causes muscle hypertrophy and very large gains in strength in older individuals. important for ADL, balance, and reducing risk of falls
fibers cluster
cluster in homogeneous groups, in contrast to the heterogeneous distribution of fiber types seen in a muscle cross-section from younger individuals
depressed protein synthesis
concurrent resistance and endurance exercise bouts could result in impaired protein synthesis following resistance exercise training. resistance increases muscle contractile protein synthesisi by activation of the IGF-1/Akt/mTOR signaling pathway. endurance increases AMPK activation and promotes mitochondrial biogenesis. active AMPK can activate a signaling molecule called tuberous sclerosis complex 1/2. active TSC 1/2 inhibits mTOR activity and impairs protein synthesis.
muscle protein synthesis
done by improving translational efficiency. primary signal is mechanical stretch (force) applied to muscle during weight lifting. triggers secondary signal of IGF-1 synthesis ad the cascade of downstream signaling events leading to increased protein synthesis. activation of important signaling molecule Akt. active Akt then activates mTOr which promotes protein synthesis by increasing translation and building more proteins. requires all essential amino acids be present in muscle in order fo synthesis to occur.
increase in size
growing fibers add new nuclei (myonuclei) within the fiber.
hypertrophy
increase in muscle fiber cross-sectional area (fiber hypertrophy). 90-95% of increase in muscle size following resistance training. gradual process that occurs during months to years of training. changes in muscle size are detectable by 3 weeks of training. weight training elicits a greater degree of hypertrophy in type 2 fibers
resistance training-induced increase in fiber cross-sectional area
increase in myofibrillar proteins (actin and myosin). increase in filaments in fiber occurs due to addition of sarcomeres in parallel to the existing sarcomeres, resulting in muscle fiber hypertrophy. addition of additional contractile proteins increases the number of myosin cross-bridges in fiber and therefore increases fiber's ability to generate force.
resistance training
increases muscular strength by changes in both the nervous system and an increase in muscle mass.
endurance exercise training
increases the oxidative capacity (mitochondrial number increases) and the antioxidant capacity in the exercised muscle fibers. promotes formation of new capillaries and therefore increases muscle capillarization.
common pain killers
interfere with resistance training-induced muscle hypertrophy. do not impede strength gains in older people engaged in resistance exercise training. some studies suggest that concurrent training and use of ibuprofen or acetaminophen may actually enhance muscle hypertrophy
VO2 max
large individual differences exist in the response to strength-training programs, and the percent gain in strength is inversely related to the initial strength
genetics
limits gains that can be achieved with training
Muscular Strength
maximal force that a muscle fo muscle group can generate and is commonly expressed as the one-repetition maximum, or 1-RM, the maximum load that can be moved through a full range of motion.
neural adaptations
occur in response to resistance training. improve ability to recruit motor units, alter motor neuron firing rates, enhance motor unit synchronization during a particular movement pattern, and result in removal of neural inhibition. result in increase in muscle force production. if you train one leg, some gains will be noticed in other leg because of neural adaptation.
prolonged periods of resistance training
promote a fast-to-slow shift in muscle fiber types within the trained muscles. strength training-induced shifts in muscle fiber types appear to be less prominent than endurance training-induced transformations because all of the change in fiber type is a movement from type 2x to 2a, with no increase in type 1
antioxidant enzyme activity
resistance exercise training can improve muscle antioxidant capacity. results of studies revealed increased activities of 2 important enzymes by almost 100%. should provide cellular protection against the oxidative damage associated with exercise-induced production of free radicals
satellite cell activation
resistance training activates satellite cells to divide and fuse with the adjacent muscle fiber to increase the number of nuclei in the fiber. constant ration between number of myonuclei and size of fiber
loss of muscle fibers
result of loss of motor neurons, so whole motor units are lost with aging.
rate of detraining in RT
slower than endurance training. most of loss of strength associated with detraining is associated with changes in the nervous system.
satellite cell
source of additional myonuclei. adult stem cell located between the sarcolemma and the outer layer of connective tissue (basal lamina) around the fiber.
concurrent training
strength development is impaired effectiveness depends on intensity, volume, frequency, and how training modes are integrated
low muscle glycogen content
successive bouts of either strength or endurance training can produce chronically low levels of muscle glycogen/ low resting levels of muscle glycogen. beginning a training session with low muscle glycogen can reduce the ability to perform subsequent resistance training sessions and impair the magnitude of the strength-training adaptations
