9 adaptations to resistance training chapter. learning objectives discover how strength is gained...
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Learning Objectives
• Discover how strength is gained through resistance training
• Note changes in the muscles and in the neural mechanisms controlling them that occur as a result of resistance training
• Learn what causes muscle soreness and how to prevent it
Resistance Training and Gainsin Muscular Fitness
Muscle is very plastic, increasing in size and strength with training and decreasing with immobilization
© BananaStock
Neural Control of Strength Gains
• Recruitment of motor units – Increased number of motor units recruited from
increased neural drive– Synchronicity of motor unit recruitment is improved
• Increased frequency of discharge from the -motor neuron
• Decrease in autogenic inhibition• Reduction in the coactivation of agonist and antagonist
muscles• Morphological changes in the neuromuscular junction
Muscle Hypertrophy
Transient hypertrophy is the increase in muscle size that develops during and immediately following a single exercise bout
– Fluid accumulation in the interstitial and intracellular space from the blood plasma
Chronic hypertrophy is the increase in muscle size after long-term resistance training
– Changes in both the size of muscle fibers (fiber hypertrophy) and the number of muscle fibers (fiber hyperplasia)
Microscopic Views of Muscle Cross Sections Before and After Training
Photos courtesy of Dr. Michael Deschene's laboratory.
Fiber Hypertrophy
• Net increase in muscle protein synthesis—possibly increasing the number of actin and myosin filaments, and increasing the number of myofibrils
• Facilitated by postexercise nutrition• Testosterone plays a role in promoting muscle growth
Fiber Hyperplasia
• Muscle fibers can split in half with intense weight training (cat research)
• Each half then increases to the size of the parent fiber• Conflicting study results may be due to differences in
the training load or mode• Satellite cells may also be involved in the generation of
new skeletal muscle fibers• Hyperplasia has been clearly shown to occur in animal
models; only a few studies suggest this occurs in humans too
The Satellite Cell Responseto Muscle Injury
Reprinted, by permission, from T.J. Hawke and D.J. Garry, 2001, “Myogenic satellite cells: Physiology to molecular biology,” Journal of Applied Physiology 91: 534-551.
Integration of Neural Activationand Fiber Hypertrophy
• Early gains in strength appear to be more influenced by neural factors
• Long-term strength increases are largely the result of muscle fiber hypertrophy
Resistance Training
Key Points• Neural adaptations always accompany strength gains• Neural mechanisms leading to strength gains include:– Increased frequency of stimulation – Recruiting more motor units– More synchronous recruitment – Decreased autogenic inhibition
• Transient muscle hypertrophy results from edema
(continued)
Resistance Training (continued)
Key Points• Chronic muscle hypertrophy reflects actual structural
changes in the muscle• Muscle hypertrophy results from an increase in the
size of the individual muscle fibers and maybe an increase in the number of muscle fibers
Muscle Atrophy and Decreased Strength With Inactivity
Immobilization• Decreased rate of protein synthesis• Decreased strength• Decreased cross-sectional area• Decreased neuromuscular activity• Affects both type I and type II fibers, with a greater
effect in type I fibers• Muscles can recover when activity is resumed
Muscle Atrophy and Decreased Strength With Inactivity
Cessation of Training• Decreased strength• Little change in fiber cross-sectional area (type II fiber
areas tend to decrease)• Maintenance training is important to prevent strength
losses
Changes in Muscle Strength With Resistance Training in Women
Adapted, by permission, from R.S. Staron et al., 1991, “Strength and skeletal muscle adaptations in heavy-resistance-trained women after detraining and retraining,” Journal of Applied Physiology 70: 631-640.
Fiber Type AlterationsWith Resistance Training
• Transition of type IIx to type IIa• Results from cross-innervation or chronic stimulation
Muscle Atrophy and Fiber Type Alterations
Key Points• Occurs when the muscle becomes inactive, as with
injury, immobilization, or cessation of training• Maintenance programs can prevent atrophy or loss of
strength• There is a transition of type IIx to type IIa fibers • One fiber type can be converted to the other fiber type
as a result of cross-innervation or chronic stimulation and possibly with training
Acute Muscle Soreness
• Results from an accumulation of the end products of exercise in the muscles or edema
• Usually disappears within minutes or hours after exercise
Delayed-Onset MuscleSoreness (DOMS)
• Soreness is felt 12 to 48 hours after a strenuous bout of exercise• Results primarily from eccentric muscle activity (e.g., downhill
running)• Is associated with:– Structural damage– Impaired calcium homeostasis leading to necrosis– Accumulation of irritants– Increased macrophage activity
• May be caused by inflammatory reaction inside damaged muscles
Electron Micrograph of a Muscle Sample Taken Immediately After a Marathon
From R.C. Hagerman et al., 1984, "Muscle damage in marathon runners," Physician and Sportsmedicine 12: 39-48.
Electron Micrograph Showing Normal Arrangement of Actin and Myosin Filaments and Z-disk Before and
Immediately After a Marathon
From R.C. Hagerman et al., 1984, "Muscle damage in marathon runners," Physician and Sportsmedicine 12: 39-48.
Armstrong’s Sequenceof Events in DOMS
1. Structural damage to the muscle cell and cell membrane
2. Impaired calcium availability, leading to necrosis3. Increased microphage activity and the accumulation of
irritants inside the cell, which stimulate free (pain) nerve endings
DOMS and Performance
• Maximal force-generating capacity is diminished but gradually returns
• Loss of strength is due to:– Physical disruption in the muscle– Failure within the excitation–contraction process– Loss of contractile proteins
Estimated Contributions of Physical Disruption, Contractile Protein Loss, and Excitation–Contraction Coupling Failure
to the Loss of Strength Following Muscle Injury
Reprinted, by permission, from G.L. Warren et al., 2001, “Excitation-contraction uncoupling: Major role in contraction-induced muscle injury,” Exercise and Sport Sciences Reviews 29: 82-87.
The Delayed Response to Eccentric Exercise of Various Physiological Markers
Adapted, by permission, from W.J. Evans and J.G. Cannon, 1991, “The metabolic effects of exercise induced muscle damage,” Exercise and Sport Sciences Reviews 19: 99-125.
Reducing Muscle Soreness
1. Reduce the eccentric component of muscle action during early training
2. Start training at a low intensity and gradually increase it
3. Begin with a high-intensity, exhaustive bout of eccentric-action exercise, which will cause much soreness initially but will decrease future pain
Muscle SorenessKey Points• Acute muscle soreness occurs late in an exercise
bout and during the immediate recovery period after an exercise bout
• Delayed-onset muscle soreness (DOMS) occurs 12 to 48 hours after exercise
• Occurs mostly with eccentric muscle action• Causes include structural damage to muscle cells
and inflammatory reactions within the muscles• Muscle soreness may be an important part of
maximizing the resistance training response
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