WK11 ( CH 14)- The Physiology of Resistance Training Flashcards
Discuss the loss of muscle mass in older individuals and how resistance training can help.
- Older people tend to suffer from sarcopenia, not only is muscle mass lost but there is also less cross section between fiber types meaning that fiber types I and II exist in homogenous groups instead of hetergenous groups as observed in younger subjects. There is an overall decline in fiber types which correlates to entire motor units being lost during aging.
- Resistance training has been shown to give strength and muscle hypertrophy for people of all ages. Which can improve balance and help older people avoid falls.
Define and explain the terms “cross education” and “neural drive”.
Cross Education- gains in strength during the first two weeks of resistance training are due primarily to nervous system functional improvements, cross education is the observation that if one limb engages in training, muscular strength increases in the untrained limb.
Neural Drive- the efferent neural output from the CNS to activated muscle fiber. Neural drive is increased in response to resistance training due to total number of neurons activated, the firing rate of the motor neuron, motor unit synchronization, and neurotransmission at the NMJ.
Define: Hyperplasia, Hypertrophy, Detraining, Muscle Atrophy, Overtraining.
Hyperplasia: increase in number of total muscle fibers within a specific muscle, this has been observed in animals but is not concrete through human studies. The two pathways of hyperplasia are muscle fiber splitting and satellite cells creating new individual fibers.
Hypertrophy: increase in muscle fiber size, primary way of increasing muscle mass. resistance training induced increases in cross sectional area of muscle fiber types are due to an increase in action and myosin filaments being deposited in sarcomeres parallel to existing sarcomeres, leading to muscle fiber hypertrophy.
Detraining: “use it or lose it”, resistance program detraining occurs at a slower rate than endurance detraining. results in muscle atrophy and loss of muscular strength mainly due to loss of nervous system adaptations.
Muscle Atrophy: a reduction in the cross-sectional area of muscle fibers resulting in a decrease in muscle mass. 7 days of limb immobilization can lead to a 7-10% loss of muscle mass.
Overtraining:resulting from a high volume of and intensity of exercise without sufficient rest and recovery, though no current evidence indicates that overtraining contributes to the inhibition of strength gains when both resistance and endurance exercise are performed.
Describe the resistance training changes and improvements in: muscle fiber type, oxidative capacity, capillary number, antioxidant enzyme activity, tendon and ligament strength, bone mineral content. See table 14.1
muscle fiber type: transition from fast to slow fibers types, especially type IIx to IIa with no change in type I fibers.
oxidative capacity and capillary number: studies are inconclusive but point to small increases in oxidative capacity and capillary number to be dependent on duration and volume of a training period with high frequencies and high volumes shown consistently to provide a small boost.
antioxidant enzymes: exercise induced production of free radicals necessitates the 100% increase seen in trained muscle antioxidant enzyme activity after 12 weeks.
tendon and ligament strength: resistance training increases the size of connective tissue, increases the size and strength of both tendons and ligaments, collagen synthesis increases within six hours of exercise and remains elevated for 48 hours, this ensures that as muscles grow tendons and ligaments are able to handle force demands.
bone mineral content: resistance training increases bone mineral content which results in more dense bones that are capable of supporting more force and not fracturing, research indicates that high stress environments such as running and jumping provide the best improvement in bone strength).
Discuss the signaling events that take place after resistance training that induce muscle growth.
the process begins with a series of cell signaling events that stimulate transcriptional activators in the sarcoplasm. The activated transcriptional activator (molecule that turns on a gene) moves from the cytosol to the nucleus and binds to the gene promoter. Activation of the gene’s promoter provides the stimulus for transcription. Transcription results in the formation of a message called messenger RNA (mRNA) which contains the genetic
information for a specific protein’s amino acid sequence. The mRNA
leaves the nucleus and travels through the sarcoplasm to the
ribosome which is the site of protein synthesis. At the ribosome, the mRNA is translated into a specific protein.
resistance training induces more ribosome synthesis which leads to more protein synthesis per molecule of mRNA not solely an increase in total mRNA.
mTOR is the primary activator of muscle protein
synthesis. Resistance exercise triggers muscle signaling events that
activate mTOR leading to increased protein synthesis. This process
begins with contraction-induced activation of a mechanoreceptor on
the fiber membrane that can activate mTOR in two ways. First,
exercise-mediated mechanoreceptor signaling promotes the
synthesis of PA, which is an mTOR activator. Second, contraction mediated
mechanoreceptor signaling activates another key mTOR
activator, Rheb. This occurs because muscle contractions activate the
enzyme, Erk, which phosphorylates the Rheb inhibitor, TSC2; this
phosphorylation removes TSC2’s inhibition of Rheb, which enables
Rheb to activate mTOR. Together, these exercise-mediated signaling
actions activate mTOR and promote muscle protein synthesis. SEE FIGURE 14.4
the amino acid leucine can also activate mTOR
Do Hormones Contribute to Resistance Training–Induced Hypertrophy?
Yes ! GH, Testosterone, and IGF-1 all promote hypertrophy by activating the mTOR signaling pathway.
Do Anti-inflammatory Drugs Impact Training-induced Hypertrophy?
studies conducted in animals indicate that it is counterintuitive to consume COX inhibitors but recent human studies conclude that pain killers do not impede strength gains in people. One study even found that concurrent use of ibuprofen or acetaminophen may enhance muscle hypertrophy, suggesting that COX pathways are involved in regulation of muscle protein content.
What is the role of satellite cells in resistance training induced hypertrophy ?
satellite cells are adult stem cell that deposit myonuclei in muscle fibers, located between the sarcolemma and basal lamina, this is done to keep up with mRNA translational demands in growing muscle.
Discuss the three major theories of how endurance exercise impedes resistance exercise benefits, as they relate to neural factors, depressed protein synthesis, and overtraining.
Neural factors: some investigators predict that concurrent training may impair neural adaptations to resistance training. However it is unclear if this is true or not.
Overtraining: no experimental evidence suggests that overtraining during concurrent exercises leads to inhibition of strength gains.
Impaired protein synthesis: endurance training may activate TSC2 which inhibits mTOR directly by inhibiting rheb, thus impairing protein synthesis. It is unclear if this is the only mechanism.
