The Mechanisms of Muscle Hypertrophy and Their Application to Resistance Training 1
- 01-19-2012, 02:58 PM
The Mechanisms of Muscle Hypertrophy and Their Application to Resistance Training 1
A jurnal i read online. so i downloaded the doc, and thought i would copy and paste it here. its a good read. enjoy.
The Mechanisms of Muscle Hypertrophy and Their Application to Resistance Training
Schoenfeld, Brad J.
Global Fitness Services, Scarsdale, New York
(from Journal of Strength and Conditioning Research, 24 (10)/2857-2873)
Contractile hypertrophy can occur either by adding sarcomeres in series or in parallel.
The majority of exercise-induced hypertrophy subsequent to traditional resistance training programs results from an increase of sarcomeres and myofibrils added in parallel. When skeletal muscle is subjected to an overload stimulus, it causes perturbations in myofibers and the related extracellular matrix. This sets off a chain of myogenic events that ultimately leads to an increase in the size and amounts of the myofibrillar contractile proteins actin and myosin, and the total number of sarcomeres in parallel. This, in turn, augments the diameter of individual fibers and thereby results in an increase in muscle cross-sectional area.
Muscle is a postmitotic tissue, meaning that it does not undergo significant cell replacement throughout life.
Satellite cells are thought to facilitate muscle hypertrophy in several ways. For one, they donate extra nuclei to muscle fibers, increasing the capacity to synthesize new contractile proteins. Because a muscle's nuclear-content-to-fiber-mass ratio remains constant during hypertrophy, changes require an external source of mitotically active cells. Satellite cells retain mitotic capability and thus serve as the pool of a myonuclei to support muscle growth. This is consistent with the concept of myonuclear domain, which proposes that the myonucleus regulates mRNA production for a finite sarcoplasmic volume and any increases in fiber size must be accompanied by a proportional increase in myonuclei. Given that muscles are comprised of multiple myonuclear domains, hypertrophy could conceivably occur as a result of either an increase in the number of domains (via an increase in myonuclear number) or an increase in the size of existing domains. Both are thought to occur in hypertrophy, with a significant contribution from satellite cells.
Structurally, IGF-1 is a peptide hormone, so named because of its structural similarities to insulin. Insulin-like growth factor receptors are found in activated satellite cells, adult myofibers, and Schwann cells.
Although the exact mechanisms of IGF-1's mode of action have not been fully elucidated, it is believed that mechano-stimulation causes the IGF-1 gene to be spliced toward MGF, which in turn “kick starts” muscle hypertrophy.
Testosterone is a cholesterol-derived hormone that has a considerable anabolic effect on muscle tissue. In addition to its effects on muscle, testosterone also can interact with receptors on neurons and thereby increase the amount of neurotransmitters released, regenerate nerves, and increase cell body size.
Although the effects of testosterone on muscle are seen in the absence of exercise, its actions are magnified by mechanical loading, promoting anabolism both by increasing the protein synthetic rate and inhibiting protein breakdown.
- 01-19-2012, 02:59 PM
The Mechanisms of Muscle Hypertrophy and Their Application to Resistance Training 2
Growth hormone is a polypeptide hormone considered to have both anabolic and catabolic properties. Specifically, GH acts as a repartitioning agent to induce fat metabolism toward mobilization of triglycerides, and stimulating cellular uptake and incorporation of amino acids into various proteins, including muscle.
Growth hormone levels spike after the performance of various types of exercise.
When combined with intense exercise, GH release is associated with marked upregulation of the IGF-1 gene in muscle so that more is spliced toward the MGF isoform.
Although a physiological basis linking cell swelling with an anabolic drive is yet to be determined, it is conceivable that increased pressure against the membrane is perceived as a threat to cellular integrity, which in turn causes the cell to initiate a signaling response that ultimately leads to reinforcement of its ultrastructure.
Given that fast-twitch fibers are most responsive to hypertrophy, it is conceivable that cellular hydration augments the hypertrophic response during resistance training that relies heavily on anaerobic glycolysis.
There are several theories as to the potential hypertrophic benefits of muscle hypoxia. For one, hypoxia has been shown to cause an increased lactate accumulation and reduced acute lactate clearance rate. This may mediate increased cell swelling, which has been shown to upregulate protein synthesis.
Nitric oxide, an ROS produced during exercise, has been shown to mediate the proliferation of satellite cells, which would presumably lead to greater skeletal muscle growth.
It is hypothesized that 3 primary factors are responsible for initiating the hypertrophic response to resistance exercise: mechanical tension, muscle damage, and metabolic stress.
It is believed that tension associated with resistance training disturbs the integrity of skeletal muscle, causing mechano-chemically transduced molecular and cellular responses in myofibers and satellite cells.
Damage can be specific to just a few macromolecules of tissue or result in large tears in the sarcolemma, basal lamina, and supportive connective tissue, and induces injury to contractile elements and the cytoskeleton.
The response to myotrauma has been likened to the acute inflammatory response to infection. Once damage is perceived by the body, neutrophils migrate to the area of microtrauma and agents are then released by damaged fibers that attract macrophages and lymphocytes. Macrophages remove cellular debris to help maintain the fiber's ultrastructure and produce cytokines that activate myoblasts, macrophages and lymphocytes. This is believed to lead to the release of various growth factors that regulate satellite cell proliferation and differentiation.
Metabolic stress manifests as a result of exercise that relies on anaerobic glycolysis for ATP production, which results in the subsequent buildup of metabolites such as lactate, hydrogen ion, inorganic phosphate, creatine, and others.
The use of high repetitions has generally proven to be inferior to moderate and lower repetition ranges in eliciting increases in muscle hypertrophy.
Whether low reps or moderate reps evoke a greater hypertrophic response has been a matter of debate, and both produce significant gains in muscle growth. However, there is a prevailing belief that a moderate range of approximately 6-12 reps optimizes the hypertrophic response.
Although low repetition sets are carried out almost exclusively by the phosphocreatine system, moderate repetition schemes rely heavily on anaerobic glycolysis.
Both testosterone and GH are acutely elevated to a greater degree from routines employing moderate rep sets as compared to those using lower repetitions, thereby increasing the potential for downstream cellular interactions that facilitate remodeling of muscle tissue.
During moderate rep training, the veins taking blood out of working muscles are compressed while arteries continue to deliver blood into the working muscles, thereby creating an increased concentration of intramuscular blood plasma. This causes plasma to seep out of the capillaries and into the interstitial spaces. The buildup of fluid in the interstitial spaces causes an extracellular pressure gradient, which causes a flow of plasma back into the muscle causing the phenomenon commonly referred to as a “pump.”
Moreover, the extra time under tension associated with a moderate repetition scheme as compared to a lower rep scheme would theoretically enhance the potential for microtrauma and fatigueability across the full spectrum of muscle fibers.
Although slow-twitch fibers are not as responsive to growth as fast-twitch fibers, they nevertheless do display hypertrophy when subjected to an overload stimulus.
Compared to full body routines, a split routine allows total weekly training volume to be maintained with fewer sets performed per training session and greater recovery afforded between sessions.
Prolonged periods of overreaching, however, can rapidly lead to an overtrained state. Overtraining has catabolic effects on muscle tissue, and is characterized by chronically decreased concentrations of testosterone and luteinizing hormone, and increased cortisol levels.
However, studies seem to show that overtraining is more a result of excessive volume than intensity.
Furthermore, the quest to train with a high volume must be balanced with performance decrements arising from lengthy exercise sessions.
Accordingly, it has been proposed that intense workouts should not last longer than one hour to ensure maximal training capacity throughout the session.
Moreover, muscles are sometimes divided into neuromuscular components-distinct regions of muscle each of which is innervated by its own nerve branch-suggesting that portions of a muscle can be called into play depending on the activity.
Studies investigating muscle activity of the long head of the biceps brachii show that MUs in the lateral aspect are recruited for elbow flexion, MUs in the medial aspect are recruited for supination, and centrally located MUs are recruited for non-linear combinations of flexion and supination. Further, the short head appears to be more active in the latter part of an arm curl (i.e., greater elbow flexion), whereas the long head is more active in the early phase.
These architectural variances of muscle give support for the need to adopt a multiplanar, multiangled approach to hypertrophy training using a variety of different exercises.
Specifically, the magnitude of postexercise hormonal elevations has been shown to be related to the extent of muscle mass involved, with multijoint movements producing larger increases in both testosterone and GH levels compared to single-joint exercises.
In all, it is estimated that over 200 muscles are activated during squat performance.
On the other hand, single-joint exercises allow for a greater focus on individual muscles compared to multijoint movements.
The use of single-joint exercises can selectively target underdeveloped muscles, improving muscular symmetry.
Moreover, the unique architecture of individual muscles suggests employing single-joint movements can elicit differing neuromuscular activation patterns that heighten overall muscular development.
Anderson and Behm found that force output was 59.6% lower when performing a chest press on an unstable surface compared to a stable surface.
An exception to the use of unstable surfaces in a hypertrophy-oriented routine involves exercises for the core musculature.
Moderate rest intervals appear to provide a satisfactory compromise between long and short rest periods for maximizing the muscle hypertrophy.
For one, training to failure is hypothesized to activate a greater number of MUs.
Training to failure also may enhance exercise-induced metabolic stress, thereby potentiating a hypertrophic response.
Linnamo et al. displayed that performing sets at 10RM to failure caused a significantly greater postexercise elevation in GH secretion compared to the same load not performed to failure.
Thus, although it seems prudent to include sets performed to failure in a hypertrophy-oriented program, its use should be periodized and/or limited to avoid an overtrained state.
Other studies, however, suggest that training at moderate speeds has greater effects on hypertrophy, perhaps through a heightened metabolic demand. Maintaining continuous muscle tension at moderate repetition speeds also has been shown to enhance muscle ischemia and hypoxia, thereby augmenting the hypertrophic response.
Although concentric and isometric contractions have been shown to produce a hypertrophic response, a majority of studies seem to show that eccentric actions have the greatest effect on muscle development. Specifically, lengthening exercise is associated with a more rapid rise in protein synthesis and greater increases in IGF-1 mRNA expression compared to shortening exercise. Moreover, isotonic and isokinetic training that does not include eccentric contractions result in less hypertrophy than those that include lengthening contractions.
There is also evidence that eccentric contractions result in additional recruitment of previously inactive MUs.
Eccentric exercise also is associated with greater muscle damage when compared to concentric and isometric contractions. This manifests as Z-line streaming, which current research suggests is indicative of myofibrillar remodeling. It has been shown that MyoD mRNA expression is specifically upregulated by eccentric contractions.
I quoted a few things from this review in my dissertation proposal. I have the full text of the actual article as well if anyone is interested.
cliffs notes please!
-Saving random peoples' nuts, one pair at at time... PCT info:
-Are you really ready for a cycle? Read this link and be honest:
*I am not a medical expert, my opinions are not professional, and I strongly suggest doing research of your own.*
Hm...that may work. My only concern is that it is copy righted material, so I wouldn't want either of us to run into any issues with that.
Other people who would like to read the article please PM me email addresses.
I will summarize the paper from what I remember reading in it, I need to re-read it again though. I will keep my summary to the actual workout rather than the mechanics behind it for simplicity's sake
1. The paper breaks rep ranges into 3: 1-5 reps, 6-12, 12+ with the recommendation of 6-12 reps being optimal
2. Research showed that Testosterone and GH increase was not noticed during the first 3 sets but was noticable with 4+ sets
3. Tempo of the lift should be explosive on the way up (concentric) and 2-3 seconds on the eccentric for maximum growth (TUT)
4. Ideal rest period for hypertrophy between sets is 60-90 seconds
5. Use of compound movements is most benefitial, but should use isolation work as well to bring up the weak parts
6. The paper recommends split routine over full body routine to reduce the number of sets performed per session. This also gives the body parts time to recover more
7. Training to failure is more productive on the short run, but detrimental if done every week. The paper suggest cycling the workouts that you do to failure every week. That way you do not train all body parts to failure every week. If training to, it is best to have deload period
8. The paper recommends cycling the workouts and not do the same workout every week
I do have many questions, but I would like to see if everyone else got the same points I did from this paper.
I could write out the need-to-know information for building muscle and losing fat on 2-3 sheets of notebook paper.
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