Hypertrophy
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Hypertrophy is the increase of the size of an organ. It should be distinguished from
hyperplasia which occurs due to cell division; hypertrophy occurs due to an increase in cell size rather than division. It is most commonly seen in
muscle that has been actively stimulated, the most well-known method being
exercise.
Hypertrophy is only desirable when it occurs in the
skeletal muscles. This is most effectively done by undertaking
resistance training, though it can also occur during other high
anaerobic exercises such as
interval training,
rowing,
cycling and
sprinting.
For hypertrophy to occur in the skeletal muscles, the muscle must be directly stimulated as discussed above. Also a diet, in which there is a
caloric surplus and abundant in
protein is required in conjunction with regular rest (8-10 hours per night). Also you should consult with your
physician before undertaking any strenuous
exercise routine.
Hypertrophy can be
pathological in many organs; for example in the
heart hypertrophy of the left
ventricle can be associated with up to a four fold risk of dying over the following 5 years. In skeletal muscle, it is usually helpful and increases strength.
Two different types of hypertrophy are common; Sarcoplasmic hypertrophy, in which sarcoplasmic fluid in the muscle cell increases rather than the contractile protein, and hence no increase in contractile strength. Myofibrillar Hypertrophy, in which there is an increase in myofibrils, and hence increase in muscular contractile strength.
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Resistance training
Resistance training typically produces a combination of the two different types of hypertrophy; contraction against 80-90% of the
one repetition maximum for a lower number of repetitions causes myofibrillated hypertrophy to dominate (as in
powerlifters, olympic lifters and strength athletes), while several repetitions against a sub-maximal load facilitates mainly sarcoplasmic hypertrophy (professional
bodybuilders and endurance athletes).
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Ventricular hypertrophy
Increased ventricular mass is an adaptation by the ventricle to increased stress, such as chronically increased volume load (preload) or increased pressure load (afterload). It is a physiological response that enables the heart to adapt to increased stress; however, the response can become pathological and ultimately lead to a deterioration in function. For example, hypertrophy is a normal physiological adaptation to exercise training that enables the ventricle to enhance its pumping capacity. This type of physiologic hypertrophy is reversible and non-pathological. Chronic hypertension causes ventricular hypertrophy. This response enables the heart to maintain a normal stroke volume despite the increase in afterload. However, over time, pathological changes occur in the heart that lead to a functional degradation and heart failure.
If the precipitating stress is volume overload, the ventricle responds by adding new sarcomeres in-series with existing sarcomeres. This results in ventricular dilation while maintaining normal sarcomere lengths. The wall thickness normally increases in proportion to the increase in chamber radius. This type of hypertrophy is termed eccentric hypertrophy.
In the case of chronic pressure overload, the chamber radius may not change; however, the wall thickness greatly increases as new sarcomeres are added in-parallel to existing sarcomeres. This is termed concentric hypertrophy. This type of ventricle is capable of generating greater forces and higher pressures, while the increased wall thickness maintains normal wall stress. This type of ventricle becomes "stiff" (i.e., compliance is reduced) which can impair filling and lead to diastolic dysfunction.
Neural Response
The first measurable effect is an increase in the neural drive stimulating muscle contraction. Within just a few days, an untrained individual can achieve measurable strength gains resulting from "learning" to use the muscle.
Genetic Response
As the muscle continues to receive increased demands, the synthetic machinery is upregulated. Although all the steps are not yet clear, this upregulation appears to begin with the ubiquitous second messenger system (including phospholipases, protein kinase C, tyrosine kinase, and others). These, in turn, activate the family of immediate-early genes, including c-fos, c-jun and myc. These genes appear to dictate the contractile protein gene response.
Protein Synthesis
Finally, the message filters down to alter the pattern of protein expression. It can take as long as two months for actual hypertrophy to begin. The additional contractile proteins appear to be incorporated into existing myofibrils (the chains of sarcomeres within a muscle cell). There appears to be some limit to how large a myofibril can become: at some point, they split. These events appear to occur within each muscle fiber. That is, hypertrophy results primarily from the growth of each muscle cell, rather than an increase in the number of cells.
Penile Hypertrophy is the continual enlargement of a males penis.
http://en.wikipedia.org/wiki/Hypertrophy