Muscle hypertrophy

Somlyo There s a problem here. In hypertrophied muscle there is an increase in rough ER because of the increase in protein production. The next problem is going to be sorting out how much of the rough ER takes up Ca2+. 

Clinical findings may include hypertrophied muscles, acne, oily skin, hirsutism in females, gynecomastia in males, and needle punctures. Edema and jaundice may develop in heavy users. Common laboratory abnormalities include elevated hemoglobin and hematocrit measurements, elevated low-density lipoprotein cholesterol and depressed high-density lipoprotein cholesterol levels. Liver function test results may be elevated, and luteinizing hormone levels are usually depressed. 

The growth of animals can be defined as an increase in mass of whole body, tissue(s), organ(s), or ceU(s) with time. This type of growth can be characterized by morphometric measurements eg, skeletal muscle or adipose tissue growth can be described by observing temporal changes in ceU number, ie, hyperplasia, and ceU size, ie, hypertrophy. Growth also includes developmental aspects of function and metaboHsm of cells and tissues from conception to maturity. 

One possible mechanism responsible for the abiHty of trenbolone acetate to stimulate skeletal muscle hypertrophy may be through enhanced proliferation and differentiation of satelHte ceUs as the result of increased sensitivity to insuHn-Hke growth factor-I (IGE-1) and fibroblast growth factor (43). 

Mechanism of Action. P-Agonists stimulate skeletal muscle growth by accelerating rates of fiber hypertrophy and protein synthesis, but generally do not alter muscle DNA content in parallel with the increases in protein accretion (133—135). This is in contrast to the effects of anaboHc steroids and ST on skeletal muscle growth. Both of the latter stimulate fiber hypertrophy and muscle protein synthesis, but also increase muscle DNA content coincident with increased protein accretion. Whether the P-agonists decrease muscle protein degradation is equivocal. 

Asthma is a complex respiratory disorder that involves mast cell degranulation, mucous secretions, and smooth muscle hypertrophy and hyperresponsiveness. Smooth muscle hyperresponsiveness has suggested some defect in the regulation of smooth muscle contractility. Therefore, a number of studies concerning asthma have centered on whether alterations in the regulation of smooth muscle contraction (Figure 4) are responsible for hyperactivity in asthmatic airway smooth muscle. 

The histopathological features of muscle samples from patients with myotonic dystrophy are not particularly distinctive. Early changes appear to be a selective atrophy of type 1 fibers, and hypertrophy of type 2 fibers, but the biochemical and/or physiological basis of these possibly related phenomena is not known. The incidence of degenerating fibers increases with age, although the presence of internally nucleated muscle fibers in early stages of the disease suggests that the muscle retains... 

Figure 16. Werdnig-Hoffman disease most muscle fibers show severe atrophy with some type 1 (dark) fibers showing hypertrophy.

Hypothyroid myopathy occurs in about 30% of patients with hypothyroidism irrespective of its cause. Muscle pain, cramps, and stiffness may be seen, and are often exacerbated by cold weather. Pseudomyotonic features of delayed muscle contraction and relaxation are common. Myoedema (the mounding phenomenon) is due to the painless, electrically silent contracture produced on direct percussion. Muscle biopsy often shows a predominance of type 1 (slow-twitch) fibers, again analogous to that seen in experimental hypothyroidism (Figure 22). Muscle hypertrophy with weakness and slowness of movement occurs in the Debre-Semelaigne syndrome seen in severely hypothyroid children, and Hoffman s syndrome is a similar condition seen in adults with hypothyroidism, but is also accompanied by painful spasms. 

Calcineurin Cytosol A calmodulin-regulated protein phosphatase. May play important roles in cardiac hypertrophy and in regulating amounts of slow and fast twitch muscles. 

O The lower urinary tract symptoms and signs of benign prostatic hyperplasia are due to static, dynamic, or detrusor factors. The static factor refers to anatomic obstruction of the bladder neck caused by an enlarged prostate gland. The dynamic factor refers to excessive stimulation of a-adrenergic receptors in the smooth muscle of the prostate, urethra, and bladder neck. The detrusor factor refers to irritability of hypertrophied detrusor muscle as a result of long-standing bladder outlet obstruction. 

Muscle fibers are incapable of mitosis. In fact, the number of muscle fibers per muscle is likely determined by the second trimester of fetal development. Therefore, enlargement of a whole muscle is not due to an increase in the number of fibers in the muscle, but rather to the hypertrophy of existing fibers. Because muscle fibers have no gap junctions between them, electrical activity cannot spread from one cell to the next. Therefore, each muscle fiber is innervated by a branch of an alpha motor neuron. A motor unit is defined as an alpha motor neuron and all of the muscle fibers that it innervates. 

Finally, several experiments indicate that excretory/secretory products (ESP), derived from newborn larvae or pepsin-HCl isolated mature muscle larvae, induce muscle cell basophilia (Blotna-Filipiak et al, 1998 Wranicz et al., 1998) or nuclear hypertrophy (Leung and Ko, 1997), respectively. Effects were observed in vivo and in vitro. Although correspondence of these general changes to biochemical or genomic characteristics of the infected cell and nuclei were not established, these observations may facilitate dissection of the parasite products that are responsible. 

Rat injection intratracheal l44CeFa — 190 veolar septa, hemorrhage, hypertrophy in bL vessel, muscle, emphysema (lung) Yes Yes No 1969b) Cember (1962 ... 

Causes of systolic dysfunction (decreased contractility) are reduction in muscle mass (e.g., myocardial infarction [MI]), dilated cardiomyopathies, and ventricular hypertrophy. Ventricular hypertrophy can be caused by pressure overload (e.g., systemic or pulmonary hypertension, aortic or pulmonic valve stenosis) or volume overload (e.g., valvular regurgitation, shunts, high-output states). 

Hypokalemia and hypomagnesemia may cause muscle fatigue or cramps. Serious cardiac arrhythmias may occur, especially in patients receiving digitalis therapy, patients with LV hypertrophy, and those with ischemic heart disease. Low-dose therapy (e.g., 25 mg hydrochlorothiazide or 12.5 mg chlorthalidone daily) rarely causes significant electrolyte disturbances. 

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