The dynamics of contraction and walls motion of the calf heart left ventricle

The echocardiographic research of the left ventricular has revealed heterogeneity of thickness of the posterior wall and interventricular septum in three parallel planes in the transverse direction of the left ventricle in calves. The amplitude of systolic motion of the left ventricle posterior wall is larger than that of the interventricular septum at the level of the mitral valve, at the level of the papillary muscles, and at the apical level. The excursion of left ventricular walls in the basal level is twice as large as the mobility of ventricular walls in the apical level. During the contraction of the myocardium, the shortness of the left ventricular transversal diameter is to great extent determined by the degree of contraction of the left ventricular wall rather than of the interventricular septum. The high contractility is revealed in calves.     

Exuberant accessory mitral valve tissue with possible true parachute mitral valve: a case report

ABSTRACT: INTRODUCTION: A parachute mitral valve is defined as a unifocal attachment of mitral valve chordae tendineae independent of the number of papillary muscles. Data from the literature suggests that the valve can be distinguished on the basis of morphological features as either a parachute-like asymmetrical mitral valve or a true parachute mitral valve. A parachute-like asymmetrical mitral valve has two papillary muscles; one is elongated and located higher in the left ventricle. A true parachute mitral valve has a single papillary muscle that receives all chordae, as was present in our patient. Patients with parachute mitral valves during childhood have multilevel left-side heart obstructions, with poor outcomes without operative treatment. The finding of a parachute mitral valve in an adult patient is extremely rare, especially as an isolated lesion. In adults, the unifocal attachment of the chordae results in a slightly restricted valve opening and, more frequently, valvular regurgitation. CASE PRESENTATION: A 40-year-old Caucasian female patient was admitted to a primary care physician due to her recent symptoms of heart palpitation and chest discomfort on effort. Transthoracic echocardiography showed chordae tendineae which were elongated and formed an unusual net shape penetrating into left ventricle cavity. The parasternal short axis view of her left ventricle showed a single papillary muscle positioned on one side in the posteromedial commissure receiving all chordae. Her mitral valve orifice was slightly eccentric and the chordae were converting into a single papillary muscle. Mitral regurgitation was present and it was graded as moderate to severe. Her left atrium was enlarged. There were no signs of mitral stenosis or a subvalvular ring. She did not have a bicuspid aortic valve or coarctation of the ascending aorta. The dimensions and systolic function of her left ventricle were normal. Our patient had a normal body habitus, without signs of heart failure. Her functional status was graded as class I according to the New York Heart Association grading. CONCLUSIONS: A recently published review found that, in the last several decades, there have been only nine adult patients with parachute mitral valve disease reported, of which five had the same morphological characteristics as our patient. This case presentation should encourage doctors, especially those involved in echocardiography, to contribute their own experience, knowledge and research in parachute mitral valve disease to enrich statistical and epidemiologic databases and aid clinicians in getting acquainted with this rare disease.     

The echocardiographic study of the rabbit heart left ventricle morpho-functional parameters

Morphometric and functional parameters of the heart left ventricle in rabbits during systole and diastole were investigated by the method of echocardiography. Morphometric parameters were studied on three levels: the mitral valve, the papillary muscles and the apical level. The internal dimension of the left ventricle uniformly decreases in three parallel planes during systole, its maximal reduction being observed on the apical level. During the contraction phase, the posterior wall thickness of the left ventricular and the interventricular septum thickness increases on the basal level to a greater extent than on the apical one. During systole, the interventricular septum movement is greater than the left ventricular posterior wall motion. During the heart cycle, the form of the left ventricular cavity changes from an ellipsoid in diastole to elliptic paraboloid in systole.     

Insights from in-vitro flow visualization into the mechanism of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy under steady flow conditions.

Hypertrophic obstructive cardiomyopathy is a heart disease characterized by a thickened interventricular septum which narrows the left ventricular outflow tract, and by systolic anterior motion (SAM) of the mitral valve which can contact the septum and create dynamic subaortic obstruction. The most common explanation for SAM has been the Venturi mechanism which postulates that septal hypertrophy, by narrowing the outflow tract, produces high velocities and thus low pressure between the mitral valve and the septum, causing the valve leaflets to move anteriorly. This hypothesis, however, fails to explain why SAM often begins early in systole, when outflow tract velocities are low or negligible or why it may occur in the absence of septal hypertrophy. The goal of this study was therefore to investigate an alternative hypothesis in which structural abnormalities of the papillary muscles act as a primary cause of SAM by altering valve restraint and thereby changing the geometry of the closed mitral apparatus and its relationship to the surrounding flow field. In order to test this hypothesis, an in vitro model of the left ventricle which included an explanted human mitral valve with intact chords and papillary muscle apparatus was constructed. Flow visualization was used to observe the ventricular flow field and the mitral valve geometry. Displacing the papillary muscles anteriorly and closer to each other, as observed clinically in patients with cardiomyopathy and obstruction produced SAM in the absence of septal hypertrophy. Flow could be seen impacting on the upstream (posterior) surface of the leaflets; such flow is capable of producing form drag forces which can initiate and maintain SAM.(ABSTRACT TRUNCATED AT 250 WORDS)     

Adaptation of cardiac structure by mechanical feedback in the environment of the cell: a model study.

In the cardiac left ventricle during systole mechanical load of the myocardial fibers is distributed uniformly. A mechanism is proposed by which control of mechanical load is distributed over many individual control units acting in the environment of the cell. The mechanics of the equatorial region of the left ventricle was modeled by a thick-walled cylinder composed of 6-1500 shells of myocardial fiber material. In each shell a separate control unit was simulated. The direction of the cells was varied so that systolic fiber shortening approached a given optimum of 15%. End-diastolic sarcomere length was maintained at 2.1 microns. Regional early-systolic stretch and global contractility stimulated growth of cellular mass. If systolic shortening was more than normal the passive extracellular matrix stretched. The design of the load-controlling mechanism was derived from biological experiments showing that cellular processes are sensitive to mechanical deformation. After simulating a few hundred adaptation cycles, the macroscopic anatomical arrangement of helical pathways of the myocardial fibers formed automatically. If pump load of the ventricle was changed, wall thickness and cavity volume adapted physiologically. We propose that the cardiac anatomy may be defined and maintained by a multitude of control units for mechanical load, each acting in the cellular environment. Interestingly, feedback through fiber stress is not a compelling condition for such control.     

Defect in oxidative phosphorylation in LV papillary muscle mitochondria of patients undergoing mitral valve replacement

Mitochondria play a pivotal role in cellular metabolism, especially in energy production. Myocardial function depends on adenosine triphosphate (ATP) supplied by oxidation of several substrates. In the adult heart, this energy is obtained primarily from fatty acid oxidation through oxidative phosphorylation (OXPHOS). With this in view, we studied OXPHOS, Total-ATPase and cytochrome content in the mitochondria of the left ventricular (LV) papillary muscles in excised mitral valves of patients who underwent mitral valve replacement (MVR). The mitochondrial OXPHOS, cytochrome content and ATPase activity were studied in 70 patients (ranging from 22 to 40 years) operated on for mitral valve disease. Control study includes 25 normal mitral valves removed at necropsy from patients who died of extracardiac causes. In the presence of glutamate and succinate as substrates, the rate of mitochondrial oxygen consumption was significantly lower in LV papillary muscles of pathological mitral valves (P<0.001) by using with and without addition of ADP. The ADP/O ratio indices for glutamate and succinate were not significantly affected. Using glutamate as substrate, respiratory control index was significantly raised (P<0.05) as compared with control. A significant reduction of total cytochrome content and ATPase activity (P<0.001) was noted in LV papillary muscles of patients operated for mitral valve disease. Our results showed that OXPHOS, cytochromes 'a', 'b', 'c+c(1)' and ATP activity are significantly impaired in LV papillary muscles in patients with pathological mitral valve. Cardiac mitochondrial oxygen consumption is a very valuable tool to investigate the regulation of cardiac mitochondrial energy metabolism. There is increasing evidence that mitochondrial diseases, such as mitochondrial cardiomyopathy, valvular disease and some myopathies, can be responsive to treatment with metabolic intermediates such as coenzyme Q(10), thiamine, prednisone, and vitamin therapy.     

兔心脏左室乳头肌的形态和动脉分布

乳头肌可因缺血、纤维化或梗塞而影响其收缩功能,并产生二尖瓣关闭不全(朱清于等,1980)。致成乳头肌功能不全最常见的原因是心肌供血不足,因此研究乳头肌的动脉,具有实用意义。一些作者(Estes,1966;Farrer-Brown,1968;Ranganathan,1969等)对人心脏乳头肌动脉来源、分支分布作过研究,但关于实验动物家兔乳头肌的动脉的研究文献尚少报道。本文为了开展实验性乳头肌梗塞的研究,对兔心脏左室乳头肌的形态、动脉来源、分布类型以及口径、血管密度等进行了研究。     

Mechanical Complications of Myocardial Infarction—Radiologic Aspects

Left ventricular aneurysm, interventricular septal defect and acute mitral valve incompetence due to papillary muscle damage are three mechanical complications which cause intractable heart failure following myocardial infarction. In each case surgical intervention can result in dramatic improvement of congestive heart failure.A hemodynamically significant left ventricular aneurysm enlarges the cardiac silhouette and frequently causes a localized protrusion as seen radiographically. Cardiac fluoroscopy will disclose an abnormal pulsation of the left ventricular border. The left ventricular angiogram establishes the diagnosis, reveals the extent of the aneurysm and may disclose a filling defect in the aneurysmal sac due to the presence of mural thrombus. Coronary arteriography shows occlusion of a major vessel, most commonly the anterior descending branch of the left coronary artery.Ischemic perforation of the interventricular septum and acute mitral incompetence due to severe papillary muscle damage both cause severe heart failure shortly after myocardial infarction. A similar pansystolic murmur accompanies both conditions, and differentiation between the two is rarely possible on the basis of the electrocardiogram or x-ray film of the chest. Ventricular cardiac catheterization and left ventricular angiocardiography are required for a correct diagnosis.     

Anatomic features of postmortem experimental ruptures of the human heart

Comparison of postmortem performed experimental cardiac ruptures with post-infarction lesions reveals uniformity of their localization. The ruptures are found to occur at places of a sharp change in the relief of the cardiac internal surface. These areas should be considered as concentrators of strain, promoting cardiac ruptures. In the left ventricle six concentrators of strain are revealed. They are: the place where the anterior part of the interventricular septum passes into the anterior wall of the left ventricle, the right edge of the papillary muscle, the left edge of the anterior papillary muscle, the left edge of the posterior papillary muscle, the right edge of the posterior papillary muscle, the place where the posterior part of the interventricular septum passes into the posterior wall of the left ventricle. Frequency of the experimental ruptures of the interventricular septum, under loading of the left ventricle, is demonstrated to depend on pressure in the right cardiac part.     

Tomographic PIV in a model of the left ventricle: 3D flow past biological and mechanical heart valves

Left ventricular flow is intrinsically complex, three-dimensional and unsteady. Its features are susceptible to cardiovascular pathology and treatment, in particular to surgical interventions involving the valves (mitral valve replacement). To improve our understanding of intraventricular fluid mechanics and the impact of various types of prosthetic valves thereon, we have developed a custom-designed versatile left ventricular phantom with anatomically realistic moving left ventricular membrane. A biological, a tilting disc and a bileaflet valve (in two different orientations) were mounted in the mitral position and tested under the same settings. To investigate 3D flow within the phantom, a four-view tomographic particle image velocimetry setup has been implemented. The results compare side-by-side the evolution of the 3D flow topology, vortical structures and kinetic energy in the left ventricle domain during the cardiac cycle. Except for the tilting disc valve, all tested prosthetic valves induced a crossed flow path, where the outflow crosses the inflow path, passing under the mitral valve. The biological valve shows a strong jet with a peak velocity about twice as high compared to all mechanical heart valves, which makes it easier to penetrate deeply into the cavity. Accordingly, the peak kinetic energy in the left ventricle in case of the biological valve is about four times higher than the mechanical heart valves. We conclude that the tomographic particle imaging velocimetry setup provides a useful ground truth measurement of flow features and allows a comparison of the effects of different valve types on left ventricular flow patterns.     

External approach to in vivo force measurement on mitral valve traction suture

BackgroundForce measurements on the mitral valve apparatus have been reported from in vivo and in vitro studies. Recent reparative techniques for ischemic mitral valve insufficiency call for papillary muscle relocation. This study describes a device to measure forces generated on traction sutures utilized for this purpose.MethodsThe transducer design was based on a modified caliper with strain gauges attached. Finite element computer simulation was employed to optimize the signal output. The system was designed to facilitate investigation of the effects of shortening GoreTex traction suture that was extended from near the fibrous trigones of the mitral valve through the papillary muscles. The suture was exteriorized out through the left ventricle in a porcine setup (n=11) and attached to the dedicated device for simultaneous papillary muscle relocation and traction suture force measurement.ResultsThe transducer demonstrated excellent signal strength, linearity, and durability. Peak force was seen at the onset of the systolic isovolumic contraction (p<0.001). Initial results indicated that this external approach can document force magnitudes comparable to previous internally measured forces in the mitral valve apparatus.ConclusionsIt has been proven feasible to measure forces in the mitral valve papillary muscle relocation sutures with an external device. The results from using this equipment will provide insight into the biomechanical requirements of relocation traction sutures and other devices utilized for papillary muscle relocation.     

Muscular Subaortic Stenosis: The Initial Left Ventricular Inflow Tract Pressure as Evidence of Outflow Tract Obstruction

Two types of intraventricular pressure differences within the left ventricle of man are described. The first is encountered in cases of muscular (or fibrous) subaortic stenosis, in which the outflow tract pressure distal to the stenosis (and proximal to the aortic valve) is low, whereas all pressures recorded in the left ventricle proximal to the stenosis, including that just inside the mitral valve (the initial inflow tract pressure) are high.The second type of intraventricular pressure difference may be recorded in patients without muscular subaortic stenosis when a heart catheter is advanced to the left ventricular wall in such a manner that it becomes imbedded or entrapped by cardiac muscle in systole. Such an entrapped catheter records a high intraventricular pressure that is believed to reflect intramyocardial tissue pressure, which normally exceeds intracavitary pressure. In such cases the initial inflow tract pressure is not high and is precisely equal to the outflow tract systolic pressure, i.e. both are recording intracavity pressure. This type of intramyocardial to intracavitary pressure difference may also be encountered in the left ventricle of dogs.The recent suggestion that intraventricular pressure differences in the left ventricle of cases of muscular subaortic stenosis are due to catheter entrapment by cardiac muscle is refuted by using the initial inflow tract pressure as the means of differentiation between the two types of intraventricular pressure differences outlined.     

Mechanical efficiency of the trout heart during volume and pressure-loading: metabolic implications of the stiffness of the ventricular tissue

In the mammalian heart the metabolic costs of pressure loading exceed those of volume loading. As evidence suggests that the opposite may be true in fish, we evaluated the metabolic costs of volume and pressure loading in the isolated trout heart and compared the results with the mammalian heart based on the biomechanical properties of cardiac muscle. The highest power output (2.33+/-0.32 mW g(-1), n=5) appeared at the highest preload pressure tested (0.3 kPa) and at an afterload of 5 kPa. At a higher afterload, power did not increase because stroke volume fell. The highest mechanical efficiency (20.7+/-2.0%, n=5) was obtained at a preload of 0.15 kPa and an afterload of 5 kPa. Further increases in preload or afterload did not increase mechanical efficiency, probably because of increases in ventricular wall stress which increased the oxygen consumed disproportionately more than the stroke work. Under pressure unloading (25% decrease in power output), mechanical efficiency was significantly higher in comparison with volume unloading. Given that stiffness of the ventricular tissue is larger in trout than in rat papillary muscles, it is suggested that the increased strain during volume loading is energetically disadvantageous for stiff muscles like those of trout, but it is advantageous when muscle stiffness is lower as it occurs in the rat papillary muscle.     

Structural finite deformation model of the left ventricle during diastole and systole

A model of left ventricular function is developed based on morphological characteristics of the myocardial tissue. The passive response of the three-dimensional collagen network and the active contribution of the muscle fibers are integrated to yield the overall response of the left ventricle which is considered to be a thick wall cylinder. The deformation field and the distributions of stress and pressure are determined at each point in the cardiac cycle by numerically solving three equations of equilibrium. Simulated results in terms of the ventricular deformation during ejection and isovolumic cycles are shown to be in good qualitative agreement with experimental data. It is shown that the collagen network in the heart has considerable effect on the pressure-volume loops. The particular pattern of spatial orientation of the collagen determines the ventricular recoil properties in early diastole. The material properties (myocardial stiffness and contractility) are shown to affect both the pressure-volume loop and the deformation pattern of the ventricle. The results indicate that microstructural consideration offer a realistic representation of the left ventricle mechanics.     

Transplantation of elastin-secreting myoblast sheets improves cardiac function in infarcted rat heart

Myoblast sheet transplantation for cardiac failure is a promising therapy to enhance cardiac function via paracrine mechanism. However, their efficacies of treatment showed a gradual decline. The gene modification of the implanted myoblast is important in improving the long-term results of the treatment. Elastin fiber enhances the extensibility of the infarcted wall and can prevent left ventricular dilation. We therefore hypothesized that the elastin gene modification of the implanted myoblast could strengthen and maintain the long-term improvement effects of cardiac function. In this study, we evaluated long-term follow-up benefits of functional myoblast sheets that secrete elastin in an infarcted model. The animal models were divided into three groups: a group transplanted with nontransfected, wild-type, skeletal myoblast-type sheets (WT-rSkM); group transplanted with myoblast sheets that secreted elastin fragments (ELN-rSkM); and a control group (ligation only). Cardiac function was examined by echocardiography, and cardiac remodeling after infarction was evaluated by histological examination. The cardiac function was significantly improved and the left ventricle end-diastolic dimensions were significantly reduced in the ELN-rSkM group. Histological analysis showed that left ventricular remodeling was attenuated in the ELN-rSkM group and that elastic fiber was formed in the epicardial area of ELN-rSkM group. The functionalization of myoblast sheet by elastin gene transfer showed the long-term improvement of cardiac function. Expressed recombinant elastin fiber prevented the dilation of the left ventricular chamber after myocardial infarction. The functional myoblast sheet transplantation maintained the treatment effect by the paracrine effect of myoblast and the formed recombinant elastin.     

Electromechanical coupling between the atria and mitral valve

Anterior leaflet (AL) stiffening during isovolumic contraction (IVC) may aid mitral valve closure. We tested the hypothesis that AL stiffening requires atrial depolarization. Ten sheep had radioopaque-marker arrays implanted in the left ventricle, mitral annulus, AL, and papillary muscle tips. Four-dimensional marker coordinates (x, y, z, and t) were obtained from biplane videofluoroscopy at baseline (control, CTRL) and during basal interventricular-septal pacing (no atrial contraction, NAC; 110-117 beats/min) to generate ventricular depolarization not preceded by atrial depolarization. Circumferential and radial stiffness values, reflecting force generation in three leaflet regions (annular, belly, and free-edge), were obtained from finite-element analysis of AL displacements in response to transleaflet pressure changes during both IVC and isovolumic relaxation (IVR). In CTRL, IVC circumferential and radial stiffness was 46 ± 6% greater than IVR stiffness in all regions (P < 0.001). In NAC, AL annular IVC stiffness decreased by 25% (P = 0.004) in the circumferential and 31% (P = 0.005) in the radial directions relative to CTRL, without affecting edge stiffness. Thus AL annular stiffening during IVC was abolished when atrial depolarization did not precede ventricular systole, in support of the hypothesis. The likely mechanism underlying AL annular stiffening during IVC is contraction of cardiac muscle that extends into the leaflet and requires atrial excitation. The AL edge has no cardiac muscle, and thus IVC AL edge stiffness was not affected by loss of atrial depolarization. These findings suggest one reason why heart block, atrial dysrhythmias, or ventricular pacing may be accompanied by mitral regurgitation or may worsen regurgitation when already present.     

Dependence of local left ventricular wall mechanics on myocardial fiber orientation: a model study.

The dependence of local left ventricular (LV) mechanics on myocardial muscle fiber orientation was investigated using a finite element model. In the model we have considered anisotropy of the active and passive components of myocardial tissue, dependence of active stress on time, strain and strain rate, activation sequence of the LV wall and aortic afterload. Muscle fiber orientation in the LV wall is quantified by the helix fiber angle, defined as the angle between the muscle fiber direction and the local circumferential direction. In a first simulation, a transmural variation of the helix fiber angle from +60 degrees at the endocardium through 0 degrees in the midwall layers to -60 degrees at the epicardium was assumed. In this simulation, at the equatorial level maximum active muscle fiber stress was found to vary from about 110 kPa in the subendocardial layers through about 30 kPa in the midwall layers to about 40 kPa in the subepicardial layers. Next, in a series of simulations, muscle fiber orientation was iteratively adapted until the spatial distribution of active muscle fiber stress was fairly homogeneous. Using a transmural course of the helix fiber angle of +60 degrees at the endocardium, +15 degrees in the midwall layers and -60 degrees at the epicardium, at the equatorial level maximum active muscle fiber stress varied from 52 kPa to 55 kPa, indicating a remarkable reduction of the stress range. Moreover, the change of muscle fiber strain with time was more similar in different parts of the LV wall than in the first simulation. It is concluded that (1) the distribution of active muscle fiber stress and muscle fiber strain across the LV wall is very sensitive to the transmural distribution of the helix fiber angle and (2) a physiological transmural distribution of the helix fiber angle can be found, at which active muscle fiber stress and muscle fiber strain are distributed approximately homogeneously across the LV wall.     

Left ventricular endocardial longitudinal and transverse changes during isovolumic contraction and relaxation: a challenge

Left ventricular (LV) longitudinal and transverse geometric changes during isovolumic contraction and relaxation are still controversial. This confusion is compounded by traditional definitions of these phases of the cardiac cycle. High-resolution sonomicrometry studies might clarify these issues. Crystals were implanted in six sheep at the LV apex, fibrous trigones, lateral and posterior mitral annulus, base of the aortic right coronary sinus, anterior and septal endocardial wall, papillary muscle tips, and edge of the anterior and posterior mitral leaflets. Changes in distances were time related to LV and aortic pressures and to mitral valve opening. At the beginning of isovolumic contraction, while the mitral valve was still open, the LV endocardial transverse diameter started to shorten while the endocardial longitudinal diameter increased. During isovolumic relaxation, while the mitral valve was closed, LV transverse diameter started to increase while the longitudinal diameter continued to decrease. These findings are inconsistent with the classic definitions of the phases of the cardiac cycle.     

An Approach to the Stepwise Management of Severe Mitral Regurgitation with Optimal Cardiac Pacemaker Function

Right ventricular apical pacing may cause or worsen mitral regurgitation (MR). Potential mechanisms for this adverse sequelae include intraventricular dyssynchrony, altered papillary muscle function, pacing-induced cardiomyopathy with left ventricular dilation, and annular dilation. In contrast, biventricular (BiV) pacing may improve MR presumably by opposing the negative effects. Whether or not left ventricular lead location is important in treating mitral regurgitation in patients with pacemakers is unknown.We report a case of severe MR and left ventricular (LV) systolic failure in a patient with right ventricular pacing. Multiple potential etiologies for the worsening valve function were noted, and a stepwise iterative optimizing scheme that included basal lateral LV pacing improved mitral valve function and ameliorated heart failure symptoms.     

Effect of endurance running on cardiac and skeletal muscle in rats

We studied the effect of resistance running on left cardiac ventricle size and rectus femoris muscle fiber composition. Ten male Wistar rats were trained on a treadmill 6 days per week for 12 weeks. Ten rats remained sedentary and served as controls. A higher endurance time (40%) and cardiac hypertrophy in the trained animals were indicators of training efficiency. Morphometric analysis of the left ventricle cross-sectional area, left ventricular wall, and left ventricular cavity were evaluated. The endurance-running group demonstrated a hypertrophy of the ventricular wall (22%) and an increase in the ventricular cavity (25%); (p<0.0001). Semi-quantitative analysis of rectus femoris fiber-type composition and of the oxidative and glycolytic capacity was histochemically performed. Endurance running demonstrated a significant (p<0.01) increase in the relative frequency of Type I (24%), Type IIA (8%) and Type IIX (16%) oxidative fibers, and a decrease in Type IIB (20%) glycolytic fibers. There was a hypertrophy of both oxidative and glycolytic fiber types. The relative cross-sectional area analysis demonstrated an increase in oxidative fibers and a decrease in glycolytic fibers (p<0.0001). Changes were especially evident for Type IIX oxidative-glycolytic fibers. The results of this study indicate that the left ventricle adapts to endurance running by increasing wall thickness and enlargement of the ventricular cavity. Skeletal muscle adapts to training by increasing oxidative fiber Type. This increase may be related to fiber transformation from Type IIB glycolytic to Type IIX oxidative fibers. These results open the possibility for the use of this type of exercise to prevent muscular atrophy associated with age or post-immobilization.