Increase In Fiber Cross-sectional Area Research Articles

Volume density and distribution of mitochondria in myocardial growth and hypertrophy

The volume density and distribution of mitochondria relative to capillaries have been measured using the technique of point counting in concentric rings, on normal and hypertrophied guinea pig myocardium. Right ventricular hypertrophy was produced by hypobaric hypoxia. In control guinea pigs right ventricular weight increased linearly with body weight. In control and hypoxic guinea pigs fiber cross sectional area (FCSA) and ventricular weight were related by a single straight line. Capillary density decreased hyperbolically with FCSA in both control and hypoxic animals. Capillary density was significantly higher ( P < 0.001) in the right ventricles of the hypoxic animals than in controls when the fibers were small but this difference disappeared as the fibers hypertrophied beyond FCSA values of 260 μm 2. Volume density of mitochondria reached a peak (29–35%) close to the capillary but then decreased significantly in the spaces farthest from the capillary (mean 25.2%). There was no significant difference in peak mitochondrial volume density in controls versus hypoxic animals. There was thus an increase in the total volume of mitochondria in these myofibers that was in direct proportion to the increases in FCSA and heart volume. The highest volume density of mitochondria was found at a distance that is approximately 15% of the total distance over which O 2 must diffuse in myocardial tissue and the peak volume density of mitochondria was thus a function of capillary density. The speculation is presented that the distribution of mitochondria may be related both to oxygen supply to the mitochondria and to the movement of high energy phosphate compounds out of mitochondria for use by myofibrils.

Volume density and distribution of mitochondria in myocardial growth and hypertrophy

The volume density and distribution of mitochondria relative to capillaries have been measured using the technique of point counting in concentric rings, on normal and hypertrophied guinea pig myocardium. Right ventricular hypertrophy was produced by hypobaric hypoxia. In control guinea pigs right ventricular weight increased linearly with body weight. In control and hypoxic guinea pigs fiber cross sectional area (FCSA) and ventricular weight were related by a single straight line. Capillary density decreased hyperbolically with FCSA in both control and hypoxic animals. Capillary density was significantly higher ( P < 0.001) in the right ventricles of the hypoxic animals than in controls when the fibers were small but this difference disappeared as the fibers hypertrophied beyond FCSA values of 260 μm 2. Volume density of mitochondria reached a peak (29–35%) close to the capillary but then decreased significantly in the spaces farthest from the capillary (mean 25.2%). There was no significant difference in peak mitochondrial volume density in controls versus hypoxic animals. There was thus an increase in the total volume of mitochondria in these myofibers that was in direct proportion to the increases in FCSA and heart volume. The highest volume density of mitochondria was found at a distance that is approximately 15% of the total distance over which O 2 must diffuse in myocardial tissue and the peak volume density of mitochondria was thus a function of capillary density. The speculation is presented that the distribution of mitochondria may be related both to oxygen supply to the mitochondria and to the movement of high energy phosphate compounds out of mitochondria for use by myofibrils.

Effect of compensatory hypertrophy studied in individual motor units in medial gastrocnemius muscle of the cat.

1. Compensatory hypertrophy of the medial gastrocnemius (MG) muscle was produced by denervating or removing its synergists (i.e., the lateral gastrocnemius, soleus, and plantaris muscles) in adult cats. Following survival times of 14-32 wk, intracellular recording and stimulation techniques were used to study the motor-unit population in MG. The data obtained were compared with results from MG motor units in normal unoperated cats of the same body size and weight. 2. Using criteria employed for normal motor units, the units in hypertrophic MG muscles were readily classified into the same groups (types FF, F(int), FR, and S) as in normal MG. There was no detectable difference in the distribution of motor-unit types after hypertrophy. 3. When compared with a normal motor-unit sample, there was a large increase in mean tetanic tension, but no significant change in twitch tension, for each motor-unit type in the hypertrophied muscles. The most marked increase was found among the fatigue-resistant type S and type FR motor units. There was no alteration of twitch contraction times or fatigue resistance in any unit type after hypertrophy. 4. For each motor-unit type, the mean homonymous (MG) group Ia EPSP amplitude was the same in normal and hypertrophic MG populations. There was, however, a significant increase in the average conduction velocity of MG motor axons in the animals with uncomplicated MG synergist removal and maximal MG hypertrophy. 5. On the basis of histochemical staining, muscle fibers from comparable sections of hypertrophic and contralateral (unoperated) MG muscles were presumptively identified as belonging to FF, FR, or S units. There was no significant difference between hypertrophic and contralateral MG muscles in the percentage of each fiber type, although there was some variability in muscle composition from one cat to another. One muscle pair was studied in detail for fiber cross-sectional area. In this cat, with marked hypertrophy by muscle weight, there was a modest increase in the mean fiber areas of histochemical S and FR muscle fibers, but no evident change in FF fibers, on the hypertrophic side. 6. MG motor units were examined in several cats in which synergist removal resulted in scarring and marked limitation of passive ankle mobility, and no evident weight gain in MG. Motor units of all types in these animals showed a decrease in twitch tension and in mean twitch/tetanus ratios, with little alteration in mean tetanic tensions. 7. The main effect of compensatory hypertrophy under the present conditions was a large increase in tetanic tension output from individual motor units due, at least in part, to an increase in fiber cross-sectional area. There was no evidence indicating any "conversion" of motor units or of their muscle fibers from one type to another.