Compensatory adaptations of skeletal muscle fiber types to a long-term functional overload.
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Biomedical subjects
Publications and source records attributed to R B Armstrong.
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The ultrastructure of fast-twitch-oxidative-glycolytic (FOG), fast-twitch-glycolytic (FG) and slow-twitch-oxidative (SO) fibers in plantaris and soleus muscles of normal and streptozotocin-diabetic rats was studied. In the diabetic animals, the mitochondria of FOG and SO fibers showed a loss of cristae and an increase in electron-dense granules. There was also an increased number of lipid droplets in close proximity to the mitochondria and the nuclei, and a separation of individual muscle nuclei to form satellite cells. Higher incidences of surface projections and sarcoplasmic splittings at the nuclear region were noticed in SO fibers. The FG fibers showed some disorientation of the T-tubular system. It is concluded that streptozotocin-diabetes has differential effects on the fine structure of the three fiber types of rat skeletal muscle.
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Succinate dehydrogenase activities of 4 skeletal muscles with widely divergent fiber compositions were determined in rats that recieved either 70 or 80 mg streptozotocin per kg body wt at various time intervals following injection. Enzyme activities in all muscles declined to a lower final level and exhibited a more rapid decay in animals receiving the larger dosage. White gastrocnemius muscle, which contains no slow-twitch fibers, experienced the greatest relative loss of activity, and soleus muscle, possessing the highest proportion of slow-twitch fibers, the smallest loss. The findings indicate that extrapancreatic effects of the drug may have been partially responsible for the differential effects of the 2 dosages on the muscles.
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The response of rat gastrocnemius muscle fibers to chronic streptozotocindiabetes was studied. Transverse sections of this muscle from normal and diabetic rats were histochemically assayed for reduced diphosphopyridine nucleotide-diaphorase, myofibrillar adenosine triphosphatase, mitochondrial alpha-glycerophosphate dehydrogenase, beta-hydroxybutyrate dehydrogenase, and alkaline phosphatase activities. Cross-sectional areas of the fiber types were measured, and fiber capillarization and populations estimated. Chemically-induced diabetes appeared to have little effect on the metabolic or morphological properties of slow-twitch fibers. However, a general dedifferentiation occurred in the 2 fast-twitch fiber populations. There was a loss of oxidative potential in the fast-twitch-oxidative-glycolytic fibers, and a significant decrease in size in the fast-twitch-glycolytic fibers. No change in the proportions of slow- and fast-twitch fibers in the muscles of diabetic rats occurred. It is concluded that hypoinsulinism has differential effects on the 3 fiber types in heterogeneous rat skeletal muscle, and that slow-twitch fibers are least affected by the diabetic condition.
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Experiences with tympanostomy tubes extending over a period of 29 years are compared with the computer-assisted analysis of a questionnaire that was submitted to 500 otolaryngologists. Ventilating tubes are being used by 99.4% of the respondents in the group and are estimated to achieve good to excellent results in 90% of patients treated. Appropriate use of tympanostomy tubes has significantly reduced the incidence of chronic ear disease. A comparison of prophylactic antibiotics and prophylactic ventilating tubes for the prevention of acute otitis media showed that 91% of the participants in the survey found ventilating tubes to be more effective than antibiotics. Benefits from ventilating tubes far outweigh the small number of tube-induced complications.
Intensive training for and competition in endurance events like the marathon are accompanied by injury to fibres in the active skeletal muscles. Evidence for the injury comes from the increases in intramuscular enzymes and myoglobin found in the blood following the exercise, from the subjective sensation of soreness in the muscles in the post-exercise period, and from direct histological examination of samples of the damaged muscles. Histological studies demonstrate that some muscle fibres undergo degenerative changes following the exercise; the necrosis is accomplished by macrophages and other phagocytic cells that invade the injured cells and the adjacent interstitium. Following the degeneration the fibers appear to be regenerated so that there is not a net loss of fibres. Precisely what initiates the cellular damage is not known, but hypotheses suggested include, 'metabolic overload' and 'mechanical strain'. Eccentric contractions are known to cause the greater amount of damage in muscles, which suggests that high local tensions in fibres may be more important than metabolic considerations in the aetiology of the injury. Training reduces the magnitude of the damage that occurs in response to a given exercise task, although competitors in endurance events may demonstrate chronic muscle injury because of increasing training intensities. Other than training, there is no compelling evidence that any drug treatment or preventative measures will lessen this form of injury.