RESUMEN
Animals with high metabolic rates are believed to have high rates of carbon and nitrogen isotopic incorporation. We hypothesized that (1) chronic exposure to cold, and hence an increase in metabolic rate, would increase the rate of isotopic incorporation of both 13C and 15N into red blood cells; and (2) that the rate of isotopic incorporation into red blood cells would be allometrically related to body mass. Two groups of sparrows were chronically exposed to either 5 or 22 degrees C and switched from a 13C-depleted C3-plant diet to a more 13C-enriched C4-plant one. We used respirometry to estimate the resting metabolic rate (VO2) of birds exposed chronically to our two experimental temperatures. The allometric relationship between the rate of 13C incorporation into blood and body mass was determined from published data. The (VO2) of birds at 5 degrees C was 1.9 times higher than that of birds at 22 degrees C. Chronic exposure to a low temperature did not have an effect on the rate of isotopic incorporation of 15N save for a very small effect on the incorporation of 13C. The isotopic incorporation rate of 13C was 1.5 times faster than that of 15N. The fractional rate of 13C incorporation into avian blood was allometrically related to body mass with an exponent similar to -1/4. We conclude that the relationship between metabolic rate and the rate of isotopic incorporation into an animal's tissues is indirect. It is probably mediated by protein turnover and thus more complex than previous studies have assumed.
Asunto(s)
Aclimatación/fisiología , Frío , Metabolismo Energético/fisiología , Gorriones/fisiología , Animales , Peso Corporal , Isótopos de Carbono/metabolismo , Eritrocitos/metabolismo , Isótopos de Nitrógeno/metabolismo , Consumo de Oxígeno , Análisis de Regresión , Gorriones/sangre , WyomingRESUMEN
In motor neurone disease changes in the functional properties of motor units, including the surface voltage, latency, conduction velocity, and response to repetitive stimulation, were investigated. Progression was marked by motor unit loss, increase in the proportion of larger motor unit potentials, and inclusion of motor unit potentials larger than normal in the remaining motor unit population. Even late in the disease, motor unit potentials with a low surface voltage persisted. The relationship between motor unit potentials, surface voltage, and latency, present in control subjects, broke down in motor neurone disease, large motor unit potentials having abnormally long latencies and small motor unit potentials unexpectedly short latencies. Amplitude decrements were more frequent and severe in motor unit potentials at later stages in the disease, particularly in those units with lower surface voltages. In one surviving motor unit potential there was evidence suggestive of functional recovery. The observations point to complex changes in the functional properties of motor units in motor neurone disease.