The insect respiratory system is composed of a network of air-filled tracheal tubes that open to the atmosphere via spiracles along the lateral sides of the body. Trachea branch throughout the body and deliver oxygen directly to tissues. Insects control respiratory gas exchange patterns by modulating the opening and closing of the spiracle valves. The function of these respiratory patterns and the complete mechanism by which the spiracle valves are controlled is unknown. The work presented here investigates (1) the airflow patterns through the tracheal system, (2) the physiological contributors to respiratory pattern and possible spiracle control mechanisms, and (3) the adaptive significance of discontinuous gas exchange in insects.
I used flow-through respirometry, video analyses of spiracle and abdominal movements, and hyperoxic tracer gases to determine if ventilating insects utilize tidal or unidirectional airflow in their respiratory system. I found that Gromphadorhina portentosa coordinates spiracular valve movements and abdominal contractions to produce unidirectional airflow through the tracheal system, with air entering through the thoracic spiracles and exiting through the posterior abdominal spiracles.
Previous studies have determined that the respiratory pattern of insects is a function of metabolic rate. However, most studies of ectotherms utilize changes in ambient temperature to manipulate metabolic rate. I exposed Rhodnius prolixus to two metabolic stimuli, changes in ambient temperature or digestion of a blood meal, and measured components of their gas exchange pattern. I found that the volume of carbon dioxide released during a spiracle opening decreased with temperature, and that R. prolixus abandoned discontinuous gas exchange at a lower metabolic rate when metabolism was increased via increased ambient temperature compared to digestion.
Lastly, I tested the longstanding “oxidative damage hypothesis” regarding the adaptive function of discontinuous gas exchange. I exposed Drosophila melanogaster to hypercapnic (6% CO2) gas treatments to prevent spiracular closure, and then measured the amount of oxidative damage (lipid peroxidation, protein carbonyl content, and superoxide dismutase activity) that accumulated in these populations versus a control group. I found that acute exposures (3 hours) of hypercapnia increased lipid peroxidation but had no effect on protein carbonyl formation or antioxidant enzyme activity. While results suggest that the discontinuous gas exchange pattern may not function to prevent excess oxidative damage, additional studies are required to investigate the chronic effects of disrupting this respiratory pattern.