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A series of five studies were conducted to examine the effect of exercise on selected pulmonary function measurements. Studies I and II determined the effect of an acute bout of exercise on various lung volumes immediately post-exercise and over a 24-hour post-exercise period. There were significant mean increases of 210 ml (20.6%) and 260 ml (20.8%) in the 5-minute post-exercise residual volume (RV) measurement for studies I and II, respectively. There also were significant mean increases of 170 ml (3.4%) and 190 ml (2.7%) in the 5-minute post-exercise total lung capacity (TLC) for studies I and II, respectively, while vital capacity (VC) remained unchanged. RV and TLC remained significantly increased over the pre-exercise values through 30 and 15 minutes of recovery, respectively. Studies III through V were undertaken to determine the physiological mechanism underlying the responses reported in studies I and II. In study III, transthoracic electrical impedance (TEI) was significantly decreased below the pre-exercise value through 30-minutes of recovery, indicating that there was an increase in thoracic fluid volume following exercise. However, TEI measurements alone cannot separate between intra- and extravascular fluid shifts. Therefore, studies IV and V attempted to identify whether the decrease in TEI and increase in RV reported in study III were due to intra- or extravascular fluid shifts. Study IV examined the TEI, RV, and TLC responses before and following exercise, as central blood volume (CBV) was experimentally increased via G-suit inflation, and decreased via venous occlusion tourniquets. The results suggest that RV is relatively insensitive to intravascular volume shifts within the thorax. Study V determined and followed the effect of an acute bout of exercise on lung diffusion capacity (D(,Lco)). D(,Lco)/V(,A) did not increase significantly following exercise, suggesting that the decrease in TEI following exercise is the result of extravascular fluid accumulation. It was concluded that a sub-clinical pulmonary edema occurs following exercise. A logical sequence of events based on the results of studies I through V was proposed as a possible explanation for the responses of RV and TLC following exercise.

Gallium arsenide (GaAs) elicited a pulmonary inflammatory response in a dose dependent manner following a single exposure. A significant influx of leukocytes (polymorphonuclear cells) was observed 24 hours after intratracheal instillation of rats and hamsters. This led to an increase in the lung/body weight ratios. An increase in pulmonary DNA and total protein accompanied these observations. Histology confirmed the presence of increased numbers of pulmonary alveolar macrophages (PAM) even 1 week after exposure to GaAs. The instillation of GaAs also appeared to produce an oxidative stress in the lung only when the animals were given the 100 mg/kg dose and not the 10 mg/kg dose. Increased glutathione peroxidase and nonprotein sulfhydryls and depletion of ascorbic acid were evidence for the oxidative stress produced in the lung. These effects were dependent on the influx of phagocytic leukocytes. Analysis of the bronchoalveolar lavage fluid (BALF) also confirmed the involvement of phagocytic leukocytes in the progression of the lesions. Acid phosphatase activities increased significantly above the control levels 24 hours after exposure. The elevation of soluble protein and alkaline phosphatase indicated that the type I pneumocyte-capillary endothelial cell interface was compromised and the type II cells were damaged, respectively. The histological evaluations confirmed this phenomenon. Alveolar wall thickening was quite characteristic of the GaAs exposure. GaAs stimulated PAM to produce the active oxygen species, superoxide anion (O₂⁻) and H₂O₂, following in vitro and in vivo exposure. The dissolution of GaAs did not produce and O₂⁻ or H₂O₂ without the presence of cells. The cytotoxicity of GaAs was comparable to other compounds that elicit collagen deposition, As₂O₃ and silica. The semiconductor properties and potential dissolution products of GaAs may both contribute to its toxicity to PAM. The differences seen in the pulmonary lesions of silica (fibrosis) and GaAs (resorption of deposited collagen) treated animals may be due to the persistence of the particles. GaAs may be cleared by dissolution and silica cannot.

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