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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.

A nonrecirculatory liver slice perifusion system has been developed and utilized for investigating glucagon-stimulated glycogenolysis in normal and diabetic states. It has been shown here that slices maintained in this system experience a controlled environment with respect to temperature and pH and remain viable throughout a three-hour experimental period based upon their maintenance of intracellular potassium levels. Although glycogen content falls by 40%, slices exhibit significant glycogenolysis in a dose-response manner upon challenge with glucagon, with maximal concentrations eliciting a 2.2-fold stimulation. This system, which permits nonrecirculatory challenge of liver tissue and subsequent analysis of both intracellular events and overall physiological responses, is extremely useful for examining hormonal mechanisms operating for glucagon, particularly at low concentrations. Using this methodology, liver slices challenged with glucagon exhibit a biphasic dose-response for glycogenolysis. While the second phase parallels cAMP (cyclic adenosine 3':5'-monophosphate) accumulation and cAMP-PK (cAMP-dependent protein kinase) activation, the first is mediated independent of cAMP. Trinitrophenylhistidine-1, homoarginine-12-glucagon (THG), which can antagonize glucagon-stimulated adenylate cyclase, exhibits 50% partial agonist activity for cAMP production and cAMP-PK but full agonism for glycogenolysis. Separation between these events is only two-fold indicating a cAMP-mediated process. [Des-amino-fYRKKE]-glucagon, ([Des-amino-His¹,D-Phe⁴,Tyr⁵,Arg¹²,Lys¹⁷·¹⁸,Glu²¹]-glucagon), another adenylate cyclase antagonist, does not stimulate cAMP or cAMP-PK up to 25 μM yet still elicits glycogenolysis. These results demonstrate that glucagon does indeed stimulate both cAMP-independent as well as cAMP-dependent glycogenolysis in normal liver. In diabetic systems, glucagon elicits attenuated adenylate cyclase activity in liver plasma membranes with reduction in basal activity and extent of stimulation. Maximal stimulation of cAMP production is also reduced by half in liver slices, but in both systems (normal vs. diabetic) EC₅₀ values for cAMP production are identical. Neither THG nor [des-amino-fYRKKE]-glucagon stimulate cAMP production or cAMP-PK in diabetic liver slices. While THG lowers blood glucose levels in vivo, [des-amino-fYRKKE]-glucagon acts as an agonist. These results suggest that the mechanisms which operate for glucagon-stimulated glycogenolysis in normal liver are attenuated in the diabetic state. Furthermore, antagonism of cAMP production alone is insufficient to antagonize glucagon's overall physiological action.

We derive the expression for the three-dimensional incoherent optical transfer function when third-order spherical aberration is present. The normalized version of the transfer function is numerically calculated for various amounts of spherical aberration. We find the effects of the aberration to be highly dependent on the spatial frequency in the longitudinal direction. We also calculate a structure content parameter, as a quality criterion, from the normalized transfer function. Remarkably, the structure content parameter dependence on spherical aberration is well-fit by a simple Cauchy curve for aberrations out to two waves at the margin.

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