The relationship between oxygen consumption and work rate in patients with airflow obstruction.

The oxygen cost of augmented ventilation is increased in patients with chronic obstructive pulmonary disease, either at rest or during exercise. Thus, if excessive demands are placed on the respiratory muscles during exercise in these patients, we postulate that the total oxygen consumption (VO2) may increase relative to the work rate compared to control subjects. The aim of this study was to examine the relationship between VO2 and work rate during exercise in patients with airflow obstruction. A retrospective analysis of data collected over 7 years was conducted. Patients with airflow obstruction (n = 131) were compared and contrasted with those in whom pulmonary function studies (spirometry, lung volumes) were normal (n = 199). Severity of airflow obstruction (ie, mild moderate, severe) was determined, using the 95 percent confidence limits for the ratio of FEV1 to FVC. Incremental exercise studies were performed on a cycle ergometer. Resting VO2 was not significantly different across the groups with airflow obstruction measured either directly or normalized for body weight. The VO2max was significantly reduced in the patients with severe airflow obstruction, compared with the normal group, as well as the patients with mild and moderate airflow obstruction. No differences were noted in the slope of VO2 plotted against work rate in the patients with airflow obstruction (regardless of the severity of the obstruction) and individuals in whom results of pulmonary function tests were normal. In addition, when gender was taken into account, there was essentially no difference in the slopes for either male or female subjects across all groups. Stepwise, linear regression failed to demonstrate any variable or variables that were strongly related to slope. We postulate that the maintenance of a normal slope of VO2 on work rate in patients with airflow obstruction, in whom the oxygen cost and work of breathing is likely increased, may mask a significant reduction in nonrespiratory VO2 (for example, to exercising skeletal muscles).

Effect of corticosteroids on diaphragm fatigue, SDH activity, and muscle fiber size.

The influence of dexamethasone on diaphragm (DIA) fatigue, oxidative capacity, and fiber cross-sectional areas (CSA) was determined in growing hamsters. One group received dexamethasone by daily subcutaneous injection for 21 days (D animals), while pair-weight (P) and free-eating controls (CTL) received saline subcutaneously. Isometric contractile properties of the DIA were determined in vitro by supramaximal direct muscle stimulation in the presence of curare. DIA fatigue resistance was determined through repetitive stimulation at 40 pulses/s for 2 min. A computer-based image-processing system was used to histochemically determine muscle fiber-type proportions, CSA, and succinate dehydrogenase activities. The medial gastrocnemius muscle (MG) was used as a limb muscle control, with histochemical studies being performed on both the superficial (s) and deep/red (r) portions. Dexamethasone markedly attenuated the normal increment in body weight over the 3-wk period. DIA fatigue resistance was significantly reduced in the D compared with CTL and P animals. Dexamethasone had no effect on fiber-type proportions of the DIA or MGr (MGs contained only type II fibers). In the DIA, the CSA of type II fibers was reduced 33% in D and 18.5% in P animals compared with CTL. Although no significant atrophy was noted in the type I DIA fibers of either D or P animals, a trend toward significance was noted in D animals compared with CTL. In the MGs, the CSA of type II fibers was reduced 33% in D and 16.5% in P animals compared with CTL. Significant atrophy of type I and II fibers of the MGr was noted in D animals compared with CTL (33.8 and 35% reductions, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Interactive effects of emphysema and malnutrition on diaphragm structure and function.

Interactive effects of emphysema (EMP) and prolonged nutritional deprivation (ND) on contractile, morphometric, and metabolic properties of hamster diaphragm muscle (DIA) were examined. Six months after induction of EMP (intratracheal elastase), saline-treated controls (CTL) and EMP hamsters of similar body weights were subjected to ND over 6 wk. Isometric contractile and fatigue properties of costal DIA were determined in vitro. DIA fibers were histochemically classified as type I or II, and fiber succinate dehydrogenase activity and cross-sectional area were determined using quantitative microscopic procedures. From histochemical sections, the number of capillaries per fiber (C/F) and per fiber cross-sectional area (C/A) were determined. ND resulted in progressive loss of body weight (ND-CTL, 23.8%; ND-EMP, 28.4%; P = NS). ND did not affect reduction in optimal length (Lo) of DIA fibers in EMP compared with CTL and ND-CTL hamsters. Maximum specific force (i.e., force/unit area) was reduced by approximately 25% in EMP animals compared with CTL. ND did not improve or exacerbate the reduction in specific force with EMP. ND attenuated improved fatigue resistance of DIA in EMP animals. No differences in fiber type proportions were noted among experimental groups. Significant atrophy of type I and II DIA fibers was noted after ND. Atrophy was proportionately greater in type II fibers of ND-EMP when referenced to EMP animals. Thus adaptive hypertrophy of type II DIA fibers in EMP animals was abolished. Fiber succinate dehydrogenase activity was significantly increased in type I and II fibers in EMP DIA. ND did not affect this metabolic adaptation of DIA fibers to persistent loads imposed by EMP.(ABSTRACT TRUNCATED AT 250 WORDS)