Comparing hospitalised, community and staff COVID-19 infection rates during the early phase of the evolving COVID-19 epidemic Dear Editor, a descriptive and modelling study. Lancet Infect Dis 2020 Apr 2 pii: S1473-3099(20)30230-9[Epub ahead of print].

To determine the effects of exercise with expiratory flow-limitation (EFL) on systemic O(2) delivery, seven normal subjects performed incremental exercise with and without EFL at approximately 0.8 l s(-1) (imposed by a Starling resistor in the expiratory line) to determine maximal power output under control (W'(max,c)) and EFL (W'(max,e)) conditions. W'(max,e) was 62.5% of W'(max,c), and EFL exercise caused a significant fall in the ventilatory threshold. In a third test, after exercising at W'(max,e) without EFL for 4 min, EFL was imposed; exercise continued for 4 more minutes or until exhaustion. O(2) consumption (V'(O)(2)) was measured breath-by-breath for the last 90 s of control, and for the first 90 s of EFL exercise. Assuming that the arterio-mixed venous O(2) content remained constant immediately after EFL imposition, we used V'(O)(2) as a measure of cardiac output (Q'(c)). Q'(c) was also calculated by the pulse contour method with blood pressure measured continuously by a photo-plethysmographic device. Both sets of data showed a decrease of Q'(c) due to a decrease in stroke volume by 10% (p < 0.001 for V'(O)(2)) with EFL and remained decreased for the full 90 s. Concurrently, arterial O(2) saturation decreased by 5%, abdominal, pleural and alveolar pressures increased, and duty cycle decreased by 43%. We conclude that this combination of events led to a decrease in venous return secondary to high expiratory pressures, and a decreased duty cycle which decreased O(2) delivery to working muscles by approximately 15%.

. Effects of rapid saline infusion on lung mechanics and airway responsiveness in humans. J Appl Physiol 95: 728-734, 2003. First published May 2, 2003 10.1152/japplphysiol.00310.2003.-Lung mechanics and airway responsiveness to methacholine (MCh) were studied in seven volunteers before and after a 20-min intravenous infusion of saline. Data were compared with those of a time point-matched control study. The following parameters were measured: 1-s forced expiratory volume, forced vital capacity, flows at 40% of control forced vital capacity on maximal (V m40) and partial (V p40) forced expiratory maneuvers, lung volumes, lung elastic recoil, lung resistance (RL), dynamic elastance (Edyn), and within-breath resistance of respiratory system (Rrs). RL and Edyn were measured during tidal breathing before and for 2 min after a deep inhalation and also at different lung volumes above and below functional residual capacity. Rrs was measured at functional residual capacity and at total lung capacity. Before MCh, saline infusion caused significant decrements of forced expiratory volume in 1 s, V m40, and V p40, but insignificantly affected lung volumes, elastic recoil, RL, Edyn, and Rrs at any lung volume. Furthermore, saline infusion was associated with an increased response to MCh, which was not associated with significant changes in the ratio of V m40 to V p40. In conclusion, mild airflow obstruction and enhanced airway responsiveness were observed after saline, but this was not apparently due to altered elastic properties of the lung or inability of the airways to dilate with deep inhalation. It is speculated that it was likely the result of airway wall edema encroaching on the bronchial lumen.

Dyspnea and leg effort are the major symptoms limiting exercise in healthy subjects and in patients with a variety of respiratory disorders. Quantitative measurement of both symptoms may be obtained by category scales such as VAS and Borg, with the latter being widely used. Furthermore, descriptor clusters of dyspnea help to assess some of the reasons for stopping exercise. The intensity of dyspnea and leg effort are similar in different disease states; this symmetry suggests that the limiting discomfort is a function of the intensity of increased motor drive to peripheral and respiratory muscles. An alternative explanation for the factors which limit exercise is that the subjects stop exercise volitionally when the discomfort associated with continuing exercise exceeds that which they are willing to tolerate. Muscle strength contributes to the intensity of dyspnea and leg effort at a given power output: the greater the muscle force, the lower the symptom. Symptoms also correlate with intensity and duration of a task by a power function in such a way that when minimizing the intensity of a given muscular task by prolonging the duration of activity, the symptom is drastically reduced. Skeletal muscle fatigue may be a factor limiting exercise tolerance both in healthy subjects and in patients with cardiorespiratory disorders. In conclusion, symptom measurement complements physiological measurements, both being essential to a comprehensive understanding of exercise tolerance.