Exertional dyspnea-related acidotic and sympathetic responses in patients with sequelae of pulmonary tuberculosis

Abstract

The objective of this study was to investigate whether exertional dyspnea correlates with exercise responses, especially arterial blood pH and plasma norepinephrine (NE) changes, in patients with sequelae of tuberculosis (TBsq). Cardiopulmonary exercise testings were performed in 49 TBsq patients and 9 controls. Each group had a break point in the dyspnea, plasma lactate, and plasma NE changes during exercise, all of which occurred at a similar exercise point. In TBsq patients in both exercise phases before and after the dyspnea break point, the dyspnea-slope (DeltaBorg scale/Deltaminute ventilation) correlated with the pH-slope (DeltapH/Deltaoxygen uptake) (r = -0.616, p < 0.0001; r = -0.629, p < 0.0001, respectively, before and after the break point) and with the NE-slope (DeltaNE/Deltaoxygen uptake) (r = 0.443, p = 0.0012; r = 0.643, p < 0.0001, respectively, before and after the break point). In TBsq patients during exercise, increases in circulating NE levels and exertional acidosis were correlated with exertional dyspnea.

Effects of Ghrelin Treatment on Exercise Capacity in Underweight COPD Patients: a substudy of a multicenter, randomized, double-blind, placebo-controlled trial of ghrelin treatment

“…The plasma norepinephrine levels seemed to be inhibited at the iso-time point (Table 3). Given the reported negative connotations of sympathetic activation in cardiac as well as respiratory disease patients [22-26], sympathetic inhibition may have positive consequences in COPD. These findings suggest that underweight patients with COPD who undergo exercise training can only increase their endurance time, efficiently decreasing $\stackrel{•}{V}{o}_2$ and plasma norepinephrine levels.…”

Takotsubo Cardiomyopathy Caused by Pulmonary Tuberculosis: A Case Report

“…Chronic infection such as pulmonary tuberculosis is not generally considered to be a common cause of TTC. However, a few reports suggest that there is a higher plasma norepinephrine concentration in pulmonary tuberculosis patients compared to normal people, which is a typical accepted pathophysiological mechanism of TTC4,5. Thus, we postulate that pulmonary tuberculosis may be a possible precipitant of TTC.…”

Differences in Physiological Response to Exercise in Patients With Different COPD Severity

“…An intimate relationship between the increase in plasma norepinephrine and dyspnea intensity during exercise has also been observed in patients with other respiratory diseases, including idiopathic pulmonary fibrosis 20 and sequelae of pulmonary tuberculosis. 21 Also, Clark et al 33 found that the administration of yohimbine increased norepinephrine release in healthy individuals, and this increase was associated with increased ventilatory response and an increased sensation of exertion during steady-state exercise. Thus, the increase in norepinephrine induced by exercise could also contribute to the increase in both ventilation and the sensation of breathlessness.…”