Mechanisms Of Exertional Dyspnea Research Articles

Inflammatory Mechanisms of Exertional Dyspnea in Southwest Asia Deployed Military Veterans

Inflammatory Mechanisms of Exertional Dyspnea in Southwest Asia Deployed Military Veterans

Mechanisms of Exertional Dyspnea in Patients with Mild COPD and a Low Resting DLCO

Patients with mild chronic obstructive pulmonary disease (COPD) and lower resting diffusing capacity for carbon monoxide (DLCO) often report troublesome dyspnea during exercise although the mechanisms are not clear. We postulated that in such individuals, exertional dyspnea is linked to relatively high inspiratory neural drive (IND) due, in part, to the effects of reduced ventilatory efficiency. This cross-sectional study included 28 patients with GOLD I COPD stratified into two groups with (n = 15) and without (n = 13) DLCO less than the lower limit of normal (<LLN; Global Lung Function Initiative criteria) and 16 healthy controls. We compared dyspnea (Borg scale), IND (by diaphragm electromyography), ventilatory equivalent for CO2 (V̇ E/V̇CO2), and respiratory mechanics during incremental cycle exercise in the three groups. Spirometry and resting lung volumes were similar between COPD groups. During exercise, dyspnea, IND and V̇ E/V̇CO2 were higher at equivalent work rates (WR) in the DLCO<LLN group compared with the other two groups (all p < 0.05). In patients with DLCO<LLN, severe respiratory mechanical constraints, indicated by end-inspiratory lung volume of approximately 90% of total lung capacity, occurred at a lower WR than the other two groups (p < 0.05). The dyspnea/IND relationship was similar across groups; therefore, the increased dyspnea at a standardized WR in the low DLCO<LLN group reflected the higher corresponding IND. Higher dyspnea ratings in patients with mild COPD and DLCO<LLN were associated with higher IND and V̇ E/V̇CO2 at a given work rate. Higher ventilatory requirements in the DLCO<LLN group accelerated dynamic mechanical abnormalities earlier in exercise, further increasing IND and dyspnea.

Mechanisms of exertional dyspnoea in symptomatic smokers without COPD.

Dyspnoea and activity limitation can occur in smokers who do not meet spirometric criteria for chronic obstructive pulmonary disease (COPD) but the underlying mechanisms are unknown.Detailed pulmonary function tests and sensory-mechanical relationships during incremental exercise with respiratory pressure measurements and diaphragmatic electromyography (EMGdi) were compared in 20 smokers without spirometric COPD and 20 age-matched healthy controls.Smokers (mean±sd post-bronchodilator forced expiratory volume in 1 s (FEV1)/forced vital capacity 75±4%, mean±sd FEV1 104±14% predicted) had greater activity-related dyspnoea, poorer health status and lower physical activity than controls. Smokers had peripheral airway dysfunction: higher phase-III nitrogen slopes (3.8±1.8 versus 2.6±1.1%·L(-1)) and airway resistance (difference between airway resistance measured at 5 Hz and 20 Hz 19±11 versus 12±7% at 5 Hz) than controls (p<0.05). Smokers had significantly (p<0.05) lower peak oxygen uptake (78±40 versus 107±45% predicted) and ventilation (61±26 versus 97±29 L·min(-1)). Exercise ventilatory requirements, operating lung volumes and cardio-circulatory responses were similar. However, submaximal dyspnoea ratings, resistive and total work of breathing were increased in smokers compared with controls (p<0.05); diaphragmatic effort (transdiaphragmatic pressure/maximumal transdiaphragmatic pressure) and fractional inspiratory neural drive to the diaphragm (EMGdi/maximal EMGdi) were also increased (p<0.05) mainly reflecting the reduced denominator.Symptomatic smokers at risk for COPD had greater exertional dyspnoea and lower exercise tolerance compared with healthy controls in association with greater airways resistance, contractile diaphragmatic effort and fractional inspiratory neural drive to the diaphragm.

Mechanisms of Exertional Dyspnea in Obesity

Mechanisms of Exertional Dyspnea in Obesity

Mechanisms of Exertional Dyspnea in Patients with Cancer.

Mechanisms of Exertional Dyspnea in Patients with Cancer.

MECHANISMS OF EXERTIONAL DYSPNEA

To understand why someone is dyspneic during exercise, we need to follow the advice of Sir Francis Bacon: "No natural phenomenon can be adequately studied in itself alone, but to be understood must be considered as it stands connected with all of nature." In the present context, this implies the careful measurement of events related to metabolism, circulation, and respiration and of the associated sensory events as these systems adapt to the strain and stress of exercise.