The primary function of perspiration is regulation of body temperature mediated by sympathetic drive, which also leads to vasodilation and tachypnea, resulting in rapid heat dissipation to maintain homeostasis . Other roles of perspiration include the excretion of toxins , maintenance of electrolyte balance, and control of microbial growth through antibacterial peptides . Our study investigates excessive perspiration, an often-neglected symptom of COPD, through objective measures and we explored its association to varying severities of COPD pulmonary dysfunction. While the causal relationship between COPD and perspiration remains unclear, we offer multiple explanations that might provide insight into their correlation.
In this study, we found there to be significantly more perspiration during exercise in COPD patients than in healthy individuals. Furthermore, perspiration rates increased with worsening ventilatory dysfunction. One possible mechanism involves elevated sympathetic excitability, which is an autonomic response driven by hypoxia and/or CO2 retention [12, 13]. Basal metabolism may also contribute to altered perspiration as evidenced by the high correlation between the basal metabolic rate and perspiration rate . The basal metabolic rate in COPD patients is significantly elevated, an observation attributed to catabolic/anabolic imbalance through catabolic hyperactivity . The basal metabolic rate in COPD patients is approximately 10% higher than that of healthy individuals . As airway resistance increases in COPD, oxygen consumption will be further elevated due to respiratory muscle load and so result in higher levels of metabolic demand at rest and during exercise [16, 17].
COPD patients expend more energy during exercise than healthy individuals, and this may contribute to increased perspiration. CPET measurements reflect both cardiopulmonary physiology and metabolic consumption [19, 20], which are inferred from such variables as peak per-kilogram O2 uptake, CO2 ventilation, and metabolic equivalents. We propose perspiration may serve as a proxy for metabolism. This is supported by the observation that increased severity of COPD is associated with higher levels of perspiration.
Some common medications indicated for COPD can significantly increase resting oxygen consumption, resulting in an elevated basal metabolic rate . Theophylline and β2-receptor agonists may synergistically increase oxygen consumption, resulting in increased metabolic rates . However, these bronchodilators also reduce airway resistance, leading to a reduction in resting oxygen consumption. The long-term effects of these COPD medications on basal metabolism have yet to be reconciled [22, 23].
In this study, we found perspiration rate in COPD patients to be closely correlated with multiple CPET variables such as peak work rate, maximum voluntary ventilation, peak O2 uptake, CO2 ventilatory equivalent, and physiological dead space. The peak work rate reflects the patient’s exercise tolerance, the maximum voluntary ventilation reflects a patient’s ventilation capacity, and the CO2 ventilatory equivalent is a normalized indicator of a patient’s ventilatory ability. When combined, these parameters can be used to assess pulmonary function with high reproducibility and accuracy and so facilitate objective comparisons between subjects [24, 25]. Based on previous reports, CO2 ventilatory equivalent is an indicator for early mortality assessment in patients with COPD [26–28]. For these reasons, the rate of perspiration in COPD patients may even have prognostic value.
While perspiration rate has been found to be correlated with age and BMI , we did not here observe such a correlation. Our results instead show the severity of dyspnea (mMRC) and ventilation dysfunction to be correlated with increased rates of perspiration in COPD patients. Additionally, the increased perspiration rate in COPD patients may be a marker of worsening lung function, increasing the severity of clinical symptoms and decreasing quality of life. The increased perspiration rate in patients with COPD may not only be a manifestation of clinical symptoms, but also can be served as an indicator of disease progression.
Our study has several limitations. The site of perspiration measurement was well-defined and placed consistently across subjects. However, all parts of the body perspire during exercise and regional contributions may differ from those produced by the back. Collecting sweat from other body parts of the body may further support our claim that altered perspiration is related to systemic autonomic dysfunction. While our perspiration measurements were made during exercise, evaluating perspiration at rest can exclude the possibility that perspiration dysfunction is linked to levels of physical activity. This may be performed through a clinical symptom survey or through measurement of perspiration during recovery phases after exercise testing. Lastly, our claims relating perspiration to severity of COPD are made from correlation, not causation. While multiple theories have been proposed, elucidating these mechanisms will require well-designed studies at the clinical and experimental levels.