Cardiorespiratory and Metabolic Kinetics During Recovery After an Incremental Test in Young Physically Active Smokers
Authors: Borrelli Marta , Doria Christian , Limonta Eloisa , Longo Stefano , Toninelli Nicholas , Cè Emiliano , Rampichini Susanna , Esposito Fabio 
Published: May 2022

BACKGROUND

Cigarette smoking is one of the most impacting risk factors for cardiopulmonary morbidity and a major cause of mortality. It is responsible for systemic modifications that alter the cardiorespiratory and metabolic behaviour at rest and during exercise. Indeed, nicotine acts as a stimulant of the sympathetic nervous system, elevating the heart rate (fH) and cardiac work. Likewise, tar impairs O2 diffusion across the alveolar‐capillary barrier, and carbon monoxide reduces O2 transport and extraction. Maximal cardiopulmonary exercise tests are commonly used to evaluate the cardiovascular and pulmonary response to exercise. Moreover, post‐exercise recovery kinetics are considered prognostic indexes of cardiovascular health. While maximal exercise tests have been already used to assess the cardiovascular and pulmonary functionality in smokers, so far, no study investigated the role of cigarette smoking after exercise cessation. Hence, this study aims to assess the pulmonary O2 uptake (V’O2) and related variables kinetics during the recovery phase after a maximum incremental test in young physically active smokers. We hypothesized that, considering the aforementioned impact of nicotine, tar and carbon monoxide, a slower recovery of the respiratory, metabolic and cardiac system may occur in smokers.

METHODS

We enrolled 7 physically active smokers (SM; age: 21±2 yr.; body mass: 77±6 kg; stature: 1.79±0.07 m; maximum V’O2 (V’O2max): 44.5±4.5 ml∙min‐1∙kg‐1; 13±5 cigarette/day for 6±2 years; mean±SD) and 9 physically active non‐smokers (CTRL; age: 24±2 yr., body mass: 77±10 kg; stature: 1.78±0.08 m; V’O2max; 46.5±6.5 ml∙min‐1∙kg‐1). After evaluating the pulmonary function by spirometry, participants performed a maximal incremental step test (25 W/2 min) on a cycle ergometer until exhaustion, followed by 5 min of active recovery at 30 W (30 rpm). Expiratory ventilation (V’E), V’O2 and fH responses were fitted off‐line by a mono‐exponential function to determine the amplitude (AMP), starting value (Y0) and time constant (τ) during the recovery phase. The peak of cardiorespiratory and metabolic variables and the maximum mechanical power were also assessed.

RESULTS

Despite similar spirometric values, SM showed lower maximum mechanical power (‐11%; P=0.05) and peak V’E (‐11%; P=0.03), and higher fH at rest (+13%; P=0.01) compared to CTRL. Moreover, SM exhibited a slower τ in V’O2 (‐18 s; P=0.01), V’E (‐23 s; P=0.04), and V’CO2 (‐24 s; P=0.05) kinetics. No differences in fH parameters were observed.

CONCLUSIONS

Even with a similar pulmonary function, cardiopulmonary exercise testing revealed smoking‐related lengthening of respiratory and metabolic recovery phase kinetics. Despite higher fH at rest, no smoking effect was found on the speed of fH recovery, possibly because of neural mechanisms, such as a preserved vagal withdrawal, or mechanical pulmonary afferents activation that immediately after maximal exercise may have counterbalanced the smoking‐induced sympathetic over‐activation.