Fourteen days of smoking cessation improves muscle fatigue resistance and reverses markers of systemic inflammation

Mohammad Z. Darabseh,Christopher I. Morse,George Welbourne,James Selfe,Hakima Aushah,Hans Degens,Thomas M. Maden-Wilkinson,Rob C. I. Wüst,Nessar Ahmed

doi:10.1038/s41598-021-91510-x

Abstract

Cigarette smoking has a negative effect on respiratory and skeletal muscle function and is a risk factor for various chronic diseases. To assess the effects of 14 days of smoking cessation on respiratory and skeletal muscle function, markers of inflammation and oxidative stress in humans. Spirometry, skeletal muscle function, circulating carboxyhaemoglobin levels, advanced glycation end products (AGEs), markers of oxidative stress and serum cytokines were measured in 38 non-smokers, and in 48 cigarette smokers at baseline and after 14 days of smoking cessation. Peak expiratory flow (p = 0.004) and forced expiratory volume in 1 s/forced vital capacity (p = 0.037) were lower in smokers compared to non-smokers but did not change significantly after smoking cessation. Smoking cessation increased skeletal muscle fatigue resistance (p < 0.001). Haemoglobin content, haematocrit, carboxyhaemoglobin, total AGEs, malondialdehyde, TNF-α, IL-2, IL-4, IL-6 and IL-10 (p < 0.05) levels were higher, and total antioxidant status (TAS), IL-12p70 and eosinophil numbers were lower (p < 0.05) in smokers. IL-4, IL-6, IL-10 and IL-12p70 had returned towards levels seen in non-smokers after 14 days smoking cessation (p < 0.05), and IL-2 and TNF-α showed a similar pattern but had not yet fully returned to levels seen in non-smokers. Haemoglobin, haematocrit, eosinophil count, AGEs, MDA and TAS did not significantly change with smoking cessation. Two weeks of smoking cessation was accompanied with an improved muscle fatigue resistance and a reduction in low-grade systemic inflammation in smokers.

Highlights

Cigarette smoking has a negative effect on respiratory and skeletal muscle function and is a risk factor for various chronic diseases
It has been reported that in diabetic people, a reduced insulin sensitivity could lead to glycation of myofibrillar proteins[14] that may be further aggravated by glycotoxins in cigarette smoke that can react with serum proteins to form advanced glycation end products (AGEs)[6]
As fatigue resistance was similar in chronic obstructive pulmonary disease (COPD) patients who had quit smoking and healthy age-matched non-smokers[27], we hypothesised that the effect of smoking on skeletal muscle fatigue is readily reversible by smoking cessation

Summary

Introduction

Cigarette smoking has a negative effect on respiratory and skeletal muscle function and is a risk factor for various chronic diseases. Part of the potential detrimental effect of cigarette smoking may be attributable to the negative impact on the oxygen delivery to tissues, including skeletal muscles, that may in turn result in exercise intolerance and a reduced muscle fatigue resistance[20,21,22]. Such an impaired oxygen delivery is at least partly attributable to the CO in the cigarette smoke that strongly binds to haemoglobin (Hb), forming carboxyhaemoglobin (COHb)[23]. As fatigue resistance was similar in COPD patients who had quit smoking and healthy age-matched non-smokers[27], we hypothesised that the effect of smoking on skeletal muscle fatigue is readily reversible by smoking cessation

Methods

Results

Conclusion