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

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.

Impact of vaping and smoking on maximum respiratory pressures and respiratory function

“…These data indicate that vaping and smoking may cause a similar degree of airway obstruction. In this study we confirmed that men have higher spirometric values, such as FEV 1 and FVC, than women, as reported previously (Mohammad Z Darabseh et al, 2021;Mead, 1980;Zakaria et al, 2019). Although it has been reported that cigarette smoking affects pulmonary function more in women than in men (Xu et al, 1994), the absence of any significant group-sex interaction indicated that in our study the effects of smoking and vaping described below were similar in men and women.…”

NMR Spectroscopy Identifies Chemicals in Cigarette Smoke Condensate That Impair Skeletal Muscle Mitochondrial Function

“…COPD patients were reported to have decreased skeletal muscle oxidative function using both in vivo [ 10 , 68 , 69 ] and ex vivo assessments [ 70 , 71 , 72 , 73 , 74 ]. Whereas COPD is often considered as a consequence of long-term smoking, several studies reported that acute cigarette smoke exposure can impair muscle mitochondrial function [ 16 , 17 ] and that short-term smoking cessation can reverse these effects [ 15 , 16 ], suggesting the presence of acute muscle mitochondrial toxicity with smoking. In the present study, we first investigated the effect of CSC on mitochondrial respiratory function and found that acute exposure of muscle mitochondria to CSC resulted in a dose-dependent impairment in mitochondrial respiration ( Figure 2 ).…”

“…However, there are reports suggesting that active exposure to tobacco smoke has direct/acute impacts on muscle health and function. For example, Darabseh et al [ 15 ] subjected active cigarette smokers to a 14-day smoking cessation protocol and observed an improvement in muscle fatigue resistance and lowered biomarkers of inflammation. In mice, ~12 weeks of cigarette smoke exposure was reported to decrease muscle mitochondrial respiration, which was reversed following 2-weeks of smoking cessation [ 16 ].…”

Concurrent Chemoradiotherapy Induces Body Composition Changes in Locally Advanced Head and Neck Squamous Cell Carcinoma: Comparison between Oral Cavity and Non-Oral Cavity Cancer

“…The LBM loss in patients with LAHNSCC undergoing CCRT is mediated by elevated levels of reactive oxygen species and pro-inflammatory cytokines, activation of proteolysis machinery including ubiquitin-dependent, calcium-dependent, and autophage/lysosome systems, decreased mitochondrial biogenesis and mass, and alteration of lipid metabolism [ 26 , 27 ]. The above mechanisms are integrated into two essential clinical factors participating in LBM loss during CCRT: patient characteristics such as age [ 28 ], tumor features [ 29 ], comorbidity [ 30 ], performance status [ 31 ], lifestyle habits [ 32 , 33 , 34 ], pretreatment nutritional status [ 35 ]; treatment-related attributes including RT treatment (dose, fraction, and duration), chemotherapy regimen [ 26 , 36 , 37 ], daily calorie delivered over the treatment course [ 9 , 37 ], and CCRT-associated toxicities [ 38 , 39 ]. The multivariate analysis in the present study showed different factors contributing to LBM loss for the OCC and NOCC subgroups: age and mean daily calorie intake for the OCC; mean daily calorie intake, BMI, and grade ¾ mucositis toxicity for the NOCC.…”