Oxidative stress and skeletal muscle dysfunction are present in healthy smokers

Abstract

Chronic exposure to cigarette smoke seems to be related to an increase of pro-inflammatory cytokines, oxidative stress and changes in muscular and physical performances of healthy smokers. However, these parameters have not yet been evaluated simultaneously in previous studies. The participants of this study were healthy males divided into two groups: smokers (n=20) and non-smokers (n=20). Inflammation was evaluated by measuring plasma levels of the cytokines IL-10, IL-6 e TNF-α, and of the soluble receptors sTNFR1 and sTNFR2. Oxidative stress was evaluated by determination of thiobarbituric acid reactive substances (TBARS) plasma levels, total antioxidant capacity of plasma and erythrocytes activity of the antioxidant enzymes superoxide dismutase (SOD) and catalase. Muscular performance was evaluated by measuring the peak torque of knee flexors and extensors, and by determining the total work of the knee extensors. Physical performance was assessed by measuring the peak oxygen uptake (VO2 peak), the maximum heart rate (HRmax) and the walking distance in the shuttle walking test. Smokers showed an increase in the levels of the sTNFR1 and TBARS and a decrease in the total antioxidant capacity of plasma, in the catalase activity and in the total work (P<0.05). IL-6, IL-10, sTNFR2, SOD, peak torque, VO2 peak, HRmax and walking distance were similar between groups. Smokers presented increased oxidative stress and skeletal muscle dysfunction, demonstrating that the changes in molecular and muscular parameters occur simultaneously in healthy smokers.

The Effect of Tobacco Smoking on Musculoskeletal Health: A Systematic Review

“…Three quasi-experimental studies investigated the biological effects of smoking. The results of those studies reported smokers had decreased local muscle O2Hb [ 206 ], thiobarbituric acid [ 211 ], and catalase [ 211 ] levels, an increase in inflammatory markers (sTNFR1) [ 211 ] and similar VO2 [ 206 , 211 ], lactate [ 206 ], superoxide dismutase (SOD) [ 211 ], and succinate dehydrogenase (SDH) activity [ 220 ], inflammatory cytokines (IL-6, IL-10, and sTNFR2), myoglobin concentration [ 220 ], and capillarization [ 220 ] during leg muscle exercises.…”

Cardiopulmonary and Muscular Interactions: Potential Implications for Exercise (In)tolerance in Symptomatic Smokers Without Chronic Obstructive Pulmonary Disease

“…Spillover of inflammatory mediators produced by lung epithelial cells in response to smoking may reach the striated muscles with negative bioenergetic consequences (Fetterman et al, 2017; Madani et al, 2018). The mitochondrion, as important source of biochemical and thermal energy, is a key target for smoking toxicity, leading to reduced respiration, decreased ATP content, and increased production of free radicals in a dose- and time-dependent manner (Neves et al, 2016; Fetterman et al, 2017; Madani et al, 2018). As a consequence, smokers may present with impaired oxidative phosphorylation (as extensively reviewed by Fetterman et al, 2017).…”

Effects of PM2.5 on Skeletal Muscle Mass and Body Fat Mass of the Elderly in Taipei, Taiwan

“…However, there is paucity of information regarding the effect of ambient PM 2.5 on human skeletal muscle and adipose tissue. Previous studies show that cigarette smoke leads to skeletal muscle cell damage, muscle protein breakdown 16 , skeletal muscle dysfunction 17 , and central obesity 18 . Because ambient PM 2.5 and cigarette smoke share some common patho-physiologic mechanisms like oxidative stress and inflammation, ambient PM 2.5 may have negative effects on muscle and adipose tissue in the elderly, a population susceptible to air pollution.…”