Logan Steele
Smoking has been linked to a range of adverse health effects, including respiratory and cardiovascular issues, cancer, and an increased risk of severe COVID-19 outcomes. Evidence also suggests that smoking contributes to skeletal muscle dysfunction and atrophy. Studies have shown that smoking can lead to muscle wasting, a reduction in muscle mass and strength, and an increased risk of sarcopenia, particularly in older individuals. The mechanisms behind these effects involve disruptions to skeletal muscle metabolism, increased inflammation and oxidative stress, impaired protein synthesis, and the activation of various intracellular signaling pathways. While the specific chemicals in cigarette smoke responsible for muscle damage have not yet been identified, research indicates that smoking reduces the number of small blood vessels supplying oxygen and nutrients to the muscles, which may be a contributing factor.
| Characteristics | Values |
|---|---|
| Muscle weakness | Loss of muscle mass |
| Smoking-induced muscle wasting | 25% smaller fiber cross-sectional area in the vastus lateralis muscle |
| Lower lean body mass | |
| Reduced muscle mass | |
| Progressive myosin breakdown | |
| Impaired muscle protein synthesis | |
| Increased expression of genes associated with impaired muscle maintenance | |
| Increased central fat storage | |
| Reduced muscle tissue | |
| Reduced muscle strength | |
| Reduced number of blood vessels in leg muscles | |
| Increased risk of sarcopenia | |
| Increased risk of chronic obstructive pulmonary disease (COPD) |
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What You'll Learn
Smoking increases the risk of sarcopenia
Smoking has been identified as a risk factor for muscle atrophy and dysfunction. Several studies in humans and animal models provide evidence that smoking results in muscle wasting. For example, a 25% smaller fiber cross-sectional area was observed in the vastus lateralis muscle of smokers, even when matched for physical activity. In addition, lean body mass is lower in smoking men compared with similarly physically active non-smoking control subjects.
Research has shown that cigarette smoke directly impairs skeletal muscle function through capillary regression and altered myofibre calcium kinetics. Components in cigarette smoke directly damage muscles by reducing the number of blood vessels in leg muscles, thereby reducing the amount of oxygen and nutrients they can receive. This can impact metabolism and activity levels, both of which are risk factors for many chronic diseases, including COPD and diabetes.
Smoking also increases the level of carbon monoxide in the body, which interferes with respiratory and muscle proteins, including hemoglobin, myoglobin, and other proteins. Smoking impairs the delivery of oxygen to the mitochondria, leading to impaired generation of adenosine triphosphate and hampered contractile function. Smoking has also been shown to impair muscle protein synthesis and to increase the expression of genes associated with impaired muscle maintenance.
Several in vivo and in vitro studies have shown that smoking can contribute to skeletal muscle damage by disrupting skeletal muscle metabolism, increasing skeletal muscle inflammation and oxidative stress, and activating various intracellular signaling pathways. Smoking can also affect the expression levels of myosin and proteins associated with catabolism. For instance, the synthesis of some muscle proteins has been shown to decrease, while the expression of muscle atrophy-related genes and myogenesis inhibitory proteins increased among smokers compared with non-smokers. Myogenesis inhibitors are members of the tumor growth factors that inhibit skeletal myogenesis and negatively regulate muscle mass. Therefore, smoking can increase the risk of sarcopenia by impairing muscle protein metabolism and increasing the expression of genes associated with disruption of muscle protein homeostasis.
In summary, smoking increases the risk of sarcopenia by impairing muscle protein metabolism, increasing muscle wasting, and disrupting muscle function.
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Cigarette smoke directly damages muscles
Cigarette smoke contains about 4000 chemicals, and while the exact ones responsible for muscle damage are unknown, it is clear that components in cigarette smoke directly damage muscles. Research from the University of California, San Diego, in conjunction with Universidade Federal do Rio de Janeiro and Kochi University, indicates that smoking decreases the number of small blood vessels that bring oxygen and nutrients to muscles in the legs. This reduction in blood vessels weakens the muscles, thereby limiting activity and exercise.
Smoking has been shown to impair muscle protein synthesis and increase the expression of genes associated with impaired muscle maintenance. It also increases the expression of muscle atrophy-related genes and myogenesis inhibitory proteins. Myogenesis inhibitors are members of the tumor growth factors that inhibit skeletal myogenesis and negatively regulate muscle mass. In addition, smoking can disrupt skeletal muscle metabolism, increase skeletal muscle inflammation and oxidative stress, and affect the expression levels of myosin and proteins associated with catabolism.
Several studies in humans and animal models provide evidence that smoking results in muscle wasting and a reduction in muscle mass. For example, a 25% smaller fiber cross-sectional area was observed in the vastus lateralis muscle of smokers, even when matched for physical activity. Similarly, in rodents, cigarette smoke exposure results in fiber atrophy, reduced muscle mass, and progressive myosin breakdown.
The impact of smoking on muscle strength is less clear. While smoking may enhance one's ability to voluntarily activate their muscles, thereby increasing force output, the chronic reduction in muscle fibre size and general muscle wasting gradually reduce maximal muscle strength over the moderate term in smokers.
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Smoking impairs muscle protein synthesis
Smoking is a major risk factor for cardiovascular disease, respiratory disease, cancer, and more severe COVID-19-related outcomes. It is also the most important risk factor for the development of chronic obstructive pulmonary disease (COPD). Patients with COPD commonly suffer from skeletal muscle dysfunction.
Several studies in humans and animal models provide evidence that smoking results in muscle wasting and atrophy. For example, a 25% smaller fiber cross-sectional area was observed in the vastus lateralis muscle of smokers, even when matched for physical activity. In addition, lean body mass is lower in smoking men compared with similarly physically active non-smoking control subjects. This, however, could also be the result of a lower food intake secondary to smoking.
Petersen et al. found that the synthesis of some muscle proteins had decreased and expression of muscle atrophy-related genes and myogenesis inhibitory proteins increased among smokers, compared with non-smokers. Myogenesis inhibitors are members of the tumor growth factors that inhibit skeletal myogenesis and negatively regulate muscle mass. Therefore, smoking can increase the risk of sarcopenia by impairing muscle protein metabolism and increasing the expression of genes associated with disruption of muscle protein homeostasis.
In a study of older smokers, relative to non-smokers, smokers demonstrated decreased cross-sectional areas of type I muscle fibers, more oxidative fiber atrophy, increased glycolytic capacity, and reduced expression of nitric oxide synthase. In a study of healthy, young (18- to 45-year-old) smokers versus non-smokers, smokers had higher levels of oxidative stress and skeletal muscle dysfunction in their dominant leg.
Smoking may affect muscle mass and strength through several mechanisms and pathways. Smoking stops new muscle proteins from being synthesized and causes existing muscle proteins to be broken down. This is mostly due to higher levels of localized muscle inflammation and reduced transport of proteins into muscle tissue.
In summary, smoking impairs muscle protein synthesis and increases the expression of genes associated with impaired muscle maintenance.
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Smoking increases muscle atrophy F-box (MAFBx)
Cigarette smoking induces skeletal muscle atrophy and dysfunction. Several studies in humans and animal models provide evidence that smoking results in muscle wasting and loss of muscle mass.
Petersen et al. found that the synthesis of some muscle proteins had decreased and the expression of muscle atrophy-related genes and myogenesis inhibitory proteins had increased among smokers compared to non-smokers. Myogenesis inhibitors are members of the tumor growth factors that inhibit skeletal myogenesis and negatively regulate muscle mass. Therefore, smoking can increase the risk of sarcopenia by impairing muscle protein metabolism and increasing the expression of genes associated with the disruption of muscle protein homeostasis.
Smoking impairs muscle protein synthesis and increases the expression of myostatin and MAFBx in muscle. The muscle growth inhibitor myostatin and muscle atrophy F-box (MAFBx) are associated with the ubiquitin/proteasome proteolytic pathway. In smokers, the quadriceps muscle displayed an increased expression of MAFBx, a muscle-specific regulating factor of ubiquitin-mediated proteolysis. Similarly, 8 weeks of cigarette smoke exposure in mice led to increased mRNA levels of MAFBx in their limb muscles. In vitro studies on smoke-exposed muscle cells (myotubes) show atrophy and loss of myosin concomitant with an increased expression of MAFBx.
The smoke-induced increase in MuRF1 expression in myotubes can also be abolished by inhibition of nuclear factor-κB (NF-κB). However, in mice exposed to cigarette smoke for 8 weeks, gastrocnemius muscle mass decreased without enhanced MuRF1-protein levels, indicating that other pathways might be involved in smoke-induced muscle wasting.
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Smoking cessation improves muscle atrophy
Smoking is a major risk factor for a variety of diseases, including cardiovascular disease, respiratory disease, cancer, and severe COVID-19 outcomes. It is also the most significant risk factor for developing chronic obstructive pulmonary disease (COPD), which is associated with skeletal muscle dysfunction.
Several studies provide evidence that smoking results in muscle wasting and atrophy. In humans, a 25% smaller fiber cross-sectional area was observed in the vastus lateralis muscle of smokers, and lean body mass is lower in smoking men compared to non-smoking controls. Additionally, in rodents and mice, cigarette smoke exposure leads to fiber atrophy, reduced muscle mass, and progressive myosin breakdown.
The negative impact of smoking on muscle health is further exacerbated when combined with vitamin D deficiency, which impairs skeletal muscle fiber hypertrophy. Smoking also affects older adults, contributing to the loss of muscle mass and strength during the aging process. It increases the risk of sarcopenia by impairing muscle protein metabolism and increasing the expression of genes associated with muscle atrophy.
However, the good news is that smoking cessation can significantly improve muscle atrophy and dysfunction. Studies in mice have shown that just one to two weeks of smoking cessation can lead to beneficial effects on skeletal muscle structure and function, with increased lean and fat mass. Similarly, in humans, a 12-week smoking cessation program resulted in gains in lean body mass and a reduction in stomach fat.
Quitting smoking as early as possible is crucial, and the knowledge that smoking cessation has positive extrapulmonary effects can be a strong motivator for smokers. Additionally, engaging in preventive behaviors such as exercise, restful sleep, healthy diets, and social interaction may help slow down the process of muscle loss.
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Frequently asked questions
Yes, smoking has been shown to cause muscle atrophy and dysfunction.
Smoking stops new muscle proteins from being synthesized and causes existing muscle proteins to break down. This leads to a reduction in muscle mass and strength.
Smoking-induced muscle atrophy can limit a person's ability to exercise and increase their risk of developing chronic diseases such as COPD and diabetes.
Yes, quitting smoking can reverse the effects of muscle atrophy. Studies have shown that even short-term smoking cessation of one to two weeks can lead to significant improvements in skeletal muscle structure and function.
