Smoking and Exercise

Introduction[edit | edit source]

Smoking takes many forms and overall is one of the most commonly used recreational drugs, along with being one of the leading causes of death in the world. Tobacco smoking is practiced by over 1 billion people in the world today [1].  Due to mainstream media coverage and the advancement of medical science and research on the topic, the negative health effects of smoking are publicized and well known to the general public.  Despite this it remains a popular fixture in today's society.  The effects that smoking has on the body, specifically implications for exercise, should be known to physical therapists as they will undoubtedly see many smokers during their time as professionals.

Cardiorespiratory Effects[edit | edit source]

Aerobic exercise challenges the body's ability to supply and handle oxygen. For example, when performing high-intensity aerobic exercise, mitochondrial reactive oxygen species' (ROS) grow in number. ROS, if left unchecked, have the ability to cause genetic mutations. However, several enzymes -- including superoxide dismutase -- are present to handle this oxidative stress caused by ROS. The body responds to chronic aerobic exercise by enhancing its ability to cope with ROS[2].

Smoking also induces an oxidative stress; however, smoking-induced oxidative stress also inhibits the body's ability to cope by suppressing the genes responsible for antioxidant production[3]. The net result of smoking-induced oxidative stress is vascular and arteriolar inflammation -- further impairing the oxygen-delivering capabilities of the body. By limiting oxygen delivery, cigarette smoking impairs the ability to generate energy through the oxidative energy system. Smoking also impairs anaerobic energy provision by altering contractile proteins, creatine kinase, and other glycolytic enzymes[4]. With th

is in mind, therapists should be weary of setting unrealistic goals for patients who are smokers.

Smoking is a huge risk factor for coronary artery disease and many other complications such as myocardial infarction and sudden death[5]. It is also associated with increased blood pressure, systemic vascular resistance, and heart rate[5].  Nicotine is one factor that stimulates epinephrine and norepinephrine release from the sympathetic nerve terminals and adrenal glands, which explains that acute cardiovascular effects may be due to adrenergic stimulation at the peripheral levels[5]. Acute cigarette smoking is associated with a significant decrease in vagal cardiac modulations which may increase the risk of complications during daily exercise or intense physical activity[5]. Acute smoking affects the cardiorespiratory responses to both submaximal and maximal exercise, which can result in an increase of sympathetic dominance at lower levels of submaximal work[5]. Clinicians should be considerate of all options and treatment plans for patients who are avid smokers.

Smoking has not only been shown to be associated with an increase in resting heart rate (HR), but also with a significantly diminished increase in HR during exercise (known as chronotropic incompetence)[6][7]. Chronotropic incompetence (CI) prevents the heart from beikeep up with increased demand during activity,and leads to progressive deterioration in exercise tolerance.  As CI worsens through habitual smoking over time, it can move beyond exercise tolerance to affect basic functional activities of daily living. CI caused by smoking has traditionally been observed in middle-aged and older adults, however a more recent study of male and female young adults (20-29 yrs) found that smokers had a significantly lower maximal HR and a significantly slower HR increase during exercise testing when compared to non-smokers[8].

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Some of the most commonly known effects of smoking are those related to the respiratory system. Smoking blocks airway passages and has significant detrimental effects on lung tissue and the lungs ability to operate at full strength. Research has shown that even second-hand smoke can have harmful effects on the lungs. During submax and maximal intensity exercise, individuals showed a significant difference in average and maximum power output of the lungs, as well as decreased average and maximum oxygen consumption following exposure to second-hand smoke[9][10]. With the lungs functioning at a lower level individuals will become exhausted more quickly during exercise and report an increased perceived exertion following exercise[9][10]. Research has also shown second-hand smoke can have significant effects at the alveolar and capillary level of the lungs by influencing the exchange of oxygen and carbon dioxide resulting in the respiratory exchange ratio elevating and eventually plateauing for up to three hours following exercise[10]. Therefore, the body is having to rely more heavily on anaerobic metoblism processes during exercise. This further supports the statement in the Cardiovascular Effects section regarding the effect of smoking on the ability of the oxidative energy system. While this information is based on second-hand smoke, an indirect or secondary source, one can imagine the magnitude in which these effects would multiply when the lungs are exposed to direct smoking.

Research looking at direct exposure to smoking has shown that moderate and heavy smokers have a decreased VO2max. There tends to be a stronger correlation in men, and the decrease in VO2max caused by smoking becomes more significant with age[11]. Furthermore, smoking just prior to exercise results in less oxygen availability at the tissue level[12].

Musculoskeletal Effects[edit | edit source]

Smoking has also been found to have a negative effect on bone mineral density which is directly related to osteoporotic fracture[13]. Smokers do not absorb supplemental or dietary calcium as well as non-smokers. Studies show that smokers on average have 20mg/day less calcium available than non-smokers. The full reason in which calcium absorption is decreased is still unclear, but one explanation is that smoking damages intestinal villi which is a major component in digestion and absorption of nutrients[13]. The decreased ability to absorb calcium leading to decreased bone mineral density increases the risk of osteoporotic fracture with exercise.

The use of cigarettes and other tobacco products has also been found to be a contributing factor to age-related muscle atrophy, which is known as sarcopenia. When compared to non-smokers of similar backgrounds those who did smoke had evidence of increased muscle tissue deterioration[14]. Type I fibers are specifically affected which would limit muscular endurance[15]. The use of tobacco products can also cause excessive amounts of adipose tissue catabolism during and after exercise. This can also lead to muscle tissue wasting in those who are nutritionally deficient. Researchers believe that this is a cause for a condition known as cachexia, condition usually seen in patients with cancer or congestive heart failure [15], in which the patient loses muscle mass uncharacteristic to aging. 

This loss of muscle mass can lead to less productivity during exercise in regards to energy output and respiration efficiency. Upper extremity muscles also serve as muscles of respiration, which should be taken into consideration while working to condition patients who are heavy smokers. A controlled trial used upper body resistance exercises to study their effects on breathing among a sample of sedentary male smokers. There was, in fact, a significant effect on forced expiration and forced vital capacity within the exercise group [16]. Clearly, smoking impacts multiple systems of the body. It is important to be aware of the interconnectedness to make improvements, such as strengthening upper extremity muscles that have been weakened due to smoking. As a result, controlled respiration can also be improved thus increasing rehabilitation productivity, exercise tolerance, and overall health.

Decrease in Exercise as Nicotine Dependence Increases[edit | edit source]

Smoking can also decrease the amount a person exercises. In a study done by Loprinzi and Walker, the variables of nicotine dependence and the amount of exercise per day were compared. They further divided the participants to account for other variables including age, gender, race, and several others. Through data analyses, this study found that there was a positive correlation between higher levels of nicotine dependence and sedentary behavior in participants 50 years of age or older. The study also found that older participants were more dependent on nicotine. [17] Individuals who smoke may exercise less and may require more motivation to participate in a more active lifestyle.

Alternative Sources of Nicotine and Their Effects on Exercise[edit | edit source]

While smoking can create adverse health issues for individuals, an athlete may be prone to the use of smokeless forms of nicotine to help with exercise performance. [18] Through smokeless forms of nicotine use, an individual may be able to obtain a greater concentration of nicotine, while being able to avoid the inhalation of harmful smoke. [18] It has been shown that nicotine has the ability to increase blood flow in muscles, as well as increase the breakdown of lipids during exercise. [19][20] This is due to "enhanced circulating levels of norepinephrine and epinephrine as well as direct action on nicotinic cholinergic receptors in adipose tissue." [20] In addition, studies have shown that nicotine use can improve cognitive function, such as "learning and memory, reaction time, and fine motor abilities." [18] Nicotine has also been found to aid in pain tolerance, which athletes could find beneficial if they participate in contact sports. [21] While nicotine has been shown to provide an ergogenic effect on exercise performance, it is still a highly addictive drug which can result in withdrawal symptoms affecting motor skills for individuals that abstain from nicotine for a short period of time. [18]

Individuals seeking nicotine without the added chemicals found in tobacco may turn to electronic cigarettes (ECIGS). ECIGS have become a popular alternative to traditional tobacco cigarettes since 2007. While most research regarding the long-term effects of ECIGS is still in infancy, several studies address ECIGS as a viable step in smoking cessation and note the reduction in negative health effects. A longitudinal study conducted over the duration of a year by Etter (2014) reported on two groups, those who just use ECIGS (vape) and those who vape and smoke traditional cigarettes. Use among the vape only group did not increase over time, while almost half of the dual users were able to quit smoking traditional cigarettes. While ECIGS may be a safer alternative to traditional cigarettes, it is important to note the specific differences and similarities between the two as they relate to exercise. [22] A study by Yan (2015) investigated nicotine intake and the acute effects of ECIGS on heart rate and blood pressure, in direct comparison to traditional tobacco use. They found that participants using ECIGS had significantly lower blood plasma levels after 30 minutes of controlled use, followed by one hour of free use. The ECIG users showed consistent levels of exhaled CO levels, heart rate, and blood pressure versus the magnified levels displayed by smokers. [23] These findings suggest ECIG users do not need to receive the same precautions as traditional smokers in regards to exercise prescription.

Exercise has been shown to reduce cravings to smoke. Roberts et al. (2015) found that vigorous exercise can drastically reduce the cravings for nicotine. The researchers believe this is due to the release of noradrenaline and cortisol. However, it is important to note that light to moderate exercise does not appear to reduce cravings for nicotine. [24] While exercise does not completely get rid of the desire to smoke, it can be a healthy and more affordable alternative to the use of other products that also help people quit smoking. A therapist should encourage patients to adopt an exercise regimen if they mention that they are trying to quit smoking. Additionally, a therapist should be able to provide the patient with an exercise plan if they request one. 

References[edit | edit source]

  1. ↑ "Tobacco Fact sheet N°339". May 2014. Retrieved 13 May 2015.
  2. ↑ Vollaard, NB, Shearman, JP, Cooper, CE. Exercise-induced oxidative stress. Sports Med 2005;35:1045-62.
  3. ↑ Garbin U, Pasini AF, Stranieri C, Cominacini M, Pasini A, Manfro S, et al. Cigarette smoking blocks the protective expression of Nrf2/ARE pathway in peripheral mononuclear cells of young heavy smokers favoring inflammation. PLoS ONE 2009;4:1-12.
  4. ↑ Barreiro E, Peinado VI, Galdiz JB, Ferrer E, Marin-Corral J, Sanchez F, et al. Cigarette smoking-induced oxidative stress: A role in chronic obstructive pulmonary disease skeletal muscle dysfunction. Am J Resp Crit Care Med 2010;182:477-88.
  5. ↑ 5.0 5.1 5.2 5.3 5.4 Fernhall B, Mendonca G, Pereira F. Effects of cigarette smoking on cardiac autonomic function during dynamic exercise. J Sport Sci 2011;29:879-86
  6. ↑ Benowitz NL. Cigarette smoking and cardiovascular disease: pathophysiology and implications for treatment. Prog Cardiovasc Dis. 2003;46:91-111.
  7. ↑ Srivastava R, Blackstone EH, Lauer MS. Association of smoking with abnormal exercise heart rate responses and long-term prognosis in a healthy, population-based cohort. Am J Med. 2000;109:20-6.
  8. ↑ Papathanasiou G, Georgakopoulos D, Papageorgiou E, Zerva E, Michalis L, Kalfakakou V, et al. Effects of smoking on heart rate at rest and during exercise, and on heart rate recovery, in young adults. Hellenic J Cardiol 2013;54:168-77.
  9. ↑ 9.0 9.1 Flouris AD, Metsios GS, Carrillo AE, Jamurtas AZ, Stivaktakis PD, Tzatzarakis MN, et al. Respiratory and immune response to maximal physical exertion following exposure to secondhand smoke in healthy adults. Plos One. 2012;7(2):e31880-e. PubMed PMID: 22355401 (accessed 4 Dec 2015).
  10. ↑ 10.0 10.1 10.2 Flouris AD, Metsios GS, Jamurtas AZ, Koutedakis Y. Cardiorespiratory and immune response to physical activity following exposure to a typical smoking environment. Heart. 2010 June 1, 2010;96(11):860-4. (accessed 4 Dec 2015).
  11. ↑ Cite error: Invalid <ref> tag; no text was provided for refs named Bernaards et al
  12. ↑ Cite error: Invalid <ref> tag; no text was provided for refs named Hansen et al
  13. ↑ 13.0 13.1 Krall EA, Dawson-Hughes B. Smoking increases bone loss and decreases intestinal calcium absorption. J Bone Miner Res 1999;14:215–20. doi: 10.1359/jbmr.1999.14.2.215
  14. ↑ Rom O, Kaisari S, Aizenbud D, Reznick A. Identification of possible cigarette smoke constituents responsible for muscle catabolism. J Muscle R and Cell Motility 2012;33(3):199-208. doi:10.1007/s10974-012-9299-4
  15. ↑ 15.0 15.1 Ide H, Tabira K. Changes in sympathetic nervous system activity in male smokers after moderate-intensity exercise. Respiratory Care 2013; 58:1892-98
  16. ↑ Singh VP, Jani H, John V, Singh P, Joseley T. Effects of upper body resistance training on pulmonary functions in sedentary male smokers. Lung India : Official Organ of Indian Chest Society 2011:28(3);169–73. doi: 10.4103/0970-2113.83971
  17. ↑ Loprinzi PD, Walker JF. Nicotine dependence, physical activity, and sedentary behavior among adult smokers. North American Journal of Medical Sciences 2015:7(3);94-9. doi: 10.4103/1947-2714.153920
  18. ↑ 18.0 18.1 18.2 18.3 Pesta DH, Angadi SS, Burtscher M, Roberts CK. The effects of caffeine, nicotine, ethanol, and tetrahydrocannabinol on exercise performance. Nutr Metabol 2013;10:71.
  19. ↑ Weber F, Anlauf M, Muller RD. Changes in muscle blood flow after smoking a cigarette determined by a new noninvasive method. Eur J Clin Pharmacol. 1989;37(5):517-20.
  20. ↑ 20.0 20.1 Andersson K, Arner P. Systemic nicotine stimulates human adipose tissue lipolysis through local cholinergic and catecholaminergic receptors. Int J Obes Relat Metab Disord : journal of the International Association for the Study of Obesity. 2001;25(8):1225-32.
  21. ↑ Jamner LD, Girdler SS, Shapiro D, Jarvik ME. Pain inhibition, nicotine, and gender. Exp Clin Psychopharm. 1998;6(1):96-106.
  22. ↑ Etter. A longitudinal study of electronic cigarette users. Addict Behav. 2014;39(2):491.
  23. ↑ Yan. Effects of using electronic cigarettes on nicotine delivery and cardiovascular function in comparison with regular cigarettes. Regul Toxicol Pharm. 2015;71(1):24.
  24. ↑ Roberts V, Gant N, Sollers JJ, Bullen C, Jiang Y, Maddison R. Effects of exercise on the desire to smoke and physiological responses to temporary smoking abstinence: a crossover trial. Psychopharmacology, 2015;232:1071-81. doi: 10.1007/s00213-014-3742-8


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