Smoking and Exercise

 Aerobic exercise challenges the body's ability to supply and handle oxygen. For example, when performing high-intensity aerobic exercise, mitochondrial reactice oxygen species' (ROS) grow in number. ROS, is left unchecked, have have the ability to cause genetic mutations. However, several enzymes -- including superoxide dismutase -- are present to handle this oxidatve stress caused by ROS.The body responds to chronic aerobic exercise by enhancing its ability to cope with ROS. [1]

Smoking also induces an oxidative stress; however, smoking-induced oxidative stress also inhibits the body's abiltiy to cope by suppressing the genes responsible for antioxidant production.[2]  The net result of smoking-induced oxidative stress is vascular and arteriolar inflammation -- further impairing the oxygen-delivering capabilties of the body. <span class="fck_mw_ref" _fck_mw_customtag="true" _fck_mw_tagname="ref" name="Garbin" /> Clearly, by limiting oxygen delivery, cigarette smoking impairs the ability to generate energy through the oxidative energy system. However, literature also suggests that smoking impairs anaerobic energy provision by altering contractile proteins, creatine kinase, and other glycolytic enzymes.[3] With this in mind, therapists should be weary of setting unrealistic goals for patients who are smokers.

Smoking is a huge risk factor coronary artery disease and many other complications such as myocardial infarction and sudden death. [59]Smoking is one of the biggest cause of death in the world. Smoking is also associated with marked, acute, and increase in blood pressure, systemic vascular resistance, and heart rate. [59] 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. [59]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. [59]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 submaimal work.[59] 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).[4][5]  Chronotropic incompetence (CI) prevents the heart from being able to keep up with increased demand during activity and therefore reach the age-appropriate maximal HR.  Since an increase in HR is key to performing exercise for any significant amount of time, CI 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.[6]

Smoking has also been found to have a negative effect on bone mineral density which is directly related to osteporotic fracture. [60] Smokers do not absorb supplemental or dietary calcium as well as non-smokers. Studies show that smokers on average have 20mg/day less available calcium 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 [60] The decreased ability to absorb calcium is directly realted to bone mineral density. Decreased bone mineral density effects the ability to exercise because increased risk of osteoportoic fractures.

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. Studies have found that when compared to non-smokers of similar backgrounds those who did smoke had evidence of increased muscle tissue deterioriation[7].Some research has also found that the use of these products can 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[8]. Researchers believe that this is a cause for a condition known as cachexia, a syndrome in which the patient loses muscle mass uncharacteristic to aging. This metabolic condition is usually seen in patients with cancer or other issues such as congestive heart failure[9].

Smoking is an overall unhealthy habit and causes many of the physiological effects described above that can hinder exercise performance, but it 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 split up 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.[10] This information shows us that individuals who smoke may exercise less and may need to be encouraged to participate in a more active lifestyle.

References[edit | edit source]

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  1. Vollaard, NB, Shearman, JP, Cooper, CE Exercise-induced oxidative stress. Sports Med 2005; 35: 1045-1062
  2. 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 favouring inflammation. PLoS ONE 2009; 4: 1-12
  3. 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: 477-488
  4. Benowitz NL. Cigarette smoking and cardiovascular disease: pathophysiology and implications for treatment. Prog Cardiovasc Dis. 2003;46: 91-111.
  5. 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: 20-26.
  6. 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.
  7. Rom, O., Kaisari, S., Aizenbud, D., &amp;amp;amp;amp;amp;amp;amp;amp;amp; Reznick, A. (2012). Identification of possible cigarette smoke constituents responsible for muscle catabolism. Journal of Muscle Research and Cell Motility, 33(3), 199-208. doi:10.1007/s10974-012-9299-4
  8. Ide H, Tabira K. Changes in sympathetic nervous system activity in male smokers after moderate-intensity exercise. Respiratory Care 2013; 58:1892-98
  9. Ide H, Tabira K. Changes in sympathetic nervous system activity in male smokers after moderate-intensity exercise. Respiratory Care 2013; 58:1892-98
  10. Loprinzi, P. D., &amp;amp; Walker, J. F. (2015). Nicotine dependence, physical activity, and sedentary behavior among adult smokers. North American Journal of Medical Sciences, 7(3), 94-99. doi: 10.4103/1947-2714.153920