Smoking??
- Thread starter urafreak
- Start date
The Terminator
New member
Cigarette smoking??? Are you looking for some justification to continue smoking, because you aren't going to find it here...
BUFFDAWG10
Rookie
That shit is nasty!!! If you quit smoking you sure will be able to train harder in the gym!
Interesting topic. I always wondered if many bodybuilders, amateur or pro, ever smoked cigarettes. Especially since lifting weights is an anaerobic rather than aerobic activity. Don't get me wrong; I sure don't recommend it. When I was in the Army, though, I saw lots of guys go straight from the gym to the bar, where they not only smoked cigarettes but sucked down shots and beers to recover from their workouts. Ouch.
Last edited:
StoneColdNTO
Administrator
But.........
.......Oh never mind...............you guys are talking about cigarettes
.........
.......Oh never mind...............you guys are talking about cigarettes
.........
hhajdo
Community Veteran
Smoking Impairs Muscle Recovery from Exercise.
Price TB, Krishnan-Sarin S, Rothman DL.
Department of Diagnostic Radiology, Yale University School of Medicine, New Haven, CT, USA.
Cigarette smoking is a leading cause of many adverse health consequences. Chronic nicotine exposure leads to insulin resistance, and may increase the risk of developing non-insulin-dependent diabetes mellitus (NIDDM) in young otherwise healthy smokers. To evaluate smoking-induced effects on carbohydate metabolism, we studied muscle glycogen recovery from exercise in a young healthy population of smokers. The study used (31)P/(13)C nuclear magnetic resonance (NMR) spectroscopy to compare muscle glycogen and glucose-6-phosphate levels during recovery in exercised gastrocnemius muscles of randomized cohorts of healthy male smokers and controls [C]. Data for the two groups were: smokers (>/=20 cigarettes/day, n=8, 24+/-2y, 173+/-3cm, 70+/-4kg) and age/weight matched non-smoking controls [C] (n=10, 23+/-1y, 175+/-3cm, 67+/-3kg). Subjects performed single-leg toe-raises to deplete glycogen to ~20mmol/l, and glycogen re-synthesis was measured during the first 4hrs of recovery. Plasma samples were assayed for glucose and insulin at rest and during recovery. Test subjects were recruited from the general community surrounding Yale University. Glycogen was depleted to similar levels in the two groups (23.5+/-1.2mmol/l, S and 19.1+/-1.3mmol.l, C). During the first hour of recovery glycogen synthesis rates were similar (13.8+/-1.1mmol/l-hr, S and 15.3+/-1.3 mmol/l-hr, C). Between hours 1 and 4 glycogen synthesis was impaired in smokers (0.8+/-0.2 mmol/l-hr, S and 4.5+/-0.5 mmol/l-hr, C, p=0.0002) compared with controls. Glucose-6-phosphate was reduced in smokers during hours 1-4 (0.105+/-0.006mmol/l, S and 0.217+/-0.019 mmol/l, C, p=0.0212). We conclude that cigarette smoking impairs the insulin dependent portion of muscle recovery from glycogen depleting exercise. This impairment likely results from a reduction in glucose uptake.
---------------------------------------
Nuklearmedizin 1980;19(5):239-43 Related Articles, Links
Effect of smoking on the central circulation at rest and during exercise as studied by radiocardiography.
Timisjarvi J, Kuikka J, Hirvonen L, Kettunen R, Koskinen M, Kari-Koskinen O, Tuominen M.
The pulmonary vessels are the first target of tobacco smoke in the circulatory system, but the functional changes occurring in the pulmonary circulation are poorly understood. Hence 46 volunteers were studied by radiocardiography under the following conditions: 1. At rest before and after smoking 2 cigarettes (15 men); 2. After repeated ergometer exercise (5 min, 100 W) with and without smoking (13 men); and 3. Control experiments under the corresponding conditions without smoking (18 subjects). A significant increase occurred in heart rate, cardiac output and systolic arterial blood pressure after smoking when at rest, but an almost significant decrease in pulmonary dispersion volume , whereas the heart rate and pulmonary capillary pressure attained significantly higher values after than before smoking in the exercise tests, with a significant decrease observed in stroke volume, pulmonary blood volume and pulmonary dispersion volume. It is concluded that smoking impairs physical performance, increases pulmonary capillary pressure and reduces pulmonary blood volume and probably the number of open capillaries.
-----------------------------------------
J Intern Med 1993 Apr;233(4):327-32 Related Articles, Links
Smoking induces insulin resistance--a potential link with the insulin resistance syndrome.
Attvall S, Fowelin J, Lager I, Von Schenck H, Smith U.
Department of Medicine, University of Goteborg, Sahlgren's Hospital, Sweden.
OBJECTIVES. The acute effect of smoking and snuffing on insulin sensitivity was studied in a group of healthy habitual smokers. DESIGN. The euglycaemic clamp technique was combined with the subcutaneous injection of a bolus (0.1 U kg-1) of fast-acting insulin (Actrapid). Randomized subjects smoked either one cigarette per hour for 6 h, took one bag-packed snuff per hour for 6 h or refrained from nicotine for 48 h before as well as during the clamp. SUBJECTS. Seven healthy smokers, four females and three males, of normal weight (BMI, mean +/- SEM, 21 +/- 0.7 kg m-2 with a range of 18.6-23.9), aged 31 +/- 2 years (range 24-35 years), who had consumed at least 20 cigarettes per day for at least 5 years were studied. They were recruited through an advertisement in a newspaper. RESULTS. The steady-state plasma nicotine levels were similar during smoking and snuffing. The insulin and glucose levels were also similar during all three clamps. Smoking, but not snuffing, impaired insulin action (P < 0.05) mainly due to a lower peripheral glucose uptake. The mean growth hormone levels during the 6-h study were more than doubled during smoking (P < 0.01) while no significant differences were seen in the other counter-regulatory hormones. CONCLUSION. Smoking (also in habitual smokers) acutely impairs insulin action and leads to insulin resistance. Thus, smoking can be of importance for the development of the insulin resistance syndrome associated with risk for cardiovascular disease.
---------------------------------------------
Diabetes Care 1996 Feb;19(2):112-8 Related Articles, Links
Acute effect of cigarette smoking on glucose tolerance and other cardiovascular risk factors.
Frati AC, Iniestra F, Ariza CR.
Department of Internal Medicine, Hospital de Especialidades del Centro Medico La Raza, Mexico City, Mexico.
OBJECTIVE: To investigate the acute effect of cigarette smoking on glucose tolerance, insulin sensitivity, serum lipids, blood pressure, and heart rate. RESEARCH DESIGN AND METHODS: This nonrandomized experimental control trial in a tertiary care center included 20 healthy chronic smokers and 20 age-, sex-, and BMI-matched healthy volunteers. Two oral glucose tolerance tests (OGTTs) were performed on each subject. Three cigarettes were smoked during the first 30 min in one of the tests. Serum glucose, insulin, and C-peptide levels were measured every 30 min; the area under the curve (AUC) and the insulin sensitivity index (ISI) were calculated; serum total cholesterol, LDL cholesterol, HDL cholesterol, and triglyceride levels were measured at 0 and 180 min; and blood pressure and heart rate were recorded every 5 min throughout 180 min. RESULTS: Smoking acutely impaired glucose tolerance: the AUC for glucose in smokers was 25.5 +/- 1.03 mmol/l (mean +/- SE) (95% CI 22.9-28) during the smoking OGTT and 21.8 +/- 0.85 mmol/l (CI 19.2-24.3) in the control OGTT (P < 0.01); in nonsmokers, it was 19.7 +/- 0.3 mmol/l (CI 18.8-20.5) in the smoking OGTT and 18.7 +/- 0.35 mmol/l (CI 17.8-19.5) in the control OGTT (P < 0.05). Smoking acutely increased serum insulin and C-peptide levels and decreased ISI only in smokers: ISI in smokers was 55 +/- 2.8 (CI 47.4-62.6) in the control OGTT and 43 +/- 2.7 (CI 35.4-50.6) in the smoking OGTT (P < 0.05). Smoking acutely caused a rise of serum total cholesterol levels in both groups and increased LDL cholesterol and triglyceride serum levels significantly only in smokers (P < 0.05). A significant rise of blood pressure and heart rate while smoking was present in all the subjects. CONCLUSIONS: Smoking acutely impaired glucose tolerance and insulin sensitivity, enhanced serum cholesterol and triglyceride levels, and raised blood pressure and heart rate. These findings support the pathogenetic role of cigarette smoking on cardiovascular risk factors.
---------------------------------------------
Insulin resistance and cigarette smoking.
Facchini FS, Hollenbeck CB, Jeppesen J, Chen YD, Reaven GM.
Department of Medicine, Stanford University School of Medicine, California.
Cigarette smoking is associated with increases in plasma triglycerides and decreases in plasma high density-lipoprotein-cholesterol concentration. These changes not only increase risk of coronary heart disease but also are secondary to resistance to insulin-stimulated glucose uptake or hyperinsulinaemia. To see whether there is a relation between cigarette smoking and insulin-mediated glucose uptake we measured plasma lipid and lipoprotein concentrations, plasma glucose and insulin response to an oral glucose challenge, and insulin-mediated glucose uptake in 40 matched healthy volunteers (20 non-smokers, 20 smokers). Smokers had significantly higher mean (SEM) very-low-density-lipoprotein triglycerides (0.66 [0.10] vs 0.39 [0.03] mmol/l, p less than 0.02) and cholesterol (0.45 [0.06] vs 0.23 [0.04] mmol/l, p less than 0.005) concentrations and lower high-density-lipoprotein cholesterol concentrations (1.16 [0.05] vs 1.51 [0.08] mmol/l, p less than 0.001). Although plasma glucose concentrations in response to the oral glucose load were similar in the two groups, plasma insulin response of the smokers was significantly higher (p less than 0.001). Finally, smokers had higher steady-state plasma glucose concentrations in response to a continuous infusion of glucose, insulin, and somatostatin (8.4 [0.2] vs 5.0 [0.3] mmol/l, p less than 0.001), despite similar steady-state plasma insulin concentrations. The findings show that chronic cigarette smokers are insulin resistant, hyperinsulinaemic, and dyslipidaemic compared with a matched group of non-smokers, and may help to explain why smoking increases risk of coronary heart disease.
---------------------------------------
Primary and secondary prevention of coronary heart disease: smoking]
[Article in German]
Meinertz T, Heitzer T.
Abteilung fur Kardiologie Universitatsklinikum Hamburg-Eppendorf Martinistrasse 52 20246 Hamburg, Germany. meinertz@uke.uni-hamburg.de
Although smoking is one of the major risk factors for the development of atherosclerosis, the exact mechanism of smoking-related vascular disease is not known. Smoking causes acute hemodynamic alterations such as increase in heart rate, systemic and coronary vascular resistance, myocardial contractility, and myocardial oxygen demand. These short-term effects could lower the ischemic threshold in smokers with coronary artery disease and contribute to the increased risk for acute cardiovascular events. Endothelial damage is thought to be an initiating event in atherosclerosis and early studies have demonstrated that long-term smoking has direct toxic effects with structural changes of human endothelial cells. Recent research has shown the importance of the functional role of the endothelium in regulating normal vascular tone, platelet-endothelial interactions, leukocyte adhesion and smooth muscle cell proliferation via synthesis and release of a variety of substances such as nitric oxide. There is strong evidence that smoking leads to endothelial dysfunction in both conductance and resistance vessels. This effect seems to be dose-related and reversible. The mechanism of endothelial dysfunction in smokers is not known, but increased degradation of nitric oxide by oxygen-derived free radicals has been suggested. In addition, smoking could cause oxidative inactivation of tetrahydrobiopterin, a critical cofactor of nitric oxide, leading to an uncoupling of the endothelial nitric oxide synthase with increased superoxide production and decreased nitric oxide bioactivity. Other pro-atherosclerotic effects of smoking are discussed. Given the enormous health hazard of tobacco use, complete abstinence from smoking should be achieved. Smoking cessation counseling should be given to healthy subjects and even more vigorously to patients with manifested disease. Every effort should be undertaken to prevent children and adolescents from starting to smoke. Brief tobacco dependence treatment is effective, and every tobacco user should be offered at least brief treatment at every office visit. More intensive treatment is more effective in producing long-term abstinence from tobacco. Nicotine replacement therapy (nicotine patches or gum), clinician-delivered social support, and skills training are the three most effective components of smoking cessation treatment.
Price TB, Krishnan-Sarin S, Rothman DL.
Department of Diagnostic Radiology, Yale University School of Medicine, New Haven, CT, USA.
Cigarette smoking is a leading cause of many adverse health consequences. Chronic nicotine exposure leads to insulin resistance, and may increase the risk of developing non-insulin-dependent diabetes mellitus (NIDDM) in young otherwise healthy smokers. To evaluate smoking-induced effects on carbohydate metabolism, we studied muscle glycogen recovery from exercise in a young healthy population of smokers. The study used (31)P/(13)C nuclear magnetic resonance (NMR) spectroscopy to compare muscle glycogen and glucose-6-phosphate levels during recovery in exercised gastrocnemius muscles of randomized cohorts of healthy male smokers
---------------------------------------
Nuklearmedizin 1980;19(5):239-43 Related Articles, Links
Effect of smoking on the central circulation at rest and during exercise as studied by radiocardiography.
Timisjarvi J, Kuikka J, Hirvonen L, Kettunen R, Koskinen M, Kari-Koskinen O, Tuominen M.
The pulmonary vessels are the first target of tobacco smoke in the circulatory system, but the functional changes occurring in the pulmonary circulation are poorly understood. Hence 46 volunteers were studied by radiocardiography under the following conditions: 1. At rest before and after smoking 2 cigarettes (15 men); 2. After repeated ergometer exercise (5 min, 100 W) with and without smoking (13 men); and 3. Control experiments under the corresponding conditions without smoking (18 subjects). A significant increase occurred in heart rate, cardiac output and systolic arterial blood pressure after smoking when at rest, but an almost significant decrease in pulmonary dispersion volume , whereas the heart rate and pulmonary capillary pressure attained significantly higher values after than before smoking in the exercise tests, with a significant decrease observed in stroke volume, pulmonary blood volume and pulmonary dispersion volume. It is concluded that smoking impairs physical performance, increases pulmonary capillary pressure and reduces pulmonary blood volume and probably the number of open capillaries.
-----------------------------------------
J Intern Med 1993 Apr;233(4):327-32 Related Articles, Links
Smoking induces insulin resistance--a potential link with the insulin resistance syndrome.
Attvall S, Fowelin J, Lager I, Von Schenck H, Smith U.
Department of Medicine, University of Goteborg, Sahlgren's Hospital, Sweden.
OBJECTIVES. The acute effect of smoking and snuffing on insulin sensitivity was studied in a group of healthy habitual smokers. DESIGN. The euglycaemic clamp technique was combined with the subcutaneous injection of a bolus (0.1 U kg-1) of fast-acting insulin (Actrapid). Randomized subjects smoked either one cigarette per hour for 6 h, took one bag-packed snuff per hour for 6 h or refrained from nicotine for 48 h before as well as during the clamp. SUBJECTS. Seven healthy smokers, four females and three males, of normal weight (BMI, mean +/- SEM, 21 +/- 0.7 kg m-2 with a range of 18.6-23.9), aged 31 +/- 2 years (range 24-35 years), who had consumed at least 20 cigarettes per day for at least 5 years were studied. They were recruited through an advertisement in a newspaper. RESULTS. The steady-state plasma nicotine levels were similar during smoking and snuffing. The insulin and glucose levels were also similar during all three clamps. Smoking, but not snuffing, impaired insulin action (P < 0.05) mainly due to a lower peripheral glucose uptake. The mean growth hormone levels during the 6-h study were more than doubled during smoking (P < 0.01) while no significant differences were seen in the other counter-regulatory hormones. CONCLUSION. Smoking (also in habitual smokers) acutely impairs insulin action and leads to insulin resistance. Thus, smoking can be of importance for the development of the insulin resistance syndrome associated with risk for cardiovascular disease.
---------------------------------------------
Diabetes Care 1996 Feb;19(2):112-8 Related Articles, Links
Acute effect of cigarette smoking on glucose tolerance and other cardiovascular risk factors.
Frati AC, Iniestra F, Ariza CR.
Department of Internal Medicine, Hospital de Especialidades del Centro Medico La Raza, Mexico City, Mexico.
OBJECTIVE: To investigate the acute effect of cigarette smoking on glucose tolerance, insulin sensitivity, serum lipids, blood pressure, and heart rate. RESEARCH DESIGN AND METHODS: This nonrandomized experimental control trial in a tertiary care center included 20 healthy chronic smokers and 20 age-, sex-, and BMI-matched healthy volunteers. Two oral glucose tolerance tests (OGTTs) were performed on each subject. Three cigarettes were smoked during the first 30 min in one of the tests. Serum glucose, insulin, and C-peptide levels were measured every 30 min; the area under the curve (AUC) and the insulin sensitivity index (ISI) were calculated; serum total cholesterol, LDL cholesterol, HDL cholesterol, and triglyceride levels were measured at 0 and 180 min; and blood pressure and heart rate were recorded every 5 min throughout 180 min. RESULTS: Smoking acutely impaired glucose tolerance: the AUC for glucose in smokers was 25.5 +/- 1.03 mmol/l (mean +/- SE) (95% CI 22.9-28) during the smoking OGTT and 21.8 +/- 0.85 mmol/l (CI 19.2-24.3) in the control OGTT (P < 0.01); in nonsmokers, it was 19.7 +/- 0.3 mmol/l (CI 18.8-20.5) in the smoking OGTT and 18.7 +/- 0.35 mmol/l (CI 17.8-19.5) in the control OGTT (P < 0.05). Smoking acutely increased serum insulin and C-peptide levels and decreased ISI only in smokers: ISI in smokers was 55 +/- 2.8 (CI 47.4-62.6) in the control OGTT and 43 +/- 2.7 (CI 35.4-50.6) in the smoking OGTT (P < 0.05). Smoking acutely caused a rise of serum total cholesterol levels in both groups and increased LDL cholesterol and triglyceride serum levels significantly only in smokers (P < 0.05). A significant rise of blood pressure and heart rate while smoking was present in all the subjects. CONCLUSIONS: Smoking acutely impaired glucose tolerance and insulin sensitivity, enhanced serum cholesterol and triglyceride levels, and raised blood pressure and heart rate. These findings support the pathogenetic role of cigarette smoking on cardiovascular risk factors.
---------------------------------------------
Insulin resistance and cigarette smoking.
Facchini FS, Hollenbeck CB, Jeppesen J, Chen YD, Reaven GM.
Department of Medicine, Stanford University School of Medicine, California.
Cigarette smoking is associated with increases in plasma triglycerides and decreases in plasma high density-lipoprotein-cholesterol concentration. These changes not only increase risk of coronary heart disease but also are secondary to resistance to insulin-stimulated glucose uptake or hyperinsulinaemia. To see whether there is a relation between cigarette smoking and insulin-mediated glucose uptake we measured plasma lipid and lipoprotein concentrations, plasma glucose and insulin response to an oral glucose challenge, and insulin-mediated glucose uptake in 40 matched healthy volunteers (20 non-smokers, 20 smokers). Smokers had significantly higher mean (SEM) very-low-density-lipoprotein triglycerides (0.66 [0.10] vs 0.39 [0.03] mmol/l, p less than 0.02) and cholesterol (0.45 [0.06] vs 0.23 [0.04] mmol/l, p less than 0.005) concentrations and lower high-density-lipoprotein cholesterol concentrations (1.16 [0.05] vs 1.51 [0.08] mmol/l, p less than 0.001). Although plasma glucose concentrations in response to the oral glucose load were similar in the two groups, plasma insulin response of the smokers was significantly higher (p less than 0.001). Finally, smokers had higher steady-state plasma glucose concentrations in response to a continuous infusion of glucose, insulin, and somatostatin (8.4 [0.2] vs 5.0 [0.3] mmol/l, p less than 0.001), despite similar steady-state plasma insulin concentrations. The findings show that chronic cigarette smokers are insulin resistant, hyperinsulinaemic, and dyslipidaemic compared with a matched group of non-smokers, and may help to explain why smoking increases risk of coronary heart disease.
---------------------------------------
Primary and secondary prevention of coronary heart disease: smoking]
[Article in German]
Meinertz T, Heitzer T.
Abteilung fur Kardiologie Universitatsklinikum Hamburg-Eppendorf Martinistrasse 52 20246 Hamburg, Germany. meinertz@uke.uni-hamburg.de
Although smoking is one of the major risk factors for the development of atherosclerosis, the exact mechanism of smoking-related vascular disease is not known. Smoking causes acute hemodynamic alterations such as increase in heart rate, systemic and coronary vascular resistance, myocardial contractility, and myocardial oxygen demand. These short-term effects could lower the ischemic threshold in smokers with coronary artery disease and contribute to the increased risk for acute cardiovascular events. Endothelial damage is thought to be an initiating event in atherosclerosis and early studies have demonstrated that long-term smoking has direct toxic effects with structural changes of human endothelial cells. Recent research has shown the importance of the functional role of the endothelium in regulating normal vascular tone, platelet-endothelial interactions, leukocyte adhesion and smooth muscle cell proliferation via synthesis and release of a variety of substances such as nitric oxide. There is strong evidence that smoking leads to endothelial dysfunction in both conductance and resistance vessels. This effect seems to be dose-related and reversible. The mechanism of endothelial dysfunction in smokers is not known, but increased degradation of nitric oxide by oxygen-derived free radicals has been suggested. In addition, smoking could cause oxidative inactivation of tetrahydrobiopterin, a critical cofactor of nitric oxide, leading to an uncoupling of the endothelial nitric oxide synthase with increased superoxide production and decreased nitric oxide bioactivity. Other pro-atherosclerotic effects of smoking are discussed. Given the enormous health hazard of tobacco use, complete abstinence from smoking should be achieved. Smoking cessation counseling should be given to healthy subjects and even more vigorously to patients with manifested disease. Every effort should be undertaken to prevent children and adolescents from starting to smoke. Brief tobacco dependence treatment is effective, and every tobacco user should be offered at least brief treatment at every office visit. More intensive treatment is more effective in producing long-term abstinence from tobacco. Nicotine replacement therapy (nicotine patches or gum), clinician-delivered social support, and skills training are the three most effective components of smoking cessation treatment.
Last edited:
gorilla_boy
Special
Smoke-free 10 days and counting...
It's gotten MUCH easier.
It's gotten MUCH easier.
