Effects of the transdermal nicotine patch on normalization of HDL-C and its subfractions.

BACKGROUND: Smoking reduces HDL-C and its subfractions, and smoking cessation leads to normalization of these lipoproteins. Nicotine replacement therapy is an important weapon employed by those attempting to quit smoking. This study examined the effects of the transdermal nicotine patch ("patch") on lipoproteins. METHODS: Ten male and 17 female smokers refrained from smoking for 77 days. The patch was utilized during the first 35 days and then removed for the remaining 42 days. Seven male and 9 female nonsmokers were controls. RESULTS: HDL-C, HDL(2)-C, and HDL(3)-C levels were significantly lower in smokers when compared with controls. These differences were sustained during the initial 35 days when using the patch. Over the following 42 days, however, these lipoproteins normalized to values similar to those of control subjects. Females who quit smoking gained 2.1 kg after the patch was removed. CONCLUSIONS: It was concluded that nicotine as administered by the transdermal nicotine patch inhibits normalization of HDL-C, HDL(2)-C, and HDL(3)-C in those who have quit smoking. Removal of the patch results in normalization of these lipoproteins. The patch appeared to prevent weight gain among female subjects.

The effect of smoking on energy expenditure and plasma catecholamine and nicotine levels during light physical activity.

A number of studies have found that cigarette smoking causes an acute increase in resting energy expenditure, but the effect on energy expenditure during light physical activity is less clear. Since both smoking and activity have been shown to increase plasma catecholamines, these could produce additive effects on energy expenditure when smoking during light physical activity. In this study, the impact of cigarette smoking on energy expenditure, cardiovascular function, plasma nicotine and plasma catecholamine levels was determined in adult male subjects at rest and while engaged in light physical activity. Smoking at rest resulted in a 3.6% increase in energy expenditure above the resting baseline; whereas the increase in energy expenditure caused by smoking during light physical activity (compared with the light physical activity baseline) was 6.3%. This increase during light physical activity was significantly greater than the increase observed at rest (p < 0.025). As expected, plasma nicotine increased with smoking during both rest and light physical activity. An increase in plasma nicotine was associated with smoking during light physical activity. When this increase was adjusted as a covariate, the difference in smoking-related energy expenditure between light physical activity and rest disappeared, suggesting nicotine accounts for the effect. Plasma epinephrine and norepinephrine levels increased with smoking and showed a significantly greater increase during light physical activity compared to rest. Cigarette smoking caused a significantly greater increase in heart rate during light physical activity than it did while at rest, but there was no significant effect of smoking on mean blood pressure. It was concluded that there is enhanced energy expenditure associated with cigarette smoking during light physical activity when compared with smoking at rest which could be due in part to smoking-induced increases in circulating plasma catecholamines and perhaps nicotine.

Smoking multiple high- versus low-nicotine cigarettes: impact on resting energy expenditure.

The thermic effect of smoking multiple cigarettes varying substantially in nicotine yield was investigated. Three treatments were imposed: nonsmoking at baseline, smoking six low-nicotine (0.8 mg nicotine) cigarettes (LOW), and smoking six high-nicotine (1.74 mg nicotine) cigarettes (HIGH). An initial increase of 6.8% in resting energy expenditure (REE) above baseline REE occurred after consumption of two consecutive cigarettes for both the HIGH and LOW treatments. With consumption of more cigarettes, the peak increase for the HIGH treatment was 9.3%, significantly greater than the peak of 5.9% for the LOW. Averaged over 2 hours, the HIGH treatment significantly increased REE by 6.9% and the LOW treatment significantly increased REE by 5.2%. Expired carbon monoxide (CO) measurements indicated that LOW cigarettes were smoked more aggressively than HIGH cigarettes. It was concluded that, initially, the nicotine yield of cigarettes is not an important influence on the thermic effect of smoking. But over a longer period and after multiple cigarettes, the nicotine yield may become an important influential factor.

Influence of worksite environmental tobacco smoke on serum lipoprotein profiles of female nonsmokers.

The purpose of this study was to examine the influence of environmental tobacco smoke (ETS) in the workplace on high-density lipoprotein cholesterol (HDL-C), HDL-C subfractions, and apolipoprotein (apo) A-I and apo B in female workers. Premenopausal women free from factors known to influence HDL-C (cigarette smoking, vigorous physical exercise, etc) who were not taking oral contraceptives, were moderate consumers of alcohol, caffeine, and dietary fat, and were between the ages of 21 and 50 years participated in one of two groups: (1) nonsmokers who had never smoked cigarettes and were generally free from ETS exposure (nonsmokers), and (2) nonsmokers who had never smoked but were subjected to concentrated doses of ETS at least 6 hours per day, 4 days per week, for at least 6 consecutive months (ETS-exposed). A third group consisting of current cigarette smokers who smoked a minimum of 20 cigarettes per day for at least the past 5 consecutive years served as smoking control (smokers). Subjects were matched by group as closely as possible with regard to criteria that can influence blood lipoprotein levels. Participants were solicited from taverns and restaurants where they were employed. It was hypothesized that individuals chronically exposed to ETS would demonstrate unfavorable lipoprotein profiles. Results showed that HDL-C, HDL2, and apo A-I were significantly (P < .05) depressed for ETS-exposed and smokers as compared with nonsmokers. Values for ETS-exposed were not different from those for smokers. Total cholesterol, triglycerides, HDL3, and apo B did not differ among the three groups. It was concluded that excessive exposure to ETS in female workers can have deleterious effects on HDL-C, HDL2, and apo A-I in nonsmokers that are similar to effects observed in cigarette smokers. It is possible that these effects increase coronary artery disease (CAD) risk.

Effect of caffeine and/or cigarette smoking on resting energy expenditure.

The thermic effect of cigarette smoking is dampened by the thermic effect of a meal, but potentiated by the thermic effect of exercise. The impact of the combined influences of caffeine and cigarette smoking is unknown. We examined the 3-h thermic response to smoking four 0.8 mg nicotine cigarettes, ingesting 200 mg of caffeine, or both, in ten fasted healthy men. Smoking four 0.8 mg nicotine cigarettes increased resting energy expenditure (REE) by 3.3% over a 3 h measurement period. Consumption of 200 mg of caffeine in the fasted condition increased REE of the smokers by 4.8% over 3 hours. Smoking four 0.8 mg cigarettes and ingesting 200 mg of caffeine significantly increased REE by 7.5% during the 3 h measurement period. At times early in the observation period, the combined thermic effect of cigarettes and caffeine was more than additive, but the effect was short-lived. A control group of nonsmokers was studied comparing REE following placebo or 200 mg of caffeine. Caffeine increased REE in the non-smoking controls 6.7%. This was not significantly different from results obtained on smokers. Fasted and non-smoking (baseline) REE was similar in smokers and non-smoking control subjects. It was concluded that the effects of caffeine on REE are additive.

Body fatness and smoking history predict the thermic effect of smoking in fasted men.

Epidemiological studies suggest that body composition and smoking history are related to degree of weight gain following smoking cessation. We hypothesized that body composition and smoking history affect the thermic effect of smoking (TES), which in turn would influence weight gain. Forty males ranging in age from 20 to 70 years smoked two cigarettes (0.8 mg nicotine yield) in 20 minutes, after which resting energy expenditure (REE) was measured during the next hour. The average change in REE (delta REE) was 4.97% (P < 0.0001), with a range of -2% to +14%. delta REE was greater than 1% in 35 subjects, less than 1% in three subjects, and reduced in two subjects. Body fatness was negatively correlated with delta REE (r = -0.68, r2 = 0.46). Multiple regression analysis indicated that body fatness (%) and pack-year history of smoking strongly predict delta REE (R = 0.82, R2 = 0.68; delta REE = 11.090-0.296 x %FAT-0.037 x pack-year). It was concluded that body fatness and smoking history substantially influence the thermic effect of smoking. In addition, this finding helps explain the wide range in TES which has been reported among subjects in many previous studies.

Potentiating effects of cigarette smoking and moderate exercise on the thermic effect of a meal.

The purposes of this study were: (i) to determine the relative thermic effects of smoking and exercise in fasted and postprandial states, and (ii) to determine whether there is a weight-controlling caloric advantage of moderate exercise in the postprandial state which might be used upon smoking cessation. The subjects were ten physically fit, young, male smokers. Twenty minutes of smoking (two cigarettes) while fasted resulted in a 6.0% (12.5 kcals/3h) increase in resting metabolic rate (RMR), and 20 minutes of walking (5.8 km/h) while fasted increased post-exercise RMR by 5.8% (11.7 kcals/3h). The thermic effect of a meal (TEM) (740 ml, 874 kcals) increased RMR 21.0% (42.3 kcals/3h), which was increased to 22.1% by smoking (45.0 kcals/3h). Exercise after a meal increased RMR 29.1% (58.1 kcals/3h). Post-prandial exercise potentiated the TEM, as the energy cost was 4.0 kcals/3h greater than the sum of the thermic effect of the meal plus the thermic effect of exercise in the fasted state. Postprandial exercise expended 112.2 kcals/20 min vs. 101.6 kcals/20 min for fasted exercise, a difference of 10.4%. The difference increased to 14.6% when the post-exercise thermic effect was included. It was concluded that the thermic effect of smoking and exercise were similar in the fasted state, but were substantially different postprandially. Moderate postprandial exercise appears to offer a substantial weight-controlling advantage when compared with fasted exercise.

Exercise and the elderly.

Data from cross-sectional studies suggest that VO2max declines in adulthood at a rate of 0.40-0.45 ml.kg-1.min-1 per year in males and 0.30 ml.kg-1.min-1 per year in females. Longitudinal studies suggest that the loss is much greater for males, approximating 1.0 ml.kg-1.min-1 per year or more. The rate of loss may be greater in sedentary compared to active individuals. The decline in VO2max with age appears to be inevitable, and a major contributing factor may be the decline in maximal cardiac output. A reduced maximal heart rate is a consistent finding, and this may be due to decreased end-organ sensitivity to catecholamines. Maximal stroke volume may or may not decrease, and physical training status may be a determining factor. The most recent evidence suggests increased dependence upon the Frank-Starling mechanism, resulting in an increased stroke volume to offset the decline in maximal heart rate. Cardiac output is thought to be maintained in this manner. Use of this mechanism may depend upon the absence of underlying disease. Therefore, investigators who vigorously screen potential subjects for occult coronary disease may report findings different from those who do not. Maximal a-vO2 difference may or may not decline in the elderly. The research is divided, and there is support for both beliefs. Several factors typical of the elderly, including a decline in muscle mass, increased blood distribution to the skin during exercise, and a potentially lower capillary/fiber ratio, would contribute to a lower a-vO2 difference. On the other hand, in those subjects with reduced cardiac output, there may be greater dependence upon a-vO2 difference during maximal exercise. Pulmonary function does not appear to limit VO2max, although the elderly may be less efficient while breathing during exercise. However, the higher ventilation and higher ventilatory equivalent for oxygen observed during submaximal exercise could be due to higher relative stress in the elderly. Elderly males and females are capable of demonstrating a training effect in response to endurance training regardless of previous physical activity patterns and current training status. The degree of change with training, expressed in relative terms, appears to be comparable to that demonstrated by younger subjects. Physiological factors contributing to an increased VO2max as a result of training appear to be similar in elderly and younger subjects, with the possible exception of no change in maximal a-vO2 difference in the elderly. This point is somewhat controversial.(ABSTRACT TRUNCATED AT 400 WORDS)

Intensity and energy cost of weighted walking vs. running for men and women.

The energy cost and intensity of exercise performed at 0% grade were determined for walking at 2, 3, and 4 mph, running at 5, 6, and 7 mph, and walking at 2, 3, and 4 mph with ankle and/or hand weights. Subjects were young moderately trained males (4) and females (3). The energy cost per kilogram of body weight was similar between sexes, and data were combined for among-treatment comparisons. Intensity of effort and energy cost per minute and per mile were increased when weight was added during walking and were increased more with hand weights compared with ankle weights regardless of speed. The average increase in O2 uptake (ml X kg-1 X min-1 X 100 g-1 of added wt) was 0.8% for ankle, 1.3% for hand, and 0.9% for ankle and hand weights. Gross energy cost per mile during weighted walking (120-158 kcal/mile) was comparable to and in some cases exceeded that of running which was independent of speed (120-130 kcal/mile). During nonweighted walking, the energy cost (kcal/mile) was significantly greater at 4 mph compared with 2 and 3 mph which did not differ. The intensity of walking at 4 mph with ankle and hand weights was comparable to running at 5 mph.

Effects of smoking cessation on weight gain, metabolic rate, caloric consumption, and blood lipids.

Thirteen sedentary adult females successfully quit smoking cigarettes for 48 days. Mean daily caloric consumption increased 227 kcal and mean weight gain was 2.2 kg. There were no measurable acute effects of smoke inhalation and no chronic net effects of smoking cessation on resting metabolic rate, as determined by oxygen consumption and respiratory exchange ratio. After 1 yr, subjects who continued to abstain gained an average of 8.2 kg. HDL-cholesterol increased 7 mg/dl in 48 days; however, this effect was lost in those who returned to smoking. Increased caloric consumption accounted for 69% of weight gained immediately following smoking cessation. Factors other than changes in caloric consumption and metabolic rate may be responsible for a significant proportion (31%) of the weight gained in individuals who quit smoking.

Gas exchange and lactate anaerobic thresholds: inter- and intraevaluator agreement.

Twenty-four coded graph sets of gas exchange variables and blood lactate concentration (LA) plotted against time at 15-s intervals were analyzed by nine evaluators who determined the gas exchange (ATGE) and LA (ATLA) anaerobic thresholds. In addition, ATGE and ATLA were determined by a linear regression computer program. Agreement between ATGE and ATLA was poor; the median intraclass correlation coefficient (ri) was 0.53. Among evaluators, ATLA agreement (median ri = 0.81) was better than ATGE agreement (median ri = 0.70). In general, the ability of any evaluator to choose similar values from duplicate plots for either ATGE (median ri = 0.97) or ATLA (median ri = 0.995) was good. There was better agreement between the mean ATLA of the evaluators and the computer ATLA (ComLA) (ri = 0.88) than between the mean ATGE of the evaluators and the computer ATGE (ComVE), (ri = 0.58). Agreement between ComVE and ComLA was poor (ri = 0.29). These results suggest that ATGE does not accurately predict ATLA and that different evaluators choose different thresholds from the same data. Further assessment of the validity and precision of ATGE based on breath-by-breath and minute-by-minute data is needed.

Cigarette smoking, exercise and high density lipoprotein cholesterol.

Cigarette smoking is associated with depressed levels of HDL-C, whereas exercise is associated with elevated levels of HDL-C. The purpose was to determine effects of smoking and exercise on blood lipids and lipoproteins in middle-aged males. It was hypothesized that smoking may attenuate the effects of exercise to elevate HDL-C. A total of 269 males (70 smokers) met all criteria for inclusion in the study population. Age, height, weight, body fatness via hydrostatic weighing, daily caloric consumption and alcohol intake, and smoking habits and history were determined. Interviews concerning physical activity patterns were conducted and cardiovascular responses to treadmill exercise were determined. Subjects were grouped as sedentary (low activity), participants in vigorous recreational activities (moderate activity) and joggers/runners (high activity). Analysis of covariance with adjustments for factors which may affect blood lipids and lipoproteins was employed. Smokers demonstrated lower HDL-C and higher total cholesterol levels than nonsmokers. High activity subjects demonstrated significantly higher HDL-C levels than the low and moderate groups which did not differ. High activity smokers did not differ from low activity nonsmokers with respect to HDL-C. This supports the proposed hypothesis. Nonsmokers were higher in weight and body fatness than smokers even though smokers consumed 288 more calories per day on the average. This suggests that smoking may account for a significant number of calories through altered metabolism or some other means.

Cigarette smoking, physical activity, and alcohol consumption: relationship to blood lipids and lipoproteins in premenopausal females.

A total of 164 premenopausal female subjects were randomly selected for evaluation from a much larger pool of volunteers. The relationships between blood lipid and lipoprotein levels as dependent variables and cigarette smoking, physical activity, and alcohol consumption were determined from partial regression coefficients. A lower HDL-C level (10.1 mg/dL) was seen in smokers v nonsmokers. For each ounce of alcohol consumed, HDL-C level was higher by 2.8 mg/dL, and greater physical activity was associated with a higher HDL-C level of 8.6 mg/dL. An analysis of covariance with covariance adjustments for age and body fat revealed that smokers who regularly exercise or consume alcohol had significantly lower HDL-C levels than nonsmokers with similar habits. Subjects who both exercise and consume alcohol demonstrated higher HDL-C levels than those who indulge in one or the other separately. Results suggest that cigarette smoking may attenuate the effects of chronic exercise or alcohol consumption, or of both, to raise HDL-C levels. Also, chronic exercise and alcohol consumption may exert an additive effect, raising HDL-C level.

Effects of prolonged warm-up exercise above and below anaerobic threshold on maximal performance.

The purpose of the present study was to determine the effects of prolonged warm-up exercise above and below anaerobic threshold (AT) on maximal performance. Warm-up exercise consisted of pedalling the Monark cycle ergometer at either 40% (Below AT) or 68% (Above AT) of VO2max for 60 min. Each maximal performance consisted of two 40 s bouts of "all out" pedalling on the Monark cycle ergometer against 5.5 kg resistance separated by a 5 min rest period. These tests were administered on two occasions without warm-up exercise and were found to be reproducible for work output and peak blood lactate concentration. Below AT warm-up exercise significantly increased core temperature with no increase in steady state blood lactate concentration and was thus representative of a desired warmed-up status. This condition did not contribute to an improved maximal performance. Above AT warm-up exercise resulted in significant increases in core temperature and steady state blood lactate concentration. Work output and peak blood lactate concentration for maximal exercise were significantly decreased. It was concluded that task specific prolonged warm-up exercise below AT does not contribute to an improved maximal performance of the type employed in the present study. Following warm-up exercise above AT, maximal performance was impaired. This was attributed to probable glycogen depletion in fast twitch muscle fibers which in turn may have contributed to a decreased lactate production.

Exercise recovery above and below anaerobic threshold following maximal work.

The purpose of this study was to determine the effects of resting and exercise recovery above [70% of maximum O2 uptake (VO2 max)] and below [40% of VO2 max] anaerobic threshold (AT) on blood lactate disappearance following maximal exercise. Blood lactate concentrations at rest (0.9 mM) and during exercise at 40% (1.3 mM) and 70% (3.5 mM) of VO2 max without preceding maximal exercise were determined on separate occasions and represented base lines for each condition. The rate of blood lactate disappearance from peak values was ascertained from single-component exponential curves fit for each individual subject for each condition using both the determined and resting base lines. When determined base lines were utilized, there were no significant differences in curve parameters between the 40 and 70% of VO2 max recoveries, and both were significantly different from the resting recovery. When a resting base line (0.9 mM) was utilized for all conditions, 40% of VO2 max demonstrated a significantly faster half time than either 70% of VO2 max or resting recovery. No differences were found between 70% of VO2 max and resting recovery. It was concluded that interpretation of the effectiveness of exercise recovery above and below AT with respect to blood lactate disappearance is influenced by the base-line blood lactate concentration utilized in the calculation of exponential half times.

Body fat content and serum lipid levels.

The relationship between the percentage of body fat and serum lipids was studied in middle-aged persons (112 men and ninety-two women) whose body fat levels were determined by hydrostatic weighing. Individuals classified as "overfat" exhibited significantly higher total serum cholesterol and total serum triglycerides than those classified as "normal fat " A trend for lower high-density-lipoprotein cholesterol levels in overfat women and higher low-density-lipoprotein cholesterol in both overfat men and women was observed. Overfat men and women had significantly higher very-low-density-lipoprotein cholesterol levels. These findings suggest that an accumulation of excess body fat may result in unfavorable serum lipid levels.

Age, diet, maximal aerobic capacity and serum lipids.

Eighty males ranging in age from 21 to 75 years were examined for maximal aerobic capacity (VO2max expressed in ml/kg x min-1), serum cholesterol (total, HDL, LDL, and VLDL-cholesterol), serum triglycerides, body fatness (%) and dietary patterns including total and constituent (protein, fat and carbohydrate) kilocalories and dietary cholesterol and alcohol intake. With age, subjects demonstrated a decreased maximal aerobic capacity, increased total serum cholesterol and LDL-cholesterol, increased serum triglycerides and body fatness. Dietary characteristics and HDL-cholesterol did not change with age. Older males (N = 27) with a mean age of 51.7 (+/- 7.2) years were matched for maximal aerobic capacity with younger males (N = 27) with a mean age of 34.2 (+/- 4.5) years. Dietary patterns and total serum cholesterol and HDL, LDL, and VLDL-cholesterol did not differ significantly between groups. Older subjects demonstrated significantly greater body fatness and serum triglycerides. It was concluded that a relationship exists between maximal aerobic capacity and serum cholesterol concentrations. This relationship did not appear to be influenced by dietary characteristics. It was further concluded that the gradual increase in body fatness with age was not attributable to quantitative or qualitative changes in caloric intake.

Recovery from maximal effort exercise: lactate disappearance and subsequent performance.

The effects of differing recovery patterns following maximal exercise on blood lactate disappearance and subsequent performance were examined. Nine subjects completed four randomly assigned experimental sessions. Each session consisted of a 5-min maximal effort performance test conducted on a Monark bicycle ergometer (T1) followed by 20 min of recovery and a second 5-min maximal effort performance test (T2). Blood lactate levels were measured during min 5, 10, 15, and 20 of recovery. Recovery patterns consisted of passive recovery (PR), active recovery below anaerobic threshold (AR less than AT), active recovery above anaerobic threshold (AR greater than AT), and active recovery above anaerobic threshold while breathing 100% oxygen (AR greater than AT + O2). Blood lactate levels prior to T2 were significantly different across treatments (P less than 0.05). Comparison among treatments and between T1 and T2 revealed no significant differences in work output. It was concluded that while lactate disappearance following severe exercise can be affected by varying the recovery pattern, elevated levels of blood lactate exert no demonstrable effect on maximal effort performance of 5-min duration.