Tony G. Babb

Fat Distribution and End-Expiratory Lung Volume in Lean and Obese Men and Women

BACKGROUND Although obesity significantly reduces end-expiratory lung volume (EELV), the relationship between EELV and detailed measures of fat distribution has not been studied in obese men and women. To investigate, EELV and chest wall fat distribution (ie, rib cage, anterior subcutaneous abdominal fat, posterior subcutaneous fat, and visceral fat) were measured in lean men and women (ie, < 25% body fat) and obese men and women (ie, > 30% body fat). METHODS All subjects underwent pulmonary function testing, hydrostatic weighing, and MRI scans. Data were analyzed for the men and women separately by independent t test, and the relationships between variables were determined by regression analysis. RESULTS All body composition measurements were significantly different among the lean and obese men and women (p < 0.001). However, with only a few exceptions, fat distribution was similar among the lean and obese men and women (p > 0.05). The mean EELV was significantly lower in the obese men (39 +/- 6% vs 46 +/- 4% total lung capacity [TLC], respectively; p < 0.0005) and women (40 +/- 4% vs 53 +/- 4% TLC, respectively; p < 0.0001) compared with lean control subjects. Many estimates of body fat were significantly correlated with EELV for both men and women. CONCLUSIONS In both men and women, the decrease in EELV with obesity appears to be related to the cumulative effect of increased chest wall fat rather than to any specific regional chest wall fat distribution. Also, with only a few exceptions, relative fat distribution is markedly similar between lean and obese subjects.

Obesity: Associations with Acute Mountain Sickness

Context A few small retrospective studies show associations between obesity and acute mountain sickness. Contribution This 24-hour study involving 9 obese and 10 nonobese men was conducted in a decompression chamber that simulated a rapid ascent to an altitude of 3658 m (12 000 ft). Obese men more often developed symptoms of mountain sickness and had lower nocturnal oxygen saturation values than did nonobese men. Cautions Although this elegant, short experiment suggests that obese men were more susceptible to acute mountain sickness, the study involved few people, simulated a steady rate of ascent, and did not simulate physical activity with altitude exposure. The Editors Rapid ascent from low to high altitude (above 2500 m or 8200 ft) often causes acute mountain sickness (AMS), a syndrome characterized by headache and other systemic symptoms, such as nausea, lassitude, and difficulty sleeping. The prevalence and severity of AMS depend on the speed of ascent, the altitude attained, preacclimatization, age, sex, exertion levels while at altitude, and the ventilatory response to acute hypoxia (1, 2). Few retrospective field studies of high altitude have reported that obesity, as evidenced by body mass index (BMI), might be associated with the development of AMS (3-7). However, this association has not been studied prospectively under controlled conditions at reasonably accessible altitudes or in individuals with mild to moderate obesity. We sought to determine whether obese individuals are more likely to develop AMS than nonobese individuals during decompression to a simulated altitude of 3658 m. We hypothesized that obese individuals were more susceptible to develop AMS than nonobese individuals during exposure to high altitudeinduced hypobaric hypoxia. Methods Participants Volunteers were recruited through local advertisements and were selected for participation on the basis of percentage body fat. Nonobese was defined as percentage body fat less than 25%. Obese was defined as a BMI of 30 kg/m2 or greater and percentage body fat of 30% or greater. None of the participants had a history of cardiovascular or respiratory abnormalities. No participant was taking long-term medications. All participants were nonsmokers. Nine obese men (mean age [SD], 35 8 years) and 10 nonobese men (mean age [SD], 34 8 years) were studied. All participants resided at sea level (100 m) in Dallas, Texas. One obese and three nonobese participants previously had mild AMS. One obese participant was exposed to a 2500-m altitude 4 days before this study; no other participant was exposed to a 1500-m or higher altitude before participating in the study. Each participant received both written and verbal explanations of the experiment before giving written consent. The Institutional Review Board of the University of Texas Southwestern Medical Center and Presbyterian Hospital of Dallas approved this study. Study Protocol The study was conducted in a large (40 ft long by 9 ft diameter) multiplace (room for >1 person) decompression chamber at the Institute for Exercise and Environmental Medicine in Dallas. The barometric pressure was held at 483 mm Hg, which is equivalent to an altitude of 3658 m (12 000 ft). The temperature (25 0.5 C), humidity (28% 1%), and concentration of CO2 (0.07% 0.02%) in the chamber were monitored continuously by trained medical staff. Four participants at a time were studied in the chamber during the 24 hours of exposure (Figure 3). Assessment of AMS According to guidelines established by the Lake Louise AMS consensus report (8), each participant completed an AMS self-report questionnaire at sea level (before decompression) and during decompression to 483 mm Hg at 6 hours, 12 hours, and 24 hours. The questionnaire included items for symptoms of headache, gastrointestinal symptoms, fatigue or weakness, dizziness or lightheadedness, and difficulty sleeping. Each symptom was graded on a scale from 0 to 3, with 0 representing no symptoms; 1, mild symptoms; 2, moderate symptoms; and 3, severe symptoms. A score of 15 was the maximum score possible. A self-score of 4 or more was an indication of AMS (8). This scoring system has been validated against the U.S. Army Environmental Symptoms Questionnaire, demonstrating similar sensitivity and specificity (9). Measurements of Sao 2 Daytime Sao 2 was measured by pulse oximetry (Ohmeda 3700 Pulse Oximeter, Datex-Ohmeda, Boulder, Colorado) at sea level and at 6 hours and 24 hours of simulated altitude. Nocturnal Sao 2 in each participant was continuously recorded in the chamber from 10:30 p.m. to 6:30 a.m. The mean nocturnal Sao 2 was calculated from values obtained every 30 minutes. Heart rate was measured at sea level and at altitude during the daytime and during sleep. Other Measurements Body composition was determined by hydrostatic weighing, and percentage body fat, fat mass, and lean mass were calculated. At sea level, all participants underwent standard spirometry (measuring lung volumes, maximal flow-volume loop, and maximal voluntary ventilation) and diffusing capacity of the lung in a whole-body plethysmograph (Model 6200, SensorMedics, Yorba Linda, California). Pulmonary function testing was performed according to the guidelines of the American Thoracic Society. Statistical Analysis Data are expressed as means (SD). The parameters of AMS score and Sao 2 were analyzed by a two-way analysis of variance (ANOVA) using SAS software, release 8.02 (SAS Institute, Inc., Cary, North Carolina), with repeated measures on one factor (altitude-time) and between-participant comparisons for the other factor (group, nonobese and obese). Comparisons were considered significant when the P value was less than 0.05. Role of the Funding Sources The funding sources had no role in the design, conduct, or reporting of the study or in the decision to submit the manuscript for publication. Results Participants The Table shows general characteristics of the participants. One participant in the obese group was removed from the chamber after 10 hours because of severe headache, nausea, and dizziness (AMS score, 8). As a result, this participant was not included in further analyses. Table. General Characteristics and Pulmonary Function of Participants at Baseline AMS Scores There was a significant interaction between altitude-time and group (P < 0.001) as a result of the two-way ANOVA. This indicated that the increase in AMS scores with altitude exposure was more pronounced in the obese participants (Figure 1). Overall, after 24 hours in the chamber, seven obese participants and four nonobese participants had an AMS score of 4 or more. The frequency of AMS symptoms at 24 hours in 18 participants was as follows: headache, 89%; gastrointestinal upset, 36%; fatigue and weakness, 36%; dizziness, 15%; and difficulty sleeping, 75%. Figure 1. Comparison of the acute mountain sickness ( AMS ) score at sea level and at simulated altitude for 24 hours in nonobese ( n = 10) and obese ( n = 8) participants. P Sao 2 There was also a significant interaction between altitude-time and group (P < 0.001) for Sao 2 as a result of the two-way ANOVA (Figure 2). This indicated that the decrease in Sao 2 with altitude exposure differed between the two groups. Figure 2. Comparison of Sao at sea level, during the daytime, and during sleep at night in nonobese ( n = 10) and obese ( n = 8) participants. o P Figure 3. Participants during simulated altitude exposure in decompression chamber. Discussion Our principal finding was that obese participants have higher AMS scores than nonobese participants during a 24-hour exposure to simulated altitude of 3658 m. Thus, obesity seems to be associated with the development of AMS. Also, the response of Sao 2 with exposure differed between nonobese and obese men; obese men had lower values than nonobese men. These findings suggest that impaired breathing during sleep may be an important pathophysiologic mechanism for the increased levels of AMS in obese individuals. Limitations Although our results suggest that obese individuals may be more susceptible to AMS, these results must be interpreted with caution. Possible limitations to generalization include the small sample size, the selected nature of the study sample, the narrow spectrum of obese participants studied, the steady rate of ascent, the lack of physical activity during altitude exposure, and the simulated environment in which the participants were studied. Obesity and AMS Obesity is characterized by an abnormally large adipose tissue mass. In particular, excess weight leads to the development of various pathophysiologic disorders and, specifically, cardiovascular and respiratory abnormalities. Obesity-related respiratory function abnormalities, such as sleep-disordered breathing and nocturnal hypercapnia and hypoxia, place obese individuals at risk for illness at higher altitudes (10-13). In addition, the prevalence of obesity in western society, especially in the United States (where 22% of the population has a BMI > 30 kg/m2 and roughly 30% of the population is overweight [14, 15]), further increases the potential for altitude-related difficulties at easily accessible high altitudes during recreational activities. A review of the literature revealed no prospective data on the effect of obesity on high-altitude illness. In our study, AMS scores increased with time during altitude exposure in both nonobese and obese participants, which is consistent with previous data demonstrating that AMS symptoms are common after 24 hours of rapid ascent to high altitude (1, 2). The severity of symptoms, however, significantly differed between nonobese and obese men, suggesting that the occurrences of AMS at high altitude may be closely related to increased body weight. Acute mountain sickness frequently occurs in travelers who rapidly ascend to an altitude of 2500 m without acclimatizing; the incidence and severity depend on the speed of asce

Dyspnea on Exertion in Obese Women Association with an Increased Oxygen Cost of Breathing

RATIONALE Although exertional dyspnea in obesity is an important and prolific clinical concern, the underlying mechanism remains unclear. OBJECTIVES To investigate whether dyspnea on exertion in otherwise healthy obese women was associated with an increase in the oxygen cost of breathing or cardiovascular deconditioning. METHODS Obese women with and without dyspnea on exertion participated in two independent experiments (n = 16 and n = 14). All participants underwent pulmonary function testing, hydrostatic weighing, ratings of perceived breathlessness during cycling at 60 W, and determination of the oxygen cost of breathing during eucapnic voluntary hyperpnea at 40 and 60 L/min. Cardiovascular exercise capacity, fat distribution, and respiratory mechanics were determined in 14 women in experiment 2. Data were analyzed between groups by independent t test, and the relationship between the variables was determined by regression analysis. MEASUREMENTS AND MAIN RESULTS In both experiments, breathlessness during 60 W cycling was markedly increased in over 37% of the obese women (P < 0.01). Age, height, weight, lung function, and %body fat were not different between the groups in either experiment. In contrast, the oxygen cost of breathing was significantly (P < 0.01) and markedly (38-70%) greater in the obese women with dyspnea on exertion. The oxygen cost of breathing was significantly (P < 0.001) correlated with the rating of perceived breathlessness obtained during the 60 W exercise in experiment 1 (r(2) = 0.57) and experiment 2 (r(2) = 0.72). Peak cardiovascular exercise capacity, fat distribution, and respiratory mechanics were not different between groups in experiment 2. CONCLUSIONS Dyspnea on exertion is prevalent in otherwise healthy obese women, which seems to be strongly associated with an increased oxygen cost of breathing. Exercise capacity is not reduced in obese women with dyspnea on exertion.

Mild-to-moderate obesity: implications for respiratory mechanics at rest and during exercise in young men.

OBJECTIVE:To investigate the effect of mild-to-moderate obesity on respiratory mechanics at rest and during exercise in obese men. We hypothesized that the simple mass loading of obesity would alter both end-expiratory lung volume (EELV) and respiratory pressures (gastric, Pga and transpulmonary, PTP) in resting body positions and during graded cycle ergometry to exhaustion.SUBJECTS:A total of 10 obese (38±5% body fat; mean±s.d.) and nine lean (18±4%) men were studied.METHODS:Body composition (by body circumferences and hydrostatic weighing) and pulmonary function were measured at rest. Breathing mechanics were measured at rest in the upright-seated position, supine, and during cycling exercise. Data were analyzed by independent t-test.RESULTS:EELV was significantly lower in the obese men in the supine (30±4 vs 37±6% total lung capacity (TLC)) and seated (39±6 vs 47±5%TLC) positions and at ventilatory threshold (35±5 vs 45±7%TLC) (P<0.01). In contrast, at peak exercise, EELV was not different between groups. Respiratory pressures (Pga and PTP) were elevated (P<0.05) during one or more phases of the breathing cycle at rest and during exercise in obese men.CONCLUSION:These data demonstrate that mild-to-moderate obesity in young men results in reduced lung volumes and alterations in respiratory mechanics when supine, seated at rest, and during exercise. During moderate exercise, obesity does not appear to limit changes in EELV; however, the regulation of EELV during heavy exercise appears to be affected.

Mechanical ventilatory constraints in aging, lung disease, and obesity : perspectives and brief review

Mechanical ventilatory constraints in aging, lung disease, and obesity; perspectives and brief review. Med. Sci. Sports Exerc., Vol. 31, No. 1 (Suppl.), pp. S12-S22, 1999. One of the most difficult tasks of cardiopulmonary exercise testing is to determine the influence of ventilatory limitations on the ventilatory response to exercise. Currently there is no generally accepted method in which to quantify the magnitude of mechanical ventilatory constraints during exercise. Nor is there agreement on how to quantify maximal ventilatory capacity. To address these issues, this article focuses on the evaluation of mechanical ventilatory constraints during exercise and provides an overview of the mechanical ventilatory constraints that are encountered with aging, lung disease, and obesity.

The Importance of the Muscle and Ventilatory Blood Pumps During Exercise in Patients Without a Subpulmonary Ventricle (Fontan Operation)

OBJECTIVES The aim of this study was to determine the relative contribution of the muscle and ventilatory pumps to stroke volume in patients without a subpulmonic ventricle. BACKGROUND In patients with Fontan circulation, it is unclear how venous return is augmented to increase stroke volume and cardiac output during exercise. METHODS Cardiac output (acetylene rebreathing), heart rate (electrocardiography), oxygen uptake (Douglas bag technique), and ventilation were measured in 9 patients age 15.8 ± 6 years at 6.1 ± 1.8 years after Fontan operation and 8 matched controls. Data were obtained at rest, after 3 min of steady-state exercise (Ex) on a cycle ergometer at 50% of individual working capacity, during unloaded cycling at 0 W (muscle pump alone), during unloaded cycling with isocapnic hyperpnea (muscle and ventilatory pump), during Ex plus an inspiratory load of 12.8 ± 1.5 cm water, and during Ex plus an expiratory load of 12.8 ± 1.6 cm water. RESULTS In Fontan patients, the largest increases in stroke volume and stroke volume index were during zero-resistance cycling. An additional increase with submaximal exercise occurred in controls only. During Ex plus expiratory load, stroke volume indexes were reduced to baseline, non-exercise levels in Fontan patients, without significant changes in controls. CONCLUSIONS With Fontan circulation increases in cardiac output and stroke volume during Ex were due to the muscle pump, with a small additional contribution by the ventilatory pump. An increase in intrathoracic pressure played a deleterious role in Fontan circulation by decreasing systemic venous return and stroke volume.

Layers of exercise hyperpnea: modulation and plasticity.

Despite the fundamental biological significance of the ventilatory response to mild or moderate physical activity (the exercise hyperpnea), we still know remarkably little concerning its underlying mechanisms. Part of the difficulty in revealing those mechanisms may arise due to confusion between multiple mechanistic layers, each contributing to the impressive degree of regulation achieved. The primary, feedforward exercise stimulus or stimuli increase ventilation in approximate proportion to changes in metabolic rate. Chemoreceptor feedback then minimizes deviations from optimal blood gas regulation, most often preventing excessive hypocapnia in non-human mammals. Recent evidence has accumulated, suggesting that adaptive control strategies including modulation and plasticity may adjust the feedforward and/or feedback contributions when blood gas homeostasis proves inadequate. In this review, we present evidence from a goat model of exercise hyperpnea concerning the existence of modulation and plasticity, and specifically mechanisms known as short-term and long-term modulation of the exercise ventilatory response. Throughout the review, we consider available evidence concerning the relevance of these mechanisms to humans. Plasticity is a property only recently recognized in the neural system subserving respiratory control, and the application of these concepts to the exercise ventilatory response in humans is in its infancy. Modulation and plasticity may confer an ability of individuals to adapt their exercise ventilatory response so that it remains appropriate in the face of life-long changes in endogenous (e.g. development, aging, onset of disease) or exogenous (e.g. altitude, wearing a breathing apparatus during physical exertion) physiological conditions.

Exercise ventilatory limitation: the role of expiratory flow limitation.

Ventilatory limitation to exercise remains an important unresolved clinical issue; as a result, many individuals misinterpret the effects of expiratory flow limitation as an all-or-nothing phenomenon. Expiratory flow limitation is not all or none; approaching maximal expiratory flow can have important effects not only on ventilatory capacity but also on breathing mechanics, ventilatory control, and possibly exertional dyspnea and exercise intolerance.

Quantification of Cardiorespiratory Fitness in Healthy Nonobese and Obese Men and Women

BACKGROUND The quantification and interpretation of cardiorespiratory fitness (CRF) in obesity is important for adequately assessing cardiovascular conditioning, underlying comorbidities, and properly evaluating disease risk. We retrospectively compared peak oxygen uptake (VO(2)peak) (ie, CRF) in absolute terms, and relative terms (% predicted) using three currently suggested prediction equations (Equations R, W, and G). METHODS There were 19 nonobese and 66 obese participants. Subjects underwent hydrostatic weighing and incremental cycling to exhaustion. Subject characteristics were analyzed by independent t test, and % predicted VO(2)peak by a two-way analysis of variance (group and equation) with repeated measures on one factor (equation). RESULTS VO(2)peak (L/min) was not different between nonobese and obese adults (2.35 ± 0.80 [SD] vs 2.39 ± 0.68 L/min). VO(2)peak was higher (P < .02) relative to body mass and lean body mass in the nonobese (34 ± 8 mL/min/kg vs 22 ± 5 mL/min/kg, 42 ± 9 mL/min/lean body mass vs 37 ± 6 mL/min/lean body mass). Cardiorespiratory fitness assessed as % predicted was not different in the nonobese and obese (91% ± 17% predicted vs 95% ± 15% predicted) using Equation R, while using Equation W and G, CRF was lower (P < .05) but within normal limits in the obese (94 ± 15 vs 87 ± 11; 101% ± 17% predicted vs 90% ± 12% predicted, respectively), depending somewhat on sex. CONCLUSIONS Traditional methods of reporting VO(2)peak do not allow adequate assessment and quantification of CRF in obese adults. Predicted VO(2)peak does allow a normalized evaluation of CRF in the obese, although care must be taken in selecting the most appropriate prediction equation, especially in women. In general, otherwise healthy obese are not grossly deconditioned as is commonly believed, although CRF may be slightly higher in nonobese subjects depending on the uniqueness of the prediction equation.

Weight Loss via Diet and Exercise Improves Exercise Breathing Mechanics in Obese Men

BACKGROUND Obesity alters breathing mechanics during exercise. Weight loss improves lung function at rest, but the effect of weight loss, especially regional fat loss, on exercise breathing mechanics is unclear. We hypothesized that weight loss, especially a decrease in abdominal fat, would improve breathing mechanics during exercise because of an increase in end-expiratory lung volume (EELV). METHODS Nine obese men were studied before and after weight loss (13% ± 8% of total fat weight, mean ± SD). Subjects underwent pulmonary function testing, underwater weighing, fat distribution estimates (MRI), and graded cycle ergometry before and after a 12-week diet and exercise program. In seven men, esophageal and gastric pressures were measured. The effects of weight loss were analyzed at rest, at ventilatory threshold (VTh), and during peak exercise by dependent Student t test, and the relationship among variables was determined by correlation analysis. RESULTS Subjects lost 7.4 ± 4.2 kg of body weight (P < .001), but the distribution of fat remained unchanged. After weight loss, lung volume subdivisions at rest were increased (P < .05) and were moderately associated (P < .05) with changes in chest, waist, and hip circumferences. At VTh, EELV increased, and gastric pressure decreased significantly (P < .05). The changes in waist circumference, hip circumference, BMI, and sum of chest, waist, and hip circumferences were also consistently and significantly correlated (P < .05) with changes in gastric pressure during exercise at VTh. CONCLUSIONS Modest weight loss improves breathing mechanics during submaximal exercise in otherwise healthy obese men, which is clinically encouraging. Improvement appears to be related to the cumulative loss of chest wall fat.