Leptin level lowers in proportion to the amount of aerobic work after four weeks of training in obesity.

Leptin values are higher in obesity. Physical exercise reduces fat mass (FM) and decreases leptin levels. Intensity of physical training seems to play a role in reducing circulating leptin. In 16 obese subjects (8 men and 8 women, age 38.6±3.9 years, BMI 35.9±1.8 kg/m(2)), leptin was sampled before and after 4 weeks of controlled training. Eight subjects (4 men and 4 women) performed an aerobic training schedule (Group A), the remainders an aerobic training program with a bout of work beyond the anaerobic threshold (AT) (Group B). Training determined a reduction in leptin levels in both groups, which was significant in Group A (12.2 vs. 27.8 µg/l, p<0.05), even when related to the change in FM (0.372 vs. 0.762 µg/l/kg, p<0.05). FM decreased significantly in Group B when compared to Group A (-7.4 vs. -2.6 kg, respectively, p<0.001). While in Group A the slight loss of FM was aggregated to a significant decrease in leptin levels, the opposite occurred in Group B. In Group A, leptin lowering was proportional to the amount of total work performed (p<0.001, R(2)=0.89). In obesity, a reduction is observed in leptin levels after short-term training, which is seemingly dissociated from concomitant decrease of FM. Aerobic training alone appears to be linked to a greater leptin reduction, which is well correlated with the amount of work performed.

Acute post-exercise oxygen uptake, hormone and plasma metabolite response in obese men.

This study aimed to compare oxygen uptake ( VO2), hormone and plasma metabolite responses during the 30 min after submaximal incremental exercise (Incr) performed at the same relative/absolute exercise intensity and duration in lean (L) and obese (O) men. Eight L and 8 O men (BMI: 22.9 ± 0.4; 37.2 ± 1.8 kg · m(-2)) completed Incr and were then seated for 30 min. VO2 was monitored during the first 10 min and from the 25-30(th) minutes of recovery. Blood samples were drawn for the determination of hormone (catecholamines, insulin) and plasma metabolite (NEFA, glycerol) concentrations. Excess post-exercise oxygen consumption (EPOC) magnitude during the first 10 min was similar in O and in L (3.5 ± 0.4; 3.4 ± 0.3 liters, respectively, p=0.86). When normalized to percent change ( VO2END=100%), % VO2END during recovery was significantly higher from 90-120 s in O than in L (p ≤ 0.04). There were no significant differences in catecholamines (p ≥ 0.24), whereas insulin was significantly higher in O than in L during recovery (p=0.01). The time-course of glycerol was similar from 10-30 min of recovery (-42% for L; -41% for O, p=0.85), whereas significantly different patterns of NEFA were found from 10-30 min of recovery between groups (-18% for L; +8% for O, p=0.03). Despite similar EPOC, a difference in VO2 modulation between groups was observed, likely due to faster initial rates of VO2 decline in L than in O. The different patterns of NEFA between groups may suggest a lower NEFA reesterification during recovery in O, which was not involved in the rapid EPOC component.

Oxygen uptake and cardiac performance in obese and normal subjects during exercise.

Work capacity and cardiopulmonary performance were studied in a group of 11 young obese subjects (BMI 39.9 kg/m2) and a group of 10 young normal subjects (BMI 22 kg/m2). First of all they underwent an incremental cycle ergometer test up to exhaustion. Subsequently, every subject of the two groups performed a constant work rate test at different work loads to estimate cardiac output (Q) below anaerobic threshold (AT) by a 20-second CO2 rebreathing method. Obese subjects had a significantly lower AT (79 vs. 109 W). The ratio between oxygen uptake and heart rate (VO2/HR) (O2 pulse) was higher in the obese group; nevertheless, this variable became significantly lower if we took into consideration the ratio between O2 pulse and kilogram fat-free body mass or kilogram body weight. Both these observations suggest that their reduced work tolerance is linked with a reduced oxygen supply to the muscles in activity. Q increased in similar ways in obese and normal subjects at the preset work rates. The ratio Q/body surface (cardiac index; CI) that we considered in order to try to minimize the differences in body sizes between the two groups, increased less in response to increasing work rates in our obese subjects than in normal subjects. As a whole, these data appear to be in line with a relatively less efficient cardiac performance during progressive work rates in obese subjects.

Haemorheological changes in obese adolescents after short-term diet.

Along with other risk factors in coronary heart and cerebrovascular disease, obesity is frequently associated with the development of atherosclerosis, a disease in which the rheological characteristics of blood are important. We studied the influence of weight reduction on haemorheological parameters of 20 obese adolescents (10 female, 10 male; aged 12-17 years) without metabolic and/or cardiovascular diseases. The control group composed 39 health non-obese subjects (19 female, 20 male; aged 13-17 years). At the beginning of the study the mean (+/- s.d.) body mass indices (BMI) of the obese adolescents were 36.0 +/- 5.3 kg/m2 in males and 36.8 +/- 5.0 kg/m2 in females. This was significantly reduced (31.5 +/- 4.9 kg/m2 in males and 32.5 +/- 4.7 kg/m2 in females) after one month following a diet of 1000 kcal/day: 25% proteins, 26% lipids and 49% carbohydrates. Before dieting, plasma fibrinogen level, whole blood viscosity at low shear rates and plasma viscosity were significantly higher in obese patients than in normal subjects, while the microhaematocrit values of the two groups were not significantly different. After dieting, plasma viscosity, the plasma fibrinogen level and the mean erythrocyte aggregation index of the patients decreased significantly compared to basal values, while whole blood viscosity did not change. Our data seem to indicate that short-term diet improves the haemorheological pattern in obese adolescents, probably as a consequence of an important metabolic rearrangement.

Metabolic aspects and sympathetic effects in the obese subject undergoing exercise testing.

An impaired plasma Epinephrine (E) and Norepinephrine (NE) response has been described in obese patients during physical exercise. Serum potassium level is influenced either by physical exercise or by the adrenergic system. We studied 12 young obese patients and 12 young controls, all without any cardio-respiratory disorders, who underwent a cycloergometric test with steps of 20 watts every four minutes until exhaustion. During the test we recorded serum potassium levels, E and NE, insulin, glucose and RQ to confirm or not the observation of the reduced adrenergic response in obese patients. During exercise, although both groups reached a not significantly different mean peak value of maximal activity, E and NE increased, more in the controls than in the obese subjects (at peak of exercise 221 +/- 44.1 vs 71 +/- 21.5 pg/ml respectively for E; 2035 +/- 164.8 vs 1141 +/- 313.7 pg/ml respectively for NE). RQ was constantly lower in the obese patients than in the normals both during and after the stress. In both groups potassium increased significantly, but the obese patients had a significantly lower increment at peak of activity when compared to the controls (delta K+: 0.52 +/- 0.11 vs 1.007 +/- 0.17 meq/l respectively, p < 0.05). Insulin and glucose had a behaviour in line with literature in both groups. The behaviour of potassium could be an index of a higher effect of beta-adrenergic system in obese patients than in normals despite the different increases of catecholamines in the two groups. This hypothesis may agree with the preferential metabolic use of fatty acids in our obese patients as indicated by RQ values.

Breathing pattern during and after maximal exercise testing in young untrained subjects and in obese patients.

More rapid and more shallow breathing (RSB) than usual, manifested by a lower tidal volume and greater breathing frequency at a given level of ventilation, may be caused by inspiratory muscle fatigue and pulmonary congestion. It has been observed during recovery in young trained adults after very high exercise levels and in middle-aged patients with cardiac disease, after their maximal work load. We studied the breathing pattern during and after exercise testing up to the maximal work capacity in a group of normal untrained, young people and in a group of young obese subjects. RSB was present in normal subjects after a work load which required a maximal O2 consumption near the theoretical value (93% in our cases) and was not present in obese patients probably because neither inspiratory muscle fatigue, nor pulmonary congestion occurs in these subjects. Maximal heart rate at peak of exercise was significantly higher in normal subjects and a direct correlation between delta Vt and maximal heart rate was found in all normal subjects. This is compatible with the hypothesis that RSB is mainly due to an initial interstitial pulmonary edema, as supposed by other authors.

Creatine kinase and creatine kinase-MB isoenzyme during and after exercise testing in normal and obese young people.

We report creatine kinase (CK) and CK-MB values during a cycloergometric test up to maximal work capacity in 10 normal subjects aged 20 to 39 years (mean body mass index, 22 kg/m2) and 11 obese patients aged 17 to 42 years (mean body mass index, 41 kg/m2), all without any cardiorespiratory diseases. Total CK was significantly higher in obese patients. The CK-MB was not significantly different between the two groups, except at the first recovery when it was increased in obese patients and decreased in normal subjects. These results could be due to more important total stress of the total musculature, especially cardiac, and especially cardiac musculature in obese patients during a physical effort. Considering the mean values of total CK of our obese patients, it may be possible that they have myocardial damage at percentages of CK-MB less than those of lean subjects generally accepted at more than 4 percent. Moreover, in obese heart patients myocardial distress during exercise testing may be present despite heart rate at peak exercise beneath the theoretic maximal.

Catecholamine-stimulated potassium transport in erythrocytes from normal and obese subjects.

The beta adrenergic-modulated Na+/K+ ATPase pump rate of red blood cells was measured in vitro in 18 non diabetic obese patients. After challenge of erythrocytes with beta adrenergic selective agonist Salbutamol, the decrement of the K+ concentration in the suspending medium was assumed to be related to the Na+/K+ ATPase pump rate or to the number of beta 2 receptors. The mean K+ uptake was markedly increased in the erythrocytes of obese patients (1.58 mEq/l SD 0.18) if compared with 38 normal subjects (1.30 mEq/l SD 0.11) and with a population of 30 atopic patients that we have previously reported to have a reduced red cells beta 2 receptor activity (1.09 mEq/L SD 0.11). These results are not consistent with the hypothesis that a reduction in the Na+/K+ ATPase pump rate (at least in red blood cells) may be responsible for decreased metabolic rates leading to obesity. Since the autonomic nervous system is involved in the regulation of the cardiovascular system, it is conceivable that an increased Na+ ATPase pump rate (or supersensitivity) may be responsible of the increased incidence of hypertension, congestive heart failure and unexplained sudden death associated with obesity in some patients.

Work capacity and cardiopulmonary adaptation of the obese subject during exercise testing.

Twelve obese patients (six male subjects) aged 17 to 42 years with a mean body mass index (BMI) of 40 kg/m2 and 12 normal subjects (six male subjects) aged 19 to 39 years with a mean BMI of 22 kg/m2 underwent a cycloergometric test until exhaustion to assess work capacity and cardiopulmonary adaptations of the two groups. Minute ventilation, expiratory gas concentrations, and heart rate, together with anaerobic threshold (AT) were determined in each subject during the test. The same subjects were then submitted to normocapnic hyperpnea at rest to assess the oxygen cost of breathing. We found that in the obese patients, the maximal sustainable work rate was not different from that of controls (120 vs 136 W) while AT was significantly lower (78 vs 110 W). Nevertheless, there was no difference in maximum VO2 and in VO2 at AT levels (expressed in milliliters per minute) indicating that cardiac, pulmonary, vascular, and muscle performance did not differ from obese to normal subjects. Greater muscular effort was needed by obese patients when moving their heavier legs and less when doing external work with a decreased gross mechanical efficiency and an identical net mechanical efficiency between the two groups.

Relationship between body mass and tolerance to physical stress in obese patients.

Eleven obese patients, 5 males; age: 17-42; body mass index (BMI): 40; % of ideal weight: 187%, and 10 normal subjects (5 males; age: 19-39; BMI: 22; % of ideal weight: 103%), both groups without heart and respiratory disorders, underwent a cycloergometric test with subsequent 20-watt increases every 4 min until exhaustion. During the test, ventilation/minute, expiratory gas concentration and heart rate were measured, and the anaerobic threshold (AT) was determined in each subject. The obese patients showed a significantly lower AT than normal subjects (p less than 0.01); showing values which decreased with the increase in the grade of obesity expressed in BMI or in percent of their ideal weight. Moreover, in the obese patients, the O2 consumption (VO2) had significantly increased compared to that of normal subjects at no resistance and at all work levels. The negative correlation between the AT value and the BMI in obese patients can attribute their increase in VO2 during stress to (1) the inertial overloading caused by obesity especially considering the adipose tissue of their legs, or (2) to their level of 'fitness' being lower than that of normal subjects.