Alberto Salvadori

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 (q̇) 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 (v̇O2/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. q̇ increased in similar ways in obese and normal subjects at the preset work rates. The ratio q̇/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.

Acylated ghrelin decreases during acute exercise in the lean and obese state

Ghrelin, the GH-secretagogue receptor ligand, is chiefly acknowledged as a central modulator of energy homeostasis. 1 In addition to promoting the drive to eat and governing long-term energy accumulation, ghrelin has been shown to influence fuel oxidation, increase the respiratory exchange ratio (RER), decrease spontaneous physical activity and enhance cardiac function. 1 In the bloodstream, ghrelin circulates both as an acylated and desacylated peptide. Ghrelin concentrations are acutely suppressed after food ingestion or glucose infusion, while fat accumulation is a long-term negative regulator. 2,3 Recent studies in lean individuals prompted debated evidence that acute exercise decreases total and acylated ghrelin levels in relation to GH concentrations and perceived appetite ratings. 4–6

Kinetics of catecholamines and potassium, and heart rate during exercise testing in obese subjects: Heart rate regulation in obesity during exercise

Background: Obesity is characterised by a marked insulin resistance which involves an abnormal regulation of K+ uptake and metabolism. Less is known about the effect of physical exercise on K+ kinetics.

Short‐term HIIT and Fatmax training increase aerobic and metabolic fitness in men with class II and III obesity

To compare the effects of two different 2‐week‐long training modalities [continuous at the intensity eliciting the maximal fat oxidation (Fatmax) versus high‐intensity interval training (HIIT)] in men with class II and III obesity.

Ventilation and its control during incremental exercise in obesity.

Background: In obesity, the addition of mass loading of the chest wall by adipose tissue decreases compliance, but its ventilation does not seem to be a limiting factor to physical performance. Plasma K+ and lactic acid are considered important determinants of ventilation during exercise. Obesity is characterized by insulin resistance. Objectives: The aim of this study was to assess ventilatory adaptations to sustained effort and the effects of lactic acid and potassium in young obese subjects. Methods: Twelve obese subjects with a body mass index of 40 (mean age 27 years, 6 males) and 12 normal subjects with a body mass index of 22 (aged 28 years, 6 males) performed a progressive cycloergometric test with increases of 20 W every 4 min to exhaustion while minute ventilation, oxygen consumption, carbon dioxide production, end-tidal oxygen pressure, and end-tidal carbon dioxide pressure were measured. Blood samples were collected at the end of every step to determine plasma K+. Lactic acid was measured at rest, 40, 80, 120 W and peak exercise (or only at peak exercise if <120 W). Before each exercise, we tested insulin sensitivity using the quantitative insulin sensitivity check index. Results: Obese subjects had lower insulin sensitivity (0.318 vs. 0.345, p < 0.01). Peak exercise was not significantly different between both groups (125 W in the obese group vs. 137 W in the control group), but the ventilatory threshold was at lower power output in the obese group compared to the controls (76 vs. 107 W, p < 0.05). Ventilation increased less in the obese group but oxygen saturation of hemoglobin remained within normal limits up to exhaustion in both groups. Ventilation was appropriate for the CO2 increase but less appropriate for the increased O2 consumption. Both K+ and lactic acid increased less in the obese group. Conclusions: In our obese subjects, ventilation was not a limiting factor during exercise. Its lower increase may be due, in addition to the characteristics of their chest walls, to insulin resistance which may limit the increase in lactic acid during effort, and to the hypertrophy of muscle fibers previously noted, which may be linked to a lower increase in plasma K+ during physical exercise.

Fat Oxidation, Hormonal and Plasma Metabolite Kinetics during a Submaximal Incremental Test in Lean and Obese Adults

This study aimed to compare fat oxidation, hormonal and plasma metabolite kinetics during exercise in lean (L) and obese (O) men. Sixteen L and 16 O men [Body Mass Index (BMI): 22.9±0.3 and 39.0±1.4 kg.m−2] performed a submaximal incremental test (Incr) on a cycle-ergometer. Fat oxidation rates (FORs) were determined using indirect calorimetry. A sinusoidal model, including 3 independent variables (dilatation, symmetry, translation), was used to describe fat oxidation kinetics and determine the intensity (Fatmax) eliciting maximal fat oxidation. Blood samples were drawn for the hormonal and plasma metabolite determination at each step of Incr. FORs (mg.FFM−1.min−1) were significantly higher from 20 to 30% of peak oxygen uptake () in O than in L and from 65 to 85% in L than in O (p≤0.05). FORs were similar in O and in L from 35 to 60% . Fatmax was 17% significantly lower in O than in L (p<0.01). Fat oxidation kinetics were characterized by similar translation, significantly lower dilatation and left-shift symmetry in O compared with L (p<0.05). During whole exercise, a blunted lipolysis was found in O [lower glycerol/fat mass (FM) in O than in L (p≤0.001)], likely associated with higher insulin concentrations in O than in L (p<0.01). Non-esterified fatty acids (NEFA) were significantly higher in O compared with L (p<0.05). Despite the blunted lipolysis, O presented higher NEFA availability, likely due to larger amounts of FM. Therefore, a lower Fatmax, a left-shifted and less dilated curve and a lower reliance on fat oxidation at high exercise intensities suggest that the difference in the fat oxidation kinetics is likely linked to impaired muscular capacity to oxidize NEFA in O. These results may have important implications for the appropriate exercise intensity prescription in training programs designed to optimize fat oxidation in O.

Dynamics of GH secretion during incremental exercise in obesity, before and after a short period of training at different work‐loads

Background  Growth hormone (GH) secretion is normally sensitive to physical exercise. Intensity and duration of exercise, fitness and age can all influence the GH response to exercise. In obesity, GH secretion is decreased both in basal conditions and in response to exercise.

The cortico-diaphragmatic pathway involvement in amyotrophic lateral sclerosis: Neurophysiological, respiratory and clinical considerations

Cortico-diaphragmatic pathway was investigated by means of transcranial magnetic stimulation (TMS), in 14 patients affected by definite amyotrophic lateral sclerosis (ALS) without clinical signs of respiratory impairment. Spirometry, gas analysis, and measurement of static inspiratory and expiratory pressures were performed in all patients. Forced vital capacity, forced expiratory volume at the first and second peak expiratory flow, sniff effort from FRC level (SNIP), maximal inspiratory and expiratory pressure at mouth (MIP/MEP), maximal transdiaphragmatic pressure (Pdimx) were considered. TMS was performed, recording by surface electrodes from hemidiaphragm, bilaterally. Latency of cortical and spinal motor-evoked potentials (Cx-MEP/Sp-MEP) and central motor conduction time (CMCT) were measured. None of the patients showed altered spirometry and gas levels. Seven patients showed decreased Pdimx and eight of MEP values. Four patients showed a delayed Sp-MEP. In one patient the Cx-MEP was abolished while the mean values of both Cx-MEP and CMCT were significantly increased (19.2+/-4.1 ms, P<0.0001; 10.8+/-4.8 ms, P<0.0001). Cx-MEP and CMCT did not show significant correlations with any of the respiratory measures. The patients with prolonged Sp-MEP, showed longer disease duration, lower Norris score, lower Pdimx and MEP values. In conclusion, cortico-diaphragmatic study is a sensitive measure to reveal subclinical diaphragmatic impairment although not correlated to respiratory measures.

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.

Lung Function and Methacholine Responsiveness among Adolescents in an Air-Polluted Area

Background: Outdoor air pollution is hazardous to human pulmonary health. Airway inflammation is an important cause of bronchial hyperresponsiveness. Information is not univocal about the potential effects of prolonged exposure to environmental air pollutants on lung function. Objectives: A cross-sectional study was performed to assess bronchial responsiveness to methacholine in children living in an air-polluted area. Afterwards, the same study protocol was repeated in children of similar age living in mountain valleys with virtually no air pollution. Methods: Every child underwent a lung function test, skin tests to common allergens, total serum levels of IgE, and a challenge to methacholine at increasing doses (PD20 FEV1). Subjects were 246 children 11–12 years old living in an air-polluted area, and 285 children 11–13 years old living in mountain valleys. Respectively, 156 and 161 were negative to skin tests and had serum total IgE <100 IU/ml, and had no asthma or other recurrent or ongoing respiratory symptoms. Results: Lung function data, adjusted for the effect of potential confounders showed significantly lower FVC, and even more so FEV1, in the children from the polluted area. After the exclusion of subjects with positive skin tests and serum total IgE >100 IU/ml and those with history of asthma or respiratory disorders, there were higher percentages of positive responses in the challenge to methacholine in children from the polluted area (28.9 vs. 15.5%, p < 0.001). Conclusions: These data may corroborate the possible importance of long exposure to air pollutants on the prevalence of bronchial aspecific hyperresponsiveness in otherwise normal children.