Mauro Cornacchia

I.R.C.C.S. Istituto Auxologico Italiano, Verbania, Piedmont, Italy

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Publications (4)12.2 Total impact

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    ABSTRACT: This study aimed to compare oxygen uptake ( V˙O2), 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. V˙O2 was monitored during the first 10 min and from the 25-30th 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 ( V˙O2END=100%), % V˙O2END 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 V˙O2 modulation between groups was observed, likely due to faster initial rates of V˙O2 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.
    Hormone and Metabolic Research 03/2014; · 2.15 Impact Factor
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    ABSTRACT: 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 (Fat max ) 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 ([Formula: see text]) in O than in L and from 65 to 85% [Formula: see text] in L than in O (p≤0.05). FORs were similar in O and in L from 35 to 60% [Formula: see text]. Fat max 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 Fat max , 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.
    PLoS ONE 01/2014; 9(2):e88707. · 3.53 Impact Factor
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    ABSTRACT: PURPOSE: It is demonstrated that aerobic exercise plays an important role in weight loss programs for obesity by increasing 24 h metabolic rate. While aerobic exercise can result in health and fitness benefits in obese subjects, also independently of weight loss, not completely clear are the effects of bouts of hard exercise on metabolic outcomes. The aim of this study was to test the hypothesis that short-term aerobic activity with anaerobic bouts might result in a greater improvement in the management of obesity than aerobic activity alone. METHODS: We studied 16 obese subjects (eight men) during a progressive cycloergometric test up to exhaustion, before and after 4 weeks of two different training schedules (6 days/week). Insulin and glycaemia, non-esterified fatty acids (NEFA) and lactic acid were sampled. Group A (eight subjects, four men) performed an aerobic cycle workout; Group B (eight subjects, four men) performed a 25 min aerobic workout followed by 5 min of anaerobic workout. All the subjects maintained their individual eating habits. RESULTS: The post-training test showed a decrease in AUCs NEFA in Group A (p < 0.05) and an increase in Group B (p < 0.05), together with an increase in lactic acid in Group A and a decrease in Group B (p < 0.01). β-cell function (HOMA2-B) revealed a reduction only in Group A (p < 0.05). Group B achieved a greatest reduction in body fat mass than Group A (p < 0.05). CONCLUSIONS: Aerobic plus anaerobic training seem to produce a greater response in lipid metabolism and not significant modifications in glucose indexes; then, in training prescription for obesity, we might suggest at starting weight loss program aerobic with short bouts of anaerobic training to reduce fat mass and subsequently a prolonged aerobic training alone to ameliorate the metabolic profile.
    European Journal of Nutrition 04/2013; · 3.13 Impact Factor
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    ABSTRACT: 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. To analyse the dynamics of GH response to a progressive cycloergometric test, conducted up to exhaustion, in adult normal subjects and obese patients, after a reconditioning program at different workloads. We studied eight lean subjects (four men, mean age 34.3 years, range 26-47 years, mean body mass index (BMI) 22.1 kg/m(2)). GH was sampled at baseline and during the last 30 s of each power output increase. Anaerobic threshold (AT) was detected by the V-slope method. The same test was carried out in 16 obese subjects (seven men, mean age 39.1 years, range 20-59 years, mean BMI 35.8 kg/m(2)) and repeated after a 4-week reconditioning program consisting of aerobic workout (Group A, eight subjects, three men, mean age 40.5 years, range 22-59 years, mean BMI 33.6 kg/m(2)), and aerobic plus anaerobic work (group B, eight subjects, four men, mean age 37.6 years, range 20-56 years, mean BMI 38.0 kg/m(2)) for 6 days/week, with no dietary restrictions. Mean exercise peak occurred at higher intensity in controls (140 vs 110 W, P < 0.05), and AT exceeded at higher work outputs than in obese subjects (102 vs 74 W, P < 0.05). In controls, GH response to exercise was prompt and further sustained after AT; in obese subjects, GH increased slowly and insignificantly before AT, thereafter it increased to lower levels than in controls (P < 0.001). Following the reconditioning period, both Group A and Group B of obese subjects failed to improve exercise performance as well as GH response to exercise before AT; beyond AT, a greater GH response to exercise occurred in Group B than Group A (7.59 ± 0.32 μg/l at peak of exercise) with significantly different Delta AUCs (Area Under the Curves) following AT: 30.5 ± 12 μg.min/l in Group A vs 124.2 ± 38 μg.min/l in Group B, P < 0.05. Our results confirm the blunted GH response to exercise in obese adults when compared to lean counterparts. With obesity, aerobic training poorly increases the GH response beyond AT, while supplemental anaerobic workload appears to increase GH response beyond AT. These observations may have implications for the prescription of physical exercise, which is one of the recommendations in the management of obesity.
    Clinical Endocrinology 10/2010; 73(4):491-6. · 3.40 Impact Factor