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Intensity of acute exercise does not affect serum leptin concentrations in young men
Abstract
We examined the effects of exercise intensity on serum leptin levels.
Seven men (age = 27.0 yr; height = 178.3 cm; weight = 82.2 kg) were tested on a control (C) day and on 5 exercise days (EX). Subjects exercised (30 min) at the following intensities: 25% and 75% of the difference between the lactate threshold (LT) and rest (0.25 LT, 0.75 LT), at LT, and at 25% and 75% of the difference between LT and VO2peak (1.25 LT, 1.75 LT).
Kcal expended during the exercise bouts ranged from 150 +/- 11 kcal (0.25 LT) to 529 +/- 45 kcal (1.75 LT), whereas exercise + 3.5 h recovery kcal ranged from 310 +/- 14 kcal (0.25 LT) to 722 +/- 51 kcal (1.75 LT). Leptin area under the curve (AUC) (Q 10-min samples) for all six conditions (C + 5 Ex) was calculated for baseline (0700-0900 h) and for exercise + recovery (0900-1300 h). Leptin AUC for baseline ranged from 243 +/- 33 to 291 +/- 56 ng x mL(-1) x min; for exercise + recovery results ranged from 424 +/- 56 to 542 +/- 99 ng x mL(-1) x min. No differences were observed among conditions within either the baseline or exercise + recovery time frames. Regression analysis confirmed positive relationships between serum leptin concentrations and percentage body fat (r = 0.94) and fat mass (r = 0.93, P < 0.01).
We conclude that 30 min of acute exercise, at varying intensity of exercise and caloric expenditure, does not affect serum leptin concentrations during exercise or for the first 3.5 hours of recovery in healthy young men.
... Leptin, özellikle enerji alımı ve metabolizmayla ilgili çok sayıda düzenleyici işlev gerçekleştirir ve bunlardan biri hipotalamo-hipofiz-adrenal (HPA) stres ekseninin aktivitesini kontrol eder. 28 Leptin, hipotalamustaki reseptörleri aracılığıyla yiyecek alımını ve enerji tüketimini etkiler. 28 Leptin, HPA eksenin 3 seviyesine etki eder. ...
... 28 Leptin, hipotalamustaki reseptörleri aracılığıyla yiyecek alımını ve enerji tüketimini etkiler. 28 Leptin, HPA eksenin 3 seviyesine etki eder. Bu seviyeler paraventriküler çekirdek, kortikotroplar ve adrenal bezdir. ...
... İştah merkezini inhibe etmek, lipogenezi durdurmak , T hücre aktivasyonun düzenlenmesinin yanı sıra enflamatuar reaksiyonların ve HPA ekseni aracılığıyla strese verilen tepkilerin düzenlenmesinde de rol alır. 28,29 Leptin, kemirgenlerde ve insanlarda vücut enerji depolarını algılamak ve düzenlemek için bir adiposit olarak işlev gören çok özel bir proteindir. Tüm vücut enerji dengesinin koordinasyonu, akut homeostatik sinyallere (örn., İnsülin, katekolaminler) ve daha uzun vadeli, kronik homeoretik sinyallere yanıt olarak enerji alımı ve harcamalarının karmaşık düzenlenmesini içerir. ...
... The effects of exercise, independently of loss of fat mass, have not been clearly established and reports on leptin response to exercise in humans have been conflicting Guerra et al. (2011e Weltman et al. (2000. Perusse et al., (1997) showed considerable interindividual differences in the leptin response to acute and chronic effects of aerobic exercise, some individuals showing either increase or reduction in leptin, others showing almost no change. ...
... Perusse et al., (1997) showed considerable interindividual differences in the leptin response to acute and chronic effects of aerobic exercise, some individuals showing either increase or reduction in leptin, others showing almost no change. Weltman et al., (2000) demonstrated that continuous exercise for 30 min, at intensities ranging from well below to well above the lactate threshold with exercise caloric expenditure ranging from 150 to 529 kcal, does not alter leptin release either during exercise itself or during 3.5 h of recovery thereafter. Other investigators have studied the effects of continuous, moderateintensity exercise on leptin concentrations and have found either no exercise-related change in circulating leptin Perusse et al. (1997) or an exercise-related decrease in blood leptin Jürimäe;Jürimäe (2005e Zaccaria et al. (2013. ...
... In the same manner, in other study Zaccaria et al. (2013) young trained males underwent a 4-h treadmill exercise at 65% of VO2max and plasma leptin levels decreased at the end of the exercise, reaching a significant reduction already after the second hour. However, our study did not concur with Weltman et al., (2000) who demonstrated that aerobic exercise for 30 min, at intensities ranging from well below to well above the lactate threshold with exercise caloric expenditure ranging from 150 to 529 kcal, does not alter leptin release either during exercise itself or during 3.5 h of recovery thereafter. Zaccaria et al., (2013) demonstrated that during a prolonged moderate intensity exercise, leptin decrease is significantly related to the total energy expenditure and norepinephrine concentrations seem to play an important role in the inhibition of leptin secretion. ...
The possible direct role of exercise intensity and duration on leptin concentrations is conflicting. The aim of this study was to evaluate the acute effects of high intensity interval (HIIE) and moderate intensity continuous (MICE) exercise on plasma leptin response. Seven young volunteers underwent three tests: 1) a treadmill graded exercise test to identify running peak velocity (PV); 2) HIIE: 5 × 2 min work bouts at 90% of PV, interspersed by 2 min of passive recovery and; 3) MICE: 30 min at 70 % of PV. Blood samples were drawn for the assays of leptin before and 30 minutes after HIIE and MICE. A 2-way repeated measures ANOVA showed a significant main effect of time [F(1,6) =17,52; p=0,006], no significant effect of condition (type of exercise) (F(1,6) = 0,16; p = 0,68) and no significant interaction (condition × time) (F(1,6)= 0,48, p=0,51). Leptin decreased 30 min after HIIE (t= 2,95, p=0,025) and MICE (t=4,18; p=0,005). There was no difference between the HIIE and MICE conditions immediately after exercise (t=0,90; p=0,40). After HIIE and MICE, leptin decreased in the same magnitude. It appears that both exercise modalities result in physical stress which is sufficient to improve short-term leptin sensibility.
... Several investigators reported that exercise may result in reductions depending on the duration and calorie expenditure whereas others have reported no change in leptin concentrations. Exercise doesn't generate decrease in leptin concentrations; Torjman et al. (1999), Weltman et al. (2000), Kraemer et al. (2002). Besides, exercise that generated decrease in leptin concentrations; Zafeiridis et al. (2003). ...
... While decreases are found in leptin levels in all studies as a result of exercises, data from investigations examining single exercise bouts suggest that serum leptin concentrations are unaltered by short duration (41 minutes or less), non-exhaustive exercise, but may be affected by short duration, exhaustive exercise (47). Weltman et al. (2000) found that 30 min of exercise at various intensities and caloric expenditure (from 150 ± 11 to 529 ± 45 kcals) in 7 healthy young men did not cause modifications in leptin levels during the exercise and during the recovery (3.5 hours) (20). Exercise programs preferred in studies have been planned as 9,10 and 12 weeks, for periods of 30 minutes and more. ...
... While decreases are found in leptin levels in all studies as a result of exercises, data from investigations examining single exercise bouts suggest that serum leptin concentrations are unaltered by short duration (41 minutes or less), non-exhaustive exercise, but may be affected by short duration, exhaustive exercise (47). Weltman et al. (2000) found that 30 min of exercise at various intensities and caloric expenditure (from 150 ± 11 to 529 ± 45 kcals) in 7 healthy young men did not cause modifications in leptin levels during the exercise and during the recovery (3.5 hours) (20). Exercise programs preferred in studies have been planned as 9,10 and 12 weeks, for periods of 30 minutes and more. ...
The aim of this study was to investigate the effect of serum leptin in rats performing various duration swimming exercises. In the study, 30 healthy albino wistar male rats with an average weight of 180-220 grams were divided into 5 groups including; control, water exercises, 15, 30 and 60 minutes swimming groups. Animals were swim-exercised for 90 days. At the end of 90 days, after performed urethane anesthesia, blood samples were taken by intracardiac way. Collected blood was analysed according to procedures. Data were analyzed by using SPSS 15. One-way anova and tukey multiple comparison test were performed in the study. The homogeneity of the variances was examined by Levene's statistic. Results showed that the leptin levels were as follows: control (1480,00 pg/ml), water exercise (705,83 pg/ml), 15 (602,33 pg/ml), 30 (396,67 pg/ ml) and 60 (435,83 pg/ml). Statistically significant difference was found between control and 30 minutes swimming group (p=0,012) and control and 60 minutes swimming group (p=0,017) (p<0,05). It is determined that 3 months of different terms (15, 30, 60 minute) of swimming exercise reduces the levels of leptin.
... Also, it has been reported that fasting adiponectin levels acutely increased after a two or three bouts of mild to moderate intensity exercises [24]. Conversely, evidence from healthy normal weight individuals suggested that short-term exercises don't modify leptin concentration levels [25,26]. No alteration of the circulating adiponectin levels following long-term exercises [27,28]. ...
... Caloric intake restriction and increasing the level of physical activities are substantial objectives of therapies prescribed for overweight or obese children [34]. Lately, there have been multiple studies demonstrated changes in serum adipokines level and lipid profile after different modes of exercise intervention focusing on the intensity or duration of training and/or diet control in young boys or girls who were overweight or obese [14,23,25], but no or very little reports have been focused on the effect the aerobic interval training against a balanced diet control regimen on the plasma adipokine levels and lipid concentration in overweight children. The purpose of the present study was to investigate changes of the plasma adipokines level, lipid profile, and HRQL after aerobic interval training and dietary control programs in overweight children. ...
... Additionally, evidence has shown that exercise training enhances adiponectin level [24]. Contrary to the results of this study, some investigators have reported no changes in leptin or adiponectin concentration following short or long term exercise training [25][26][27][28]. The controversial leptin and adiponectin responses to exercise training probably caused by variable sample sizes, different age groups, different degrees of obesity and/or different intensities and duration of exercise training. ...
Background: Lately, childhood obesity has gained more attention. The present study constructed to compare the effectiveness of aerobic interval exercises and dietary control on plasma adipokines level, lipid profile and the health-related quality of life in overweight or obese children.
Methods: Thirty-seven overweight or obese children at the age from 10-18 years were recruited and randomly classified into aerobic interval exercises (AIE) and dietary control (DC) groups. The Training load for AIE group was eight weeks of an intermittent short high intense burst of exercises throughout a regular training program primarily consisted of treadmill training. Whereas, subjects in the DC group were engaged in a balanced dietary plan. Plasma adipokines, lipid profile, and the health-related quality of life were assessed before and after the intervention.
Results: Both groups were similar at the baseline (p>0.05). Within the AIE group; leptin, adiponectin and all lipid
profile measures significantly changed (p<0.05). But, within the DC group, only leptin, high-density lipoprotein cholesterol (HDL-Cho) and low-density lipoprotein cholesterol (LDL-Cho) levels have been significantly changed (p<0.05). Further, the health-related quality of life (HRQL) indicated significant differences within both groups (p<0.05) with regard to both physical and psychosocial health. Finally, significant differences of leptin, HDL-Cho, LDL-Cho levels and the psychosocial health (p<0.05) were recorded between both groups in favor of the AIE group.
Conclusion: However, both aerobic interval training and balanced dietary control are useful to improve plasma adipokines level, lipid profile, and the HRQL in overweight or obese children. But, aerobic interval training is more helpful.
Keywords: Childhood obesity, Aerobic interval exercises, Dietary control, Plasma adipokines, Lipid profile, Health-related quality of life
... It is accepted that chronic exercise resulting in weight reduction corres0onds to a decline in leptin concentrations (18,21,24). 7Vhere is tnore contToversy surrounding the effects of acuLte exercise bouts and the corresponding changes, or lack thereof, in leptin concentrations (2,3,13,22,25). ...
... Weltman et al. (25) recently reported tha regardless of exercise intensity, leptin concentrations were unchanged during a 3.5-h recovery period after 30 niin of aerobic exercise. Weltman's data are corroborated by similar negative findings after other acute exercise bouts reported by other researchers (7,11,12,18,19). ...
... Unfortunately, the only other acute postexercise leptin studies that are available for comparison are for aerobic exercise. Although the majority of these previous studies have failed to observe any effect of exercise on leptin (7,11,12,18,19,25), our data support and extend the recent findings of Essig et al. (3), who also reported a delayed effect of exercise on leptin concentrations after treadmill running at 70% VO 2 mn , and those of Elias et al. (2), who reported a decrease after a treadmill run to exhaustion. Essig et al. (3) found a decrease in plasma leptin only at 48 h after exercise, but not at 0 or 24 h. ...
... In our meta-analysis, we did not find any differences between the effect of ET, ST, and CT on leptin and adiponectin concentrations in overweight and obese adults. A possible explanation for our results is that the changes in these parameters are not related to the type of exercise, but to the change in body weight [70,71] or the duration [72,73] and intensity [74] of the intervention. In a three-year weight loss study, Madsen et al. [70] indicated that weight loss greater than 10% can improve the levels of circulating adiponectin, as well as inflammatory parameters in obese subjects. ...
... Studies on the effects of acute exercise and the corresponding changes or lack thereof in leptin levels are less conclusive. In the study by Weltman et al. [72], 30 min of exercise at various intensities and caloric expenditures did not appear to be sufficient to affect leptin concentrations during exercise, or 3.5 h after training in healthy young men. On the other hand, Nindl et al. [73] indicated that, after acute strength exercises with an energy expenditure of 855 ± 114 kcals, leptin concentrations were lower compared to the control nine hours following the exercise. ...
The aim of this meta-analysis was to compare the effects of endurance, strength, and combined training on inflammatory markers and adipokine concentrations in overweight and obese adults. We performed a literature search of the Cochrane Library, PubMed, Scopus, and Web of Science databases and identified 24 randomised control trials published prior to June 2021. Our findings indicate that endurance training was significantly more beneficial than strength training in reducing C-reactive protein (CRP) (standard mean difference (SMD): −1.317, 95% confidence intervals (CI): −2.565, −0.070, p = 0.0385), interleukin 6 (IL-6) (SMD: −0.363, 95% CI: −0.648, −0.078, p = 0.0126), and visfatin (SMD: −0.618, 95% CI: −1.015, −0.222, p = 0.0023) concentrations. Moreover, combined training was more beneficial than strength training alone in lowering tumour necrosis factor-alpha (TNF-α) levels (SMD: 0.890, 95% CI: −0.301, 1.478, p = 0.0030). There were no differences between the effects of different types of training programmes on adiponectin and leptin concentrations. In conclusion, compared with strength training, endurance training is more effective in lowering CRP, IL-6, and visfatin concentrations, while combined training is more beneficial in reducing TNF-α levels in overweight and obese adults. Further studies are needed to determine which type of training has a better effect on adiponectin and leptin concentrations in this population.
... The exercises with sufficient intensity, which may alter the balance of energy consumption, may also lead to changes in leptin levels (8). Because, the exercise is a strong stimulant for the secretion of many hormones and has been suggested to also affect serum leptin (SL) levels (9). Exercise doesn't only increase energy consumption, but also decrease the fatty mass. ...
... Findings showing the increasing effects of leptin on food intake and energy metabolism have led to the need to investigate the relationships between leptin levels and exercise (15). But unfortunately, despite the potential importance of pediatric exercise metabolism, a limited number of studies are currently available on this topic (1,9). On the other hand, there are almost no studies that investigate the effect of acute exercise on SL levels of the pre-puberty girls. ...
Objective: The aim of this study was to determine the relationship between serum leptin (SL) level, which is the sensor of changes in energy intake and consumption, and maximal oxygen consumption (VO 2max) level in pre-puberty swimmer girls. Methods: Voluntary participants were divided into swimmer group (n: 16) and the control group (n: 15). Bruce protocol was used for acute exercise effect. Body composition, VO 2max and SL concentrations of the study group were measured before and after acute exercise. The paired-samples t-test and independent samples t-test were used for intra-and inter-group comparisons. The linear relations between the VO 2max and SL levels were determined by Pearson correlation coefficient. The level of significance was used at 0.05. Results: There was a significant difference between the SL level and test stage, test duration, HR of test-end, and VO 2max variables in both groups (p<0.05). There was a high level of negative correlation between VO 2max and SL levels in both groups after exercise (SG, r=-0.63; p<0.01, and CG, r=-0.60; p<0.05, respectively). Conclusion: Acute exercise resulted in decreased SL levels of both groups. It was concluded that regular swimming sports has a positive effect on body composition, VO 2max , and SL values of pre-pubertal girls.
... Long term, moderate exercise has been observed to suppress serum leptin levels based on the decrease in body fat percentage represented by BMI (body mass in-dex) (Sutken et al. 2006). Indeed, a large number of studies have been reported that short-term training sessions (<12 weeks) do not have an impact on leptin levels so long as they do not reduce fat mass (Kohrt et al. 1996;Gutin et al. 1999;Okazaki et al. 1999), while long-term training sessions (>12 weeks) decrease leptin levels (Torjman et al. 1999;Weltman et al. 2000;Kraemer and Castracane 2007). ...
... However, the volume of exercise and the amount of energy consumed are effective on changing the serum leptin level (Gomez-Merino at al. 2002). Thus, while a large number of the researchers have reported that exercise can cause a decrease in leptin concentrations based on the duration and calorie consumption (Leal-Cerro et al. 1998;Zafeiridis et al. 2003;Sutken et al. 2006) others have claimed that in general exercise which is short termed (<60 minutes) and which has an energy consumption of less than 800 kg calories does not change leptin concentrations (Torjman et al. 1999;Weltman et al. 2000;Kraemer et al. 2002;Bouassida et al. 2009). ...
The purpose of this paper is to compare the anaerobic power values and sprint performances of football players playing in different positions and to evaluate the association between these. A total of 40 male football players participated in the study voluntarily. For this aim, 20, 30 and 45.72 m sprint tests, vertical jump and Wingate anaerobic power tests were performed on the football players. The results of this study showed that there were significant differences for all the sprint tests. Moreover, statistically significant positive correlation was found between all the sprint tests, while statistically significant negative correlation was found between sprint and vertical jump tests. In addition, a negative correlation was found between 30 m sprint and peak power values. Also, the negative correlation found between the sprint and vertical jump values brings to mind that vertical jump trainings can be used to improve the ability of speed.
... Given that physical activity increases the activity of cardiovascular, breathing and the energy-generating systems, it can affect the OXA secretion (12). This has been shown in several studies in order to evaluate the role of physical activity in OXA secretion of non-human subjects (9,13). In addition, some studies reported no change in OXA levels after physical activity in animal specimens (13,14). ...
... This has been shown in several studies in order to evaluate the role of physical activity in OXA secretion of non-human subjects (9,13). In addition, some studies reported no change in OXA levels after physical activity in animal specimens (13,14). ...
... Long term, moderate exercise has been observed to suppress serum leptin levels based on the decrease in body fat percentage represented by BMI (body mass in-dex) (Sutken et al. 2006). Indeed, a large number of studies have been reported that short-term training sessions (<12 weeks) do not have an impact on leptin levels so long as they do not reduce fat mass (Kohrt et al. 1996;Gutin et al. 1999;Okazaki et al. 1999), while long-term training sessions (>12 weeks) decrease leptin levels (Torjman et al. 1999;Weltman et al. 2000;Kraemer and Castracane 2007). ...
... However, the volume of exercise and the amount of energy consumed are effective on changing the serum leptin level (Gomez-Merino at al. 2002). Thus, while a large number of the researchers have reported that exercise can cause a decrease in leptin concentrations based on the duration and calorie consumption (Leal-Cerro et al. 1998;Zafeiridis et al. 2003;Sutken et al. 2006) others have claimed that in general exercise which is short termed (<60 minutes) and which has an energy consumption of less than 800 kg calories does not change leptin concentrations (Torjman et al. 1999;Weltman et al. 2000;Kraemer et al. 2002;Bouassida et al. 2009). ...
The purpose of the present study is to investigate the association among the leptin levels and aerobic capacities of footballers, wrestlers and sedentary group. The study included a total of 130 volunteers (43 footballers, 41 wrestlers and 46 sedentary). The results showed a statistically significant difference between footballers and the sedentary group in terms of leptin levels both male and female. Leptin levels of the females were significantly higher than the males for all groups while MaxVO2 levels of the males were significantly higher than the males for all groups. The correlations between serum leptin levels and MaxVO2 levels of both males and females were no significant in all groups. Besides, as the aerobic capacity of the groups who did sports increased, their serum leptin levels decreased. Consequently, it can be ascertained that serum leptin levels of footballers and wrestlers are lower than those of the sedentary group and this difference is caused by the athletes’ aerobic capacities.
... Moreover, a greater decrease in leptin occurred with a decreased percentage of body fat. Weltman et al. [79] showed that physical activity of various levels of intensity and caloric expenditure (from 150 ± 11 to 529 ± 45 kcal) in 7 healthy young men did not affect the leptin concentration during exercise but also during convalescence (3.5 h). Our research showed statistically significantly lower leptin levels in older people qualified to the high physical fitness group (4.9 ± 1.2 ng/mL) compared to in the low physical fitness group (6.8 ± 2.5 ng/mL, Table 4). ...
An active lifestyle is of key importance for reduction of obesity and inflammation, as well as circulating levels of adipokines. Therefore, the aim of our study was to assess the relationship of physical fitness with chronic inflammatory status, and to evaluate biomarkers useful in the analysis of adipose tissue dysfunction. Sixty-three older adults (69.6 ± 5.1 years) were allocated to a high n = 31 (women n = 23 and men n = 8 male) or low physical fitness n = 32 (women n = 29 and men n = 3) group based on gait speed values (1.4–1.8 m/s or ≤ 1.3 m/s). The gait speed correlated with hand grip strength (rs = 0.493, p = 0.0001) and with leptin level (R = -0.372, p = 0.003), which shows the benefits of physical activity on muscle strength and circulating adipokines. In low physical fitness group, 58.1% individuals had adiponectin to leptin ratio (Adpn/Lep) < 0.5 revealing dysfunction of adipose tissue and high cardiometabolic risk; 20% of the group were obese with BMI ≥ 30 kg/m². In high physical fitness group, 25.8% of individuals had Adpn/Lep ≥ 1.0 i.e., within the reference range. Markers of systemic inflammation were significantly related to physical fitness: CRP/gait speed (rs = -0.377) and HMGB-1/gait speed (rs = -0.264). The results of the ROC analysis for Adpn (AUC = 0.526), Lep (AUC = 0.745) and HMGB-1 (AUC = 0.689) indicated their diagnostic potential for clinical prognosis in older patients. The optimal threshold values corresponded to 1.2 μg/mL for Adpn (sensitivity 74.2%, specificity 41.9%, OR = 1.4, 95%Cl 0.488–3.902), 6.7 ng/mL for Lep (sensitivity 56.2%, specificity 93.5%, OR = 14.8, 95%Cl 3.574–112.229), 2.63 mg/L for CRP (sensitivity 51.6%, specificity 84.3%, OR = 4.4, 95% Cl 1.401- 16.063) and 34.2 ng/mL for HMGB-1 (sensitivity 62.0%, specificity 86.6%, OR = 12.0, 95%Cl 3.254—61.614). The highest sensitivity and specificity were observed for Leptin and HMGB-1. The study revealed changes in inflammatory status in older adults at various levels of physical fitness and demonstrated diagnostic usefulness of adipokines in the assessment of adipose tissue inflammation.
... Generally, studies have reported that short-term exercise does not reduce leptin levels, and decreased leptin levels are also associated with circadian rhythm. [27,28] It has been determined that long-term exercises significantly reduce leptin levels, and the duration and form of exercise are important. [25,29,30] In this study, it was observed that feeding a high-fat diet significantly increased leptin levels, but exercise was not very effective in reducing leptin levels. ...
Aim: This study was performed to investigate the effect of exercise on serum resistin and leptin values in rats fed with a high-fat diet.
Material and Method: 24 Wistar albino male rats were used in the study. They were randomly divided into 4 groups, with 6 rats in each group. The groups were determined as the control group (C), exercise group (E), high-fat diet (HFD) group, and high-fat diet + exercise (HFDE) Group.
Results: When the findings obtained in this study were evaluated statistically, it was determined that the resistin values were similar in the C, E and HFDE groups, and higher in the HFD group compared to the other groups. It was observed that resistin value increased with high-fat diet and decreased with exercise. When evaluated in terms of leptin levels, the C and E groups showed similarity, while the HFD and HFDE groups showed similarity with each other. Although exercise decreased the leptin level, which was highly increased with a high-fat diet, it was not statistically significant.
Conclusion: It has been determined that feeding with a high-fat diet causes an increase in serum resistin and leptin levels, and exercise provides a significant decrease in resistin values, but is not effective in leptin levels.
... 60 dakikanın altında olan kısa süreli akut egzersizlerin, kandaki leptin seviyesinde herhangi bir değişikliğe sebebiyet vermediği veya çok az kayda değer olmayan değişikliklerin söz konusu olduğu belirtilmektedir (45,46). Bazı araştırmalarda ise; leptin düzeyinde azalma tespit edilmesi (47,48), gün içerisindeki ritimsel hareketlere veya hermokonsantrasyona bağlı bir değişken olarak düşünülmektedir. ...
GIRIŞ Yirmi birinci yüzyılın önemli sağlık problemlerinden biri olan ve son yıllarda dün-yanın her yerinde insan sağlığını önemli düzeyde tehdit eden obezite, toplum sağ-lığı açısından olumsuz yükselişine devam etmektedir. Obezite terminolojik olarak birçok farklı bakış açısına göre tanımlanmış olsa da, kısaca vücutta anormal yağ birikmesi şeklinde ortaya çıkan aşırı kilo alma veya şişman olma şeklinde ifade etmek mümkündür. Obezite sonuçları itibari ile sadece bireyin yaşam kalitesini olumsuz etkilemek-le kalmaz aynı zamanda dünya toplumlarının sağlık harcamalarına daha fazla kaynak aramaya mahkûm eder. Ayrıca obezite ile birlikte ortaya çıkan hastalık-lar ve bu hastalıklara yakalanan insanların bir sonraki insan nesline aktaracakları sağlıksız genetik mirasının da, sağlıksız bir neslin oluşmasına sebep olacağı göz ardı edilmemelidir. Obezitenin yaygınlığı ve riski artarken Dünya Sağlık Örgütü (DSÖ) başta olmak üzere, durumun ciddiyetinin farkında olan toplumlar obezite ile mücadele etme konusunda önemli kaynaklar aramaktadırlar. Bu mücadele çalışmaları arasında önemli olduğunu düşündüğümüz ve özellikle DSÖ'nün ısrarla üzerinde durduğu bireylerin inaktif yaşamdan uzak, aktif bir yaşam tarzı benimsemeleri yönündedir. Dolayısıyla egzersiz ve spor bilimcilere göre aktif yaşam tarzının önemli olduğunu ve bireylerin ancak egzersiz ile birlikte obezite karanlığından aydınlığa doğru çıka-bileceğini, ayrıca kaybedilen sağlıklı beden mirasını yeniden kazanabileceğimizi vurgulamaktadır. Bu noktada insanoğlunun sağlığı konusunda endişe duyan bilim insanları obezitenin önce nasıl engelleneceği ve daha sonra tamamen nasıl orta-dan kaldırılacağı konusunda birçok çalışma yapmaktadırlar.
... On the other hand, in women after menopause, the main source of fat tissue Armataz (the enzyme that converts androgens to estrogens) and increasing the size and number of fat cells in obese patients may contribute to the strengthening of Aromatase androgens. Furthermore, the increase in adipose tissue by increasing blood fats and reducing harmful levels of adiponectin and insulin levels and insulin-like growth factor type (IGF-1) which is involved in breast tumor progression and is related to Mutagenic activity [15]. ...
The aim of this study was to determine the effect of regular physical activity in water with and without ginger supplementation on adiponectin levels in women with breast cancer. The population of the study, 98 women with a mean age of breast cancer patients (48±8.5), weight (76±9)kg and fat mass (8.41±4) formed that voluntarily participated in this study that 40 people of them were selected as sample. subjects were randomly divided into four groups (Group 1: placebo, Group 2: Selected exercises in water placebo, Group 3 and Group 4 supplementation Ginger: Ginger supplements selected exercises in water) were divided into groups of ginger supplements and exercise The Water Department ginger supplements daily for 6 weeks orally 4 capsules (750mg) were used. Programs supplement group ginger exercise and water exercise group placebo juice containing a combination of increased intensity and distance training, with 50% to 75% heart rate reserve for 60 to 75 minutes in a pool with a width of 15 meters and a depth of 4m, 4 times a week 6 weeks was performed. Fasting blood samples were collected at pre-test and post-test. The result of the study All findings using the statistical software in SPSS23 and evaluated p<0.05. Ginger supplements or exercise in water increase adiponectin was compared to baseline. However, the exercise group in water exercise with ginger showed a much better effect on the inflammatory marker adiponectin and blood, than the exercise group in water with placebo or the ginger group alone. The findings show that a protective effect of non-pharmacological strategies such as exercise in water and plant anti-inflammatory agents such as ginger has been detected in inflammatory and metabolic responses in obese women with breast cancer.
... For both anaerobic and aerobic exercise, leptin levels increased substantially only in the HBF group and reached a peak 6 h after exercise. Most studies investigating the effects of short-term exercise on leptin report a reduction or no changes in leptin levels [54][55][56][57][58][59][60][61]. For example, a transient decline in leptin levels (6-14%) in individual subjects, up to 120 min post exercise, was shown in men and women 18-55 years of age and with a BMI corresponding to that of the HBF group in the current study after a treadmill test following the Bruce protocol to exhaustion [31,62]. ...
Human adipocytes release multiple adipokines into the bloodstream during physical activity. This affects many organs and might contribute to the induction of inflammation. In this study, we aimed to assess changes in circulating adipokine levels induced by intense aerobic and anaerobic exercise in individuals with different adipose tissue content. In the quasi-experimental study, 48 male volunteers (aged 21.78 ± 1.98 years) were assigned to groups depending on their body fat content (BF): LBF, low body fat (<8% BF, n = 16); MBF, moderate body fat (8–14% BF, n = 19); and HBF, high body fat (>14% BF, n = 13). The volunteers performed maximal aerobic effort (MAE) and maximal anaerobic effort (MAnE) exercises. Blood samples were collected at five timepoints: before exercise, immediately after, 2 h, 6 h, and 24 h after each exercise. The selected cytokines were analyzed: adiponectin, follistatin-like 1, interleukin 6, leptin, oncostatin M, and resistin. While the participants’ MAnE and MAE performance were similar regardless of BF, the cytokine response of the HBF group was different from that of the others. Six hours after exercise, leptin levels in the HBF group increased by 35%. Further, immediately after MAnE, resistin levels in the HBF group also increased, by approximately 55%. The effect of different BF was not apparent for other cytokines. We conclude that the adipokine exercise response is associated with the amount of adipose tissue and is related to exercise type.
... With regard to short-term (<60 min) studies, Elias et al. (2000) observed a decline in plasma leptin in males after graded treadmill exercise to exhaustion, and suggested that this may be associated with an elevated production in non-esterified fatty acids during exercise, which has been shown to be inversely correlated with leptin levels (Duclos et al., 1999). Weltman et al. (2000) reported that 30 min of exercise at, above, and below lactate threshold, an index of accelerated metabolism and exercise intensity, did not alter serum leptin concentrations in young males either during exercise or recovery. Perusse et al. (1997) reported no change in leptin levels in 51 untrained men and 46 untrained women following a 10-to12-min maximal exercise test on a cycle ergometer. ...
In this review, the current understanding of leptin’s role in energy balance, glycemic regulation, and cognitive function is examined, and its involvement in maintaining the homeostatic “harmony” of these physiologies is explored. The effects of exercise on circulating leptin levels are summarized, and the results of clinical application of leptin to metabolic disease and neurologic dysfunction are reviewed. Finally, pre-clinical evidence is presented which suggests that synthetic peptide leptin mimetics may be useful in resolving not only the leptin resistance associated with common obesity and other elements of metabolic syndrome, but also the peripheral insulin resistance characterizing type 2 diabetes mellitus, and the central insulin resistance associated with certain neurologic deficits in humans.
... In this context, the effect of physical exercise on leptin concentrations has been studied. Several studies suggest that short-term exercises (<60 min) and exercises that generated energy expenditure lower than 800 kcal do not modify serum concentrations of leptin (40,194,383). Instead, long-term and high-intensity exercise lower leptin concentrations in trained males running on a treadmill burning 800 and 1500 kcal (97). ...
Obesity is a global epidemic in developed countries accounting for many of the metabolic and cardiorespiratory morbidities that occur in adults. These morbidities include type 2 diabetes, sleep-disordered breathing (SDB), obstructive sleep apnea, chronic intermittent hypoxia, and hypertension. Leptin, produced by adipocytes, is a master regulator of metabolism and of many other biological functions including central and peripheral circuits that control breathing. By binding to receptors on cells and neurons in the brainstem, hypothalamus, and carotid body, leptin links energy and metabolism to breathing. In this comprehensive article, we review the central and peripheral locations of leptin's actions that affect cardiorespiratory responses during health and disease, with a particular focus on obesity, SDB, and its effects during early development. Obesity-induced hyperleptinemia is associated with centrally mediated hypoventilation with decrease CO2 sensitivity. On the other hand, hyperleptinemia augments peripheral chemoreflexes to hypoxia and induces sympathoexcitation. Thus, "leptin resistance" in obesity is relative. We delineate the circuits responsible for these divergent effects, including signaling pathways. We review the unique effects of leptin during development on organogenesis, feeding behavior, and cardiorespiratory responses, and how undernutrition and overnutrition during critical periods of development can lead to cardiorespiratory comorbidities in adulthood. We conclude with suggestions for future directions to improve our understanding of leptin dysregulation and associated clinical diseases and possible therapeutic targets. Lastly, we briefly discuss the yin and the yang, specifically the contribution of relative adiponectin deficiency in adults with hyperleptinemia to the development of metabolic and cardiovascular disease. © 2020 American Physiological Society. Compr Physiol 10:1047-1083, 2020.
... Here some studies found no changes 210,212,213 whereas others reported decreases 71,167,211 in leptin levels in response to exercise. ...
This narrative review summarizes current knowledge on the effects of physical activity (PA) on adipokine levels in individuals with overweight and obesity. Approximately 90 investigations including randomized control, cross‐sectional and longitudinal studies that reported on the effects of a single session of PA (acute) or long‐term PA (chronic) on adipokine levels in individuals with overweight/obesity were reviewed. The findings support the notion that there is consensus on the benefits of chronic exercise training—regardless of the mode (resistance vs. aerobic), intensity and cohort (healthy vs. diabetes)—on adipokine levels (such as tumour necrosis factor‐alpha, interleukin‐6, adiponectin, visfatin, omentin‐1 and leptin). However, several confounding factors (frequency, intensity, time and type of exercise) can alter the magnitude of the effects of an acute exercise session. Available evidence suggests that PA, as a part of routine lifestyle behaviour, improves obesity complications by modulating adipokine levels. However, additional research is needed to help identify the most effective interventions to elicit the most beneficial changes in adipokine levels in individuals with overweight/obesity.
... [10] Hickey et al. proposed that stability of leptin concentration immediately after short-term exercises is due to delayed exercise effect; [11] in this regard, Weltman et al. also did not find any decrease in leptin concentration during 3.5 h of recovery following 30 min of high-intensity exercise in seven healthy young men. [12] Another investigation conducted by Torjman et al. also did not observe any decrease in leptin concentration after 60 min of treadmill activity performed at 50% of maximal oxygen consumption by six healthy men. [13] The delayed effect of exercise may explain the reason of no change in leptin concentration immediately after a short-term exercise. ...
Aim: This study aimed to determine the delayed effect of one session of concurrent exercise on serum leptin and resistance insulin levels of sedentary men. Materials and Methods: Fifteen healthy young men with a mean age of 22.9 ± 1.7 years and a body mass index of 23.3 ± 1 kg/m2 voluntarily participated in this experimental research. They participated in one session of concurrent exercise including 20 min of aerobic running on a treadmill at 60%–70% maximum oxygen uptake plus a resistance exercise at the intensity of 70% of 1-repetition maximum with ten repetitions per set to second round. Blood serum leptin, glucose, insulin, and insulin resistance index were assessed before, 24, 48, and 72 h after the exercise program.Results: The results showed that leptin level did not change statistically significantly immediately and 72 h after the exercise termination (P > 0.05) but did decrease statistically significantly 24 and 48 h after the exercise program (P ≤ 0.05). The result also showed that insulin and insulin resistance levels decreased statistically significantly immediately after the exercise and lasted for up to 48 h postexercise (P ≤ 0.05); however, it returned to its initial value after 72 h of recovery (P > 0.05). Conclusions: It was concluded that energy use in one session of concurrent exercise might reduce leptin levels up to 48 h of recovery. In addition, a decrease in insulin, a known inducer of leptin expression in adipocytes, occurs before the decrease in leptin. This change may mediate the decrease of leptin concentration.
... In our study, it is surprising that there is no decrease in leptin levels despite the decrease in weight loss with HIIT exercise. However, there are other publications in the literature that suggest that exercise does not decrease leptin levels (Weltman 2000, Bouassida 2006, Torjman 1999. We also found that HIIT exercise in PCOS did not alter vaspin levels. ...
Aim: We aimed to investigate the metabolic effects of HIIT exercise on PCOS patients and how it affects adiponectin, vaspin and leptin.
Material and methods: Twenty women with PCOS were included in the study and were divided into two groups. HIIT program was applied for 10 PCOS and Medium Intensity Continuous Training (MICT) program was applied for other 10 PCOS. At the beginning and at the end of the study, total cholesterol, low-density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), triglyceride(TG), insulin, Adiponectin, Leptin, Vaspin levels of both PCOS groups were evaluated.
Results: When PCOS patients by performed HIIT exercise for 12 weeks, we found that the levels of leptin and vaspin did not change while adiponectin levels increased. Moreover serum levels of insulin, TG, total cholesterol, LDL-C decreased but levels of HDL-C increased.
Conclusion: HIIT increased in the adiponectin levels in women with PCOS and provided more weight loss.
... Egzersiz sonrasında büyüme hormonu ve norepinefrin konsantrasyonu artmasına rağmen her iki egzersizde de leptin konsantrasyonu sabit kalmıştır. Weltman ve ark.[44]7 sağlıklı genç erkekte leptin hormonunu, enerji tüketimleri ve şiddetleri birbirlerinden farklı olan (150±11 ile 529±45 kcal) 30 dakikalık egzersiz esnasında ve toparlanmada (3.5 saat) değişmediğini rapor etmişlerdir. Bouassida ve ark. ...
LEPTİN HORMONU: EGZERSİZ VE OBEZİTE İLE İLİŞKİSİ ÖZET Leptin vücut ağırlığının düzenlenmesinde anahtar rol oynadığı düşünülen, 16 kDa molekül ağırlığına ob gen ürünü protein yapılı bir hormondur. Leptin, sempatik sinir sistemi aktivasyonunu ve lipolizi atrrırarak enerji harcanımını arttırmaktadır. Ayrıca hipotalamus üzerinde etkili olarak iştahı baskılamaktadır. Bu derleme egzersizinin leptin konsantrasyonu üzerindeki etkilerini ve leptinin vücut ağırlığı düzenlenmesi, ve obezite üzerindeki etkilerini kapsayan güncel bilgileri içermektedir. İnsan denekleri üzerinde yapılan çalışmalarda egzersiz esnasındaki leptin konsantrasyonu verileri oldukça çelişkilidir. Araştırmalar leptin konsantrasyonunun değişmediğini, arttığını ve azaldığını rapor etmektedirler. Sonuç olarak fiziksel egzersiz ile plazma leptin konsantrasyonu arasındaki ilişki tam olarak aydınlatılabilmiş değildir. Bunun temel nedeni yapılmış olan araştırmalarda kullanılan egzersiz şiddeti, sıklığı ve süresindeki farklılıklar olabilir. Anahtar Kelimeler: Leptin, Obezite, Egzersiz, Enerji Homeostazisi, Besin Alımı LEPTIN HORMONE: RELATIONSHIP WITH EXERCISE AND OBESITY ABSTRACT Leptin the product of the ob gene is a proteohormone with a molecular mass of 16 kDa that is thought to play a key role in the regulation of body weight. Leptin increases energy expenditure by enhancing sympathic nervous activity and lypolysis. It also suppresses appetite by acting on the hypothalamus. This review will attempt to update the knowledge of leptin on the body weight regulation, obesity and the effect of exercise on leptin concentration. Controversial data on leptin concentration during exercise in human subjects have been published. Studies have reported increases, decreases or no change in leptin concentrations. It can be concluded that the relationship between physical exercise and the plasma concentration of leptin is not clear. The reasons for discrepancies among studies could be the differences in duration, intensity and frequency of the exercise employed in each study.
... Zoladz et al., [118] who conducted a research on 8 healthy males, examined leptin after maximal incremental exercise on a full stomach, and submaximal incremental exercise on an empty stomach. Growth hormone and norepinephrine concentration increased after exercise, but leptin concentration didn't change after both exercises.Weltman et al., [108] reported that leptin hormone didn't change during and in recovery (3.5 hours) after 30 min exercises with different calorie burn and intensities (150±11 with 529±45 kcal) among 7 healthy young males. Bouassida et al., reported that plasma leptin concentration didn't decrease during 45second supramaximal exercise done at 120% of peak aerobic strength among physically active 12 females and 5 males. ...
Background: Obesity is spreading all around the world rapidly, especially in developed and developing countries, due to physical inactivity related to technological developments and increase in the consumption on energy rich food. Discovery of the new stimulants that affect various parts of the hypothalamus and produced from some peripheral tissues, and understanding of their functions better increase our knowledge of energy homeostasis. Objective: Especially, the discovery of obese gene (16kDa, ob) product released from adipose tissue, discovery of leptin known as satiety hormone, the discovery of ghrelin known as hunger hormone, and the discovery of obestatin, which is the product of the same gene with ghrelin and thought to resist the effects of ghrelin on food intake started a new era about the opinions on obesity. Results: Exercise is a non-pharmacological method used by itself or along with food-intake limitation in obesity treatment and body weight control. This review will attempt to update the knowledge of ghrelin, leptin and obestatin on the body weight regulation and the effect of exercise training on ghrelin, leptin and obestatin concentration. In conclusion, Conclusion: findings of the current studies on acute and chronic exercise conducted on human subjects that examined the effect of exercise on ghrelin, leptin and obestatin contradict with each other. Some of these differences may have resulted from differences between intensity, duration, and type of the exercise, or the features of the subjects, different research designs such as time of food intake. For this reason, many more studies using various subject groups and different methods are required in the subject field.
... Egzersiz sonrasında büyüme hormonu ve norepinefrin konsantrasyonu artmasına rağmen her iki egzersizde de leptin konsantrasyonu sabit kalmıştır. Weltman ve ark.[44]7 sağlıklı genç erkekte leptin hormonunu, enerji tüketimleri ve şiddetleri birbirlerinden farklı olan (150±11 ile 529±45 kcal) 30 dakikalık egzersiz esnasında ve toparlanmada (3.5 saat) değişmediğini rapor etmişlerdir. Bouassida ve ark. ...
LEPTİN HORMONU: EGZERSİZ VE OBEZİTE İLE İLİŞKİSİ ÖZET Leptin vücut ağırlığının düzenlenmesinde anahtar rol oynadığı düşünülen, 16 kDa molekül ağırlığına ob gen ürünü protein yapılı bir hormondur. Leptin, sempatik sinir sistemi aktivasyonunu ve lipolizi atrrırarak enerji harcanımını arttırmaktadır. Ayrıca hipotalamus üzerinde etkili olarak iştahı baskılamaktadır. Bu derleme egzersizinin leptin konsantrasyonu üzerindeki etkilerini ve leptinin vücut ağırlığı düzenlenmesi, ve obezite üzerindeki etkilerini kapsayan güncel bilgileri içermektedir. İnsan denekleri üzerinde yapılan çalışmalarda egzersiz esnasındaki leptin konsantrasyonu verileri oldukça çelişkilidir. Araştırmalar leptin konsantrasyonunun değişmediğini, arttığını ve azaldığını rapor etmektedirler. Sonuç olarak fiziksel egzersiz ile plazma leptin konsantrasyonu arasındaki ilişki tam olarak aydınlatılabilmiş değildir. Bunun temel nedeni yapılmış olan araştırmalarda kullanılan egzersiz şiddeti, sıklığı ve süresindeki farklılıklar olabilir. Anahtar Kelimeler: Leptin, Obezite, Egzersiz, Enerji Homeostazisi, Besin Alımı LEPTIN HORMONE: RELATIONSHIP WITH EXERCISE AND OBESITY ABSTRACT Leptin the product of the ob gene is a proteohormone with a molecular mass of 16 kDa that is thought to play a key role in the regulation of body weight. Leptin increases energy expenditure by enhancing sympathic nervous activity and lypolysis. It also suppresses appetite by acting on the hypothalamus. This review will attempt to update the knowledge of leptin on the body weight regulation, obesity and the effect of exercise on leptin concentration. Controversial data on leptin concentration during exercise in human subjects have been published. Studies have reported increases, decreases or no change in leptin concentrations. It can be concluded that the relationship between physical exercise and the plasma concentration of leptin is not clear. The reasons for discrepancies among studies could be the differences in duration, intensity and frequency of the exercise employed in each study.
... Zoladz et al., [118] who conducted a research on 8 healthy males, examined leptin after maximal incremental exercise on a full stomach, and submaximal incremental exercise on an empty stomach. Growth hormone and norepinephrine concentration increased after exercise, but leptin concentration didn't change after both exercises.Weltman et al., [108] reported that leptin hormone didn't change during and in recovery (3.5 hours) after 30 min exercises with different calorie burn and intensities (150±11 with 529±45 kcal) among 7 healthy young males. Bouassida et al., reported that plasma leptin concentration didn't decrease during 45second supramaximal exercise done at 120% of peak aerobic strength among physically active 12 females and 5 males. ...
Background: Obesity is spreading all around the world rapidly, especially in developed and developing countries, due to physical inactivity related to technological developments and increase in the consumption on energy rich food. Discovery of the new stimulants that affect various parts of the hypothalamus and produced from some peripheral tissues, and understanding of their functions better increase our knowledge of energy homeostasis. Objective: Especially, the discovery of obese gene (16kDa, ob) product released from adipose tissue, discovery of leptin known as satiety hormone, the discovery of ghrelin known as hunger hormone, and the discovery of obestatin, which is the product of the same gene with ghrelin and thought to resist the effects of ghrelin on food intake started a new era about the opinions on obesity. Results: Exercise is a non-pharmacological method used by itself or along with food-intake limitation in obesity treatment and body weight control. This review will attempt to update the knowledge of ghrelin, leptin and obestatin on the body weight regulation and the effect of exercise training on ghrelin, leptin and obestatin concentration. In conclusion, Conclusion: findings of the current studies on acute and chronic exercise conducted on human subjects that examined the effect of exercise on ghrelin, leptin and obestatin contradict with each other. Some of these differences may have resulted from differences between intensity, duration, and type of the exercise, or the features of the subjects, different research designs such as time of food intake. For this reason, many more studies using various subject groups and different methods are required in the subject field.
... Short-term (≤60 min) exercises do not have or have a little effect on serum leptin levels [30][31]. But long-term exercises (>60 min) causes a decrease at serum leptin level [32-33-34]. ...
This study aims to investigate the effect of acute handball training on the irisin, leptin, insulin and blood lipids. 19 male handball players, who are between 15-17, regularly train and play for Turkish Super Young League, have been volunteer for this research. All of the members of this research group are healthy and play handball for at least 3 years. Blood samples have been drawn from players before and after training (30 min. warming, 10 min. stretching and 80 min. handball training). Arithmetic average, standard deviation and frequency distribution techniques have been used for analyzing data as descriptive statistics. A significant change have been detected at total cholesterol, triglyceride, HDL, LDL, AST, ALT, irisin and leptin parameters but not at VLDL when the pre-test and post-test compared. It has been concluded that the blood lipid levels generally change by the training and acute exercise. However, the glucose level increases and insulin level decreases after exercise. According to results, an increase has been observed at irisin level but a decrease has been observed at leptin level during the exercise. Additionally, irisin and leptin interaction may occur in different ages and metabolisms. It has been suggested that irisin and leptin interactions should be investigated deeper for more comprehensive data.
... Regarding exercise, a study performed in rowers showed a decline in circulating leptin concentrations immediately after maximal rowing (Jurimae & Jurimae, 2005). Moreover, reduced leptin levels were observed after one bout of long-term ET session (>60 min) that stimulates NEFA release (Desgorces et al., 2004;Duclos et al., 1999), or after exercise with significant levels of energy expenditure (higher than 800 kcal) (Leal-Cerro et al., 1998;Zaccaria et al., 2002); however, several others studies reported no effects of acute exercise in the levels of leptin of healthy trained or untrained individuals (Ferguson et al., 2004;Olive & Miller, 2001;Perusse et al., 1997;Weltman et al., 2000). Regarding chronic exercise, both ET Perusse et al., 1997) and RT (Fatouros et al., 2005) programs seem to result in reduced fat mass accompanied by lower leptin concentrations in healthy individuals. ...
... In contrast to the findings on leptin and nesfatin-1, baseline irisin levels normalised to total body weight were significantly higher in the trained group compared to those of the untrained group in the of some previous studies [11,18], but it contrasts with findings of exercise-induced decreases in leptin levels [9]. Based on the finding of individual-based variations in leptin levels (i.e. ...
The aims of this study were to investigate the impacts of acute aerobic exercise on circulating levels of hormones associated with energy metabolism, namely leptin, nesfatin-1 and irisin, in trained and untrained male subjects and to determine whether the timing of the exercise (i.e. morning or night) amplified these impacts. Thirty trained (19.2±0.7 years) and 30 untrained (19.5±0.6 years) male subjects performed two aerobic running exercises (3 days between tests) to 64-76% of the subjects’ maximal heart rate for about 30 min. Pre- and post-exercise venous blood samples were taken and analysed for leptin, nesfatin-1 and irisin using enzyme-linked immunosorbent assay (ELISA). Paired samples and independent samples t-tests were used to analyse data. Irisin levels increased in all the subjects (p<0.001). In both groups, nesfatin-1 levels increased significantly after the night-time exercise (p<0.05). Importantly, leptin and nesfatin-1 levels varied among the trained and untrained groups: Both leptin and nesfatin-1 levels increased in 4 (13%) and 12 (40%) subjects, respectively, after the morning exercises, and they increased in 9 (30%) and 10 (33%) subjects, respectively, after the night-time exercise. They decreased in 5 (16%) and 7 (23%) subjects, respectively, after the morning exercise and in 6 (20%) and 3 (10%) subjects, respectively, after the night-time exercise. Exercise may result in increased energy consumption by altering irisin levels. However, due to variations among individuals, increasing leptin and nesfatin-1 levels by reducing food intake may not be applicable.
... In this respect, there are also studies in the literature showing that short-term exercise (<60 min.) has no effect on serum leptin levels (Weltman et al., 2000;Essing et al., 2000;Houmard et al., 2000;Olive and Milller, 2001;Sütken et al., 2006;Yamaner et al, 2010). The aim of this study is to investigate the effects of four weeks training on plasma leptin levels and body fat percentages in junior female judokas. ...
... This hormone is the main peptide secreted from the adipose tissue; its serum concentration is an important index in the regulation of food intake and energy consumption. Various factors might influence gene expression and plasma leptin level, including exercise and physical activities (6). The effects of physical activity on the leptin level have recently been a hotly debated issue. ...
... In this respect, there are also studies in the literature showing that short-term exercise (<60 min.) has no effect on serum leptin levels (Weltman et al., 2000;Essing et al., 2000;Houmard et al., 2000;Olive and Milller, 2001;Sütken et al., 2006;Yamaner et al, 2010). The aim of this study is to investigate the effects of four weeks training on plasma leptin levels and body fat percentages in junior female judokas. ...
The purpose of this study is to investigate the effects of four weeks judo training on plasma leptin levels. Twenty-five female national team athletes with a mean age of 18.12±1.12 years; body weight of 62.72±22.72 kg; body height of 164.28±7.28 cm, BMI of 23.17±6.28 kg/m 2; training experience of 6.56±5.44 years participated in this study. The data were collected from junior female judokas who trained six times in a week for two hours daily. Physical measurements and blood samples were taken before and after four weeks of training including technical, tactical and physical preparations. Body fat percentages were measured by using the Tanita Bioimpedance BC-418 (Tokio, Japan). Statistical Package for Social Science 15.0 (SPSS) was used to analyse the obtained results. Before and after the training, paired samples t-test was used to evaluate the differences between serum leptine and body fat percentages. Results of this study showed that pre-training serum leptin levels were significantly lower than post-training levels (p<0.01). There was also significant decrease in body fat percentages after four week training (p<0.01). Four weeks judo training results in a decrease in total body fat and serum leptin level in junior female judokas. It may be considered that lowered serum leptin levels were due to the decrease of the body fat percentage after four weeks training.
... Kısa süreli (! 60 dakika) egzersizler serum leptin düzeylerinde değişikliğe yol açmaz ya da çok az değişiklik yapar (25)(26)(27)(28). Bazı çalışmalarda (27,29) serum leptin düzeylerinde azalma bulunması, gün içi ritme ya da hemokonsantrasyona atfedilebilir. ...
Amaç: Bu derlemede egzersizin leptin konsantrasyonları üzerine etkilerini gözden geçirmek amaçlanmıştır. Ana bulgular: Leptin yiyecek alımını azaltırken enerji tüketimini artırır. Leptin düzeyleri yağ dokusu miktarı ile ilişkilidir. Leptin düzeyi kısa süreli akut egzersizlerle değişmezken uzun süreli akut egzersizlerle azalır. Bu azalma egzersizden yaklaşık 48 saat sonra açığa çıkar. Yağ kitlesi kaybı yapmayan kısa süreli (!12 hf) antrenmanlar leptin düzeylerini değiştirmezken uzun süreli (" 12hf) egzersizler leptin düzeylerini azaltır. Sonuç: Egzersizin enerji dengesine ve vücut yağ kitlesine yaptığı güçlü etkiler leptin salgılanmasını değiştirebilir. Anahtar kelimeler: Leptin, egzersiz, antrenman, vücut yağı The effects of exercise on leptin concentrations Objective: It was aimed to review the effects of exercise on leptin concentrations. Main findings: Leptin decreases food intake and increases energy expenditure. Leptin levels are positively correlated with body fat mass. Short term acute exercises do not cause to change leptin concentrations, but long term acute exercises cause to decrease it and this occurs approximately 48 hours after the exercise. Short term exercise training (!12 wk) does not change leptin levels, but induces loss of fat mass. Long term exercise training (" 12 wk) reduces leptin levels. Conclusion: Strong impacts of exercise on energy balance and fat mass alternations can change leptin secretion.
... Regarding the effect of exercise on leptin levels, there is no consensus in the literature, since some studies have found no changes in levels [84,106,116,121,123] whereas others report a reduction [53,81,83,90,110]. A few studies have described increased levels of circulating leptin [21,60]. ...
A number of studies to better understand the complex physiological mechanism involved in regulating body weight have been conducted. More specifically, the hormones related to appetite, leptin and ghrelin, and their association to obesity have been a focus of investigation. Circadian patterns of these hormones are a new target of research. The behaviour of these hormones in individuals subject to atypical working times such as shiftwork remains unclear. Shiftwork is characterized by changes in biological rhythms and cumulative circadian phase changes, being associated with high rates of obesity and metabolic syndrome. Truck drivers, who work irregular shifts, frequently present a high prevalence of obesity, which might be associated with work-related factors and/or lifestyle. In this context, the aim of this paper was to discuss the relationship of body mass index, appetite-related hormones and sleep characteristics in truck drivers who work irregular shifts compared with day workers.
... Quanto à intensidade, alguns autores 26,27 demonstram que somente exercícios físicos realizados em alta intensidade são capazes de reduzir os níveis de leptina circulante. Diferentemente, outros pesquisadores demonstraram que a intensidade do exercício aeróbio não modifica os níveis plasmáticos de leptina logo após o esforço, nem após a recuperação 27,28 . ...
INTRODUÇÃO/OBJETIVO:
O presente estudo se propôs a verificar a influência do exercício físico aeróbio associado aos exercícios de resistência sobre os níveis séricos de leptina e percentual de gordura corporal de adultos com sobrepeso ou obesidade.
MÉTODOS:
O grupo de estudos foi composto por 15 pessoas, cinco homens e 10 mulheres, com média de idade de 52 anos, com sobrepeso ou obesidade de acordo com critérios da Organização Mundial de Saúde. O programa de exercícios físicos foi realizado três vezes na semana, durante 14 semanas. Era constituído de alongamento, 30 minutos de exercício aeróbio de intensidade moderada e exercícios de resistência muscular localizada. Os dados obtidos foram analisados por meio de estatística descritiva e teste "t" de Student, adotando-se um nível de significância de 5%.
RESULTADOS:
Os resultados demonstraram redução no peso corpóreo, índice de massa corporal (IMC) e leptinemia em resposta às atividades físicas, porém somente a redução na leptinemia foi significativa (p<0,05).
CONCLUSÃO:
O protocolo de exercícios adotado foi eficaz na redução dos níveis séricos de leptina em adultos com sobrepeso ou obesidade. Acredita-se que um maior tempo de intervenção com exercícios físicos traga melhores resultados sobre a composição corporal e normalização da leptinemia sérica.
Intellectual disability is characterized by limitations in cognitive development that impact an individual's ability to learn. 1 Individuals with intellectual disabilities typically have limited attention spans and difficulties in acquiring information and expressing emotions and opinions due to deficits in cognitive and intellectual capabilities. 2,3 Moreover, insufficient engagement in physical and social activities hinders their capacity for independent living, leading to health concerns such as obesity caused by unhealthy eating behaviors, including excessive consumption, selective eating, and frequent intake of high-calorie foods. 4,5 Furthermore, decreased physical activity levels are associated with diminished physical fitness and Results: A total of 3,968 records were identified, with 14 studies meeting the inclusion criteria. Of these, 6 studies focused on children and adolescents, while 8 studies involved adults. Significant improvements were observed in physical fitness, motor performance, mobility skills, pelvic alignment, abdominal obesity, blood lipids, spontaneity, physical self-concept, adaptive behavior , and social competence for children and adolescents. For adults, notable improvements were reported in balance, physical fitness, physical activity levels , upper limb function, inflammatory markers, blood lipids, adaptive behavior, satisfaction, stress reduction, self-efficacy, emotional function, and cognitive function. Conclusion: Exercise programs provided by community welfare centers in Korea have a significant positive impact on the physical, psychological, and mental health of individuals with intellectual disabilities. These programs are essential for enhancing the quality of life for this population.
Several types of hormones exert control over appetite in humans. This narrative review explores the effects of exercise and training on the concentrations of gastrointestinal hormones in healthy and obese individuals. It focuses on the major hormones of appetite regulation: ghrelin, glucagon-like peptide 1, peptide YY, cholecystokinin, leptin, and oxyntomodulin. In normal-weight and overweight individuals, responses to most of these hormones depend on the intensity of exercise and training. However, findings in obese individuals are limited in number and, to some degree, contradictory. Although some gastrointestinal hormones have been studied extensively (eg, leptin), most have not been investigated systematically. Further research is required to confirm the effectiveness of exercise and training on gut hormones and to better understand the effect of gut hormones on appetite and hunger suppression in individuals with obesity. Investigations to elucidate the impact of various forms of exercise that have recently engaged the public interest, eg, high-intensity interval training or concurrent aerobic and resistance training, are warranted.
Gestational diabetes mellitus (GDM) is described as glucose intolerance of variable intensities that begins or is first diagnosed during pregnancy and usually resolves during the first postpartum weeks. It is generally accepted that women with GDM exhibit eminent insulin resistance and are at high risk for developing type 2 diabetes mellitus (T2DM) after delivery. The mechanism responsible for the development of T2DM is unclear, but obesity and weight-related factors are strongly implicated. Adipocyte-derived cytokines (adipokines) provide an important link between obesity-related disorders and insulin resistance. Insulin resistance during pregnancy and at postpartum has been partially explained by the influence of adipokines derived from fat tissue as leptin. A positive association between leptinemia and insulinemia has been reported in numerous studies of obese and non-obese humans. Experimentally, increased insulin levels may stimulate leptin production in adipocytes, and vice versa; an increase in leptin levels may lead to insulin resistance and alter β-cell secretory capacity.
Kaveh Hariri Asli and others/ Book Description: This book provides new methods to novel applications of existing methods to gain understanding of the material and/or structural behavior of new and advanced systems. The authors provide innovative chapters on the growth of educational, scientific, and research activities among athletes and provides a medium for mutual communication between international sports academia. This book publishes significant research reporting new methodologies and important applications in the fields of anthropometric measuring and software. Software and anthropometric-based research findings to date contribute to the scholarly debates over mortality trends, the nature of slavery, and the outcomes of industrialization and economic development. On the other hand, these ideas were included in the proper analysis to provide a dynamic response to the shortcomings of body motion. This book also describes advanced technology and high speed detectors/equipment to determine the operational procedures to avoid hazards on human health, economics and human biology. Consequently, the results within this book will help to reduce the risk of sport injuries. (Imprint: Nova)
and others) Book Description: This book provides new methods to novel applications of existing methods to gain understanding of the material and/or structural behavior of new and advanced systems. The authors provide innovative chapters on the growth of educational, scientific, and research activities among athletes and provides a medium for mutual communication between international sports academia. This book publishes significant research reporting new methodologies and important applications in the fields of anthropometric measuring and software. Software and anthropometric-based research findings to date contribute to the scholarly debates over mortality trends, the nature of slavery, and the outcomes of industrialization and economic development. On the other hand, these ideas were included in the proper analysis to provide a dynamic response to the shortcomings of body motion. This book also describes advanced technology and high speed detectors/equipment to determine the operational procedures to avoid hazards on human health, economics and human biology. Consequently, the results within this book will help to reduce the risk of sport injuries. (Imprint: Nova)
Purpose:
To examine the effects of 3 days of intermittent fasting (3d-IF: abstaining from eating/drinking from dawn to sunset) on physical performance and metabolic responses to repeated-sprints (RS).
Methods:
Twenty-one active males performed an RS-test [2 sets: 5×5-second maximal-sprints with 25 seconds of recovery between sprints and 3 minutes of recovery between sets on an instrumented treadmill] in two conditions: counter-balanced fed/control session (CS) and fasting session (FS assessed on the 3rd day of IF; sessions: 4pm to 6pm, 7 days in-between). Biomechanical and biochemical markers were assessed pre- and post-exercise.
Results:
Significant main effects of IF were observed for sprints: maximal-speed (P=0.016), mean-speed (P=0.015), maximal-power (P=0.035), mean-power (P=0.049), vertical stiffness (P=0.032), and vertical center of mass displacement (P=0.047). Sprint speed and vertical stiffness decreased during the first and second sprints of set-2 (P=0.030). Post-exercise insulin decreased in CS (P=0.023) but not in FS (P=0.230). Free-fatty acid levels were higher in FS than that of CS at pre- (P<0.001) and at post-exercise (P=0.009). HDL-cholesterol was higher at post-exercise in FS (1.32±0.22-mmol.l-1) compared with that of CS (1.26±0.21-mmol.l-1, P=0.039). The triglyceride concentration was decreased in FS (P<0.05) compared with that of CS.
Conclusion:
The findings were that 3d-IF impaired speed and power through a decrease in vertical stiffness during the initial runs of the second set. The findings of the present study confirmed the benefits of 3d-IF: improved HDL-C and TG profiles while maintaining TC and LDL-C levels. Moreover, improving muscle power might be a key factor to retain a higher vertical stiffness and to partly counteract the negative effects of intermittent fasting. FS showed beneficial changes in biochemical marker levels from an overall health point of view.
Maintaining balance and stability for performing daily activity as well as sport skills is necessary. Despite such an important task in life, man had not been able to examine all the details of maintaining balance and many questions including how balance is established still remains unanswered. The purpose of this study was to compare two dimensional balance control strategy on two hands in elite male and female gymnasts. Ten male subjects with age of 18.21±1.10 yr, height of 165.69±4.21 cm, weight of 60.38±3.89 kg and another 10 female subjects with age of 15.03±0.78 yr, height of 155.81±3.8 cm, and weight of 46.10±2.4 kg participated in this study. Eight spherical reflective markers were placed on the anatomical landmark of upper extremities as well as on thigh in order to represent the segments. Using the three motion analyzer system equipped with three cameras and one force plate, the execution of balance on two hands for five seconds was recorded. Kinematics data including the position, speed and acceleration angles of segments and body joints was analyzed by Winanalyze software and kinetic data (force) was calculated by Bioware software. Anthropometric measures of each subject including segment’s mass, its center position, the length of each segment was determined. By defining a five segmental model (hand, elbow, arm, torso and lower extremity) through the inverse dynamic in Matlab software, the torque for wrist, elbow, shoulder, and hip joints for both groups was calculated. Statistical data analysis was performed by using MANOVA and independent t-test at p≤0.05. The most angular changes in both male and female groups were observed in wrist of both genders, whereas the shoulder, hip, knee and elbow joints were observed, consequently. The most changes in torque was observed in both gender followed by elbow, shoulder, and thigh, respectively. Due to results, the strategy of two dimensional control during the execution of balance on two hands in men and women is wrist, elbow, shoulder, and hip.
Introduction: Obesity results in some diseases such as of atherosclerosis diabetic and thereforeinfluence on the immune system, greatly. Given the undeniable role of sport in general health, the aim ofthis present study was to assay the effects of regular exercise on serum levels of immunoregulators factors(leptin, tumor necrosis factor- α (TNF- α) and interleukin-6) in obese and lean men.Material and methods: 37 male subjects divided two groups of obese and lean with body compositionanalyzer. Blood samples were taken 48 h before starting the aerobic training program. Then, both groupsperformed the aerobic training program included running with 65-85% of individual maximum heart rateon treadmill for 3 sessions per week, 30 minutes per session and 2 consecutive months. Then anotherblood sample was taken following the training period. Serum levels of leptin, TNF- α and interleukin-6of all subjects before and after the training period were measured using standard biochemical methodsfrom all the subjects and all the parameters were measured in both groups again.Results: Our results showed that the aerobic training resulted in a significant decrease in leptin levelsin obese (p=0.000) and non obese (p=0.004) peoples and also a significant decrease in TNF- α (p=0.042)in lean people. However, the aerobic training had no significant influence in the levels of interleukin-6 inboth groups.Conclusion: The results showed that regular and light aerobic exercises could decrase leptin levels inboth obese and lean men, but have differential effects on levels of TNF- α in both groups. These effectsmay influence functions of immune system and metabolism in obese and lean men in a different way.
Introduction: This study was conducted to determine the effect of twelve weeks of aerobic training on serum levels of leptin, vaspin, total antioxidant capacity (TAC) and malondialdehyde (MDA) in obese middle-aged women. Materials and Methods: In this quasi-experimental study, 30 sedentary, middle-aged women (mean±SD age 48.30±3.02 yr, body mass index 30.89±3.23 kg/m2 and body fat 32.88 ±2.71%) were randomized into the experimental (n=15) and control (n=15) groups. The experimental group performed twelve weeks aerobic training (3 times per week at an intensity of 65-75 % of maximum heart rate reserve). Blood samples were collected 24h before and 48h after the training. Data was analyzed by Student's t-test (P< 0.05). Results: Results showed a significant decrease in serum levels of leptin and MDA (P values 0.009 and 0.01 respectively) while TAC significantly increased (P=0.01) in the experimental group. Body fat percentage significantly decreased in the experimental group (0.0001), but serum vaspin levels were not significantly different between the two groups (P=0.93). Conclusions: Regular aerobic training is associated with weight loss and reduced body fat in obese women. As leptin production occurs in adipose tissue, subsequent decrease in body fat percent, serum leptin levels also occurred. On the other hand, aerobic training can improve oxidation/anti-oxidation in the body by reducing MDA concentration and increasing TAC.
Objective: Exercise activity could be an amendment to polycystic ovary syndrome (PCOS). However the acute and chronic effects of various exercise intensities on serum leptin levels are ambiguous. This study investigates the acute and chronic responses of various intensities of exercise on serum leptin levels and weights of female rats with PCOS. Methods: In this semi-empirical study, 80 adult Wistar rats (185±22 gr) after PCOS induction were divided into two groups. Group 1 participated in an exercise program at an intensity of 50%-55% maximal oxygen consumption (20 m/min), 70%-75% maximal oxygen consumption (28 m/min) and 80%-85% maximal oxygen consumption (34 m/min). Group 2 participated in an eight-week training program, three days a week for 60 minutes. One-way analysis of variance test (ANOVA) was used to compare differences between groups. Significance was p<0.05. Results: In the acute training group, there was no change in weight in the subgroups of group 1. In group 2, training reduced in the medium intensity 2 compared to the PCOS control 2 groups. Serum leptin levels did not respond to one session of exercise at various intensities in group 1 subgroups. Leptin levels significantly reduced in the medium intensity 2 group compared to the PCOS control 2 (p=0.044) group. Conclusion: One exercise session does not seem to significantly affect serum leptin levels. Exercise training at medium intensity probably can reduce leptin levels and weight in subjects as a non-pharmaceutical alternative in PCOS patients.
The impact of chronic training on pituitary function is best understood by a basic appraisal of the neuroendocrine physiology of any given individual axis and the more complex interactive pathophysiology among axes [1–12]. Interaxes interactions have received relatively little attention. Even evaluating a single neuroendocrine axis in its dynamic state is a complicated challenge, given combined feedforward and feedback activities among the key control loci within any given axis [13, 14]. For example, in the case of the growth hormone (GH) and insulin-like growth factor 1 (IGF-1) axis, hypothalamic GH-releasing hormone (GHRH) secreted by arcuate nuclei stimulates pituitary GH secretion acutely, whereas the somatostatinergic system originating in the paraventricular nuclei opposes GHRH action [15]. These two neuronal inputs are reciprocally interconnected by intrahypothalamic synapses and common impinging neuromodulator pathways [14]. In addition, secreted GH feeds back on brain GH receptors, stimulating somatostatin secretion and possibly inhibiting GHRH release. Available GH secreted into the bloodstream triggers IGF-1 production in various target tissues, and circulating IGF-1 is capable of inhibiting pituitary GH secretion indirectly and directly (see Fig. 4.1). Such feedforward (GHRH’s driving GH secretion) and feedback (GH’s inhibiting its own secretion, IGF-1’s inhibiting GH secretion, and so forth) dynamic control mechanisms in principle can be modified by the effects of exercise at one or more levels within the axis. Moreover, multiple determinants modulate neuroendocrine responses to training, such as the body composition of the individual, concurrent stress and/or weight loss, gender, diet and energy balance, concomitant drug or hormone use, age, puberty, pregnancy, and/or lactational status [16–18].
Ten collegiate rowers performed discontinuous incremental exercise to their tolerable limit on two occasions: once on a rowing ergometer and once on a treadmill. Ventilation and pulmonary gas exchange were monitored continuously, and blood was sampled from a venous catheter located in the back of the hand or forearm for determination of blood lactate ([La]) and plasma epinephrine ([Epi]) and norepinephrine ([NE]) concentrations. Thresholds for lactate (LT), epinephrine (Epi-T), and norepinephrine (NE-T) were determined for each subject under each condition and defined as breakpoints when plotted as a function of O2 uptake (VO2). For running, LT (3.76 +/- 0.18 l/min) was lower (P < 0.05) than Epi-T (4.35 +/- 0.14 l/min) and NE-T (4.04 +/- 0.19 l/min). For rowing, LT (3.35 +/- 0.16 l/min) was lower (P < 0.05) than Epi-T (3.72 +/- 0.22 l/min) and NE-T (3.70 +/- 0.18 l/min) and was lower (P < 0.05) than LT for running. Within each mode of exercise, Epi-T and NE-T did not differ. Because LT occurred at a significantly lower VO2 than either Epi-T or NE-T, we conclude that catecholamine thresholds, per se, were not the cause of LT. However, for both modes of exercise LT occurred at a plasma [Epi] of approximately 200-250 pg/ml (rowing, 221 +/- 48 pg/ml; running, 245 +/- 45 pg/ml); these concentrations are consistent with the plasma [Epi] reported necessary for eliciting increments in blood [La] during Epi infusion at rest. Plasma [NE] at LT differed significantly between modes (rowing, 820 +/- 127 pg/ml; running, 1,712 +/- 217 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
The factors responsible for the variability in plasma leptin levels observed among individuals with similar body compositions remain unclear. To examine the impact of dietary variables, we compared the changes in leptin levels induced by fasting and dietary fat restriction with the expected decrease following a significant loss in adipose mass. A 21.4 +/- 3.7% weight loss led to a 76.3 +/- 8.1% decrease in mean plasma leptin level (25.2 +/- 9.3 to 6.1 +/- 3.4 ng/mL, P = 0.0001) in a group of 9 obese males. Despite a weight loss of only 2.6 +/- 0.8%, mean plasma leptin levels fell by 61.9 +/- 25.2% (8.5 +/- 4.5 to 2.4 +/- 0.5 ng/mL, P < 0.01) in 7 nonobese females subjected to 3 days of fasting. Leptin levels in fasted subjects returned to baseline within 12 h of refeeding. Individual high- and low-fat meals given to 19 subjects after an overnight fast had no effect on plasma leptin levels. Reduction in dietary fat content from 37-10% of total calories for 7 weeks was also without effect on plasma leptin levels in these subjects. We conclude that plasma leptin levels primarily reflect total adipose mass, rather than meal consumption or dietary energy source, but that the reduction in leptin levels with ongoing fasting is disproportionate to the reduction in adipose mass. The ability of fasting to deactivate this presumed physiological satiety system may have been advantageous in environments characterized by rapid changes in food availability.
Leptin, the product of the ob gene, is a recently discovered hormone secreted by adipocytes that regulates food intake and energy expenditure. Growth hormone (GH) secretion is markedly influence by body weight being markedly suppressed in obesity and underweight. The aim of the present study was to study whether leptin can act as a metabolic signal connecting the adipose tissue with the growth hormone axis. We administered leptin antiserum (10 ul, i.c.v.) or normal rabitt serum (NRS; 10 ul, i.c.v.) to freely moving fed rats. Furthermore we assessed the effect of leptin administration (10 ug, i.c.v.) on fed and fasted rats. Spontaneous GH secretion was assessed over 6 hours with blood samples taken every 15 min. Administration of leptin antiserum led to a decrease in spontaneous GH secretion as assessed by the area under the curve (AUC) (168+/-72 ng/ml/6h) in comparison to NRS-treated rats (813+/-179 ng/ml/6h, p<0.01). While leptin administration (10 ug/rat; i.c.v.) to normal fed rats did not modify spontaneous GH secretion, leptin administration to fasted rats led to a reversal of the inhibitory effect exerted by fasting on GH secretion (AUC, 1650+/-351 ng/ml/6h vs 77+/-32 ng/ml/6h, p<0.01). This data suggests that leptin is a metabolic signal that regulates GH secretion.
Leptin, the protein product of the ob gene, may be involved in the regulation of energy balance. Although a clear relationship between energy intake and plasma leptin concentrations has been demonstrated in humans, little is known about the effect of exercise on leptin metabolism. In the present study, we evaluated abdominal adipose tissue leptin production in vivo by arteriovenous balance at rest and during 60 min of moderate-intensity cycle ergometer exercise (50% of maximal heart rate) in five sedentary male subjects (mean age 38.4 +/- 1.7 yr, body mass index (28.4 +/- 4.2 kg/m2). Blood samples were taken simultaneously from an abdominal vein, draining sc adipose tissue, and a radial artery, at rest and every 10 min during exercise. Adipose tissue blood flow was determined by the xenon washout technique. Plasma leptin concentrations did not change throughout exercise and were the same as the values obtained during resting conditions. Average net adipose tissue leptin production rates during exercise (3.07 +/- 0.89 ng/100 g-1.min-1) also were similar to resting values (3.86 +/- 0.95 ng/100 g-1.min-1). These results demonstrate that plasma leptin concentrations and leptin production do not change during an acute bout of moderate-intensity aerobic exercise.
The acute (single bout of exercise) and chronic (exercise training) effects of exercise on plasma leptin were investigated in 97 sedentary adult men (n = 51) and women (n = 46) participating in the HERITAGE Family Study. Exercise training consisted of a standardized 20-wk endurance training program performed in the laboratory on a computer-controlled cycle ergometer. Maximal oxygen uptake, body composition assessed by hydrostatic weighing, and fasting insulin level were also measured before and after training. Pre- and posttraining blood samples were obtained before and after completion of a maximal exercise test on the cycle ergometer. Exercise training resulted in significant changes in maximal oxygen uptake (increase in both genders) and body composition (reduction of fat mass in men and increase in fat-free mass in women). There were considerable interindividual differences in the leptin response to acute and chronic effects of exercise, some individuals showing either increase or reduction in leptin, others showing almost no change. On average, leptin levels were not acutely affected by exercise. After endurance training was completed, leptin levels decreased significantly in men (from 4.6 to 3.9 ng/ml; P = 0.004) but not in women. However, after the training-induced changes in body fat mass were accounted for, the effects of exercise training were no longer significant. Most of the variation observed in leptin levels after acute exercise or endurance training appears to be within the confidence intervals of the leptin assay. We conclude that there are no meaningful acute or chronic effects of exercise, independent of the amount of body fat, on leptin levels in humans.
The effect of endurance training on plasma leptin levels was investigated in 15 obese male subjects (age 37.3 +/- 5.2 yr, body weight 96.5 +/- 13.6 kg, and body mass index 29.8 +/- 3.0 kg/m2) in a weight loss and exercise program. After 4 mo of treatment consisting of a very low energy diet (VLED) and endurance exercise training (3-4 times weekly, 1 h sessions, moderate intensity), two groups were formed. One group continued the exercise sessions (trained subjects, n = 7) and the other group stopped with the exercise program (control, n = 8). Measurements of anthropometry, aerobic power, and fasted blood samples were executed at fixed time points (0, 2, 4, 10, and 16 mo). With partial regression analysis, keeping the changes in insulin and body fat percentage constant, it was shown that the number of hours of exercise training was significantly correlated with changes in leptin levels, during the 16-mo period (r = 0.56, P < 0.05). Changes in insulin levels were significantly related to the changes in leptin levels (r = 0.47, P < 0.05), which were less for changes in body fat percentage (r = 0.42, P = 0.07). During the VLED, the change in insulin concentration affected leptin levels significantly (r = 0.79) but changes in body fat percentage were not noted. It is concluded that endurance exercise training decreased plasma leptin levels independently of changes in plasma insulin levels and body fat percentage.
Leptin is a hormone produced by the adipocytes to regulate food intake and energy expenditure at the hypothalamic level. It is commonly accepted that the main determinants of leptin secretion are the net amount of body fat and the mean size of adipocytes. On the contrary, important vectors of energy flux in the organism, such as food intake and energy expended on exercise, are not thought to be regulators of that secretion. To understand whether leptin is regulated by an acute energy expenditure such as strenuous exercise, 29 male athletes who had trained for marathon running were studied before and after a marathon run and compared with 22 nonobese, age-, sex-, and body mass index (BMI)-matched sedentary controls. Controls and marathon athletes showed no differences in BMI or fat-free mass. Marathon runners showed a strong reduction in total fat mass (6.2 +/- 0.4 kg; 9.1 +/- 0.5% of body fat) compared with controls (12.3 +/- 0.5 kg; 16.1 +/- 0.5% of body fat; P < 0.05). This difference in body composition was paralleled by a mean serum leptin level that in marathonians (2.9 +/- 0.2 micrograms/L) was significantly (P < 0.05) reduced compared with that in controls (5.1 +/- 0.6 micrograms/L). It is remarkable that the ratio of leptin per kg body fat, showed a very good agreement between the two groups, 0.40 +/- 0.04 microgram/L.kg for controls and 0.46 +/- 0.03 microgram/L.kg for marathonians. In the two groups, leptin was correlated with both body weight, BMI, and fat mass (P < 0.001). The marathon trajectory was the standard 42.195 km accomplished in an average time of 3 h, 17 min, 7 s, with a calculated energy expenditure of over 2800 Cal. After the marathon run, a water imbalance occurred, with a significant decrease in body weight and an increase in serum albumin. A significant (P < 0.05) reduction in leptin values was observed after the run (2.6 +/- 0.2 micrograms/L) compared with before (2.9 +/- 0.2 micrograms/L), which was more relevant considering the relative hemoconcentration. In conclusion, 1) compared with sedentary subjects, leptin levels are reduced in male marathon runners in parallel with the relevant reduction in total body fat; 2) expressed as a ratio of leptin per kg body fat, no differences were observed between marathonians and controls; and 3) after an energy expenditure of 2800 Cal in the marathon run, a reduction in leptin levels occurred. Strong changes in energy expenditure may regulate serum leptin levels in man.
The effects of short-term moderate physiological changes in energy flux and energy balance, by exercise and over- or underfeeding, on a 24h plasma leptin profile, were investigated.
Subjects were studied over 24h in four randomized conditions: no exercise/energy balance (energy intake (EI)=energy expenditure (EE)=11.8+/-0.8 MJ); exercise/energy balance (EI=EE=15.1+/-0.6 MJ); exercise/negative energy balance (EI=11.8+/-0.8 MJ, EE=15.1+/-0.8 MJ); exercise/positive energy balance (El=18.6+/-0.7 MJ, EE=15.1+/-0.6 MJ).
Eight healthy, lean men (age: 23.5+/-7.0y, body fat 14.1+/-5.4%, body mass index (BMI): 21.4+/-2.3 kg/m2).
Blood was sampled every hour during the daytime (09.00-23.00h) and every two hours during the night (01.00-09.00h) for analysis of plasma leptin, insulin, glucose, FFA and catecholamines.
Plasma leptin levels were highest around 01.00h (mean+/-s.e.m. 4.9+/-2.0 ng/ml) and lowest around 11.00 h. (2.3+/-0.7 ng/ml). An increased 24h EE, induced by exercise under conditions of energy balance, significantly decreased the peak and average 24h plasma leptin concentration. A positive energy balance, by overfeeding, resulted in a significantly higher amplitude of the 24h plasma leptin curve, compared to a condition of energy balance.
Exercise decreases peak and average 24h plasma leptin concentration and a moderately positive energy balance increases the amplitude of the 24h plasma leptin profile. These effects are not acute, but are manifest within 24h. The variations of average 24h FFA and average 24h glucose concentrations almost fully explained the variation in average 24h leptin concentration across trials.
In subjects who maintain a constant body mass, the increased energy expenditure induced by exercise must be compensated by a similar increase in energy intake. Since leptin has been shown to decrease food intake in animals, it can be expected that physical exercise would increase energy intake by lowering plasma leptin concentrations. This effect may be secondary either to exercise-induced negative energy balance or to other effects of exercise. To delineate the effects of moderate physical activity on plasma leptin concentrations, 11 healthy lean subjects (4 men, 7 women) were studied on three occasions over 3 days; in study 1 they consumed an isoenergetic diet (1.3 times resting energy expenditure) over 3 days with no physical activity; in study 2 the subjects received the same diet as in study 1, but they exercised twice daily during the 3 days (cycling at 60 W for 30 min); in study 3 the subjects exercised twice daily during the 3 days, and their energy intake was increased by 18% to cover the extra energy expenditure induced by the physical activity. Fasting plasma leptin concentration (measured on the morning of day 4) was unaltered by exercise [8.64 (SEM 2.22) 7.17 (SEM 1.66), 7.33 (SEM 1.72) 1 microg x l(-1) in studies 1, 2 and 3, respectively]. It was concluded that a moderate physical activity performed over a 3-day period does not alter plasma leptin concentrations, even when energy balance is slightly negative. This argues against a direct effect of physical exercise on plasma leptin concentrations, when body composition is unaltered.
We investigated the response of leptin to short-term fasting and refeeding in humans. A mild decline in subcutaneous adipocyte ob gene mRNA and a marked fall in serum leptin were observed after 36 and 60 h of fasting. The dynamics of the leptin decline and rise were further substantiated in a 6-day study consisting of a 36-h baseline period, followed by 36-h fast, and a subsequent refeeding with normal diet. Leptin began a steady decline from the baseline values after 12 h of fasting, reaching a nadir at 36 h. The subsequent restoration of normal food intake was associated with a prompt leptin rise and a return to baseline values 24 h later. When responses of leptin to fasting and refeeding were compared with that of glucose, insulin, fatty acids, and ketones, a reverse relationship between leptin and β-OH-butyrate was found. Consequently, we tested whether the reciprocal responses represented a causal relationship between leptin and β-OH-butyrate. Small amounts of infused glucose equal to the estimated contribution of gluconeogenesis, which was sufficient to prevent rise in ketogenesis, also prevented a fall in leptin. The infusion of β-OH-butyrate to produce hyperketonemia of the same magnitude as after a 36-h fast had no effect on leptin. The study indicates that one of the adaptive physiological responses to fasting is a fall in serum leptin. Although the mediator that brings about this effect remains unknown, it appears to be neither insulin nor ketones.
Leptin, the product of the ob gene, is a recently discovered hormone secreted by adipocytes that regulates food intake and energy expenditure. Growth hormone (GH) secretion is markedly influenced by body weight being markedly suppressed in obesity and underweight. The aim of the present study was to study whether leptin can act as a metabolic signal connecting the adipose tissue with the growth hormone axis. We administered leptin antiserum (10 ul, i.c.v.) or normal rabbit serum (NRS; 10 ul, i.c.v.) to freely moving fed rats. Furthermore we assessed the effect of leptin administration (10 ug, i.c.v.) on fed and fasted rats. Spontaneous GH secretion was assessed over 6 hours with blood samples taken every 15 min. Administration of leptin antiserum led to a decrease in spontaneous GH secretion as assessed by the area under the curve (AUC) (168 ± 72 ng/ml/6h) in comparison to NRS-treated rats (813 ± 179 ng/ml/6 h, p < 0.01). While leptin administration (10 ug/rat; i.c.v.) to normal fed rats did not modify spontaneous GH secretion, leptin administration to fasted rats led to a reversal of the inhibitory effect exerted by fasting on GH secretion (AUC, 1650 ± 351 ng/ml.6 h vs77 ± 32 ng/ml/6 h, p < 0.01). This data suggests that leptin is a metabolic signal that regulates GH secretion.
OBJECTIVE
Growth hormone (GH) secretion declines with age and is affected by body composition. The signal that mediates the latter relationship remains ill-defined. Leptin, the protein product of the adipocyte specific ob gene, is thought to accurately reflect fat mass and could therefore be a candidate to influence GH secretion. We have therefore investigated the relationship between GH status, leptin and body composition in normal and GH-deficient elderly subjects.DESIGNGH secretion was assessed by 20-minute sampling over 24 hours and serum leptin concentrations were measured in a single morning, fasted sample.PATIENTSTwenty-one GH deficient elderly patients (61–83 years) and 22 gender- and BMI-matched controls (61–88 years).MEASUREMENTSBody composition was assessed by dual-energy X-ray absorptiometry (DEXA). GH was measured in an ultrasensitive chemiluminescent assay and serum leptin was determined by radioimmunoassay.RESULTSLeptin was correlated with percentage body fat in both sexes (male r = 0.75, female r = 0.89, both P < 0.001). Male patients had increased fat mass (FM) (P < 0.01) and leptin concentrations (P < 0.05) but similar lean mass (LM) compared with controls. However, leptin concentration per unit FM was identical in both groups (P = 0.3). In contrast, female patients had lower LM (P < 0.05) but similar FM to controls, yet their leptin concentration per unit FM was twice that of the controls (P < 0.05). In multiple linear regression (MLR) leptin was determined positively by FM and negatively by LM (controls r 2 = 76%; patients r 2 = 73%, both P < 0.0001). When controlled for gender, GH secretion in the controls was correlated negatively with leptin (r = −0.68, P < 0.01) and negatively with percentage body fat (r = −0.73, P < 0.01). In MLR, using leptin as a marker of body composition, 66% of the variability in GH secretion in the controls could be explained by gender (38%) and by leptin (28%).CONCLUSIONS
Both decreased lean mass and increased fat mass raise serum leptin concentrations in normal and growth hormone-deficient elderly subjects. Leptin is therefore a marker of body composition rather than fat mass alone. The influence of body composition on growth hormone secretion in the elderly may be mediated through leptin, acting as a peripheral signal from adipose tissue to decrease GH secretion.
We hypothesized that circulating GH would increase only if a threshold of work intensity [corresponding to the anaerobic or lactate threshold (LT)] was exceeded. Ten healthy male volunteers (18-35 yr) first performed ramp-type progressive cycle-ergometer exercise to determine the LT and the maximal oxygen uptake. On subsequent mornings after an overnight fast, each subject performed bouts of 1, 5, and 10 min constant work rate exercise of either high intensity (above LT) or low intensity (below LT). A 1-h interval separated exercise bouts. Gas exchange (breath-by-breath), GH, immunoreactive insulin, glucose, lactate, pyruvate, and epinephrine and norepinephrine were measured at regular intervals. After the 10-min bouts of high compared with low intensity exercise, lactate was 7.2 +/- 3.7 mmol/L vs. 1.4 +/- 1.3, P less than 0.05; epinephrine was 1,113 +/- 519 pmol/L vs. 496 +/- 273, P less than 0.05; and norepinephrine was 7.89 +/- 3.45 nmole/L vs. 2.83 +/- 1.34, P less than 0.05. GH did not increase significantly from preexercise baseline during low intensity exercise (e.g., GH after 10-min low intensity exercise changed from baseline values by 1.5 +/- 2.0 micrograms/L, NS). Although lactate was elevated after 5-min of high intensity exercise, peak GH was significantly elevated (mean increase above baseline of 7.7 +/- 2.4 micrograms/L, P less than 0.05) only after 10 min of high intensity exercise (increases in 9 of 10 subjects). The GH increase occurred despite simultaneous increases in both IRI and glucose. A minimum duration of 10 min, high intensity exercise consistently increased circulating GH in adult males.
Fifteen male runners were tested on two occasions to determine the reliability of a continuous incremental level running treadmill protocol (C), with 3-min stages, for lactate threshold (LT) and fixed blood lactate concentration (FBLC) (2.0 mM, 2.5 mM, 4.0 mM) assessment. Test-retest (T-RT) reliability coefficients for velocity at LT, 2.0 mM, 2.5 mM, and 4.0 mM were r = 0.89, 0.91, 0.95, and 0.95, respectively (velocity ranged from 215.3 m/min at LT to 273.6 m/min at 4.0 mM). Mean differences in T-RT velocity values ranged from 0.7 m/min (at LT) to 6.0 m/min (at 2.5 mM; 252.3 m/min vs 258.3 m/min; NS) and the standard errors of measurement were less than +/- 10.0 m/min. Similar results were observed for VO2, with T-RT r values ranging from r = 0.82 (at LT) to r = 0.88 (at 2.0 mM) (VO2 ranged from 47.2 ml/kg.min-1 at LT to 60.9 ml/kg.min-1 at 4.0 mM; VO2 peak = 65.6 ml/kg.min-1). Mean differences in T-RT VO2 values were less than 1.4 ml/kg.min-1 (NS) and the standard errors of measurement were less than +/- 2.95 ml/kg.min-1. Interinvestigator and intrainvestigator reliability coefficients were high and ranged from r = 0.91 to r = 0.99. Validity of C was assessed in an additional 16 male runners who completed C and a criterion discontinuous (D) protocol (using a series of 10-min stages) for LT and FBLC assessment. Results indicated that C and D resulted in similar VO2 and velocity values at LT and FBLC.(ABSTRACT TRUNCATED AT 250 WORDS)
This investigation examined the relationship among plasma catecholamines, the blood lactate threshold (TLa), and the ventilatory threshold (TVE) in highly trained endurance athletes. Six competitive cyclists and six varsity cross-country runners performed a graded exercise test via two different modalities: treadmill running and bicycle ergometry. Although maximal oxygen consumption (VO2 max) did not differ significantly for the cyclists for treadmill running and cycling (64.6 +/- 1.0 and 63.5 +/- 0.4 ml O2.kg-1-min-1, respectively), both TLa and TVE occurred at a relatively earlier work load during the treadmill run. The opposite was true for the runners as TLa and TVE appeared at an earlier percent of VO2max during cycling compared with treadmill running (60.0 +/- 1.7 vs. 75.0 +/- 4.0%, respectively, TLa). The inflection in plasma epinephrine shifted in an identical manner and occurred simultaneously with that of TLa (r = 0.97) regardless of the testing protocol or training status. Although a high correlation (r = 0.86) existed for the shift in TVE and TLa, this relationship was not as strong as was seen with plasma epinephrine. The results suggest that a causal relationship existed between the inflection in plasma epinephrine and TLa during a graded exercise test. This association was not as strong for TVE and TLa.
Leptin, the gene product of the obese gene, may play an important role in regulating body weight by signalling the size of the adipose tissue mass. Plasma leptin was found to be highly correlated with body mass index (BMI) in rodents and in 87 lean and obese humans. In humans, there was variability in plasma leptin at each BMI suggesting that there are differences in its secretion rate from fat. Weight loss due to food restriction was associated with a decrease in plasma leptin in samples from mice and obese humans.
C57BL/6J mice with a mutation in the obese (ob) gene are obese, diabetic, and exhibit reduced activity, metabolism, and body temperature. Daily intraperitoneal injection of these mice with recombinant OB protein lowered their body weight, percent body fat, food intake, and serum concentrations of glucose and insulin. In addition, metabolic rate, body temperature, and activity levels were increased by this treatment. None of these parameters was altered beyond the level observed in lean controls, suggesting that the OB protein normalized the metabolic status of the ob/ob mice. Lean animals injected with OB protein maintained a smaller weight loss throughout the 28-day study and showed no changes in any of the metabolic parameters. These data suggest that the OB protein regulates body weight and fat deposition through effects on metabolism and appetite.
Leptin, the product of the ob gene, is a hormone secreted by adipocytes. Animals with mutations in the ob gene are obese and lose weight when given leptin, but little is known about the physiologic actions of leptin in humans.
Using a newly developed radioimmunoassay, wer measured serum concentrations of leptin in 136 normal-weight subjects and 139 obese subjects (body-mass index, > or = 27.3 for men and > or = 27.8 for women; the body-mass index was defined as the weight in kilograms divided by the square of the height in meters). The measurements were repeated in seven obese subjects after weight loss and during maintenance of the lower weight. The ob messenger RNA (mRNA) content of adipocytes was determined in 27 normal-weight and 27 obese subjects.
The mean (+/- SD) serum leptin concentrations were 31.3 +/- 24.1 ng per milliliter in the obese subjects and 7.5 +/- 9.3 ng per milliliter in the normal-weight subjects (P < 0.001). There was a strong positive correlation between serum leptin concentrations and the percentage of body fat (r = 0.85, P < 0.001). The ob mRNA content of adipocytes was about twice as high in the obese subjects as in the normal-weight subjects (P < 0.001) and was correlated with the percentage of body fat (r = 0.68, P < 0.001) in the 54 subjects in whom it was measured. In the seven obese subjects studied after weight loss, both serum leptin concentrations and ob mRNA content of adipocytes declined, but these measures increased again during the maintenance of the lower weight.
Serum leptin concentrations are correlated with the percentage of body fat, suggesting that most obese persons are insensitive to endogenous leptin production.
We investigated the response of leptin to short-term fasting and refeeding in humans. A mild decline in subcutaneous adipocyte ob gene mRNA and a marked fall in serum leptin were observed after 36 and 60 h of fasting. The dynamics of the leptin decline and rise were further substantiated in a 6-day study consisting of a 36-h baseline period, followed by 36-h fast, and a subsequent refeeding with normal diet. Leptin began a steady decline from the baseline values after 12 h of fasting, reaching a nadir at 36 h. The subsequent restoration of normal food intake was associated with a prompt leptin rise and a return to baseline values 24 h later. When responses of leptin to fasting and refeeding were compared with that of glucose, insulin, fatty acids, and ketones, a reverse relationship between leptin and beta-OH-butyrate was found. Consequently, we tested whether the reciprocal responses represented a causal relationship between leptin and beta-OH-butyrate. Small amounts of infused glucose equal to the estimated contribution of gluconeogenesis, which was sufficient to prevent rise in ketogenesis, also prevented a fall in leptin. The infusion of beta-OH-butyrate to produce hyperketonemia of the same magnitude as after a 36-h fast had no effect on leptin. The study indicates that one of the adaptive physiological responses to fasting is a fall in serum leptin. Although the mediator that brings about this effect remains unknown, it appears to be neither insulin nor ketones.
As one of the postulated roles of the ob gene product, leptin, is regulation of energy balance and preservation of normal body composition, we investigated the effect of acute and chronic calorie excess (weight gain) on serum leptin in humans. Two protocols were employed: 1) acute (12-h) massive (120 Cal/kg) voluntary overfeeding of eight healthy individuals; and 2) chronic overfeeding to attain 10% weight gain, with its subsequent maintenance for additional 2 weeks, involving six normal males. In the acute experiments (protocol 1), circulating leptin rose by 40% over baseline (P < 0.01) during the final hours of overfeeding; this increase persisted until the next morning. At the point of achievement and the 2-week maintenance of 10% weight gain (protocol 2), a more than 3-fold rise in the basal leptin concentration was observed (P < 0.01). A direct linear relationship was found between the magnitude of the leptin response to weight gain and the percent gain of body fat (r = 0.88; P < 0.01). In summary, 1) in contrast to normal food intake (8), short term massive overfeeding is associated with a moderate elevation of circulating leptin levels that persists until next feeding cycle is initiated; and 2) a 10% weight gain causes different changes in the body composition, and the resulting rise in circulating leptin parallels the increase in the percentage of body fat. In conclusion, these studies document acute elevation of leptin in response to positive energy balance and suggest that developing resistance to leptin is associated with bigger fat deposition during weight gain in humans.
The aim of this study was to evaluate the effects of exercise training and hormone replacement therapy (HRT) on serum leptin levels in older women. Previously sedentary, healthy women, aged 60-72 yr, were assigned to control (n = 16), exercise (n = 17), HRT (n = 15), or exercise + HRT (n = 13) groups. Exercise training consisted of a 2-month flexibility-exercise program followed by a 9-month exercise program that included walking, jogging, and stair climbing. HRT consisted of 11 months of continuous conjugated estrogens (0.625 mg/day) and medroxyprogesterone acetate (5 mg/day) for 13 days every third month. Body composition was assessed by dual-energy x-ray absorptiometry, and serum insulin levels were measured in the fasted state and in response to a glucose challenge. Leptin levels were reduced by 23 +/- 25% and 22 +/- 27% (both P < 0.01) in response to exercise and exercise + HRT, respectively. There was no effect of HRT on leptin. Fat mass was the strongest predictor of serum leptin concentration, both before (r = 0.81; P < 0.001) and after (r = 0.85; P < 0.001) the study period, and the change in fat mass in the exercisers was significantly correlated with the change in leptin (r = 0.55; P < 0.01). There did not seem to be an effect of exercise, independent of the reduction in fat mass, on leptin. Insulin levels were significantly correlated with leptin levels, but this was not independent of the association with adiposity. The curvilinear relationship between leptin level and fat mass and the finding that the ratio of leptin mass to fat mass decreased after weight loss suggest that fat cell size is an important determinant of circulating leptin levels.
We measured plasma leptin concentrations by RIA in 204 normal weight and obese subjects, aged 18-80 yr, using full-length recombinant human leptin as a standard. Fasting levels between 1.2-97.9 ng/mL were observed. The plasma leptin concentration was highly correlated with percent body fat (r = 0.710; P < 0.0001) and was 3 times as high in women as in men (17.1 vs. 5.8 ng/mL; P < 0.0001). Circulating leptin was inversely related to age and was reduced 53% in subjects over age 60 yr. A statistical model containing percent body fat, gender, and age accounted for 65% of the variance in plasma leptin levels. Leptin was not independently related to abdominal fat distribution, plasma lipids and lipoproteins, chronic energy intake, diet composition, plasma insulin, or maximum oxygen consumption. However, plasma leptin was reduced by 26% in 5 obese subjects who consumed a 1000-Cal diet for 10 days (P = 0.004). We conclude that circulating leptin rises continuously with increasing adiposity. Gender, age, and short term caloric restriction may be important secondary regulators of plasma leptin.
Leptin, the product of the ob gene, has been reported to be related to body fat in humans (Considine et al. N. Engl. J. Med. 334: 292, 1996). However, little is known about the physiology of this putative satiety signal in humans. The purpose of the present study was to determine whether leptin is related to body fat content in relatively lean endurance-trained adults. In addition, the effect of acute exercise on circulating leptin concentration was studied. Thirteen male runners, whose mean age, height, weight, %fat, and maximal oxygen consumption (VO2max) were 32.2 +/- 2.5 yr, 176.2 +/- 1.6 cm, 71.9 +/- 6.9 kg, 9.7 +/- 0.9%, and 62.9 +/- 2.2 ml.kg-1.min-1, respectively, were studied. Blood samples were obtained after an overnight fast and again immediately after the completion of a 20-mile run at 70% VO2max under controlled environmental conditions. Serum leptin was closely related to fat mass (r = 0.92) in the runners. Acute exercise had no detectable effect on serum leptin levels (PRE = 2.19 +/- 0.32 ng/ml, POST = 2.14 +/- 0.36 ng/ml). These data indicate that, even at a biological extreme of body fat, circulating leptin concentration is closely related to fat content. Furthermore, the data suggest that, in trained individuals with low leptin concentrations, acute exhaustive exercise has no immediate effect on circulating leptin concentration.
Obesity is a complex disease which results from the interaction of multiple genes and the environment. The recently discovered genes for leptin (ob gene) and the leptin receptor appear to play a major regulatory role in body energy balance and adipose tissue deposition. Furthermore, defects in the ob gene and leptin receptor gene have been demonstrated to be the cause of obesity in several rodent models. These observations raise the possibility that human obesity may also be due to defects in the leptin signal system. This review will summarize the current findings on the ob gene, leptin and the leptin receptor in both animals and humans. These observations will be discussed in the context of potential defects in the system and the possibility that these defects result in obesity in humans.
Leptin, the product of the ob gene, is elevated in obese humans and appears to be closely related to body fat content. The purpose of the present investigation was to determine the effect of aerobic exercise training on systemic leptin levels in humans. Eighteen sedentary middle-aged men (n = 9) and women (n = 9) who did not differ in aerobic capacity (29.4 +/- 1.2 vs. 27.5 +/- 1.2 ml x kg(-1) x min(-1)) or insulin sensitivity index (3.41 +/- 1.12 vs. 4.88 +/- 0.55) were studied. Fat mass was significantly lower in females vs. males (21.83 +/- 2.25 vs. 26.99 +/- 2.37 kg, P < 0.05). Despite this, fasting serum leptin was significantly higher in the females vs. males (18.27 +/- 2.55 vs. 9.88 +/- 1.26 ng/ml, P < 0.05). Serum leptin concentration decreased 17.5% in females (P < 0.05) after 12 wk of aerobic exercise training (4 day/wk, 30-45 min/day) but was not significantly reduced in males. Fat mass was not altered after training in either group. In contrast, both aerobic capacity (+13% males, +9.1% females) and insulin sensitivity (+35% males, +82% females) were significantly improved subsequent to training. These data suggest that 1) women have higher circulating leptin concentrations despite lower fat mass and 2) exercise training appears to have a greater effect on systemic leptin levels in females than in males.
Serum leptin and free fatty acid concentrations were determined in two groups of subjects undergoing strenuous exercise: 12 men who fasted overnight and then pedaled a stationary ergometer for 2 hours, and 14 nonfasting ultramarathon runners. Blood samples were collected before exercise, immediately after cessation of exercise, and 6 to 24 hours after the end of the exercise period. Two hours of strenuous pedaling following an overnight fast significantly reduced mean leptin levels by 8.3%; free fatty acids were highly increased and correlated well with the decrease in serum leptin (r = .737, P = .01). After 6 hours of rest and refeeding, leptin concentrations recovered to preexercise levels and free fatty acid concentrations were decreased to less than preexercise levels. A similar decrease in serum leptin levels (12.3%) occurred in subjects who fasted overnight and then for a period corresponding to the cycle exercise period. The prolonged exercise of an ultramarathon significantly reduced leptin concentrations by 32% in comparison to prerace levels; free fatty acid concentrations were highly increased, but did not correlate with the change in serum leptin concentrations (r = .366, P = .20). Leptin and free fatty acid concentrations all trended toward prerace levels in blood samples collected 18 to 24 hours after cessation of racing. The results suggest that the negative energy balance of exercise can reduce serum leptin concentrations, but that the significant decrease occurs only at extremes of severity/duration of the exercise-induced negative balance. The possible physiological role of reduced leptin concentrations in response to energy balance and the role of free fatty acids in mediating the response are discussed.
Leptin is a recently discovered hormone that appears as a regulator of energy balance. It is important to know whether leptin concentrations are changed under conditions of altered energy homeostasis. Consequently, we examined the effects of exercise with fasting and exercise with feeding on circulating leptin concentrations in healthy men and in type 1 diabetic patients with normal body weight and well controlled diabetes.
Leptin concentrations were determined with radioimmunoassay.
During a 3-h cycle ergometer exercise with fasting, leptin decreased by 42% (P < 0.01) in nine healthy men and by 23% (P = 0.05) in eight male type 1 diabetic patients. Leptin fell equally by 12% (P < 0.03) both in nine healthy men and in eight male type 1 diabetic patients who were studied as a resting control group. The absolute fall in leptin in healthy men was similar in the exercise and resting control groups (0.8 +/- 0.1 microgram.L-1 vs 0.8 +/- 0.2 microgram.L-1). However, due to lower leptin concentration before the exercise, the relative decrease (42%) was greater than during the resting control study (12%, P < 0.005). This difference was not seen in the diabetic patients. Fasting leptin concentration correlated positively with BMI (r = 0.75, P < 0.001) and fasting insulin (r = 0.71, P < 0.01) in healthy men as well as with insulin level (r = 0.54, p < 0.05) in type 1 diabetic patients. When exercise was performed with feeding, and this was associated with a significant rise in serum cortisol level (marathon run, 14 healthy men and 7 type 1 diabetic patients), leptin concentration did not change significantly.
1) During morning hours, leptin decreases both in healthy men and in type 1 diabetic patients, reflecting a diurnal variation of leptin concentration and the effect of fasting on leptin concentration. 2) The fall in leptin during morning hours is augmented by physical exercise in healthy men. 3) If exercise is performed with feeding and associated with a rise in serum cortisol level, leptin concentration remains unchanged. These data suggest that although exercise may reduce circulating leptin levels, the effect is small and can be counterbalanced by feeding or a rise in serum cortisol concentration.
To investigate the effects of exercise intensity on growth hormone (GH) release, 10 male subjects were tested on 6 randomly ordered occasions [1 control condition (C), 5 exercise conditions (Ex)]. Serum GH concentrations were measured in samples obtained at 10-min intervals between 0700 and 0900 (baseline) and 0900 and 1300 (exercise+ recovery). Integrated GH concentrations (IGHC) were calculated by trapezoidal reconstruction. During Ex subjects exercised for 30 min (0900-0930) at one of the following intensities [normalized to the lactate threshold (LT)]: 25 and 75% of the difference between LT and rest (0.25LT and 0.75LT, respectively), at LT, and at 25 and 75% of the difference between LT and peak (1.25LT and 1.75LT, respectively). No differences were observed among conditions for baseline IGHC. Exercise+recovery IGHC (mean +/- SE: C = 250 +/- 60; 0.25LT = 203 +/- 69; 0.75LT = 448 +/- 125; LT = 452 +/- 119; 1.25LT = 512 +/- 121; 1.75LT = 713 +/- 115 microg x l(-1) x min(-1)) increased linearly with increasing exercise intensity (P < 0.05). Deconvolution analysis revealed that increasing exercise intensity resulted in a linear increase in the mass of GH secreted per pulse and GH production rate [production rate increased from 16. 5 +/- 4.5 (C) to 32.1 +/- 5.2 microg x distribution volume(-1) x min(-1) (1.75LT), P < 0.05], with no changes in GH pulse frequency or half-life of elimination. We conclude that the GH secretory response to exercise is related to exercise intensity in a linear dose-response pattern in young men.
Leptin levels in human and rodent: measurement of plasma leptin and ob RNA in obese and weight reduced subjects
- J Halaas
- E Ravussin
MAFFEI, M. J., J. HALAAS, E. RAVUSSIN, et al. Leptin levels in human and rodent:
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ACSM's Guidelines for Exercise Testing and Prescription
- American College
- Sports
- Medicine
AMERICAN COLLEGE OF SPORTS MEDICINE. ACSM's Guidelines for
Exercise Testing and Prescription. Baltimore: Williams & Wilkins, 1995, p. 163.