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Review on leptin and adiponectin responses and adaptations to acute and chronic exercise
  1. A Bouassida,
  2. K Chamari,
  3. M Zaouali,
  4. Y Feki,
  5. A Zbidi,
  6. Z Tabka
  1. Laboratoire des adaptations cardio-circulatoires, respiratoires, métaboliques et hormonales à l'exercice musculaire, Faculté de Médecine Ibn El Jazzar, Sousse, Tunisia
  1. Correspondence to Dr A Bouassida, Laboratoire des adaptations cardio-circulatoires, respiratoires, métaboliques et hormonales à I'exercice musculaire, Faculté de Médecine Ibn El Jazzar, Sousse, 4002 Tunisia; bouassida_anissa{at}yahoo.fr

Abstract

Leptin and adiponectin represent two newly discovered adipose tissue derived hormones; that are both associated with health status and glucose and free fatty acid (FFA) metabolism. Moreover, acute and chronic exercises affect body composition, carbohydrate and lipid metabolism. It is thus interesting to evaluate the effects of physical exercise and training on leptin and adiponectin levels. It seems that leptin concentration is not modified after short-term exercise (<60 min) or exercise that generates an energy expenditure lower than 800 kcal. Leptin levels decrease after long-term exercise (≥60 min) stimulating FFA release, or after exercise that generates energy expenditure higher than 800 kcal. Adiponectin concentration presents a delayed increase (30 min) after short-term intense exercise (<60 min) performed by trained athletes. For adiponectin, limited data suggest that adiponectin concentration presents a delayed increase (30 min) after short-term intense exercise (<60 min) performed by trained athletes. It seems that adiponectin concentrations do not change in response to long-term exercise (≥60 min). Short-term training (<12 weeks) and long-term training (≥12 weeks) show contrasting results regarding leptin and adiponectin. Most training studies which improve fitness levels and affect body composition could decrease leptin and increase adiponectin concentrations.

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Adipose tissue is not only a passive energy store but also an active endocrine organ that produces biologically active substances termed “adipocyto-kines.”1 These adipocytokines include several novel and highly active molecules abundantly released by adipocytes, as leptin, adiponectin, resistin, apelin or visfatin, as well as some more classical molecules, like tumour necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6).1 2

This review focuses on leptin and adiponectin. Both are associated with regulation of energy balance and insulin action.3,,5 As exercise reduces risk factors for cardiovascular disease and type 2 diabetes,6 it is interesting to study the effects of exercise on leptin and adiponectin. Exercise is also a potent facilitator for the maintenance of healthy levels of body fat and insulin sensitivity.3 In this review, we discuss leptin and adiponectin first by summarising their roles in carbohydrate and lipid metabolism, and then by considering the effects of acute and chronic exercise on each of these peptides.

Leptin

Leptin, one of the first identified adipocytokines,7,,9 is a 16 kDa adipocyte-derived cytokine, encoded by the ob gene.7 Adipocytes are the primary sites of leptin expression, although leptin is also expressed in gastric wall, vascular cells, placenta, ovary, liver and skeletal muscle.10,,12 Leptin levels vary with the diurnal cycle and provide more feedback on fat mass at night13 than during daylight hours.14

Leptin promotes body mass loss by acting on receptors within the hypothalamus15 16 to decrease food intake and to increase sympathetic nervous system activity.17 Leptin could inhibit food intake in a complex, multifactorial manner that is reported to involve citing its action on cocaine amphetamine-related transcript (CART),18 pro-opiomelanocortin (POMC),18 neuropeptide Y (NPY),19 agouti-related peptide (AgRP) (Schwartz)19 in the arcuate nucleus (Arc). AMP-activated kinase (AMPK)20 and acetyl-coenzyme A carboxylase (ACC)11 20 are also involved in leptin cell signalling as well as Janus kinase (JAK),21 signal transduction and activation of transcription 3 (STAT3), and a supressor of cytocine signalling 3 (SOCS3).21 Leptin has a complementary effect on satiety through the sympathetic and direct-induced increase in fatty acid disposal for metabolism.22,,24

Leptin receptors (OB-R) are expressed in a number of different tissues, and this may explain their widespread range of actions;25 26 receptors are particularly prominent within skeletal muscle and liver.27 Different splice variants of the receptors may be relevant for different signalling pathways.2 OB-Rb (long isoforms), the major signalling receptor, is expressed in hypothalamus, monocytes, lymphocytes, endothelial cells, smooth muscle cells and pancreatic beta cells. The OB-Ra (short isoform) serves blood-brain barrier transport.2

Adiponectin

Adiponectin has various names. It has been referred to as an adipocyte complement-related protein of 30 kDa (ACRP30), adipoQ, adipose most abundant gene transcript 1 (apM1) and gelatinbinding protein of 28 kDa (GBP28). It is also an adipocyte-derived protein.28,,30 Circulating adiponectin concentrations increase with age31 and represent a relatively abundant plasma protein specifically secreted from adipose tissue. It is found in the circulation at relatively high levels in healthy human subjects (~2 to 10 μg/ml).32 33 In contrast to other adipokines, adiponectin expression is reduced in overweight subjects.34 Adiponectin levels are (1) negatively correlated with percentage body fat, central fat distribution, fasting plasma insulin and oral glucose tolerance, and (2) positively correlated with glucose disposal during euglycaemic insulin clamp.35 Adiponectin levels are also significantly lower in patients with coronary artery disease36 37 and in people with insulin resistance and type 2 diabetes.38 This suggests a possible association of reduced adiponectin in vasculopathic and diabetic states.39 Adiponectin is also associated with cardiovascular health—reduced circulating adiponectin levels are correlated with increased prevalence and severity of atherosclerosis.40 In addition, adiponectin stimulates food intake and decreases energy expenditure during fasting through its effects in the central nervous system.41 Two receptors for adiponectin, termed AdipoR1 and AdipoR2, have been cloned. AdipoR1 is produced primarily in skeletal muscles, whereas AdipoR2 is primarily found in hepatic tissues.42

Effects of leptin on carbohydrate and lipid metabolism

In skeletal muscle, the acute stimulatory effect of leptin on fatty acid oxidation is due, at least in part, to a direct rapid and transient stimulation of AMP-activated protein kinase (AMPK) in skeletal muscle.43 The greatest effect is in oxidative fibres.44 Leptin (10 mg/ml) has increased free fatty acid (FFA) oxidation in isolated mouse soleus muscle by 42%.45 Also, leptin-induced increase in fatty acid catabolism has been mediated by decreased skeletal muscle lipid deposition.27 Short-term leptin treatment (10 mg/kg/day for 10 days) in high-fat fed rats has altered muscle fatty acid metabolism by increasing fatty acid uptake and oxidation relative to pair feeding alone.46 This has resulted in a decrease in the fatty acid esterification–oxidation ratio. Leptin has also increased glucose uptake in skeletal muscle tissue in vivo47 48 and in a myotube cell line in vitro49 (fig 1).

Figure 1

Actions of leptin on skeletal muscle and liver. IL-6, interleukin 6; TNF-α, tumour necrosis factor-α.

In liver, leptin has direct effects on gluconeogenesis.50 Intracerebroventricular leptin infusion for 7 days in rats does not change leptin plasma levels but decreases triacylglyceride content and favours fatty acid uptake and oxidation in the liver. These results suggest that leptin, acting in the central nervous system, exerts tissue-specific effects that limit fat tissue mass and lipid accumulation in non-adipose tissues. This would mitigate against the development of obesity and type 2 diabetes.51 Intravenous leptin infusion decreases liver triacylglyceride secretion and increases hepatic fatty acid oxidation.52 The literature describing the effects of leptin on hepatic glucose metabolism provides conflicting results. For example, ob/ob mice display elevated hepatic gluconeogenesis,53 but there may be more data overall suggesting that leptin reduces hepatic gluconeogenesis.50 54 55

Effects of adiponectin on carbohydrate and lipid metabolism

In skeletal muscle, adiponectin has potent effects on carbohydrate and lipid metabolism (fig 2). Adiponectin stimulates fatty acid oxidation and improves insulin sensitivity in humans and rats, due in part to the activation of AMP and subsequent deactivation of acetyl coenzyme-A carboxylase (ACC).56 57 Ceddia et al58 showed that globular adiponectin increased glucose uptake in skeletal muscle cells via GLUT4 translocation and subsequently reduced the rate of glycogen synthesis and shifted glucose metabolism toward lactate production. These effects are consistent with increased phosphorylation of AMP kinase and acetyl-coenzyme A carboxylase and oxidation of fatty acids induced by globular adiponectin. Globular adiponectin stimulates glucose transport in isolated skeletal muscle, as well as in cultured myocytes.59 60

Figure 2

Actions of adiponectin on liver, heart and skeletal muscle. IL-6, interleukin 6; TNF-α, tumour necrosis factor-α.

In liver, adiponectin also modulates carbohydrate and lipid metabolism (fig 2). Specifically, it increases liver fatty acid oxidation56 and decreases insulin resistance by decreasing triglyceride content in muscle and liver in obese mice.51 A moderate rise in circulating levels of adiponectin inhibits the expression of hepatic gluconeogenic enzymes (phosphoenolpyruvate carboxykinase and glucose-6-phosphatase) and the rate of endogenous glucose production.61

In the heart, adiponectin contributes to glucose and lipid metabolism62 63 (fig 2). Adiponectin is synthesised and secreted by isolated murine and human cardiomyocytes.64 Adiponectin treatment significantly enhances glucose and fatty acid uptake by the cardiomyocytes.64 Globular adiponectin increases fatty acid oxidation in isolated perfused newborn rabbit heart.65 Furthermore, adiponectin induces phosphorylation of AMPK in cultured cardiomyocytes,66 since AMPK is known to stimulate glucose uptake and translocation of the cardiomyocyte glucose transporter GLUT4 to the cell surface.62 It seems possible that the adiponectin-dependent increase in glucose uptake in cardiomyocytes is mediated by AMPK activation.67

Acute exercise and leptin

Several studies have analysed the effects of a single bout of exercise on leptin concentration (table 1). For short-term exercise (<60 min), in obese females, walking at 60–80% of the heart rate maximum (HRM) for 45 min did not alter leptin concentrations,68 although it decreased insulin resistance. There was a decline in leptin concentrations in trained rowers immediately after and 30 min after maximal rowing exercise (30 min).69 Thus, leptin was sensitive to short-term intensive exercise when all major muscles were involved. Similarly, significantly lowered leptin concentrations were shown in sedentary middle-aged male and females after 20 min of vigorous running.70 Nevertheless, after 1 h of supine recovery, leptin levels returned to basal values. These authors indicated the existence of a relationship between stressful physical exercise and plasma leptin levels in middle-aged subjects.70 Serum leptin concentrations have been analysed in healthy males after four conditions: control and three acute resistance exercise protocols.71 Serum leptin concentrations after 30 min of recovery exhibited similar reductions from baseline after the resistance protocols that were comparable with fasting-induced reduction in the control session. Indeed, resistance exercise protocols did not result in serum leptin changes when sampled immediately or after 30 min postexercise. These observations underline the importance of using a resting session when evaluating the effect of exercise on leptin concentrations to control for fasting- and/or circadian rhythm-induced leptin reductions.71 Our group showed72 that short supramaximal exercise performed by physically active males and females did not modify plasma leptin and insulin concentrations but increased cortisol concentrations. Under these conditions, leptin production seemed insensitive to exercise (≥60 min): serum leptin concentrations were analysed after three competitive endurance races performed by 45 males who participated in one of three competitive endurance races: a half-marathon run (estimated energy expenditure “EE” ~1400 kcal), a ski-alpinism race (estimated EE ~5000 kcal), and an ultramarathon race (estimated EE ~7000 kcal).73 Only prolonged endurance exercise involving high energy expenditure (over 1400 kcal) (eg, alpine skiing and ultramarathon race) induced a marked reduction in circulating serum leptin levels.73 A 4 h resting trial was compared with a 2 h run followed by a 2 h resting trial.74 There was a 30% reduction in postexercise resting leptin concentrations with respect to control conditions. The investigators indicated significant inverse correlations between leptin and glycerol as well as free fatty acid levels.74 Trained males completing 60 min of running at approximately 70% of VO2max showed a delayed decrease in leptin concentrations at 24 h and 48 h after the exercise.75 The leptin response did not appear to be related to changes in insulin or glucose concentrations. The same subjects underwent a maximal graded running exercise, and leptin levels did not decline immediately after, or 24 or 48 h after, exercise.75 Two hours and 24 h after 90 min of rowing at 70–75% of VO2max, leptin concentrations were lowered in the drills of eleven trained rowers.76 An immediate exercise effect was observed on the levels of FFA until 2 h postexercise, which did not persist after a longer recovery.76

Table 1

Acute studies of exercise and leptin

Thus, it appears that lowered leptin concentrations were observed after long-term exercise (≥60 min) that stimulates FFA release, or after exercise that generates an energy expenditure higher than 800 kcal. These decreases could be contributed to by the circadian rhythm of leptin. A role of FFA levels via increased lipolysis could also be suggested. Therefore, it appears that leptin concentrations were not modified after short-term exercises (<60 min) or exercises that generated an energy expenditure lower than 800 kcal.77 78

Acute exercise and adiponectin

Six acute bout of exercise studies have reported the effects of various kinds of exercises (running, cycling, rowing) on adiponectin concentrations79,,84 (table 2).

Table 2

Acute studies of exercise and adiponectin

Short-term exercise (<60 min)

In a recent study, the plasma adiponectin response to a maximal 6000 m rowing ergometer test achieved by highly trained male rowers was studied.79 Adiponectin was unchanged immediately after exercise when uncorrected for plasma volume changes but was decreased when adjusted for plasma volume changes. Adiponectin concentrations rose significantly above the preexercise value after 30 min of recovery (in both uncorrected and corrected for plasma volume expressions). However, no changes occurred in plasma leptin and insulin concentrations. These results suggest that plasma adiponectin is altered as a result of maximal acute exercise in highly trained athletes.79 Another recent study determined acute adiponectin response to a 6.5 km rowing at the individual anaerobic threshold in trained athletes.80 Adiponectin was unchanged immediately after the exercise and significantly increased above pre-exercise values after 30 min of recovery. Leptin concentrations remained unchanged immediately after exercise and significantly decreased after 30 min of recovery. Plasma insulin was significantly reduced immediately after exercise and remained lower than pre-exercise values after the 30 min recovery period. These authors concluded that plasma adiponectin is sensitive in the first 30 min of recovery to the effects of short-term exercise at individual anaerobic threshold when all major muscle groups are involved.80 Nine overweight subjects performed a 45 min submaximal exercise (65% of VO2max). Adiponectin concentration was measured prior to exercise, immediately after as well as 24 and 48 h after exercise.81 Authors noted that there were no significant changes in adiponectin across time. Insulin sensitivity increased, and insulin concentration decreased significantly only immediately after exercise. The results of this study indicated that a submaximal aerobic exercise did not result in significant changes in adiponectin up to 48 h postexercise in overweight subjects.81 To investigate the acute effects of running on adiponectin in healthy men, subjects ran at 79% of VO2max for 30 min.82 Although there was a significant increase in adiponectin after exercise, it was no longer significant after correction for plasma volume shifts. These authors suggested that 30 min of heavy continuous running does not stimulate an increase in the production and the release of adiponectin, and that the small increases in adiponectin concentrations resulting from the exercise may be attributed to normal plasma volume shifts.82

Long-term exercise (≥60 min)

The effect of a single cycling exercise (60 min at 65% of VO2max) on adiponectin response in healthy men and women was studied.83 Postexercise, neither male nor female subjects exhibited changes in adiponectin or leptin concentrations. It was concluded that acute exercise does not affect adiponectin concentrations in women and in men.83 Some researchers aimed to determine changes in plasma adiponectin concentration and adiponectin receptor 1 and 2 mRNA expression in skeletal muscle during and after 120 min exercise at 50% of VO2max under normal, fasting conditions and pharmacological inhibition of adipose tissue lipolysis.84 The authors reported no changes in plasma adiponectin levels and in adiponectin receptors 1 and 2 in response to either experiment. Plasma FFA concentrations and total fat oxidation rates were substantially reduced in the pharmacological group. Investigators concluded that plasma adiponectin concentrations and adiponectin receptor 1 and 2 mRNA expression in muscle are not affected by changes in adipose tissue lipolysis and/or plasma FFA concentrations.84

Thus, limited data suggested that adiponectin concentrations presented a delayed increase (30 min) after short-term intense exercise (<60 min): at individual anaerobic threshold or maximal performed only by trained subjects. It seems that adiponectin concentrations do not change in response to longterm exercise (≥60 min).

Chronic exercise and leptin

A number of studies have investigated the effects of training on leptin concentration. These studies have tended to report either no effect of training on leptin concentration or a reduction in leptin levels (table 3).

Table 3

Chronic studies of exercise and leptin

Short-term training (<12 weeks)

Circulating leptin levels decreased after 2 weeks skiing expedition in well-trained males.85 The changes in leptin were accompanied by decreased waist circumferences and insulin sensitivity.85 The study of obese females reported that 4 weeks of walking resulted in a reduced insulin resistance and leptin concentrations.68 Three weeks of increased training stress followed by a 2-week tapering period in highly trained rowers induced significant reductions in fasting leptin levels.86 Plasma leptin concentration was significantly increased at the end of the 2-week tapering period with respect to the value measured after the 3 weeks of training but remained significantly lower compared with the pretraining value. Authors suggested that leptin may be sensitive to the rapid and pronounced changes in training load. A greater training time is associated with lowered leptin concentration in highly trained male rowers.86

In spite of significant reductions in fat mass and serum-free testosterone, serum leptin concentrations were not significantly altered by 6 weeks' strength training performed by 12 physical education students.87 Changes in leptin concentrations were examined in 13 male collegiate distance runners with overtraining syndrome before and after an 8-day strenuous training camp. Plasma leptin was not significantly changed after the training camp.88 This stability of leptin concentrations occurred with significant changes in body fat percentages, in serum testosterone and in serum cortisol. The authors concluded that the change in blood leptin level is independent of the changes in cortisol, testosterone and fat percentage in highly trained male athletes in the state of overtraining syndrome.88

Long-term training (≥12 weeks)

The effects of a 12-week aerobic training programme was examined in obese females89 and in obese premenopausal women, respectively.90 In both studies, leptin significantly decreased after endurance training, and these decreases in leptin concentrations were associated with fat mass loss. Serum leptin concentrations were measured in 36 overweight men (BMI, 28.9 (2.3)) after a 1-year aerobic exercise programme.91 Leptin, insulin, BMI and percentage body fat were significantly reduced after this long-term training. This study indicated that chronic mild aerobic exercise training significantly lowers serum leptin concentrations and thus may improve the leptin resistance observed in overweight men.91 Trained rowers performed two exercise sessions of 90 min each (70–75% of VO2max) separated by 36 weeks of intense endurance training.76 Leptin concentrations were measured in both sessions before, at the end and after 2 and 24 h of recovery. In the first session, compared with the pre-exercise levels, the plasma leptin concentration was significantly lower after a 120 min and a 24 h recovery. After the second session, the leptin levels were significantly reduced after a 120 min recovery but returned to pre-exercise levels after a 24 h recovery. Thus, training modified leptin levels. The FFA and leptin levels were correlated after 24 h in the first session and after 2 h in the second session. The training effect was apparent for catecholamines (epinephrine, norepinephrine, dopamine), particularly for norepinephrine. The authors suggested that the amplitude of the norepinephrine response to exercise induced an increase in fat use and a rapid leptin recovery after the second exercise. The sensitivity of leptin to changes in the fat stores may be improved after training.76 In older men (65–78 years), leptin was examined through resistance-training adaptations over the course of a year.92 Men were randomly assigned to four different training groups: control group and low-, moderate- and high-intensity training. Energy expenditure during exercise, VO2max and strength were improved in all training groups in a training intensitydependent manner. Likewise, skinfold sum and BMI decreased to a greater degree with a high-intensity training group as compared with a moderate-intensity training group. Leptin was reduced for all training groups. The authors concluded that resistance training and detraining may alter leptin response in an intensity-dependent manner. Leptin changes were strongly correlated to anthropometric changes.92

Thus, short-term training (<12 weeks) and long-term training (≥12 weeks) have disparate effects concerning leptin concentration. Exercise training protocols that result in reduced fat mass are generally accompanied by lower leptin concentrations. Reductions in leptin levels have also been attributed to alterations in energy balance, insulin sensitivity and lipid metabolism.

Chronic exercise and adiponectin

Ten studies that analysed the effects of chronic exercise on adiponectin concentrations are summarised in table 4.

Table 4

Chronic studies of exercise and adiponectin

Short-term training (<12 weeks)

The effect of 10 weeks' aerobic training on adiponectin concentrations was considered in young and middle-aged women.93 After the training programme, serum adiponectin concentrations, VO2max and insulin sensitivity were increased in both groups. The authors concluded that the improved insulin sensitivity could involve increased adiponectin levels in exercise-trained women.93

In obese 25–35-year-old women (BMI=31.5 (4.1) kg/m2), diet combined with supervised physical activity (9 weeks) did not alter adiponectin levels.94 After the intervention, fasting insulin concentrations, body mass, BMI, subcutaneous and visceral adipose tissue decreased significantly. However, adiponectin and IL-6 remained unchanged. In this study, the morphological changes were insufficient to raise adiponectin concentration.94 Similarly, aerobic training (8 weeks) and aerobic-resistance training (5 months) on adiponectin levels in young obese men (BMI=31.1 (4.2) kg/m2) did not modify adiponectin concentrations.95 After the aerobic training, fat mass and ventilatory threshold (VT) were significantly improved. The aerobic-resistance training exhibited significant reduction in body mass, BMI, percentage body fat and fat mass, and showed a significantly increased VT and VO2max. These findings indicate that to increase the adiponectin level, the improvement in body composition of young obese men is more important than the way training is performed.95

Long-term training (≥12 weeks)

Plasma adiponectin concentrations, insulin sensitivity and body composition were analysed in upper-body obese insulinresistant, non-diabetic adults before and after 19 weeks of a diet/exercise programme.96 This therapy reduced body fat, visceral fat and improved insulin sensitivity, and increased adiponectin, whereas TNF-α, IL-6 and resistin did not change. These findings do not support an endocrine role for resistin, TNF-α and IL-6 in mediating changes in insulin resistance after a diet/exercise programme. These data indicated that of the adipokine/inflammatory markers that were measured, only adiponectin was consistently related to insulin sensitivity and body fat distribution, but changes in adiponectin were not predicted by changes in insulin sensitivity.96 Severely obese subjects (mean BMI=45.8 kg/m2) completed a 15-week intervention including a hypocaloric diet and exercise.97 Plasma blood samples, adipose tissue and skeletal muscle biopsies were obtained before and after the programme. The intervention reduced body mass and increased insulin sensitivity. Plasma CRP, IL-6 and adiponectin increased, but the exercise treatment did not affect adiponectin receptor 1 and 2 mRNA in adipose tissue or skeletal muscle. It was concluded that diet modification coupled with exercise increased adiponectin levels. Moreover, low levels of adiponectin in adipose tissue and plasma of the severely obese subjects appear not to be related to increases in macrophage infiltration in adipose tissue but instead to inhibitory effects of TNF-α and IL-6 released from the macrophages in the adipose tissue.97 Adiponectin levels were increased after 7-month aerobic exercise programme in eight young obese female subjects (BMI>25 kg/m2).98 The subjects' exercise training decreased BMI, percentage body fat, leptin and TNF-α. Thus, this exercise-training programme was of a sufficient caloric expenditure and duration to reduce body fat and increase adiponectin concentrations in young obese female subjects.98 In a study on obese men and women (mean age 63 years), subjects completed 12 weeks of aerobic training.99 Training improved fitness levels, reversed insulin resistance and reduced fat mass, subcutaneous fat, abdominal fat and leptin concentration but did not affect circulating adiponectin levels. These findings are different from those of other training studies that have shown increases in adiponectin with training-induced weight loss and improvement in insulin sensitivity. Authors indicated that exercise successfully targets and reduces visceral fat, and enhances glucose tolerance, making it a highly effective treatment strategy for insulin resistance in older obese people.99 In another study, 12 obese male subjects (BMI=33.6 (1.2) kg/m2) were investigated before and following 3 months of dynamic strength training.100 After training, total body mass, adiponectin, IL-6 and TNF-α remained unchanged. The wholebody glucose disposal rate increased by 24% (p<0.05), and plasma levels of leptin decreased by 21% (p<0.05). In these obese subjects, the increase in insulin sensitivity was not associated with training-induced modifications in plasma levels adipokines supposedly involved in the development of insulin resistance.100 Plasma leptin concentration was assessed in elite rowers after a 12-week preparatory rowing period.101 This training programme significantly increased physical fitness and aerobic power. Fasting adiponectin did not change during the training period. Likewise, body fat percentage, body mass, leptin, insulin, growth hormone and glucose values were not significantly changed after the training period. The authors surmised that fasting adiponectin does not change throughout a prolonged training period in elite male rowers despite substantial changes in training volume.101 Overweight and obese adolescents completed a 12-week aerobic training programme that improved cardiorespiratory fitness (VO2max) by 18%.102 Although body mass and percentage body fat did not change, lean body mass and insulin sensitivity were increased with training. However, serum adiponectin, IL-6 and C-reactive protein (CRP) did not change, and the authors concluded that the improvement in insulin sensitivity was not related to changes in adiponectin.

Thus, short-term training (<12 weeks) and long-term training (≥12 weeks) studies showed disparate findings. It does not appear that adiponectin concentrations were inevitably affected by morphological and hormonal changes occurring after different kind of training programmes. Indeed, in certain cases, adiponectin levels remained unaffected after aerobic and resistance training in spite of decreased body fat or BMI, on the one hand. It appears mostly that training improving fitness levels and reducing body mass and body fat will increase resting adiponectin levels, on the other hand. Moreover, it seems that the changes in insulin sensitivity by exercise training are independent of adiponectin alterations.

The heterogeneity of the findings concerning the effects of acute and chronic exercises on leptin and adiponectin concentrations may be related to one or more factors including morphological changes, hormonal modifications, changes in insulin sensitivity, time of sampling, studied populations (trained, untrained, obese), variation in plasma volume shifts, nutritional status and other unknown factors at the moment.

Conclusion

The studies suggested that leptin and adiponectin responses and adaptations differ in acute and chronic exercises. Acute exercise studies: for leptin, it appears that a lowered leptin concentration was observed after long-term exercise (≥60 min) that stimulates FFA release, or after exercise that generates an energy expenditure higher than 800 kcal. Therefore, it seems that the leptin concentration is not modified after short-term exercise (<60 min) or exercise that generates an energy expenditure lower than 800 kcal. For adiponectin, limited data suggest that adiponectin concentration presents a delayed increase (30 min) after short-term intense exercise (<60 min) performed by trained athletes. It seems that adiponectin concentrations do not change in response to long-term exercise (≥60 min). In chronic exercise studies, for leptin and adiponectin, short-term training (<12 weeks) and long-term training (≥12 weeks) have disparate effects. Exercise training protocols that result in reduced fat mass are generally accompanied by lower leptin concentrations. It appears mostly that training improving fitness levels and reducing body mass and body fat will increase resting adiponectin levels. In fact, there is some support for the use of training at an adequate duration and intensity to produce substantive changes in fitness levels and in body composition to decrease circulating leptin and raise circulating adiponectin.

Further investigations are needed. First, indeed, augmented adiponectin levels were observed so far in two studies of acute heavy exercise performed by trained subjects. This indicates that exercise is not necessarily ineffective in this regard but highlights the necessity for more strongly designed studies. Second, longterm, well-designed chronic training studies, which measure and control dietary intake and visceral adiposity and assess distal health outcomes, should be conducted. Particular attention should be focused on high-risk groups including overweight children, adolescents and adults, and metabolic syndrome type-2 diabetes, and may assume critical importance for long-termhealth outcomes in the general population.

What is already known on this topic

  • ▶. This study reviews the evidence that leptin and adiponectin are involved in carbohydrate and lipid metabolism.

  • ▶. The effect of acute and chronic exercises on leptin and adiponectin concentrations revealed disparate findings.

What this study adds

  • ▶. To date, only two acute studies have indicated a delayed (30 min) increase in adiponectin concentrations.

  • ▶. This review includes four tables that included the majority of recent studies, in order to define more clearly the effects of acute and chronic exercises on leptin and adiponectin concentrations.

References

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Footnotes

  • Funding This work was supported by the “Ministère de la Recherche Scientifique, de la Technologie et du Développement des Compétence, Tunisia.”

  • Competing interests None.

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