| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Department of Physical Education and Sports Science, Democritus University of Thrace (I.G.F., P.T., I.D., K.T.), Komotini 69100, Greece; Diabetes and Metabolism Unit (S.T., D.L., A.M.), and Department of Biochemistry (M.M.), Henry Dunant Hospital, Athens 11526, Greece; Department of Physical Education and Sports Sciences, University of Thessaly (A.Z.J.), Trikala 42100, Greece; and Department of Pediatrics, University Hospital of Alexandroupolis (M.S.), Dragana, Alexandroupolis 68100, Greece
Address all correspondence and requests for reprints to: Dr. Ioannis G. Fatouros, Department of Physical Education and Sports Science, 7th km of of National Road Komotini-Xanthi, Komotini 69100, Greece. E-mail: fatouros{at}otenet.gr.
 |
Abstract |
|---|
 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Objective: The objective of this study was to investigate leptin and adiponectin responses in elderly males after exercise training and detraining.
Design: The study design was a 1-yr randomized controlled trial.
Setting: The study was performed at the Laboratory of Physical Education and Sport Science Department.
Participants: Fifty inactive men [age, 65–78 yr; body mass index (BMI), 28.7–30.2 kg/m2] were recruited from a volunteer database by word of mouth and fliers sent to medical practitioners, physiotherapists, and nursing homes in the local community.
Intervention(s): Participants were randomly assigned to a control (n = 10), low-intensity (n = 14), moderate-intensity (n = 12), or high-intensity training (HI; n = 14) group. Resistance training (6 months, 3 d/wk, 10 exercises/three sets) was followed by 6 months of detraining.
Main Outcome Measure(s): Strength, exercise energy cost, skinfold sum, body weight, maximal oxygen consumption, resting metabolic rate (RMR), and plasma leptin and adiponectin were determined at baseline and after training and detraining.
Results: Strength, maximal oxygen consumption, RMR, and exercise energy cost increased (P < 0.05) after training in an intensity-dependent manner. Skinfold sum and BMI were reduced by resistance training (P < 0.05), with HI being more effective (P < 0.05) than moderate-intensity/low-intensity training. Leptin was diminished (P < 0.05) by all treatments, whereas adiponectin increased (P < 0.05) only in HI. Detraining maintained training-induced changes only in HI. The percent leptin decrease was associated (P < 0.05) with the percent BMI decrease and the percent RMR increase, whereas the percent adiponectin increase was associated (P < 0.05) with the percent BMI decrease.
Conclusions: Resistance training and detraining may alter leptin and adiponectin responses in an intensity-dependent manner. Leptin and adiponectin changes were strongly associated with RMR and anthropometric changes.
|
Introduction |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Aging increases body fat and leptin levels (9), although this increase seems disproportionate to the augmented adiposity seen with aging (10). Leptin administration reduced visceral adiposity in aging rats (9), an effect that has not been shown in humans (4).
Exercise extends the average life span by reducing the incidence of cardiovascular and other degenerative diseases while increasing functional performance in aging individuals (11, 12). Chronic exercise disrupts energy balance, sympathoadrenal input, as well as hormonal and metabolic homeostasis, which may influence leptin levels at rest or during exercise. Regular exercise seems to create energy deficits that help to regulate body weight and fat on a long-term basis in older individuals (13) and reduces aging-related sarcopenia in the elderly (14, 15). The vast majority of previous studies examined the effects of acute, but not chronic, exercise on the serum leptin concentration. Although resistance exercise induces marked metabolic and endocrine changes (16), significant energy flux perturbations (17), acidosis, and altered carbohydrate metabolism (18), only limited information is available regarding the effects of resistance training (RT) on leptin and adiponectin responses in young or old adults. Circulating leptin levels remained unchanged after acute aerobic exercise (19, 20) and decreased (21) or remained unaltered (22) with acute resistance exercise in young adults. However, exercise eliciting significant energy expenditure may decrease plasma leptin (23). The basal leptin response is attenuated or remains unaltered after endurance training (23), whereas it decreases with combined resistance and endurance training independently of changes in body composition and weight (24). The only study that examined the effects of RT on the leptin response in the elderly revealed an up-regulation associated with fat mass reduction (25).
Adiponectin, an adipose tissue-derived protein, is released into circulation and is inversely correlated with body mass index (BMI) and body fat levels and distribution (26). Adiponectin levels increased (27), decreased (28), or remained unaltered (29) in healthy humans, whereas they increased in patients with cardiovascular or metabolic diseases after aerobic exercise training (26, 30, 31). However, to our knowledge, there are no data available regarding adiponectin responses to RT in the elderly.
Therefore, the purpose of the present investigation was to study leptin and adiponectin responses and their association with potential metabolic changes 1) after prolonged resistance exercise training and detraining, and 2) as a function of resistance exercise intensity.
|
Subjects and Methods |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Fifty older men volunteered to participate in a 48-wk training/detraining study. Subjects were recruited from a volunteer database by word of mouth and fliers sent to medical practitioners, physiotherapists, and nursing homes in the local community. Written informed consent was signed by all participants. Procedures were performed in accordance with the Helsinki Declaration for the ethical treatment of human subjects. Ethics approval was given by the institutional review board for human research. The physical characteristics of the subjects are shown in Table 1
.
|
The inclusion criteria were availability to participate in measurements for 48 wk; complete inactivity before the study for at least 10 yr before the study [maximal oxygen consumption (VO2max), <20 ml/kg·min; score of <9.0 in the Modified Baecke Questionnaire for Older Adults; Table 1
] (32, 33); weight stability (±2 kg) 6 months before entry; absence of restraining orthopedic/neuromuscular diseases; resting blood pressure less than 160/100 mm Hg; no use of tobacco, aspirin, alcohol-containing beverages, or lipid-altering medications; and no history of diabetes (controlled by history, use of medications, and initial screening; fasting plasma glucose, 
7 mmol/liter).
Study design
A four-group, randomized, repeated measures, controlled trial was employed. During their first visit, subjects were medically screened and had their resting energy expenditures (REE) and anthropometric profiles measured. At the second visit, subjects underwent a progressive diagnostic treadmill test to exhaustion to evaluate their VO2max and were given 5-d diet recall forms to complete. Thereafter, subjects underwent two familiarization sessions with RT. During the fifth and sixth visits, fasting blood samples were collected, and maximal strength and exercise energy cost were measured. Thereafter, subjects were randomly assigned to one of four groups: control (C; n = 10), low-intensity RT (LI; n = 14), moderate-intensity RT (MI; n = 12), and high-intensity RT (HI; n = 14). Subjects trained for 24 wk. After training, subjects underwent a 24-wk detraining period in which no exercise training was performed. Blood collection and measurement of strength, REE, exercise energy cost, and VO2max were repeated at the end of training and detraining.
Measurements
Anthropometric variables. Height and weight were measured, and BMI was determined using standard procedures (11). Skinfold thickness was measured sequentially, in triplicate, at chest, biceps, triceps, subscapula, abdomen, suprailiac, calf, and thigh by the same investigator using a skinfold caliper (Harpenden, HSK-BI, British Indicators, West Sussex, UK) and a standard technique (32). The sum of the eight skinfolds was used as an index of body fatness. Waist and hip circumferences were obtained in duplicate with a Gullick II tape, and the waist to hip ratio (WHR) was determined.
Measurement of VO2max. VO2max was determined during graded exercise testing using a modified version of the Bruce protocol (32). An Oxycon Champion pulmonary gas exchange system (Minjhardt, The Netherlands) was used to evaluate the participants’ VO2max. Oxygen uptake (VO2) was measured continuously via breath by breath analysis with the use of a computerized system. To ascertain that VO2max had been attained, standard criteria had to be met (32).
REE and respiratory quotient (RQ). REE and RQ were determined while subjects were in a semirecumbent position in the morning for 45 min after an overnight fast. VO2/CO2 production rates were measured from expired air samples collected via a ventilated hood system (Vmax29c, Sensormedics). After a 10-min stabilization period, 20 consecutive 1-min measurements were taken and averaged. Energy expenditure was calculated by the Weir equation (34) and expressed per 24 h.
Isotonic strength assessment. Maximal strength (1RM) was measured bilaterally with subjects positioned on leg extension (lower body strength) and lat pull down (upper body strength) equipment (Universal Machines, Irvine, CA) after a familiarization period (control for large early gains in strength due to motor learning and reduce injury risk) using standard procedures (11, 35). The intraclass correlation coefficient estimated for test-retest trials within the same week was 0.92.
Biochemical analyses
Fasting blood samples were collected at rest (baseline) and after training and detraining. Subjects abstained from physical exercise for the last 48 h before testing. Blood was collected into Vacutainers (Becton Dickinson, Franklin Lakes, NJ) containing SST Gel (Becton Dickinson), EDTA, or heparin and was immediately placed on ice and centrifuged (4 C, 1500 x g, 15 min). The serum or plasma obtained was stored in multiple aliquots at –75 C until assayed (in duplicate).
Serum leptin was determined by an ELISA with a commercially available kit (EIA-2395, DRG, Marburg, Germany) with a 5.9% intraassay precision, a 6.8% interassay accuracy, and a sensitivity of 0.5 ng/ml. Plasma adiponectin was analyzed with a commercially available RIA (Linco Research, Inc., St. Charles, MO), with a 6.9% intraassay precision, a 7.8% interassay accuracy, and a sensitivity of 0.5 ng/ml. Insulin was measured with an immunoassay (Access Immunoassay System, Beckman Coulter, Fullerton, CA), with a 4.9% intraassay precision, a 3.8% interassay accuracy, and a sensitivity of 0.5 µU/ml. Glucose was determined by the glucose oxidase method (Sigma-Aldrich Corp., St Louis, MO) with 3.8% and 4.9% inter- and intraassay coefficients of variation, respectively.
Dietary records
Subjects were prescreened by a trained dietician before participation to ensure compliance with the typical American Heart Dietary intake recommendations (five men were excluded based on this criterion) using 5-d diet recalls. Macronutrient composition and energy content were analyzed using the computerized nutritional analysis system ScienceTech Diet 200A (Science Technologies, Athens, Greece) (36).
Exercise training
Subjects trained under supervision three times per week for 24 wk. After a warm-up (11), subjects trained for approximately 60 min. Blood pressure and heart rate were monitored throughout training and recovery. Subjects executed eight resistance exercises (Universal Machines) selected to stress the major muscle groups in the following order: chest press, leg extension, shoulder press, leg curls, latissimus pull down, leg press, arm curls, and triceps extension: two sets per exercise (wk 1–8) and three sets per exercise thereafter (training intensity was maintained at 45–50% of 1RM in LI, at 60–65% of 1RM in MI, and at 80–85% of 1RM in HI; Table 1) (32). The 1RM of each exercise was retested every 4 wk so that resistance could be adjusted properly (11). There were rest periods of 2, 4, and 6 min between sets (for LI, MI, and HI, respectively) (11). Participants also performed abdominal crunches and lower back exercises: one set/six repetitions (wk 1–4), two sets/eight repetitions (wk 5–12), three sets/10 repetitions (wk 13–20), and four sets/10–12 repetitions (wk 21–24).
Energy cost of the exercise protocols
Energy expenditure during a single exercise session was determined using a portable indirect calorimetry system (VmaxST, Sensormedics, Yorba Linda, CA) at baseline, after training, and after detraining. Subjects performed the RT protocol used during training (three sets per exercise) and at the intensity used during training. The analyzer was fitted snuggly about the subject’s shoulders using a breathable Velcro shoulder mount. A facemask that covered the mouth and nose of the participant was attached to a bidirectional digital turbine flow meter and fastened on the participant by the use of a mesh hairnet and Velcro straps. Breath by breath O2 and CO2 gas exchanges were measured and stored within the unit’s computer system (averaged over 20-sec intervals). The energy cost of the exercise program was estimated using a constant value of 5.05 kcal/liter oxygen (32). Subjects were required to fast for 12 h, engage in no physical activity for 24 h before testing, and be well hydrated and well rested.
Detraining
After completion of the RT program, subjects in LI, MI, and HI were instructed to resume their normal lifestyles and avoid any type of systematic exercise for 24 wk. Subjects were contacted systematically to ensure that they were not engaged in regular exercise. However, eight subjects (three in LI, three in MI, and two in HI) were excluded for excessive activity during detraining.
Statistical analysis
Results were expressed as the mean ± SD. Between-group differences were analyzed by Kruskal-Wallis and Mann-Whitney U tests for continuous variables, and 
2 test was used for categorical variables as appropriate. Within-group differences were evaluated by Friedman and Wilcoxon tests. Bivariate correlations were estimated by Spearman test. Partial correlations were performed to estimate the association of leptin and adiponectin responses independent of BMI changes. All tests were two-tailed, and P < 0.05 was considered significant. Data analysis was performed using SPSS software (version 10.0, SPSS, Inc., Chicago, IL).
|
Results |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
). There were no differences between groups in age, BMI, WHR, skinfold sum, and strength (Tables 3 and 4). Mean exercise energy cost (Table 5) was significantly lower in HI compared with LI and MI (P < 0.001).
|
|
|
|
During training, all exercise groups demonstrated a decrease (P < 0.01) in BMI (1.2–1.7%; Table 3). However, between groups, BMI values were not different. Similarly skinfold sum decreased (1.5–2.9%) in MI and HI (P = 0.04 and P = 0.005, respectively). WHR decreased (P < 0.05) only in HI after training, but returned to baseline after detraining. BMI and skinfold sum increased (P < 0.01) in all groups, but reached baseline values only in LI and MI.
Changes in muscular strength
There were no differences in strength between groups at baseline (Table 4). Leg strength increased (P < 0.05) in exercise groups after training (48%, 73%, and 99% in LI, MI, and HI, respectively), with HI inducing greater (P < 0.001) gains than the other groups, and MI being more effective than LI (P < 0.05). Trunk strength increased in all exercise groups (33%, 70%, and 106% in LI, MI, and HI, respectively), with HI demonstrating greater (P < 0.05) improvement than the other groups, and MI being more effective than LI (P < 0.05). Detraining caused a decline (P < 0.05) in strength in all exercise groups. Specifically, leg strength was reduced in HI (25%), MI (42%), and LI (83%). Trunk strength was reduced (P < 0.05) in HI (20%), and MI (36%), but returned to pretraining values in LI.
Changes in glucose, HOMAIR, and RQ
Glucose (Table 2) declined (P < 0.05) with training in all exercise groups, with no differences detected between groups. Glucose returned to pretraining levels after detraining. HOMAIR decreased (4–29%) in all exercise groups (P < 0.05); the percent decrease was significantly higher in HI compared with the other groups (P < 0.05). After detraining, HOMAIR increased in all exercise groups (15–39%; P < 0.05). However, no significant differences were observed between groups in the percent HOMAIR increase. RQ values remained unaltered by both training and detraining.
Changes in leptin and adiponectin levels
Leptin (Table 2) decreased (3–19%) with training in all exercise groups (P < 0.01). However, absolute leptin levels and percent decrease from baseline were higher (P < 0.001, by Kruskal-Wallis test) in HI compared with other groups. Furthermore, leptin levels after training remained lower in HI even after BMI or skinfold sum adjustment. At detraining, although leptin increased (6–10%) in all exercise groups, it remained significantly lower (P < 0.01) than baseline in HI despite the fact that the percent leptin rise was higher (P < 0.01) in HI. Adiponectin increased in MI (P = 0.03, by Friedman test) and HI (P = 0.006, by Friedman test). After detraining, adiponectin decreased, reaching baseline values only in MI. In HI, adiponectin levels remained higher (P = 0.028) than baseline values.
After training, the percent leptin decrease correlated with the percent BMI decrease (r = 0.6; P < 0.001), skinfold sum (r = 0.59; P < 0.001), RMR (r = –0.58; P < 0.001), energy cost per training session (r = –0.59; P < 0.005), HOMAIR (r = 0.46; P < 0.01), VO2max (r = –0.35; P = 0.05), and adiponectin (r = –0.47; P < 0.05). After adjustment for BMI and skinfold sum changes, training-induced leptin responses correlated with the RMR percent increase (r = –0.44; P = 0.03 and r = –0.6; P = 0.002), the HOMAIR percent decrease (r = 0.37; P = 0.04 and r = 0.51; P = 0.003), and the exercise energy cost percent increase (r = 0.59; P = 0.003). The adiponectin percent increase after training was associated with skinfold sum changes (r = –0.64; P = 0.001), VO2max (r = 0.5; P = 0.01), and HOMAIR percent decrease (r = –0.4; P = 0.05) and was marginally associated with BMI (r = –0.37; P = 0.07). After adjustment for skinfold sum changes, the association of adiponectin responses with VO2max remained significant (r = 0.3; P = 0.05).
After detraining, the leptin percent increase correlated with the BMI percent increase (r = 0.51; P = 0.03) and the RMR percent decrease (r = –0.59; P < 0.001) and marginally with the HOMAIR percent increase (r = 0.34; P = 0.056). After adjustment for BMI changes, leptin responses correlated with the RMR percent decrease (r = –0.46; P = 0.009). Adiponectin responses demonstrated no significant association with either BMI or VO2max percent changes after detraining.
Changes in energy cost of exercise session, RMR, and VO2max
During training, the energy cost per training session (Table 5) increased (P < 0.05) in all groups (12.4–30.6%). The energy cost increase was higher in HI compared with LI and MI (P < 0.01). REE (Table 2) increased (P < 0.05) in all exercise groups (2.9–8.6%). The percent increase from baseline was higher (P < 0.001, by Kruskal-Wallis test) in HI compared with other groups. After detraining, RMR decreased (P < 0.05) in all exercise groups (1.7–4.7%). In MI and HI, RMR remained higher (P < 0.05) compared with baseline after detraining. VO2max increased (P < 0.05) in all groups (4.2–10.2%). The VO2max percent increase was higher (P < 0.05) in HI compared with the other groups. After detraining, VO2max returned to pretraining values in LI, but remained above (P < 0.05) baseline in MI and HI.
|
Discussion |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Leptin responses to training
Leptin is believed to play a crucial role in energy balance (2). It is not certain how circulating leptin reacts to exercise training, because most studies that investigated this association produced conflicting results. Leptin has been shown to decrease after cardiovascular exercise training in type 2 diabetes (37) or healthy controls (38, 39), especially when exercise was accompanied by conditions of energy deficiency (40). In contrast, other investigations revealed that cardiovascular exercise training (20–36 wk) had no impact in circulating leptin levels in older (41, 42) or younger (43, 44) subjects. The relationship between RT and leptin was examined in only one study (25), which revealed a marked leptin increase. However, in that study subjects ingested megestrol acetate, which stimulates appetite and weight gain in underweight elderly. Therefore, the present investigation is the first to demonstrate a decrease in leptin levels (3–19%) in older men after RT of various protocol configurations. The conflicting results produced by human studies on the relationship between leptin levels and exercise are attributed to the different training protocols used (intensity, volume, duration, subject’s initial conditioning status, and energy balance conditions). Short-term exercise protocols may induce little or no effect on leptin levels (38) except under conditions of energy deficiency (40). Studies that demonstrated a leptin decline after exercise training were mainly confined to untrained populations (43, 44).
RT counteracts aging-induced deterioration in muscular mass, strength, and power; improves the functional status of older adults (45); and reduces frailty in the elderly (11, 14, 15, 45). However, the association between leptin and RT in older humans has drawn very limited attention. Acute resistance exercise induces a delayed (9–13 h after exercise) decline in circulating leptin levels (21, 22). Intense resistance exercise is expected to induce a leptin decline due to elevated glucose uptake by peripheral tissues in the presence of lactate, induced acidosis, augmented sympathoadrenal input and energy expenditure, glycogen depletion, and glycolysis inhibition (22, 46). Muscle glycogen was not assessed in this study, but similar resistance exercise protocols cause a significant rise in blood lactate (5- to 11-fold), suggesting an increased glycogenolytic rate (22) and a decrease (20–40%) in muscle glycogen stores (17). Future studies should address the association of alterations in sympathetic nervous system activity and glucose metabolism with leptin responses after RT.
Another mechanism that could explain the training-induced leptin decline is the reduction of body weight and fat as a result of a disruption in balance between energy intake and expenditure. Aging is associated with declines in physical activity and REE and an increase in body fat stores (47). Exercise training increases total energy expenditure by up-regulating the direct energy cost of physical activity and elevating REE, which may lead to decreased body fat stores that ultimately will depress leptin secretion (48, 49). This response could be partially due to a rise in the norepinephrine appearance rate (48, 50). The RT-induced leptin decline in the present study was accompanied by decreases in BMI and skinfold sum and significant increases in REE and exercise energy cost independent of intensity. In fact, training-induced leptin responses correlated with REE and exercise energy cost increase after adjustment for BMI and skinfold sum changes, indicating a possible association among leptin, RMR, and exercise energy expenditure. However, this association does not establish a cause and effect relationship. Furthermore, BMI and skinfold measurement may pose a limitation in the present study as accurate measures of body fat content and lean mass change compared with dual-energy x-ray absorptiometry, computed tomography, or magnetic resonance imaging. BMI is not a very sensitive measure to track body composition changes where lean and fat masses vary in opposite directions, whereas skinfolds lack reproducibility. Hence, it is possible that adjustment for BMI and skinfolds still leaves some residual confounding. Nevertheless, the hypothesis that adipokine changes relate to adiposity changes cannot be rejected.
The training effects on leptin, REE, and exercise energy cost were intensity dependent. Although MI and HI induced a significant change in leptin, REE, and exercise energy cost, HI elicited a more pronounced response in these variables. Repetitive muscular contractions during resistance exercise may generate peripheral feedback signals to the central nervous system, modulating energy requirements (21). Furthermore, the excess postoxygen consumption and increased energy expenditure produced by resistance exercise of high to moderate intensity (51) may cause a disruption in energy homeostasis resulting in a reduction in the leptin concentration (21). This is of particular importance, because guidelines for exercise prescription for older adults suggest intensity ranges similar to those used in the present study (32).
Adiponectin responses to training
Adiponectin has been reported to improve insulin sensitivity and affect carbohydrate and lipid metabolism (52, 53). In the present study, MI and HI, but not LI, RT increased adiponectin circulating levels.
The adiponectin response to exercise training is not well documented. Adiponectin remained unaltered (29), increased (26, 27, 30, 31), or decreased (28) after prolonged endurance training (low to moderate intensity, three to five exercise sessions per week for 10–24 wk), whereas adiponectin responses to RT have not been investigated. An increase in adiponectin after RT may be attributed to an enhancement of insulin sensitivity caused by training. Insulin reduces adiponectin mRNA levels in adipocytes in a dose- and time-dependent manner (54), whereas adiponectin increases insulin sensitivity by increasing fat oxidation, reducing circulating fatty acid levels and intracellular triglycerides in liver and muscle (55). However, there are studies in the literature reporting an unchanged adiponectin response despite a training-induced enhancement of insulin action (29, 56). In the present investigation, an increase in adiponectin after exercise training was associated with improvement of insulin sensitivity. Interventions that decrease body weight and/or fat may elevate adiponectin levels (26). Previous work reported that weight loss induced by nutritional and exercise interventions elicited an augmented adiponectin response (29), indicating that body weight/composition changes may be necessary to increase adiponectin concentration (57). Marked weight loss (21%) after gastric partition surgery caused a 46% increase in serum adiponectemia (58). In the present study, RT induced body weight and fat loss of smaller (2–3%) magnitude compared with that found in previous investigations (26, 29). As stated, the use of BMI, weight, and skinfolds poses a limitation in accurate assessment of body compositional change, because muscle mass increased and body fat decreased simultaneously in this study. However, even limited weight loss induced by sibutramine (5.4%) and orlistat treatment (2.5%) led to increased serum adiponectin levels (59). Recently, long-term caloric restriction elicited a minimal weight loss and an enhanced adiponectin response (60). It is possible that cytokine reduction (TNF-
and IL-6) after training and/or weight loss regimens might be responsible for the up-regulated adiponectin responses. Future research should address this hypothesis by studying training effects on gene expression of various adipocytokines in adipose tissue.
Leptin and adiponectin responses to detraining
A 6-month training cessation reversed exercise-induced leptin and adiponectin responses. Both adipocytokines remained significantly different from baseline in HI, suggesting a possible intensity threshold to maintain training-induced adaptations. This is the first attempt to determine resistance detraining effects on adipocytokine levels in the elderly. The leptin change correlated with the detraining-induced REE decrease, revealing an association between these two parameters and indicating that training-induced reductions in body weight/composition due to a disruption in energy balance may lead to leptin attenuation. The fact that body weight/fat and REE remained elevated during detraining suggests that training gains were of sufficient magnitude to preserve positive adaptations in older men. Nevertheless, BMI and skinfold measurements may not assess body composition changes accurately, and dual-energy x-ray absorptiometry would be a more appropriate choice for future studies attempting to determine the mechanisms responsible for leptin and adiponectin changes after exercise training.
Adiponectin remained elevated only in HI during detraining, demonstrating no association with changes observed in body weight, skinfold sum, or REE. The fact that the body weight decline was not completely abolished by detraining in HI may indicate that this exercise protocol could offer a sufficient stimulus for adiponectin to remain higher than pretraining values. It is evident that more work is needed to determine the factors that affect adipocytokine responses to RT and detraining.
In conclusion, RT and detraining alter leptin and adiponectin responses in older men in an intensity-dependent manner. Leptin and adiponectin responses to RT in older males appear to be associated with body weight and/or composition alterations, REE increase, and exercise energy cost elevation.
|
Acknowledgments |
|---|
|
Footnotes |
|---|
Abbreviations: BMI, Body mass index; HI, high-intensity training; HOMAIR, homeostasis model assessment of insulin resistance; LI, low-intensity training; MI, moderate-intensity training; REE, resting energy expenditure; 1RM, maximal strength; RMR, resting metabolic rate; RQ, respiratory quotient; RT, resistance training; VO2max, maximal oxygen consumption; WHR, waist to hip ratio.
Received February 7, 2005.
Accepted August 2, 2005.
|
References |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
, growth hormone, and IL-6 in 3T3–L1 adipocytes. Horm Metab Res 35:147–152[CrossRef][Medline]
, and leptin in elderly men ingesting megestrol acetate: a randomized cotrolled trial. J Gerontol Med Sci 58A:165–170.
This article has been cited by other articles:
 |
|
 |
|
  A. Chatzinikolaou, I. Fatouros, A. Petridou, A. Jamurtas, A. Avloniti, I. Douroudos, G. Mastorakos, C. Lazaropoulou, I. Papassotiriou, S. Tournis, et al. Adipose Tissue Lipolysis Is Upregulated in Lean and Obese Men During Acute Resistance Exercise Diabetes Care, July 1, 2008; 31(7): 1397 - 1399. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Ahmadizad, A. H. Haghighi, and M. R. Hamedinia Effects of resistance versus endurance training on serum adiponectin and insulin resistance index Eur. J. Endocrinol., November 1, 2007; 157(5): 625 - 631. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. R. Kraemer and V. D. Castracane Exercise and Humoral Mediators of Peripheral Energy Balance: Ghrelin and Adiponectin Experimental Biology and Medicine, February 1, 2007; 232(2): 184 - 194. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Bluher, J. W. Bullen Jr., J. H. Lee, S. Kralisch, M. Fasshauer, N. Kloting, J. Niebauer, M. R. Schon, C. J. Williams, and C. S. Mantzoros Circulating Adiponectin and Expression of Adiponectin Receptors in Human Skeletal Muscle: Associations with Metabolic Parameters and Insulin Resistance and Regulation by Physical Training J. Clin. Endocrinol. Metab., June 1, 2006; 91(6): 2310 - 2316. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Moriconi, M. Kraenzlin, B. Muller, U. Keller, C. P. G. Nusbaumer, S. Stohr, M. Tamm, and J. J. Puder Body Composition and Adiponectin Serum Concentrations in Adult Patients with Cystic Fibrosis J. Clin. Endocrinol. Metab., April 1, 2006; 91(4): 1586 - 1590. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
