Sympathetic Neural Adaptation to Hypocaloric Diet With or Without Exercise Training in Obese Metabolic Syndrome Subjects
Sympathetic Neural Adaptation to Hypocaloric Diet With or Without Exercise Training in Obese Metabolic Syndrome Subjects Nora E. Straznicky 1 , Elisabeth A. Lambert 1 , Paul J. Nestel 2 , Mariee T. McGrane 1 , Tye Dawood 1 , Markus P. Schlaich 3 , Kazuko Masuo 1 , Nina Eikelis 1 , Barbora de Courten...
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Published in | Diabetes (New York, N.Y.) Vol. 59; no. 1; pp. 71 - 79 |
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Main Authors | , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Alexandria, VA
American Diabetes Association
01.01.2010
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Subjects | |
Online Access | Get full text |
ISSN | 0012-1797 1939-327X 1939-327X |
DOI | 10.2337/db09-0934 |
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Abstract | Sympathetic Neural Adaptation to Hypocaloric Diet With or Without Exercise Training in Obese Metabolic Syndrome Subjects
Nora E. Straznicky 1 ,
Elisabeth A. Lambert 1 ,
Paul J. Nestel 2 ,
Mariee T. McGrane 1 ,
Tye Dawood 1 ,
Markus P. Schlaich 3 ,
Kazuko Masuo 1 ,
Nina Eikelis 1 ,
Barbora de Courten 4 ,
Justin A. Mariani 5 ,
Murray D. Esler 1 ,
Florentia Socratous 3 ,
Reena Chopra 1 ,
Carolina I. Sari 1 ,
Eldho Paul 6 and
Gavin W. Lambert 1
1 Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia;
2 Cardiovascular Nutrition Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia;
3 Neurovascular Hypertension and Kidney Disease Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia;
4 Clinical Physiology Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia;
5 Heart Failure Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia;
6 Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Victoria, Australia.
Corresponding author: Nora E. Straznicky, nora.straznicky{at}bakeridi.edu.au .
Abstract
OBJECTIVE Sympathetic nervous system (SNS) overactivity contributes to the pathogenesis and target organ complications of obesity.
This study was conducted to examine the effects of lifestyle interventions (weight loss alone or together with exercise) on
SNS function.
RESEARCH DESIGN AND METHODS Untreated men and women (mean age 55 ± 1 year; BMI 32.3 ± 0.5 kg/m 2 ) who fulfilled Adult Treatment Panel III metabolic syndrome criteria were randomly allocated to either dietary weight loss
(WL, n = 20), dietary weight loss and moderate-intensity aerobic exercise (WL+EX, n = 20), or no treatment (control, n = 19). Whole-body norepinephrine kinetics, muscle sympathetic nerve activity by microneurography, baroreflex sensitivity,
fitness (maximal oxygen consumption), metabolic, and anthropometric measurements were made at baseline and 12 weeks.
RESULTS Body weight decreased by −7.1 ± 0.6 and −8.4 ± 1.0 kg in the WL and WL+EX groups, respectively (both P < 0.001). Fitness increased by 19 ± 4% ( P < 0.001) in the WL+EX group only. Resting SNS activity decreased similarly in the WL and WL+EX groups: norepinephrine spillover
by −96 ± 30 and −101 ± 34 ng/min (both P < 0.01) and muscle sympathetic nerve activity by −12 ± 6 and −19 ± 4 bursts/100 heart beats, respectively (both P < 0.01), but remained unchanged in control subjects. Blood pressure, baroreflex sensitivity, and metabolic parameters improved
significantly and similarly in the two lifestyle intervention groups.
CONCLUSIONS The addition of moderate-intensity aerobic exercise training to a weight loss program does not confer additional benefits
on resting SNS activity. This suggests that weight loss is the prime mover in sympathetic neural adaptation to a hypocaloric
diet.
Footnotes
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore
be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received June 28, 2009.
Accepted October 4, 2009.
© 2010 American Diabetes Association |
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AbstractList | Sympathetic Neural Adaptation to Hypocaloric Diet With or Without Exercise Training in Obese Metabolic Syndrome Subjects
Nora E. Straznicky 1 ,
Elisabeth A. Lambert 1 ,
Paul J. Nestel 2 ,
Mariee T. McGrane 1 ,
Tye Dawood 1 ,
Markus P. Schlaich 3 ,
Kazuko Masuo 1 ,
Nina Eikelis 1 ,
Barbora de Courten 4 ,
Justin A. Mariani 5 ,
Murray D. Esler 1 ,
Florentia Socratous 3 ,
Reena Chopra 1 ,
Carolina I. Sari 1 ,
Eldho Paul 6 and
Gavin W. Lambert 1
1 Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia;
2 Cardiovascular Nutrition Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia;
3 Neurovascular Hypertension and Kidney Disease Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia;
4 Clinical Physiology Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia;
5 Heart Failure Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia;
6 Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Victoria, Australia.
Corresponding author: Nora E. Straznicky, nora.straznicky{at}bakeridi.edu.au .
Abstract
OBJECTIVE Sympathetic nervous system (SNS) overactivity contributes to the pathogenesis and target organ complications of obesity.
This study was conducted to examine the effects of lifestyle interventions (weight loss alone or together with exercise) on
SNS function.
RESEARCH DESIGN AND METHODS Untreated men and women (mean age 55 ± 1 year; BMI 32.3 ± 0.5 kg/m 2 ) who fulfilled Adult Treatment Panel III metabolic syndrome criteria were randomly allocated to either dietary weight loss
(WL, n = 20), dietary weight loss and moderate-intensity aerobic exercise (WL+EX, n = 20), or no treatment (control, n = 19). Whole-body norepinephrine kinetics, muscle sympathetic nerve activity by microneurography, baroreflex sensitivity,
fitness (maximal oxygen consumption), metabolic, and anthropometric measurements were made at baseline and 12 weeks.
RESULTS Body weight decreased by −7.1 ± 0.6 and −8.4 ± 1.0 kg in the WL and WL+EX groups, respectively (both P < 0.001). Fitness increased by 19 ± 4% ( P < 0.001) in the WL+EX group only. Resting SNS activity decreased similarly in the WL and WL+EX groups: norepinephrine spillover
by −96 ± 30 and −101 ± 34 ng/min (both P < 0.01) and muscle sympathetic nerve activity by −12 ± 6 and −19 ± 4 bursts/100 heart beats, respectively (both P < 0.01), but remained unchanged in control subjects. Blood pressure, baroreflex sensitivity, and metabolic parameters improved
significantly and similarly in the two lifestyle intervention groups.
CONCLUSIONS The addition of moderate-intensity aerobic exercise training to a weight loss program does not confer additional benefits
on resting SNS activity. This suggests that weight loss is the prime mover in sympathetic neural adaptation to a hypocaloric
diet.
Footnotes
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore
be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received June 28, 2009.
Accepted October 4, 2009.
© 2010 American Diabetes Association Sympathetic nervous system (SNS) overactivity contributes to the pathogenesis and target organ complications of obesity. This study was conducted to examine the effects of lifestyle interventions (weight loss alone or together with exercise) on SNS function. Untreated men and women (mean age 55 +/- 1 year; BMI 32.3 +/- 0.5 kg/m(2)) who fulfilled Adult Treatment Panel III metabolic syndrome criteria were randomly allocated to either dietary weight loss (WL, n = 20), dietary weight loss and moderate-intensity aerobic exercise (WL+EX, n = 20), or no treatment (control, n = 19). Whole-body norepinephrine kinetics, muscle sympathetic nerve activity by microneurography, baroreflex sensitivity, fitness (maximal oxygen consumption), metabolic, and anthropometric measurements were made at baseline and 12 weeks. Body weight decreased by -7.1 +/- 0.6 and -8.4 +/- 1.0 kg in the WL and WL+EX groups, respectively (both P < 0.001). Fitness increased by 19 +/- 4% (P < 0.001) in the WL+EX group only. Resting SNS activity decreased similarly in the WL and WL+EX groups: norepinephrine spillover by -96 +/- 30 and -101 +/- 34 ng/min (both P < 0.01) and muscle sympathetic nerve activity by -12 +/- 6 and -19 +/- 4 bursts/100 heart beats, respectively (both P < 0.01), but remained unchanged in control subjects. Blood pressure, baroreflex sensitivity, and metabolic parameters improved significantly and similarly in the two lifestyle intervention groups. The addition of moderate-intensity aerobic exercise training to a weight loss program does not confer additional benefits on resting SNS activity. This suggests that weight loss is the prime mover in sympathetic neural adaptation to a hypocaloric diet. OBJECTIVE--Sympathetic nervous system (SNS) overactivity contributes to the pathogenesis and target organ complications of obesity. This study was conducted to examine the effects of lifestyle interventions (weight loss alone or together with exercise) on SNS function. RESEARCH DESIGN AND METHODS--Untreated men and women (mean age 55 ± 1 year; BMI 32.3 ± 0.5 kg/[m.sup.2]) who fulfilled Adult Treatment Panel III metabolic syndrome criteria were randomly allocated to either dietary weight loss (WL, n = 20), dietary weight loss and moderate-intensity aerobic exercise (WL+EX, n = 20), or no treatment (control, n = 19). Whole-body norepinephrine kinetics, muscle sympathetic nerve activity by microneurography, baroreflex sensitivity, fitness (maximal oxygen consumption), metabolic, and anthropometric measurements were made at baseline and 12 weeks. RESULTS--Body weight decreased by -7.1 ± 0.6 and -8.4 ± 1.0 kg in the WL and WL+EX groups, respectively (both P < 0.001). Fitness increased by 19 ± 4% (P < 0.001) in the WL+EX group only. Resting SNS activity decreased similarly in the WL and WL+EX groups: norepinephrine spillover by -96 ± 30 and -101 ± 34 ng/min (both P < 0.01) and muscle sympathetic nerve activity by -12 ± 6 and -19 ± 4 bursts/100 heart beats, respectively (both P < 0.01), but remained unchanged in control subjects. Blood pressure, baroreflex sensitivity, and metabolic parameters improved significantly and similarly in the two lifestyle intervention groups. CONCLUSIONS--The addition of moderate-intensity aerobic exercise training to a weight loss program does not confer additional benefits on resting SNS activity. This suggests that weight loss is the prime mover in sympathetic neural adaptation to a hypocaloric diet. OBJECTIVE--Sympathetic nervous system (SNS) overactivity contributes to the pathogenesis and target organ complications of obesity. This study was conducted to examine the effects of lifestyle interventions (weight loss alone or together with exercise) on SNS function. RESEARCH DESIGN AND METHODS--Untreated men and women (mean age 55 [+ or -] 1 year; BMI 32.3 [+ or -] 0.5 kg/[m.sup.2]) who fulfilled Adult Treatment Panel III metabolic syndrome criteria were randomly allocated to either dietary weight loss (WL, n = 20), dietary weight loss and moderate-intensity aerobic exercise (WL+EX, n = 20), or no treatment (control, n = 19). Whole-body norepinephrine kinetics, muscle sympathetic nerve activity by microneurography, baroreflex sensitivity, fitness (maximal oxygen consumption), metabolic, and anthropometric measurements were made at baseline and 12 weeks. RESULTS--Body weight decreased by -7.1 [+ or -] 0.6 and -8.4 [+ or -] 1.0 kg in the WL and WL+EX groups, respectively (both P < 0.001). Fitness increased by 19 [+ or -] 4% (P < 0.001) in the WL+EX group only. Resting SNS activity decreased similarly in the WL and WL+EX groups: norepinephrine spillover by -96 [+ or -] 30 and -101 [+ or -] 34 ng/min (both P < 0.01) and muscle sympathetic nerve activity by -12 [+ or -] 6 and -19 [+ or -] 4 bursts/100 heart beats, respectively (both P < 0.01), but remained unchanged in control subjects. Blood pressure, baroreflex sensitivity, and metabolic parameters improved significantly and similarly in the two lifestyle intervention groups. CONCLUSIONS--The addition of moderate-intensity aerobic exercise training to a weight loss program does not confer additional benefits on resting SNS activity. This suggests that weight loss is the prime mover in sympathetic neural adaptation to a hypocaloric diet. Sympathetic nervous system (SNS) overactivity contributes to the pathogenesis and target organ complications of obesity. This study was conducted to examine the effects of lifestyle interventions (weight loss alone or together with exercise) on SNS function.OBJECTIVESympathetic nervous system (SNS) overactivity contributes to the pathogenesis and target organ complications of obesity. This study was conducted to examine the effects of lifestyle interventions (weight loss alone or together with exercise) on SNS function.Untreated men and women (mean age 55 +/- 1 year; BMI 32.3 +/- 0.5 kg/m(2)) who fulfilled Adult Treatment Panel III metabolic syndrome criteria were randomly allocated to either dietary weight loss (WL, n = 20), dietary weight loss and moderate-intensity aerobic exercise (WL+EX, n = 20), or no treatment (control, n = 19). Whole-body norepinephrine kinetics, muscle sympathetic nerve activity by microneurography, baroreflex sensitivity, fitness (maximal oxygen consumption), metabolic, and anthropometric measurements were made at baseline and 12 weeks.RESEARCH DESIGN AND METHODSUntreated men and women (mean age 55 +/- 1 year; BMI 32.3 +/- 0.5 kg/m(2)) who fulfilled Adult Treatment Panel III metabolic syndrome criteria were randomly allocated to either dietary weight loss (WL, n = 20), dietary weight loss and moderate-intensity aerobic exercise (WL+EX, n = 20), or no treatment (control, n = 19). Whole-body norepinephrine kinetics, muscle sympathetic nerve activity by microneurography, baroreflex sensitivity, fitness (maximal oxygen consumption), metabolic, and anthropometric measurements were made at baseline and 12 weeks.Body weight decreased by -7.1 +/- 0.6 and -8.4 +/- 1.0 kg in the WL and WL+EX groups, respectively (both P < 0.001). Fitness increased by 19 +/- 4% (P < 0.001) in the WL+EX group only. Resting SNS activity decreased similarly in the WL and WL+EX groups: norepinephrine spillover by -96 +/- 30 and -101 +/- 34 ng/min (both P < 0.01) and muscle sympathetic nerve activity by -12 +/- 6 and -19 +/- 4 bursts/100 heart beats, respectively (both P < 0.01), but remained unchanged in control subjects. Blood pressure, baroreflex sensitivity, and metabolic parameters improved significantly and similarly in the two lifestyle intervention groups.RESULTSBody weight decreased by -7.1 +/- 0.6 and -8.4 +/- 1.0 kg in the WL and WL+EX groups, respectively (both P < 0.001). Fitness increased by 19 +/- 4% (P < 0.001) in the WL+EX group only. Resting SNS activity decreased similarly in the WL and WL+EX groups: norepinephrine spillover by -96 +/- 30 and -101 +/- 34 ng/min (both P < 0.01) and muscle sympathetic nerve activity by -12 +/- 6 and -19 +/- 4 bursts/100 heart beats, respectively (both P < 0.01), but remained unchanged in control subjects. Blood pressure, baroreflex sensitivity, and metabolic parameters improved significantly and similarly in the two lifestyle intervention groups.The addition of moderate-intensity aerobic exercise training to a weight loss program does not confer additional benefits on resting SNS activity. This suggests that weight loss is the prime mover in sympathetic neural adaptation to a hypocaloric diet.CONCLUSIONSThe addition of moderate-intensity aerobic exercise training to a weight loss program does not confer additional benefits on resting SNS activity. This suggests that weight loss is the prime mover in sympathetic neural adaptation to a hypocaloric diet. Sympathetic nervous system (SNS) overactivity contributes to the pathogenesis and target organ complications of obesity. This study was conducted to examine the effects of lifestyle interventions (weight loss alone or together with exercise) on SNS function. Untreated men and women (mean age 55 +/- 1 year; BMI 32.3 +/- 0.5 kg/m(2)) who fulfilled Adult Treatment Panel III metabolic syndrome criteria were randomly allocated to either dietary weight loss (WL, n = 20), dietary weight loss and moderate-intensity aerobic exercise (WL+EX, n = 20), or no treatment (control, n = 19). Whole-body norepinephrine kinetics, muscle sympathetic nerve activity by microneurography, baroreflex sensitivity, fitness (maximal oxygen consumption), metabolic, and anthropometric measurements were made at baseline and 12 weeks. Body weight decreased by -7.1 +/- 0.6 and -8.4 +/- 1.0 kg in the WL and WL+EX groups, respectively (both P < 0.001). Fitness increased by 19 +/- 4% (P < 0.001) in the WL+EX group only. Resting SNS activity decreased similarly in the WL and WL+EX groups: norepinephrine spillover by -96 +/- 30 and -101 +/- 34 ng/min (both P < 0.01) and muscle sympathetic nerve activity by -12 +/- 6 and -19 +/- 4 bursts/100 heart beats, respectively (both P < 0.01), but remained unchanged in control subjects. Blood pressure, baroreflex sensitivity, and metabolic parameters improved significantly and similarly in the two lifestyle intervention groups. The addition of moderate-intensity aerobic exercise training to a weight loss program does not confer additional benefits on resting SNS activity. This suggests that weight loss is the prime mover in sympathetic neural adaptation to a hypocaloric diet. |
Audience | Professional |
Author | Gavin W. Lambert Mariee T. McGrane Elisabeth A. Lambert Tye Dawood Reena Chopra Paul J. Nestel Nora E. Straznicky Florentia Socratous Nina Eikelis Barbora de Courten Murray D. Esler Markus P. Schlaich Carolina I. Sari Eldho Paul Kazuko Masuo Justin A. Mariani |
Author_xml | – sequence: 1 givenname: Nora E. surname: Straznicky fullname: Straznicky, Nora E. organization: Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia – sequence: 2 givenname: Elisabeth A. surname: Lambert fullname: Lambert, Elisabeth A. organization: Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia – sequence: 3 givenname: Paul J. surname: Nestel fullname: Nestel, Paul J. organization: Cardiovascular Nutrition Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia – sequence: 4 givenname: Mariee T. surname: McGrane fullname: McGrane, Mariee T. organization: Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia – sequence: 5 givenname: Tye surname: Dawood fullname: Dawood, Tye organization: Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia – sequence: 6 givenname: Markus P. surname: Schlaich fullname: Schlaich, Markus P. organization: Neurovascular Hypertension and Kidney Disease Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia – sequence: 7 givenname: Kazuko surname: Masuo fullname: Masuo, Kazuko organization: Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia – sequence: 8 givenname: Nina surname: Eikelis fullname: Eikelis, Nina organization: Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia – sequence: 9 givenname: Barbora surname: de Courten fullname: de Courten, Barbora organization: Clinical Physiology Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia – sequence: 10 givenname: Justin A. surname: Mariani fullname: Mariani, Justin A. organization: Heart Failure Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia – sequence: 11 givenname: Murray D. surname: Esler fullname: Esler, Murray D. organization: Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia – sequence: 12 givenname: Florentia surname: Socratous fullname: Socratous, Florentia organization: Neurovascular Hypertension and Kidney Disease Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia – sequence: 13 givenname: Reena surname: Chopra fullname: Chopra, Reena organization: Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia – sequence: 14 givenname: Carolina I. surname: Sari fullname: Sari, Carolina I. organization: Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia – sequence: 15 givenname: Eldho surname: Paul fullname: Paul, Eldho organization: Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Victoria, Australia – sequence: 16 givenname: Gavin W. surname: Lambert fullname: Lambert, Gavin W. organization: Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia |
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CODEN | DIAEAZ |
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ClassificationCodes | 8000141 |
ContentType | Journal Article |
Copyright | 2015 INIST-CNRS COPYRIGHT 2010 American Diabetes Association COPYRIGHT 2010 American Diabetes Association Copyright American Diabetes Association Jan 2010 2010 by the American Diabetes Association. |
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Keywords | Endocrinopathy Physical exercise Human Obesity Diabetes mellitus Nutrition disorder Metabolic diseases Cardiovascular disease Metabolic syndrome Sympathetic nervous system Feeding Diet Autonomic nervous system Nutritional status Adaptation |
Language | English |
License | CC BY 4.0 Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details. |
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Snippet | Sympathetic Neural Adaptation to Hypocaloric Diet With or Without Exercise Training in Obese Metabolic Syndrome Subjects
Nora E. Straznicky 1 ,
Elisabeth A.... Sympathetic nervous system (SNS) overactivity contributes to the pathogenesis and target organ complications of obesity. This study was conducted to examine... OBJECTIVE--Sympathetic nervous system (SNS) overactivity contributes to the pathogenesis and target organ complications of obesity. This study was conducted to... |
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SubjectTerms | Acclimatization - physiology Aerobic exercises Aerobics Aerobiosis Biological and medical sciences Blood Pressure Body Size Body Weight Care and treatment Diabetes Diabetes. Impaired glucose tolerance Diet Diet, Reducing Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Exercise Female Fitness training programs Fundamental and applied biological sciences. Psychology Health aspects Humans Hypertension Insulin resistance Intervention Life Style Lifestyles Male Medical sciences Metabolic diseases Metabolic syndrome Metabolic Syndrome - complications Middle Aged Miscellaneous Muscle, Skeletal - physiopathology Nervous system Norepinephrine - metabolism Obesity Obesity - complications Obesity - physiopathology Obesity - rehabilitation Original Other metabolic disorders Pathogenesis Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ Physical fitness Research design Sympathetic Nervous System - physiopathology Treatment Outcome Vertebrates: nervous system and sense organs Weight control Weight loss Women |
Title | Sympathetic Neural Adaptation to Hypocaloric Diet With or Without Exercise Training in Obese Metabolic Syndrome Subjects |
URI | http://diabetes.diabetesjournals.org/content/59/1/71.abstract https://www.ncbi.nlm.nih.gov/pubmed/19833893 https://www.proquest.com/docview/216473482 https://www.proquest.com/docview/733849154 https://pubmed.ncbi.nlm.nih.gov/PMC2797947 |
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