BRIEF REPORT
Reactive Oxygen Species Response to Exercise Training and Weight Loss in Sedentary Overweight and Obese Female Adults Vittorio E. Bianchi, MD; Paul M. Ribisl, PhD
■ PURPOSE: Reactive oxygen species (ROS) are implicated in cardiovascular disease and in the pathogenesis of type 2 diabetes and its complications, and it has been shown to increase insulin resistance. The purpose of this study was to examine the effect of aerobic exercise training and weight loss on ROS in overweight and obese patients as applied in a community clinical setting. ■ METHODS: Fifty healthy female clinic patients (M ± SEM: age, 41.0 ± 1.8 years; body mass index, 28.2 ± 0.8 kg/m2), free of cardiovascular events and not on drug therapy were evaluated before and after 3 months of dietary restriction (∼150 to 300 kcal/day deficit) and aerobic training (3 days/week for 1 hour at ∼75% V˙O2max). Measures included ROS, maximal power (kg/min) on cycle ergometry, postexercise heart rate recovery responses at 1 and 2 minutes, and selected anthropometric and hematologic variables.
K E Y
W O R D S
community setting intervention exercise training oxidative stress reactive oxygen species weight loss
■ RESULTS: Significant (P < .01) improvements were observed after aerobic training and weight loss in body weight in kilograms (−7.1%); maximal power in kg/min (+32.6%), ROS in U.CARR (Carratelli units) (−25.7%); and heart rate recovery 1 minute in beats per minute (−37.6%) following the program. Significant improvements were also noted in other anthropometric, cardiovascular, and hematologic measures.
Author Affiliations: Center for Clinical Nutrition, Metabolism, and Physical Performance, San Marino, Italy (Dr Bianchi), and Department of Health and Exercise Science, Wake Forest University, Winston-Salem, North Carolina (Dr Ribisl).
■ CONCLUSIONS: A 12-week program of nutritional and exercise intervention in overweight/obese sedentary women improves levels of oxidative stress when accompanied by weight loss and improved fitness. More than restricted caloric intake, physical activity at a relatively high intensity was effective in improving cardiovascular risk markers. The reduction in ROS may be an additional mechanism by which physical activity may contribute to preventing metabolic syndrome and subsequent atherosclerotic disease.
The authors declare no conflicts of interest.
Oxidative stress has been defined as an impaired balance between free radical production and antioxidant capacity, which results in an accumulation of oxidative products and is a well-recognized mechanism in many pathological conditions.1 A consequence of the www.jcrpjournal.com
Correspondence: Paul M. Ribisl, PhD, Department of Health and Exercise Science, Wake Forest University, 303 Gymnasium, Winston-Salem, NC 27109 ([email protected]). DOI: 10.1097/HCR.0000000000000114
excess free radical production is the generation of reactive oxygen species (ROS), which is correlated with increased cytokine release and other inflammatory markers, eventually leading to endothelial dysfunction. Oxidative stress is increased only in adipose Exercise Training and Weight Loss in Female Adults / 263
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
JCRP-D-13-00168.indd 263
12/06/15 4:42 AM
tissue, which is the major source of elevated plasma ROS2 and represents an important pathogenic mechanism of the metabolic syndrome (MetS).1 The production of ROS increases selectively in adipose tissue among obese individuals and recent studies have suggested that in nondiabetic human subjects, fat accumulation is closely correlated with markers of systemic oxidative stress and systemic oxidative stress strongly correlates with body mass index (BMI).3 While the formation of ROS and secretion of antioxidants are independently regulated by exercise and diet, little is known about their combined effect. The purpose of this study was to examine the effect of aerobic exercise training and weight loss on ROS in overweight and obese female patients enrolled in an outpatient clinical program.
METHODS This study was conducted in a health clinic in which unfit and overweight/obese patients volunteered to be part of a medically supervised weight loss program using diet and exercise. Fifty females (M ± SEM: age, 41.0 ± 1.8 years; height, 1.60 ± 0.06 m; weight, 72.2 ± 1.93 kg; BMI, 28 ± 0.76 kg/m2), who were free of cardiovascular disease and not on drug therapy, were evaluated before and after 3 months of dietary restriction and aerobic training.
Anthropometric and Dietary Measures Height and weight were measured with a stadiometer and physician’s balance scale and waist (level of the iliac crest) and hip (level of the symphysis pubis and the greatest gluteal protuberance) circumferences were measured using a metal tape. Three-day dietary records were maintained by each participant and were analyzed using NutriGenie software, (NutriGenie, Stanford, CA) providing total kcals and kcals from protein, carbohydrate, and fat (saturated, monounsaturated, and polyunsaturated).
Graded Exercise Testing Each subject was administered a graded exercise test to determine fitness level and cardiovascular response to exercise. The test was conducted on a Monark (model 839) ergometer with a brief warm-up followed by 2 minutes at 150 kg/min. Depending on the response, the load was then increased to the second stage for 2 minutes and thereafter by 150 kg/min each 2-minute stage until exhaustion. During the test, heart rate (HR, beats/min), systolic and diastolic blood pressures (SBP/DBP mmHg), and ratings of perceived exertion were taken during the final 30 seconds of
each stage. Immediately upon termination of the exercise test, minute-by-minute recovery HR and SBP/ DBP values were obtained in the sitting position for 3 minutes, or until the subject had recovered sufficiently. Heart rate recovery (HRR) was defined as the difference between HRpeak and the HR at 1 and at 2 minutes of recovery (HRR 1 m; HRR 2 m). Peak exercise capacity in metabolic equivalents (METs) was estimated from the final workload and body weight using the YMCA formula.4
Hematologic Measures Reactive oxygen species was measured by a capillary test, using the D-ROMS method.5 Total cholesterol, triglycerides, glucose, and insulin values were obtained and analyzed using a standardized medical hematology laboratory procedure using venipuncture samples. Steady state beta cell function and insulin resistance were estimated using Homeostasis Model Assessment (HOMA), as calculated using the standard formula: HOMA1-IR = [FPI (mU/L) × FPG (mmol/L)]/22.5.
Dietary and Exercise Interventions Patients were encouraged to follow their regular diet and it was strongly recommended that the patients not use supplements, and no supplementation was prescribed. The dietary prescription was based on the 2005 US Department of Agriculture Guideline recommendations as well as individualized on body weight and BMI. A balanced diet (∼15% protein, ∼30% fat, and ∼55% CHO) with reduced caloric intake (∼150300 kcal/day deficit) was prescribed and patients maintained food records to encourage adherence. The exercise prescription was set at a minimum of 3 days/ week for 1 hour at ∼75% V˙O2max.
Statistical Analysis Data are expressed as mean ± SEM. Comparisons between baseline and 3 month values were performed using paired t tests with a P value < .01 being considered as statistically significant. NCSS software was used for all statistical analyses (NCSS, Kaysville, UT).
RESULTS Anthropometric, metabolic, and cardiovascular data at baseline and postintervention are presented in Table 1.
Anthropometric Significant improvements were noted in body weight, BMI, waist circumference, hip circumference, and waist/hip ratio.
264 / Journal of Cardiopulmonary Rehabilitation and Prevention 2015;35:263-267
www.jcrpjournal.com
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
JCRP-D-13-00168.indd 264
12/06/15 4:42 AM
T a b l e 1 • Baseline and Postintervention Anthropometric, Exercise, and Hematologic Data (M ± SEM) Baseline
Postintervention
P Value
BMI, kg/m2
28.2 ± 0.8
26.2 ± 0.7
Reactive Oxygen Species Response to Exercise Training and Weight Loss in Sedentary Overweight and Obese Female Adults Vittorio E. Bianchi, MD; Paul M. Ribisl, PhD
■ PURPOSE: Reactive oxygen species (ROS) are implicated in cardiovascular disease and in the pathogenesis of type 2 diabetes and its complications, and it has been shown to increase insulin resistance. The purpose of this study was to examine the effect of aerobic exercise training and weight loss on ROS in overweight and obese patients as applied in a community clinical setting. ■ METHODS: Fifty healthy female clinic patients (M ± SEM: age, 41.0 ± 1.8 years; body mass index, 28.2 ± 0.8 kg/m2), free of cardiovascular events and not on drug therapy were evaluated before and after 3 months of dietary restriction (∼150 to 300 kcal/day deficit) and aerobic training (3 days/week for 1 hour at ∼75% V˙O2max). Measures included ROS, maximal power (kg/min) on cycle ergometry, postexercise heart rate recovery responses at 1 and 2 minutes, and selected anthropometric and hematologic variables.
K E Y
W O R D S
community setting intervention exercise training oxidative stress reactive oxygen species weight loss
■ RESULTS: Significant (P < .01) improvements were observed after aerobic training and weight loss in body weight in kilograms (−7.1%); maximal power in kg/min (+32.6%), ROS in U.CARR (Carratelli units) (−25.7%); and heart rate recovery 1 minute in beats per minute (−37.6%) following the program. Significant improvements were also noted in other anthropometric, cardiovascular, and hematologic measures.
Author Affiliations: Center for Clinical Nutrition, Metabolism, and Physical Performance, San Marino, Italy (Dr Bianchi), and Department of Health and Exercise Science, Wake Forest University, Winston-Salem, North Carolina (Dr Ribisl).
■ CONCLUSIONS: A 12-week program of nutritional and exercise intervention in overweight/obese sedentary women improves levels of oxidative stress when accompanied by weight loss and improved fitness. More than restricted caloric intake, physical activity at a relatively high intensity was effective in improving cardiovascular risk markers. The reduction in ROS may be an additional mechanism by which physical activity may contribute to preventing metabolic syndrome and subsequent atherosclerotic disease.
The authors declare no conflicts of interest.
Oxidative stress has been defined as an impaired balance between free radical production and antioxidant capacity, which results in an accumulation of oxidative products and is a well-recognized mechanism in many pathological conditions.1 A consequence of the www.jcrpjournal.com
Correspondence: Paul M. Ribisl, PhD, Department of Health and Exercise Science, Wake Forest University, 303 Gymnasium, Winston-Salem, NC 27109 ([email protected]). DOI: 10.1097/HCR.0000000000000114
excess free radical production is the generation of reactive oxygen species (ROS), which is correlated with increased cytokine release and other inflammatory markers, eventually leading to endothelial dysfunction. Oxidative stress is increased only in adipose Exercise Training and Weight Loss in Female Adults / 263
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
JCRP-D-13-00168.indd 263
12/06/15 4:42 AM
tissue, which is the major source of elevated plasma ROS2 and represents an important pathogenic mechanism of the metabolic syndrome (MetS).1 The production of ROS increases selectively in adipose tissue among obese individuals and recent studies have suggested that in nondiabetic human subjects, fat accumulation is closely correlated with markers of systemic oxidative stress and systemic oxidative stress strongly correlates with body mass index (BMI).3 While the formation of ROS and secretion of antioxidants are independently regulated by exercise and diet, little is known about their combined effect. The purpose of this study was to examine the effect of aerobic exercise training and weight loss on ROS in overweight and obese female patients enrolled in an outpatient clinical program.
METHODS This study was conducted in a health clinic in which unfit and overweight/obese patients volunteered to be part of a medically supervised weight loss program using diet and exercise. Fifty females (M ± SEM: age, 41.0 ± 1.8 years; height, 1.60 ± 0.06 m; weight, 72.2 ± 1.93 kg; BMI, 28 ± 0.76 kg/m2), who were free of cardiovascular disease and not on drug therapy, were evaluated before and after 3 months of dietary restriction and aerobic training.
Anthropometric and Dietary Measures Height and weight were measured with a stadiometer and physician’s balance scale and waist (level of the iliac crest) and hip (level of the symphysis pubis and the greatest gluteal protuberance) circumferences were measured using a metal tape. Three-day dietary records were maintained by each participant and were analyzed using NutriGenie software, (NutriGenie, Stanford, CA) providing total kcals and kcals from protein, carbohydrate, and fat (saturated, monounsaturated, and polyunsaturated).
Graded Exercise Testing Each subject was administered a graded exercise test to determine fitness level and cardiovascular response to exercise. The test was conducted on a Monark (model 839) ergometer with a brief warm-up followed by 2 minutes at 150 kg/min. Depending on the response, the load was then increased to the second stage for 2 minutes and thereafter by 150 kg/min each 2-minute stage until exhaustion. During the test, heart rate (HR, beats/min), systolic and diastolic blood pressures (SBP/DBP mmHg), and ratings of perceived exertion were taken during the final 30 seconds of
each stage. Immediately upon termination of the exercise test, minute-by-minute recovery HR and SBP/ DBP values were obtained in the sitting position for 3 minutes, or until the subject had recovered sufficiently. Heart rate recovery (HRR) was defined as the difference between HRpeak and the HR at 1 and at 2 minutes of recovery (HRR 1 m; HRR 2 m). Peak exercise capacity in metabolic equivalents (METs) was estimated from the final workload and body weight using the YMCA formula.4
Hematologic Measures Reactive oxygen species was measured by a capillary test, using the D-ROMS method.5 Total cholesterol, triglycerides, glucose, and insulin values were obtained and analyzed using a standardized medical hematology laboratory procedure using venipuncture samples. Steady state beta cell function and insulin resistance were estimated using Homeostasis Model Assessment (HOMA), as calculated using the standard formula: HOMA1-IR = [FPI (mU/L) × FPG (mmol/L)]/22.5.
Dietary and Exercise Interventions Patients were encouraged to follow their regular diet and it was strongly recommended that the patients not use supplements, and no supplementation was prescribed. The dietary prescription was based on the 2005 US Department of Agriculture Guideline recommendations as well as individualized on body weight and BMI. A balanced diet (∼15% protein, ∼30% fat, and ∼55% CHO) with reduced caloric intake (∼150300 kcal/day deficit) was prescribed and patients maintained food records to encourage adherence. The exercise prescription was set at a minimum of 3 days/ week for 1 hour at ∼75% V˙O2max.
Statistical Analysis Data are expressed as mean ± SEM. Comparisons between baseline and 3 month values were performed using paired t tests with a P value < .01 being considered as statistically significant. NCSS software was used for all statistical analyses (NCSS, Kaysville, UT).
RESULTS Anthropometric, metabolic, and cardiovascular data at baseline and postintervention are presented in Table 1.
Anthropometric Significant improvements were noted in body weight, BMI, waist circumference, hip circumference, and waist/hip ratio.
264 / Journal of Cardiopulmonary Rehabilitation and Prevention 2015;35:263-267
www.jcrpjournal.com
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
JCRP-D-13-00168.indd 264
12/06/15 4:42 AM
T a b l e 1 • Baseline and Postintervention Anthropometric, Exercise, and Hematologic Data (M ± SEM) Baseline
Postintervention
P Value
BMI, kg/m2
28.2 ± 0.8
26.2 ± 0.7
