HIGHLIGHTED TOPIC Role of Exercise in Reducing the Risk of Diabetes and Obesity
Inactivity, exercise, and visceral fat. STRRIDE: a randomized, controlled
study of exercise intensity and amount
Cris A. Slentz,1Lori B. Aiken,3Joseph A. Houmard,5Connie W. Bales,2,4Johanna L. Johnson,3
Charles J. Tanner,5Brian D. Duscha,1and William E. Kraus3
1Divisions of Cardiology and2Geriatrics,3Duke Center for Living, Duke University Medical Center, Durham;4Geriatric
Research, Education, and Clinical Center, Durham Veterans Administration Medical Center, and5Department of Exercise
and Sports Science and Human Performance Laboratory, East Carolina University, Greenville, North Carolina
Submitted 1 February 2005; accepted in final form 22 June 2005
Slentz, Cris A., Lori B. Aiken, Joseph A. Houmard, Connie W.
Bales, Johanna L. Johnson, Charles J. Tanner, Brian D. Duscha,
and William E. Kraus. Inactivity, exercise, and visceral fat.
STRRIDE: a randomized, controlled study of exercise intensity and
amount. J Appl Physiol 99: 1613–1618, 2005. First published July 7,
2005; doi:10.1152/japplphysiol.00124.2005.—Despite the importance
of randomized, dose-response studies for proper evaluation of effec-
tive clinical interventions, there have been no dose-response studies
on the effects of exercise amount on abdominal obesity, a major risk
factor for metabolic syndrome, diabetes, and cardiovascular disease.
One hundred seventy-five sedentary, overweight men and women
with mild to moderate dyslipidemia were randomly assigned to
participate for 6 mo in a control group or for ?8 mo in one of three
exercise groups: 1) low amount, moderate intensity, equivalent to
walking 12 miles/wk (19.2 km) at 40–55% of peak oxygen consump-
tion; 2) low amount, vigorous intensity, equivalent to jogging 12
miles/wk at 65–80% of peak oxygen consumption; or 3) high amount,
vigorous intensity, equivalent to jogging 20 miles/wk (32.0 km).
Computed tomography scans were analyzed for abdominal fat. Con-
trols gained visceral fat (8.6 ? 17.2%; P ? 0.001). The equivalent of
11 miles of exercise per week, at either intensity, prevented significant
accumulation of visceral fat. The highest amount of exercise resulted
in decreased visceral (?6.9 ? 20.8%; P ? 0.038) and subcutaneous
(?7.0 ? 10.8%; P ? 0.001) abdominal fat. Significant gains in
visceral fat over only 6 mo emphasize the high cost of continued
inactivity. A modest exercise program, consistent with recommenda-
tions from the Centers for Disease Control/American College of
Sports Medicine (CDC/ACSM), prevented significant increases in
visceral fat. Importantly, a modest increase over the CDC/ACSM
exercise recommendations resulted in significant decreases in visceral,
subcutaneous, and total abdominal fat without changes in caloric
Studies of Targeted Risk Reduction Interventions through Defined
Exercise; exercise training; visceral fat; exercise amount
THE PREVALENCE OF OVERWEIGHT and obesity is high and contin-
ues to rise, presenting ever-increasing challenges for individ-
uals and health professionals. Overweight individuals are at
increased risk for cardiovascular disease, diabetes, and other
health disorders (2, 5, 14, 21, 24). The location of the excess
weight is of particular importance, because the strength of the
relation between central obesity and disease risk is well doc-
umented (6, 13, 17, 30, 32), with visceral fat often considered
the major culprit (3, 4, 12, 20, 22, 23). In addition, several
studies have also shown a significant relationship between
abdominal subcutaneous fat and metabolic risk factors (1, 8,
18–20). It is important for interventions designed to reduce
abdominal obesity to monitor their effects on both visceral and
Controversy exists regarding the minimal and/or optimal
amount of exercise needed for health benefits. Interestingly,
despite the importance of centrally located body fat, there are
few if any prospective exercise training studies that compare
the effects of different amounts and intensities of exercise on
changes in parameters of central obesity. Studies of Targeted
Risk Reduction Interventions through Defined Exercise, a
randomized, controlled clinical trial, was prospectively de-
signed to investigate, in an 8-mo training study, the separate
effects of the amount of exercise and exercise intensity on
cardiovascular risk factors in overweight men and women with
mild to moderate dyslipidemia. This report summarizes the
effects of exercise amount and intensity on visceral, subcuta-
neous, and total abdominal fat.
A complete description of the Studies of Targeted Risk Reduction
Interventions through Defined Exercise design, hypotheses, recruit-
ment strategies, methods, and preliminary recruiting results are pub-
lished elsewhere (16).
Subjects. Subjects (n ? 330) from Durham, Greenville, and sur-
rounding communities in North Carolina met inclusion criteria and
were randomized into the study. Sixty-eight percent (225) completed
the 8-mo study. Of the 225 completers, 78% (n ? 175) had complete
pre- and poststudy computed tomography (CT) scan data, and the data
from these subjects were included in this analysis. There were no
differences in any variables measured between those in the subgroup
who had CT scans and those who did not have scans. Inclusion criteria
were 40–65 yr of age, sedentary (exercise ?2 times/wk), overweight
or mildly obese (body mass index of 25–35 kg/m2) with mild to
moderate lipid abnormalities [either low-density lipoprotein (LDL)
cholesterol of 130–190 mg/dl or high-density lipoprotein (HDL)
cholesterol of ?40 mg/dl for men or ?45 mg/dl for women]. Women
were postmenopausal. Exclusion criteria were diabetes, hypertension,
other metabolic or musculoskeletal diseases, current use of or intent to
Address for reprint requests and other correspondence: W. E. Kraus,
Division of Cardiology, Dept. of Medicine, PO Box 3327, Duke Univ. Medical
Center, Durham, NC 27710 (e-mail: firstname.lastname@example.org).
The costs of publication of this article were defrayed in part by the payment
of page charges. The article must therefore be hereby marked “advertisement”
in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
J Appl Physiol 99: 1613–1618, 2005.
First published July 7, 2005; doi:10.1152/japplphysiol.00124.2005.
8750-7587/05 $8.00 Copyright © 2005 the American Physiological Societyhttp://www.jap.org 1613
control group and the beneficial effects of the high-amount
exercise were observed in men and women.
1. Abate N, Garg A, Peshock R, Stray-Gundersen J, and Grundy S.
Relationships of generalized and regional adiposity to insulin sensitivity in
men. J Clin Invest 96: 88–98, 1995.
2. Caterson I, Hubbard V, Bray G, Grunstein R, Hansen B, Hong Y,
Labarthe D, Seidell JC, and Smith S. Prevention conference VII.
Obesity, a worldwide epidemic related to heart disease and stroke group
III: worldwide comorbidities of obesity. Circulation 110: 476–483, 2004.
3. Couillard C, Bergeron N, Pascot A, Almeras N, Bergeron J, Tremblay
A, Prud’homme D, and Despres JP. Evidence for impaired lipolysis in
abdominally obese men: postprandial study of apolipoprotein B-48- and
B-100-containing lipoproteins. Am J Clin Nutr 76: 311–318, 2002.
4. Despres JP, Coillard C, Gagnon J, Bergeron J, Leon A, Rao D,
Skinner J, Wilmore J, and Bouchard C. Race, visceral adipose tissue,
plasma lipids, and lipoprotein lipase activity in men and women (HERI-
TAGE). Arterioscler Thromb Vasc Biol 20: 1932–1938, 2000.
5. Eckel R, York D, Rossner S, Hubbard V, Caterson I, Sachiko T,
Hayman L, Mullis R, and Blair S. Prevention conference VII. Obesity,
a worldwide epidemic related to heart disease and stroke, executive
summary. Circulation 110: 2968–2975, 2004.
6. Folsom A, Kushi L, Anderson K, Mink P, Olson J, Hong C, Sellers T,
Lazovich D, and Prineas R. Associations of general and abdominal
obesity with multiple health outcomes in older women. Arch Intern Med
160: 2117–2128, 2000.
7. Frayn K. Visceral fat and insulin resistance—causative or correlative?
Br J Nutr 83: 71–77, 2000.
8. Goodpaster B, Thaete F, Simoneau J, and Kelley D. Subcutaneous
abdominal fat and thigh muscle composition predict insulin sensitivity
independently of visceral fat. Diabetes 46: 1579–1585, 1997.
9. Haskell W. What to look for in assessing responsiveness to exercise in a
health context. Med Sci Sports Exerc 33: S454–S458, 2001.
10. Houmard J, Tanner C, Slentz C, Duscha B, McCartney J, and Kraus
W. Effect of the volume and intensity of exercise training on insulin
sensitivity. J Appl Physiol 96: 101–106, 2004.
11. Irwin ML, Yasui Y, Ulrich CM, Bowen D, Schwartz RS, Yukawa M,
Aiello E, Potter JD, and McTiernan A. Effect of exercise on total and
intra-abdominal body fat in postmenopausal women: a randomized con-
trolled trial. JAMA 289: 323–330, 2003.
12. Janssen I, Fortier A, Hudson R, and Ross R. Effects of energy-
restrictive diet with or without exercise on abdominal fat, intermuscular
fat, and metabolic risk factors in obese women. Diabetes Care 25:
13. Kissebah AH and Krakower GR. Regional adiposity and morbidity.
Physiol Rev 74: 761–811, 1994.
14. Klein S, Burke L, Bray G, Blair S, Allison D, Pi-Sunyer X, Hong Y,
and Eckel R. Clinical implications of obesity with specific focus on
cardiovascular disease. A statement for professionals from the American
Heart Association on nutrition, physical activity, and metabolism. Circu-
lation 110: 2952–2967, 2004.
15. Kraus W, Houmard J, Duscha B, Knetgzer K, Wharton M, McCart-
ney J, Bales C, Henes S, Samsa G, Otvos J, Kulkarni K, and Slentz C.
Exercise training amount and intensity effects on plasma lipoproteins: a
randomized, controlled trial. NEJM 347: 1483–1492, 2002.
16. Kraus W, Torgan C, Duscha B, Norris J, Brown S, Cobb F, Bales C,
Annex B, Samsa G, Houmard J, and Slentz C. Studies of a targeted risk
reduction intervention through defined exercise (STRRIDE). Med Sci
Sports Exerc 33: 1774–1784, 2001.
17. Lemieux I, Pascot A, Coillard C, Lamarche B, Tchernof A, Almeras
N, Bergeron J, Gaudet D, Tremblay A, Prud’homme D, Nadeau A,
and Despres JP. Hypertriglyceridemic waist—a marker of the athero-
genic metabolic triad (hyperinsulinemia; hyperapolipoprotein B; small,
dense LDL) in men? Circulation 102: 179–184, 2000.
18. Martin M and Jensen M. Effects of body fat distribution on regional
lipolysis in obesity. J Clin Invest 88: 609–613, 1991.
19. Misra A, Garg A, Abate N, Peshock R, Stray-Gundersen J, and
Grundy S. Relationship of anterior and posterior subcutaneous abdominal
fat to insulin sensitivity in nondiabetic men. Obes Res 5: 93–99, 1997.
20. Miyazaki Y, Glass L, Triplitt C, ZWajcberg E, Mandarino L, and
Defronzo R. Abdominal fat distribution and peripheral and hepatic insulin
resistence in Type 2 diabetes mellitus. Am J Physiol Endocrinol Metab
283: E1135–E1143, 2002.
21. Mullis R, Blair S, Arrone L, Bier D, Denke M, Dietz W, Donato K,
Drewnowski A, French S, Howard B, Robinson T, Swinburn B, and
Weschsler H. Prevention conference VII. Obesity, a worldwide epidemic
related to heart disease and stroke. Group IV: prevention/treatment.
Circulation 110: 484–488, 2004.
22. Nguyen-Duy TB, Nichaman M, Church T, Blair S, and Ross R.
Visceral fat and liver fat are independent predictors of metabolic risk
factors in men. Am J Physiol Endocrinol Metab 284: E1065–E1071, 2003.
23. Nieves DJ, Cnopp M, Retzlaff B, Walden CE, Brunzell JD, Knopp
RH, and Kahn SE. The atherogenic lipoprotein profile associated with
obesity and insulin resistance is largely attributable to intra-abdominal fat.
Diabetes 52: 172–179, 2003.
24. NIH. Clinical guidelines on the identification, evaluation, and treatment of
overweight and obesity in adults: the evidence report. Obes Res 6, Suppl
2: 51–209, 1998.
25. Pascot A, Lemieux S, Lemieux I, Prud’homme D, Tremblay A,
Bouchard C, Nadeau A, Couillard C, Tchernof A, Bergeron J, and
Despres JP. Age-related increase in visceral adipose tissue and body fat
and the metabolic risk profile of premenopausal women. Diabetes Care
22: 1471–1478, 1999.
26. Passmore J. Human energy expenditure. Physiol Rev 35: 801–808, 1955.
27. Pate R, Pratt M, Blair S, Haskell W, Macera C, Bouchard C, Buchard
C, Buchner D, Ettinger W, Heath G, and King A. Physical activity and
public health. A recommendation from the Centers for Disease Control
and Prevention and the American College of Sports Medicine. JAMA 273:
28. Peiris AN, Sothmann MS, Hoffmann RG, Hennes MI, Wilson CR,
Gustafson AB, and Kissebah A. Adiposity, fat distribution, and cardio-
vascular risk. Ann Intern Med 110: 867–872, 1989.
28a.Ravussin E and Smith SR. Increased fat intake, impaired fat oxidation,
and failure of fat cell proliferation result in ectopic fat storage, insulin
resistance, and Type 2 diabetes mellitus. Ann NY Acad Sci 967: 363–378,
29. Ross R, Dagnone D, Jones PJH, Smith H, Paddags A, Hudson R, and
Janssen I. Reduction in obesity and related comorbid conditions after
diet-induced weight loss or exercise-induced weight loss in men. Ann
Intern Med 133: 92–103, 2000.
30. Seidell JC and Bouchard C. Visceral fat in relation to health: is it a major
culprit or simply an innocent bystander? Int J Obes 21: 626–631, 1997.
31. Slentz C, Duscha B, Johnson J, Ketchum K, Aiken L, Samsa G,
Houmard J, Bales C, and Kraus W. Effects of the amount of exercise on
body weight, body composition, and measures of central obesity.
STRRIDE—a randomized controlled study. Arch Intern Med 164: 31–39,
32. Van Pelt R, Evans E, Schechtman K, Ehsani A, and Kohrt W.
Contributions of total and regional fat mass to risk for cardiovascular
disease in older women. Am J Physiol Endocrinol Metab 282: E1023–
INACTIVITY, EXERCISE, AND VISCERAL FAT
J Appl Physiol • VOL 99 • OCTOBER 2005 • www.jap.org