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J Appl Physiol 101: 893-897, 2006. First published May 25, 2006; doi:10.1152/japplphysiol.00260.2006
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Elevated peak exercise systolic blood pressure is not associated with reduced exercise capacity in subjects with Type 2 diabetes

Patrice Brassard, Annie Ferland, Valérie Gaudreault, Nadine Bonneville, Jean Jobin, and Paul Poirier

Institut Universitaire de Cardiologie et de Pneumologie, Centre de Recherche de l'Hôpital Laval, Université Laval, Québec, Canada

Submitted 28 February 2006 ; accepted in final form 24 May 2006


   ABSTRACT
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 ABSTRACT
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 GRANTS
 REFERENCES
 
Subjects with Type 2 diabetes without cardiovascular disease have a reduced exercise capacity compared with nondiabetic subjects. However, the mechanisms responsible for this phenomenon are unknown. The purpose of this study was to evaluate the impact of exercise systolic blood pressure (SBP) response on diverse exercise tolerance parameters in Type 2 diabetic subjects. Twenty-eight sedentary men with Type 2 diabetes were recruited for this study. Subjects were treated with oral hypoglycemic agents and/or diet. Evaluation of glycemic control and peak exercise capacity were performed for each subject. The subjects were divided into two groups according to the median value of peak SBP (210 mmHg) measured in each subject. We observed a 13, 13, and 16% reduction in the relative peak oxygen uptake (VO2 peak), absolute VO2 peak, and peak work rate in the low- compared with the high-peak SBP group [26.95 (SD 5.35) vs. 30.96 (SD 3.61) ml·kg–1·min–1, 2.5 (SD 0.4) vs. 2.8 (SD 0.6) l/min, and 169 (SD 34) vs. 202 (SD 32) W; all P < 0.05]. After adjusting for age, relative VO2 peak was still significantly different (P < 0.05). There were similar peak respiratory exchange ratio (RER) [1.20 (SD 0.08) vs. 1.16 (SD 0.07); P = 0.24] and peak heart rate [160 (SD 20) vs. 169 (SD 15) beats/min; P = 0.18] between the low- compared with the high-SBP group. No difference in glycemic control was observed between the two groups. The results reported in this study suggest that in subjects with Type 2 diabetes without cardiovascular disease, an elevated exercise SBP is not associated with reduced exercise capacity and its modulation is probably not related to glycemic control.

peak oxygen uptake; Type 2 diabetic patients; high blood pressure response

THE STUDY OF OXYGEN UPTAKE (VO2) during an incremental exercise protocol reflects the integration of numerous body functions in response to an imposed work stimulus (28). The VO2 measured at maximal exercise, i.e., maximal or peak VO2 (VO2 max or VO2 peak), is very important in clinical practice because it is related to survival (19). In subjects with Type 2 diabetes, a reduced VO2 max has been reported compared with nondiabetic subjects (23, 24). However, the mechanisms responsible for this phenomenon remain unclear. Presence of endothelial dysfunction (10, 27) and abnormalities of cardiac function such as diastolic dysfunction (21) may be related to this reduced exercise capacity. Furthermore, subtle hemodynamic changes in response to exercise appearing early in the time course of diabetes might also have a negative influence on exercise capacity.

Type 2 diabetes is related to arterial stiffness (6), which in turn is associated with increased afterload (6), leading to an elevated systolic blood pressure (SBP) (4). An exaggerated SBP response to exercise is associated with a lower cardiorespiratory fitness level in women (12). In contrast, athletes are known to develop an elevated blood pressure (BP) response in association with a higher exercise capacity compared with nonathletes (9). In fact, a positive relationship between the exercise BP response and left ventricular (LV) mass has been documented in this population (9). However, the influence of early hemodynamic changes induced by diabetes, such as the presence of an elevated exercise SBP response on exercise capacity in subjects with Type 2 diabetes without cardiovascular disease, is unknown.

The aim of the present study was to evaluate the impact of an elevated SBP in response to peak exercise on different parameters related to exercise capacity in sedentary subjects with Type 2 diabetes without cardiovascular disease. We hypothesized that subjects with higher exercise SBP would have a reduced exercise capacity.


   MATERIALS AND METHODS
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 ABSTRACT
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 GRANTS
 REFERENCES
 
Study Population

Twenty-eight sedentary men with Type 2 diabetes were recruited for this study. All subjects had Type 2 diabetes treated with oral hypoglycemic agents (metformin, glyburide, glyclazide) and/or diet. No subject was on insulin. Exclusion criteria were a documented presence of cardiovascular disease and hypertension, all forms of complications related to diabetes and cardiovascular related medication. No subject presented macroalbuminuria. The study was approved by the local hospital ethics committee in accordance with the Declaration of Helsinki, and all subject gave signed informed consent.

Evaluations

Blood sampling.   At subjects' arrival at the laboratory, a 18-gauge polyethylene catheter was inserted into a forearm vein for blood sampling. Blood samples were drawn at rest from subjects 30 min before the exercise protocol for the measurement of fasting blood glucose (FBG) and glycated hemoglobin (HbA1c), after an 8-h overnight fast. FBG was assayed using the hexokinase method (Roche Diagnosis, Indianapolis, IN). HbA1c was assayed using the ion-exchange high-performance liquid chromatography method (Bio-Rad, Hercules, CA).

Exercise protocol.   Exercise capacity was evaluated for each subject using an incremental protocol of 15 W/min after a warm-up period of 1 min at 15 W and 2 min at 30 W, performed on an electromagnetically braked cycle ergometer (Corival, Lode, The Netherlands) at a pedaling rate of 50–70 rpm. Expired air was continuously collected for the determination of VO2, carbon dioxide production (VCO2), pulmonary ventilation (VE), and the respiratory exchange ratio (RER) (VCO2/VO2) on a breath-by-breath basis (Medgraphics, CPX Ultima, St. Paul, MN). Heart rate (HR) was obtained using electrocardiographic monitoring during the test. Subjects exercised until volitional exhaustion. Peak exercise (VO2 peak) was defined as the mean VO2 recorded in the last 15 s of the incremental exercise protocol concurrent with a RER ≥1.15. The exercise protocol was always performed in the fasting state at the same time of the day at 20°C room temperature.

BP.   After 15 min of quiet rest in a supine position, resting BP was then measured with the subject seated using an automated sphygmomanometer with headphone-circuit option (model 412, Quinton Instrument, Bothell, WA). BP during exercise was measured every 2 min throughout the maximal exercise protocol using the same automated sphygmomanometer as for the evaluation of resting BP. The subjects were divided into two groups according to the median value of peak SBP measured in each subject.

Statistical Analysis

A Student's unpaired t-test and a one-way analysis of covariance were used to evaluate the peak exercise parameters differences between the groups. The Mann-Whitney test was used for data not normally distributed. The hypoglycemic regimen in the two groups were compared using the Fisher's exact test. The Pearson's correlation was used to assess associations between variables. All data are presented as means (SD) unless otherwise specified. A value of P < 0.05 was considered statistically significant.


   RESULTS
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 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
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Baseline characteristics of each group separated on the basis of the median peak exercise SBP are presented in Table 1. There was no statistical difference in all baseline characteristics between groups. Also, there was no statistical difference in the proportions of subjects on hypoglycemic agents. However, the subjects in the high-peak SBP group tended to be younger [50 (SD 10) vs. 56 (SD 8) yr; P = 0.08], whereas a trend for a lower resting SBP was observed in the low-peak SBP group (<210 mmHg) compared with the high-peak SBP group (>210 mmHg) [130 (SD 11) vs. 139 (SD 14) mmHg; P = 0.06].


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  		Table 1. Baseline characteristics of the groups according to median peak systolic blood pressure

 
Table 2 presents results from the peak exercise capacity evaluation (VO2 peak). Per study design, there was a difference between the peak SBP between groups (P < 0.001). A reduced increment in SBP (peak SBP minus resting SBP) during exercise was observed in the low-peak SBP group compared with the high-peak SBP group [63 (SD 21) vs. 98 (SD 17) mmHg; P < 0.001]. We observed a 13% reduction in the relative and absolute VO2 peak and a 16% reduction in the peak work rate in the low- compared with the high-peak SBP (all P < 0.05). An elevated rate-pressure product (SBP x HR) was also observed in subjects with higher peak SBP (P < 0.001). After adjusting for age, relative VO2 peak was still significantly higher in subjects with higher peak SBP (P < 0.05).


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  		Table 2. Exercise capacity parameters observed in the groups according to median peak systolic blood pressure

 
Significant relationships were observed between the resting SBP (r = 0.422), absolute VO2 peak (r = 0.405), exercise duration (r = 0.414), peak work rate (r = 0.454), and peak exercise SBP (all P < 0.05) (Fig. 1). Whereas there was a significant inverse relation between age and absolute values of VO2 peak (r = –0.612; P < 0.001) and a trend between age and relative values of VO2 peak (r = –0.332; P = 0.08), there was no significant relation between age and peak SBP. No difference in the glycemic control (FBG and HbA1c) was observed between the two groups.


Figure 1
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  		Fig. 1. A: relationship between peak oxygen uptake (VO2 peak) and peak exercise systolic blood pressure (SBP) B: relationship between exercise duration and peak exercise SBP. C: relationship between total work rate and peak exercise SBP.

 

   DISCUSSION
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
GRANTS
 REFERENCES
 
These results suggest that, in subjects with Type 2 diabetes without cardiovascular disease, an elevated exercise SBP is not associated with reduced exercise capacity. Furthermore, SBP modulation during exercise is not related to glycemic control in our sample. To our knowledge, the present study is the first to evaluate the impact of diverse exercise SBP responses on parameters related to exercise capacity in subjects with Type 2 diabetes.

The presence of an elevated SBP response during exercise may be a predictor of future hypertension (17, 18, 26). In contrast, an elevated SBP response to exercise has been also observed in endurance- and strength-trained athletes as well as in subjects with prehypertension, and it seems to be positively associated with exercise capacity (7, 25). In the present study, important parameters related to exercise capacity, namely absolute VO2 peak, exercise duration, and peak work rate, were positively related to peak exercise SBP. In addition, subjects with an elevated SBP (>210 mmHg) in response to peak exercise presented higher VO2 peak compared with subjects with lower SBP (<210 mmHg) even after adjustment for age. The literature regarding the BP response to exercise in subjects with diabetes is sparse. A greater diastolic BP (DBP) in response to submaximal exercise has been reported in Type 2 diabetes (2) while an exaggerated SBP has also been documented in normoalbuminuric Type 1 (3) as well as in Type 2 diabetic patients (13).

Type 2 diabetes is related to reduced LV systolic volume, altered myocardial and diastolic functions and increased arterial stiffness (6, 11, 22). These are all important parameters related to BP regulation, and they are potential contributors to the reduced exercise capacity documented in diabetic individuals. The elevated peak exercise SBP observed in our subjects is probably partly associated with the arterial stiffness observed in subjects with diabetes (4, 6). In theory, a cascade of events will take place after the appearance of arterial stiffness: 1) increased afterload, 2) reduced stroke volume, 3) LV remodeling, 4) increased SBP, 5) diastolic dysfunction, 6) reduced exercise performance, and 7) systolic dysfunction (6, 8). So, how can we reconcile the positive results related to elevated peak SBP observed in our subjects with the reported harmful impacts of diabetes on the cardiovascular function that should normally lead to a reduced exercise performance?

A plausible explanation could be that a relatively more important LV remodeling, induced by diabetes and triggered more specifically by arterial stiffness (6), might be present and induce a transitory adaptive beneficial impact, i.e., a higher cardiac output compared with subjects with lower exercise SBP, before the appearance of diastolic dysfunction. This might override the deleterious impact induced by diabetes on LV function. In athletes, a positive relationship has been reported between a nonpathological LV hypertrophy with a preserved diastolic function (15) and elevated exercise SBP and exercise capacity (9). On the other hand, Poirier et al. (21) demonstrated that diastolic dysfunction influences negatively exercise capacity in subjects with Type 2 diabetes. In other words, the impact of a relatively more important increased LV mass in subjects with higher exercise SBP, potentially induced by arterial stiffness to compensate for an increase in afterload, could have a transitory positive and relatively more important adaptive impact on exercise SBP and exercise capacity than arterial stiffness per se compared with subjects with lower exercise SBP. This positive influence on exercise capacity is probably lost with the appearance of diastolic dysfunction (21). Figure 2 illustrates a hypothetic schematic representation regarding this enhanced, or preserved, exercise capacity observed in subjects with higher peak exercise SBP.


Figure 2
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  		Fig. 2. Schematic representation of the parameters influencing exercise capacity in patients with higher peak exercise SBP.

 
BP response appears to be related to blood glucose control (16). Indeed in the resting state, the presence of hyperglycemia led to an increase in SBP and DBP independently of endogenous insulin in 20 patients with Type 2 diabetes (16). A reduced availability of nitric oxide has been suggested as a potential explanation (16). However, in our two groups with a marked difference in peak exercise SBP, there was no significant difference between short-term (FBG) as well as long-term (HbA1c) blood glucose control, suggesting that the BP modulation observed during exercise in these subjects may not have been influence by blood glucose exposure per se.

The principal limitation of the present study is the absence of a control group of nondiabetic subjects. Consequently, we used the terms elevated and high SBP instead of exaggerated SBP because we did not compare our results with a "normal" exercise response obtained from a control group. Nevertheless, the goal of this study was to investigate the impact of an elevated exercise SBP on exercise capacity in subjects with Type 2 diabetes. Therefore, the group with peak exercise SBP below 210 mmHg could be considered as control subjects because 210 mmHg is a clinically relevant cutoff regarding the exercise-induced hypertensive response (14). Of note, age might have influenced at some point our results but the higher exercise capacity observed in our subjects with higher exercise SBP is still present compared with subjects with lower exercise SBP after adjustment for age. Also, even if all the subjects were carefully screened in light of our inclusion and exclusion criteria, we cannot rule out the possibility that the differences observed in our groups were related to the insulin resistance state and/or the presence of LV diastolic dysfunction. Furthermore, it is already known that the resting SBP represents an independent predictor of exercise SBP, which explains over 40% of the interindividual variability (1). In this study, the resting SBP was also related to peak SBP, but it explained only 17% of the variance. Because there was no significant difference in terms of resting or peak exercise HR, it seems unlikely that sympathetic overactivity might have accounted for our results. However, we cannot exclude the possibility that a subtle change in sympathovagal activity, i.e., sympathetic predominance, might have influenced our findings (22). Finally, we cannot ignore that these differences might be related to whether the maximal effort was attained or not because we used VO2 peak instead of VO2 max. However, this is unlikely because our two groups reached similar RER both above 1.15, and it was recently shown that VO2 peak is likely to be a valid index of VO2 max (5).

Further research is needed to evaluate whether 1) these results represent an increase or a preservation of exercise performance, 2) LV remodeling is related to increased peak SBP and exercise capacity in these subjects, and 3) these results will be influenced in subjects with LV diastolic function.

In conclusion, our results suggest that, in subjects with Type 2 diabetes without cardiovascular disease, an elevated exercise SBP is not associated with reduced exercise capacity and that its modulation is probably not related to glycemic control.


   GRANTS
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 GRANTS
REFERENCES
 
This work was supported in part by the Canadian Diabetes Association and the Quebec Heart Institute Foundation. P Brassard is the recipient of a graduate research scholarship in pharmacy (PhD) from the Rx & D Health Research Foundation Awards Program funded in partnership with the Canadian Institutes of Health Research (CIHR). A. Ferland is supported by the CIHR. P. Poirier is a clinician-scientist of the Fonds de la Recherche en Santé du Québec.


   FOOTNOTES
 

Address for reprint requests and other correspondence: P. Poirier, Institut Universitaire de Cardiologie et de Pneumologie, Centre de Recherche Clinique/Hôpital Laval, 2725 Chemin Ste-Foy, Sainte-Foy, Québec, Canada G1V 4G5 (e-mail: paul.poirier{at}crhl.ulaval.ca)

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.


   REFERENCES
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 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
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  1. Bassett DR Jr, Duey WJ, Walker AJ, Torok DJ, Howley ET, and Tanaka H. Exaggerated blood pressure response to exercise: importance of resting blood pressure. Clin Physiol 18: 457–462, 1998.[CrossRef][ISI][Medline]
  2. Brett SE, Ritter JM, and Chowienczyk PJ. Diastolic blood pressure changes during exercise positively correlate with serum cholesterol and insulin resistance. Circulation 101: 611–615, 2000.[Abstract/Free Full Text]
  3. Cavan D, O'Donnell MJ, Parkes A, Lewis H, Lawson N, Chapman J, and Barnett AH. Abnormal blood pressure response to exercise in normoalbuminuric insulin dependent diabetic patients. J Hum Hypertens 5: 21–26, 1991.[ISI][Medline]
  4. Chen CH, Nakayama M, Nevo E, Fetics BJ, Maughan WL, and Kass DA. Coupled systolic-ventricular and vascular stiffening with age: implications for pressure regulation and cardiac reserve in the elderly. J Am Coll Cardiol 32: 1221–1227, 1998.[Abstract/Free Full Text]
  5. Day JR, Rossiter HB, Coats EM, Skasick A, and Whipp BJ. The maximally attainable VO2 during exercise in humans: the peak vs. maximum issue. J Appl Physiol 95: 1901–1907, 2003.[Abstract/Free Full Text]
  6. Devereux RB, Roman MJ, Paranicas M, O'Grady MJ, Lee ET, Welty TK, Fabsitz RR, Robbins D, Rhoades ER, and Howard BV. Impact of diabetes on cardiac structure and function: the Strong Heart Study. Circulation 101: 2271–2276, 2000.[Abstract/Free Full Text]
  7. Fazio S, Palmieri EA, Izzo R, Affuso F, Romano M, Riccio G, Pilato G, Trimarco B, and De Luca N. An exaggerated systolic blood pressure response to exercise is associated with cardiovascular remodeling in subjects with prehypertension. Ital Heart J 6: 886–892, 2005.[Medline]
  8. Hayat SA, Patel B, Khattar RS, and Malik RA. Diabetic cardiomyopathy: mechanisms, diagnosis and treatment. Clin Sci (Lond) 107: 539–557, 2004.[Medline]
  9. Karjalainen J, Mantysaari M, Viitasalo M, and Kujala U. Left ventricular mass, geometry, and filling in endurance athletes: association with exercise blood pressure. J Appl Physiol 82: 531–537, 1997.[Abstract/Free Full Text]
  10. Kingwell BA. Nitric oxide-mediated metabolic regulation during exercise: effects of training in health and cardiovascular disease. FASEB J 14: 1685–1696, 2000.[Abstract/Free Full Text]
  11. Kizu A, Koyama H, Tanaka S, Maeno T, Komatsu M, Fukumoto S, Emoto M, Shoji T, Inaba M, Shioi A, Miki T, and Nishizawa Y. Arterial wall stiffness is associated with peripheral circulation in patients with type 2 diabetes. Atherosclerosis 170: 87–91, 2003.[CrossRef][ISI][Medline]
  12. Kokkinos PF, Andreas PE, Coutoulakis E, Colleran JA, Narayan P, Dotson CO, Choucair W, Farmer C, and Fernhall B. Determinants of exercise blood pressure response in normotensive and hypertensive women: role of cardiorespiratory fitness. J Cardiopulm Rehabil 22: 178–183, 2002.[CrossRef][Medline]
  13. Kumagai S, Kai Y, Hanada H, Uezono K, and Sasaki H. Relationships of the systolic blood pressure response during exercise with insulin resistance, obesity, and endurance fitness in men with type 2 diabetes mellitus. Metabolism 51: 1247–1252, 2002.[CrossRef][ISI][Medline]
  14. Lauer MS, Levy D, Anderson KM, and Plehn JF. Is there a relationship between exercise systolic blood pressure response and left ventricular mass? The Framingham Heart Study. Ann Intern Med 116: 203–210, 1992.[ISI][Medline]
  15. Lewis JF, Spirito P, Pelliccia A, and Maron BJ. Usefulness of Doppler echocardiographic assessment of diastolic filling in distinguishing "athlete's heart" from hypertrophic cardiomyopathy. Br Heart J 68: 296–300, 1992.
  16. Marfella R, Nappo F, De Angelis L, Paolisso G, Tagliamonte MR, and Giugliano D. Hemodynamic effects of acute hyperglycemia in type 2 diabetic patients. Diabetes Care 23: 658–663, 2000.[Abstract/Free Full Text]
  17. Matthews CE, Pate RR, Jackson KL, Ward DS, Macera CA, Kohl HW, and Blair SN. Exaggerated blood pressure response to dynamic exercise and risk of future hypertension. J Clin Epidemiol 51: 29–35, 1998.[CrossRef][ISI][Medline]
  18. Miyai N, Arita M, Miyashita K, Morioka I, Shiraishi T, and Nishio I. Blood pressure response to heart rate during exercise test and risk of future hypertension. Hypertension 39: 761–766, 2002.[Abstract/Free Full Text]
  19. Myers J, Gullestad L, Vagelos R, Do D, Bellin D, Ross H, and Fowler MB. Clinical, hemodynamic, and cardiopulmonary exercise test determinants of survival in patients referred for evaluation of heart failure. Ann Intern Med 129: 286–293, 1998.[Abstract/Free Full Text]
  20. Poirier P, Garneau C, Bogaty P, Nadeau A, Marois L, Brochu C, Gingras C, Fortin C, Jobin J, and Dumesnil JG. Impact of left ventricular diastolic dysfunction on maximal treadmill performance in normotensive subjects with well-controlled type 2 diabetes mellitus. Am J Cardiol 85: 473–477, 2000.[CrossRef][ISI][Medline]
  21. Poirier P, Bogaty P, Philippon F, Garneau C, Fortin C, and Dumesnil JG. Preclinical diabetic cardiomyopathy: relation of left ventricular diastolic dysfunction to cardiac autonomic neuropathy in men with uncomplicated well-controlled type 2 diabetes. Metabolism 52: 1056–1061, 2003.[CrossRef][ISI][Medline]
  22. Regensteiner JG, Bauer TA, Reusch JE, Brandenburg SL, Sippel JM, Vogelsong AM, Smith S, Wolfel EE, Eckel RH, and Hiatt WR. Abnormal oxygen uptake kinetic responses in women with type II diabetes mellitus. J Appl Physiol 85: 310–317, 1998.[Abstract/Free Full Text]
  23. Regensteiner JG, Sippel J, McFarling ET, Wolfel EE, and Hiatt WR. Effects of non-insulin-dependent diabetes on oxygen consumption during treadmill exercise. Med Sci Sports Exerc 27: 875–881, 1995.[Medline]
  24. Scharhag J, Schneider G, Urhausen A, Rochette V, Kramann B, and Kindermann W. Athlete's heart: right and left ventricular mass and function in male endurance athletes and untrained individuals determined by magnetic resonance imaging. J Am Coll Cardiol 40: 1856–1863, 2002.[Abstract/Free Full Text]
  25. Singh JP, Larson MG, Manolio TA, O'Donnell CJ, Lauer M, Evans JC, and Levy D. Blood pressure response during treadmill testing as a risk factor for new-onset hypertension. The Framingham heart study. Circulation 99: 1831–1836, 1999.[Abstract/Free Full Text]
  26. Stehouwer CDA, Lambert J, Donker AJM, and van Hinsbergh VWM. Endothelial dysfunction and pathogenesis of diabetic angiopathy. Cardiovasc Res 34: 55–68, 1997.[Abstract/Free Full Text]
  27. Wasserman K, Hansen JE, Sue DY, Casaburi R, and Whipp BJ. Principles of Exercise Testing and Interpretation Including Pathophysiology and Clinical Applications. Philadelphia, PA: Lippincott, Williams & Wilkins, 1999.



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