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Eur J Appl Physiol (2007) 100:437–444 DOI 10.1007/s00421-007-0446-3

O R I G I N A L A R T I CL E

Endurance training improves post-exercise cardiac autonomic modulation in obese women with and without type 2 diabetes Arturo Figueroa · Tracy Baynard · Bo Fernhall · Robert Carhart · Jill A. Kanaley

Accepted: 11 March 2007 / Published online: 4 April 2007 © Springer-Verlag 2007

Abstract Obesity and type 2 diabetes (T2D) are associated with abnormal cardiovascular autonomic function and increased risk for cardiac complications, especially after exercise. Since improvements at rest are not always observed after training, we investigated changes in resting and post-exercise autonomic function in obese women with and without T2D after16-week of walking training. Heart rate (HR) variability (HRV) and baroreXex sensitivity (BRS) were measured at rest and 20 min after a 20 min bout of treadmill exercise at 65% VO2 peak in obese women with (n = 8) and without T2D (n = 12) before and after training. HRV was analyzed by frequency-domain [high- (HF) power and low-frequency (LF)] and BRS by the sequence method. Exercise training induced similar signiWcant changes in VO2 peak, resting systolic blood pressure (SBP) and post-exercise autonomic function in both groups. Training increased VO2 peak (6%; P < 0.01) and

decreased resting SBP (8%; P < 0.001). Increased postexercise HR recovery (5%; P < 0.001), HF power (14%; P < 0.05), LF power (14%; P < 0.05) and BRS (86%; P < 0.001) were also observed. Resting autonomic function and post-exercise SBP were not altered after training. In conclusion, endurance training reduced blood pressure without changes in HRV and BRS at rest, but training increased HRV and BRS during the recovery of acute endurance exercise indicating an improved post-exercise autonomic modulation of HR, which was similar in obese women with and without T2D. Keywords Exercise recovery · Walk training · Autonomic nervous system · Obesity · Type 2 diabetes · BaroreXex sensitivity

Introduction

A. Figueroa (&) Department of Nutrition, Food and Exercise Sciences, Florida State University, Tallahassee, FL 32306, USA e-mail: [email protected] T. Baynard · J. A. Kanaley Department of Exercise Sciences, Syracuse University, Syracuse, NY 13244, USA B. Fernhall Department of Kinesiology, University of Illinois, Urbana-Champaign, IL 61820, USA R. Carhart Department of Medicine/Cardiology, SUNY Upstate Medical University, Syracuse, NY 13210, USA

Both heart rate (HR) variability (HRV) and baroreXex sensitivity (BRS) are non-invasive methods of evaluating cardiac autonomic function. HRV analyzes the beat-to-beat variation in R–R interval (Task Force 1996), and BRS quantiWes the capacity of the eVective autonomic control of the HR in response to changes in blood pressure (BP) (Cevese et al. 2001; Loimaala et al. 2003). Post-exercise HR returns to the pre-exercise levels (HR recovery) due to adjustments in cardiac parasympathetic and sympathetic activity (Pober et al. 2004) partially, controlled by the arterial baroreXex (Terziotti et al. 2001). Recover of parasympathetic tone and BRS to pre-exercise levels occurs between 15 and 60 min after moderate intensity exercise (Piepoli et al. 1993; Terziotti et al. 2001; Raczak et al. 2005). A mechanism for the increased risk of sudden cardiac death in vulnerable populations after acute exercise

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(Albert et al. 2000) may be an increased excitability of the sinus node as a result of reduced parasympathetic reactivation and increased sympathetic activity (Piepoli et al. 1993). Thus, evaluation of exercise recovery dynamics is important. Aging (Monahan et al. 2000), obesity (Alvarez et al. 2005) and type 2 diabetes (T2D) (Gerritsen et al. 2001; Loimaala et al. 2003; Schroeder et al. 2005) are conditions associated with reduced HRV and BRS. Diabetic metabolic abnormalities are associated with progressive cardiac autonomic dysfunction (Schroeder et al. 2005), which leads to increased risk of mortality in overweight individuals with diabetes compared to non-diabetic individuals (Gerritsen et al. 2001). Whether endurance training can reverse the eVect of obesity and T2D on autonomic function is not known. Several studies have reported improvements in resting HRV and BRS after exercise training in non-diabetic individuals (Pagani et al. 1988; Levy et al. 1998; Amano et al. 2001; Melanson and Freedson 2001; Gulli et al. 2003; Lee et al. 2003; Ueno and Moritani 2003; Hautala et al. 2004; Jurca et al. 2004; Okazaki et al. 2005). Conversely, other studies have shown no eVect of exercise training in resting HRV and BRS in healthy middle-aged and older individuals (Boutcher and Stein 1995; Loimaala et al. 2000; Perini et al. 2002). In patients with T2D, exercise training has improved BRS, resting HR and glucose control without aVecting HRV (Loimaala et al. 2003). These disparate results on autonomic adaptations to exercise training may be related to the fact that the evaluation has been done at rest rather than after a physiological perturbation such as exercise (Yamamoto et al. 2001). A decrease in HR at rest and 20 min post-exercise recovery has been attributed to improved HRV in healthy young males after training (Yamamoto et al. 2001). Therefore, the decreased risk of sudden death observed during and up to 30 min after vigorous exercise in habitual exercises (Albert et al. 2000) may be attributed to improved post-exercise autonomic function. Although reduced cardiac autonomic function is associated with increased mortality in patients with high cardiovascular risk at rest (La Rovere et al. 2002) and post-exercise (Albert et al. 2000), the eVect of exercise training on post-exercise cardiac autonomic function in individuals with greater cardiovascular risk has not been determined. The purpose of this study was to evaluate the eVects of a 16-week moderate intensity endurance training on resting and post-exercise HRV and BRS in obese women with and without T2D. We hypothesized that exercise training will produce greater improvements in autonomic function in women with T2D than in non-diabetic women due to a greater autonomic dysfunction.

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Methods Subjects Twenty-eight obese [body mass index (BMI) ¸ 30 kg/m2] women with type 2 diabetes (T2D, n = 10) and without T2D (obese, n = 18) participated in this study. Patients had been diagnosed with T2D from 1 to 7 years before entering the study. Exclusionary criteria included current smoking, known diseases: coronary artery, peripheral vascular, renal, adrenal, pituitary, thyroid, and stage 2 hypertension (>160/ 100 mm Hg). Medications included the following: oral hypoglycemic agents (6 T2D), angiotensin-converting enzyme inhibitors (3 T2D and 1 obese), statins (1 T2D and 1 obese). Individuals on insulin, -blockers, or individuals participating in regular physical activity during the previous 6 months were also excluded from the study. Postmenopausal women on hormone replacement therapy (1 T2D, 1 obese) were included. Premenopausal women were studied in the Wrst 10 days of the menstrual cycle to avoid the possible eVect of endogenous female sex hormones on HRV during the luteal phase (Saeki et al. 1997). All subjects gave written informed consent prior to their inclusion. The Syracuse University’s Institutional Review Boards approved the protocol. Study protocol Each subject underwent maximal and submaximal treadmill exercise tests, body composition assessment and blood draw. The maximal test screened for cardiac abnormalities and determined exercise capacity. Autonomic function was evaluated before and after a 20-min bout of exercise at 65% VO2 peak. After the 16 weeks of training, all subjects repeated the tests under the same condition at the same time of day. Maximal exercise test Peak oxygen consumption (VO2 peak) was measured with a treadmill protocol as previously described (Kanaley et al. 2003). The subjects started walking at 2.5 mph for 2 min and speed was increased 0.5 mph every 2 min until 3.5 mph was reached. The grade was increased by 2% every 2 min until exhaustion. A continuous 12-lead ECG recording was performed throughout the test to evaluate for cardiac abnormalities. Oxygen consumption was measured continuously using a metabolic cart (Cosmed Quark b2, Rome, Italy). A test was considered maximal if two of the following parameters were met: VO2 did not increase more than 150 ml with increased workload, respiratory exchange ratio (RER value) > than 1.10, rate of perceived exertion (RPE) > 17 and heart rate § 10 beats/min of age-predicted maximum.

Eur J Appl Physiol (2007) 100:437–444

Submaximal exercise Subjects reported to the laboratory with a minimum of 3 h after their last meal and abstained from caVeine and medication that aVects HR and BP for at least 12 h. Subjects were asked to refrain from moderate or intense exercise 48 h prior to the test. Following at least 15 min of quiet rest, cardiovascular parameters were collected for 5 min in the supine position. Thereafter, subjects exercised on a treadmill for 20 min at »65% of the previously determined peak VO2 before training. The responses to submaximal treadmill exercise were reevaluated at the same pre-training absolute intensity (i.e., 65% of untrained VO2max) because endurance training reduces HR and BP at the same absolute intensity, which will make more apparent the eVects on autonomic control. Immediately after exercise, subjects were placed in the supine position and the post-exercise measurements were collected between 20 and 25 min after exercise cessation. A metronome was used to set the breathing frequency at 12 breaths/min (0.2 Hz) during data recording. Autonomic measurements Continuous ECG and BP recordings were obtained from a modiWed CM5 lead sampled by a data acquisition system (Biopac, Santa Barbara, CA, USA) and from the left middle Wnger using a Portapres device (TNO Biomedical Instrumentation, Amsterdam, The Netherlands), respectively. The ECG and BP signals were sampled at a frequency of 1,000 and 200 Hz, respectively, and stored on a computer for future analyses. Both signals were manually inspected and sporadic ectopic beats and technical artifacts were linearly interpolated using the WinCPRS software (Absolute Aliens Oy, Turku, Finland). Fast Fourier transformation was used to obtain power spectrums of the R–R interval (RRI) (Pagani et al. 1986; Malliani et al. 1991) high-frequency (HF, 0.15–0.4 Hz) and low-frequency (LF, 0.04–0.15 Hz) (Task Force 1996). The HF power is an indicator of parasympathetic modulation of the sinus node (Pagani et al. 1986). The LF component is mediated by both sympathetic and parasympathetic activities and the LF/HF ratio is an index of sympathovagal balance (Task Force 1996; Cevese et al. 2001). Spontaneous BRS was evaluated by the sequence method. The time series of pulse intervals (PI) and SBP were scanned with the winCPRS software to identify sequences in which PI and SBP concurrently increased (up sequences) or decreased (down sequences) for three or more consecutive beats (Legramante et al. 2002). For each sequence, a regression line is computed from changes in SBP and PI of at least 1 mmHg and 5 ms per beat,

439

respectively. Only sequences with a correlation >0.80 were considered and the mean slope of all sequences in a 5-min period was accepted as an index of BRS for rest and postexercise recovery. Data acquisition and subsequent analysis were conducted following the recommendations of the Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology (Task Force 1996). Exercise training The 16-week exercise training was a partially supervised home-based program with subjects walking at 65% VO2 peak, 3 days/week on their own and one supervised session on a treadmill in the laboratory. Exercise intensity was monitored by Polar heart rate monitors and RPE during the supervised and unsupervised sessions, respectively. This allowed us to verify their training intensity, served as motivational tool, and allowed us to increase the training workload as subjects became more Wt. Subjects walked for 30 min at the beginning of the study and this was increased to 45 min/day at the 8-week mark. Subjects Wlled activity logs daily and we check the records on daily and weekly basis. Blood sampling and analysis Subject reported to the laboratory at 0700 hours after a 12 h overnight fast. Venous blood samples were analyzed for hemoglobin A1c (HbA1c) concentration (Diabetes Technologies Inc, Thomasville, GA, USA). Plasma glucose concentrations were determined using the glucose oxidase method with the YSI 2300 Stat (Yellow Springs Instruments, Inc., Yellow Springs, OH, USA). Blood samples for insulin were placed in EDTA tubes, centrifuged (2,300 rpm), aliquotted, and stored at ¡80°C for later analysis. Plasma insulin concentration was determined using commercially available radioimmunoassay kits (Diagnostic Products Corp., Los Angeles, CA, USA). The intra- and inter-assay CV for the insulin assays were 7.6 and 8.9%, respectively. Insulin sensitivity was calculated using the oral glucose insulin sensitivity (OGIS) index (Mari et al. 2001). Body composition Height and weight were measured and BMI (kg/m2) was calculated. Percentage of body fat and lean body mass were calculated by air displacement plethysmography (ADP) using the Bod Pod (Life Measurements Inc, Concord, CA). Compared to hydrostatic weighing, measures of % fat by ADP are accurate and reliable for overweight/obese individuals (Vescovi et al. 2001).

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Statistical analysis All statistical analyses were performed with SPSS version 13.0 (SPSS Inc., Chicago, IL, USA). Because LF and HF power were not normally distributed, they were transformed using the natural logarithm (Ln) before statistical analysis. Group diVerences of the description variables were analyzed using unpaired t tests. Comparison between and within groups was performed by two-way (group £ time) ANOVA with repeated measures at rest and 20 min post-exercise [group (T2D vs. obese) £ rest or 20-min (before vs. after training)]. Values are shown as mean § SEM, and statistical signiWcance was set at P < 0.05. Results Twenty-four of the original 28 subjects completed the training program; however data of an additional four subjects were excluded from the analysis due to inadequate signal. Compliance to the program was 86%. There were no signiWcant diVerences between the groups at baseline for any measure of anthropometry and resting cardiovascular function (Table 1). Fasting glucose levels were higher in obese women with type 2 diabetes than non-diabetic women (P < 0.01). Fasting insulin concentrations were similar in both groups, but insulin sensitivity was higher (P < 0.01) in non-diabetic women than in women with T2D. There was no group by time eVect for BMI, percentage of body fat, lean body mass, HbA1c, plasma glucose,

plasma insulin, insulin sensitivity, and resting HR, HF power, LF power, LF/HF, and BRS. However, there was a similar increase (P < 0.01; 6%) in VO2 peak for both groups after training. Also, resting SBP decreased (P < 0.01; 8%) similarly in both groups after training (Table 1). There was no diVerence in mean VO2 (% of peak) during the submaximal acute bout of exercise before (63.1 § 1.4%) and after (61.4 § 2.2%) training. There was no signiWcant group by time interaction for any variable during the post-exercise recovery. There was a training eVect for post-exercise HR, HF power, LF power, and BRS (Fig. 1). In both T2D and obese groups, respectively, post-exercise measures for HR decreased (P < 0.01) from 82 § 4 to 78 § 4 and from 81 § 3 to 77 § 3 beats/ min; HF power increased (P < 0.05) from 4.4 § 0.6 to 5.2 § 0.4 and from 4.4 § 0.3 to 5.3 § 0.3 Ln ms2; LF power increased (P < 0.05) from 4.3 § 0.5 to 4.7 § 0.4 and from 4.3 § 0.2 to 4.9 § 0.3 Ln ms2; and BRS increased (P < 0.001) from 6.3 § 1.4 to 10.5 § 2.1 and from 6.6 § 0.6 to 9.0 § 0.9 ms/mm Hg. There was no signiWcant training eVect on post-exercise SBP (T2D = 115 § 3 vs. 114 § 2 and obese = 118 § 4 vs. 117 § 4 mm Hg). Discussion This present study demonstrated that the eVect of exercise training on cardiac autonomic function in obese women with T2D did not diVer from the obese non-diabetic women. The main Wnding of this study was that increases in

Table 1 Baseline subject characteristics and resting cardiovascular function at baseline and after 16 weeks of endurance training Type 2 diabetes (n = 8) Baseline

Obese (n = 12) 16 weeks

Baseline

16 weeks

Age (years)

50 § 1

Body mass index (kg/m2)

35.2 § 1.7

34.6 § 1.7

48 § 2 37.6 § 1.4

37.4 § 1.5

Body fat (%)

44.9 § 2.3

44.1 § 3.6

47.6 § 1.1

46.6 § 0.9

Lean body mass (kg)

49.4 § 1.6

47.7 § 1.5

53.4 § 1.8

54.1 § 1.7

Hemoglobin A1c (%)

7.5 § 0.4

7.1 § 0.5

6.1 § 0.5

5.3 § 0.1

Glucose (mmol/l)

7.9 § 0.699

7.6 § 0.699

5.2 § 0.1

5.1 § 0.2

Insulin (pmol/l)

21.4 § 8.7

15.4 § 4.2

28.3 § 15.1

13.3 § 5.8

Insulin sensitivity (ml min¡1 m¡2)

364 § 239

387 § 289

481 § 16

479 § 14

VO2 peak (ml kg¡1 min¡1)

21.9 § 1.0

23.6 § 1.1**

21.4 § 0.6

22.9 § 1.2**

Systolic BP (mmHg)

120 § 4

113 § 4**

125 § 5

112 § 5**

Heart rate (beats/min)

77 § 4

76 § 3

74 § 2

72 § 2

HF power (Ln ms2)

4.4 § 0.4

5.2 § 0.4

5.2 § 0.2

5.3 § 0.3

LF power (Ln ms2)

4.4 § 0.4

4.8 § 0.2

4.6 § 0.2

4.9 § 0.4

LF/HF (ratio)

1.01 § 0.06

0.93 § 0.05

0.89 § 0.04

0.95 § 0.05

BRS (ms/mmHg)

7.5 § 1.2

8.2 § 1.8

8.8 § 0.6

7.4 § 0.8

Values are mean § SEM BP blood pressure, HF high-frequency, LF low-frequency, BRS baroreXex sensitivity SigniWcantly diVerent from obese non-diabetic women at 9 P < 0.01; 99 P < 0.001; ** P < 0.01 for within group analysis

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Eur J Appl Physiol (2007) 100:437–444 T2D

Obese

T2D

A 2

85

**

80 75

**

Before

13

4.5

*

BRS (ms/mm Hg)

2

*

5.5

*

4.5

After

C LF power (Ln ms )

5.5

3.5

70 Before

Obese

*

B HF power (Ln ms )

90

Heart rate (beats/min)

Fig. 1 Changes in heart rate (a), high-frequency (HF) power (b), low-frequency (LF) power (c), and baroreXex sensitivity (BRS) (d) before and after 16-week of endurance training in obese women with T2D and obese non-diabetic women. Values are mean § SEM. SigniWcantly diVerent from before training at * P < 0.05, ** P < 0.01, and *** P < 0.001 level

441

12

After

***

D

11 10 9 8

***

7 6 5

3.5

Before

BRS and parasympathetic control of the heart rate after 16 weeks of moderate walking training are evident only during the recovery of an acute bout of exercise but not at rest. In the present study, the only eVect of exercise training at rest was a reduction in systolic blood pressure. The observed hypotensive eVect of exercise training is similar to the change reported previously in hypertensive patients (Pagani et al. 1988; Davy et al. 1997), T2D patients (Loimaala et al. 2003) and overweight middle-aged individuals (Pescatello and Kulikowich 2001). A reduction in sympathetic activity has been suggested as a mechanism responsible for the reduction in resting BP (Pagani et al. 1988); however, the training-induced eVect on resting BP may occur in the absence of changes in autonomic function (Bowman et al. 1997; Davy et al. 1997; Perini et al. 2002; Loimaala et al. 2003), in accordance with our Wndings. Moreover, our study demonstrates that post-exercise BP did not change after exercise training, although there were changes in post-exercise autonomic control. These data suggest that the eVects of exercise training on BP at rest and during the post-exercise period are not inXuenced by the eVects on cardiac autonomic control. Consistent with previous research (Boutcher and Stein 1995; Davy et al. 1997; Loimaala et al. 2000; Perini et al. 2002), our data demonstrate that resting autonomic function was not aVected by exercise training. Exercise interventions using moderate intensities have not improved resting autonomic function in healthy middle-aged and older individuals (Davy et al. 1997; Loimaala et al. 2000; Perini et al. 2002). Conversely, Jurca et al. (2004) showed an improvement in HF power of HRV at rest after 8 weeks of training at moderate intensity in postmenopausal women with low VO2max. Longer training periods (5 months to 5 years)

After

Before

After

(Loimaala et al. 2000; Uusitalo et al. 2004) or higher exercise intensity (Okazaki et al. 2005) than the used in this study have not improved resting baroreXex gain in the LF band and HF power of HRV in older individuals. These observations suggest that long duration and high intensity are less likely to be the main determinants for the lack of training eVect on resting autonomic function in middleaged and older individuals. Because only moderate weight loss are needed to improve BRS (Alvarez et al. 2005) and vagal activity (Rissanen et al. 2001) at rest, it cannot be ruled out that the eVect of training on autonomic function observed in previous studies (Levy et al. 1998; Gulli et al. 2003; Jurca et al. 2004) may have been inXuenced by body fat loss (Amano et al. 2001). Our Wndings of unchanged body weight and autonomic function are in agreement with previous studies (Davy et al. 1997; Loimaala et al. 2000; Perini et al. 2002). Our results indicate that endurance training did not inXuence resting autonomic function in obese women in the absence of fat loss. Improvements in cardiac autonomic function after exercise training are evident when physiological perturbations such as the Valsalva maneuver (Monahan et al. 2000; Cooke et al. 2002) and submaximal exercise (Yamamoto et al. 2001) are used rather than a simple measure at rest. Although no changes were observed in resting autonomic function with exercise training, our data demonstrate a beneWcial eVect on post-exercise cardiac autonomic modulation. We found a lower (5%) HR during the post-exercise recovery period after training. Exercise training accelerates HR recovery by enhancing post-exercise cardiovagal activity (Yamamoto et al. 2001). Post-exercise HF power, an indicator of cardiac parasympathetic regulation of HR (Pagani et al. 1986), was increased (14%) in our subjects after training. Likewise, Yamamoto et al. (2001) observed a

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faster HR recovery at 20 min post-exercise due to enhanced post-exercise vagal activity after training. Therefore, the training-induced enhancement of post-exercise HF power improved HR recovery after acute exercise. A diVerent interpretation has been proposed to explain the increase in LF power after training (Gulli et al. 2003). Cevese et al. (2001) suggested that LF oscillations of HRV are induced by sympathetic vascular tone which stimulates baroreXex activity. Two longitudinal studies have reported enhancement of resting LF power after endurance training in obese individuals and older women (Amano et al. 2001; Gulli et al. 2003). Exercise training increased both resting LF and HF power in obese individuals (Amano et al. 2001). Although Gulli et al. (2003) found enhanced resting LF power without changes in HF power after training, they attributed the lower resting HR and higher LF power to improved BRS (Gulli et al. 2003). Because enhanced cardiovagal tone and reduced HR are indicators of increased cardiac autonomic control, our results suggest that the increase in post-exercise LF power might be a beneWcial training adaptation accounted for by enhanced BRS. Thus, if the enhanced BRS improved parasympathetic activity in both the LF and in the HF components of HRV similarly, no change in the LF/HF ratio could be interpreted as either improvement in vagal activity or no change in sympathetic activity. Improvement in resting BRS after training has been reported in middle-aged men with T2D (Loimaala et al. 2003). We did not detect changes in BRS at rest; however, improvements in the post-exercise recovery were apparent. Yamamoto et al. (2001) suggested that the beneWcial changes in post-exercise cardiac autonomic function after exercise training was probably due to improved BRS. Our data showed that the enhanced post-exercise HR recovery and cardiovagal activity after training are accompanied with enhanced BRS. To the best of our knowledge, this study is the Wrst to examine the eVects of endurance training on post-exercise BRS. This improved post-exercise autonomic modulation of HR may have the potential to reduce the risk of cardiac complications observed after acute vigorous exercise (Albert et al. 2000) as the changes observed have been associated with reduced cardiac mortality in high risk individuals (La Rovere et al. 2002). Previous studies have shown reduced cardiac autonomic function in patients with T2D (Gerritsen et al. 2001; Loimaala et al. 2003; Schroeder et al. 2005) and non-diabetic obese individuals (Alvarez et al. 2005). The beneWcial eVect of exercise training (Howorka et al. 1997) and glycemic control (Burger et al. 1999) on HRV improvement is more evident in diabetic patients with early autonomic neuropathy compared with patients without this dysfunction. In contrast to our hypothesis, obese women with and without T2D had similar autonomic function along with similar

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physical characteristics and levels of HbA1c throughout the study. Because peak aerobic capacity was similar in our groups, it is unlikely that women with T2D had diastolic dysfunction, a clinical evidence of diabetic cardiomyopathy characterized by autonomic dysfunction and exercise intolerance (Maser and Lenhard 2005). The Wnding of comparable autonomic function in non-diabetic obese and T2D patients with no evidence of neuropathy has been previously described (Huggett et al. 2005). Our study extends these Wndings and shows that endurance training induced the same cardiovascular eVects in obese women with and without T2D. Our results are applicable to obese women with T2D with no autonomic neuropathy and relatively good glycemic control. Further studies are needed to investigate the eVects of exercise training on BRS in those with diabetic complications. It could be argued that the improved autonomic modulation observed after training may be due to the use of the same absolute workloads after training, which may represent less cardiovascular stress. Although there was an increase in VO2 peak (»1.6 ml kg¡1 min¡1) with training, the relative intensity of the acute bout of exercise before (63%) and after (61%) training was similar. Changes in VO2 were similar than those previously reported in men with T2D (Loimaala et al. 2003). Therefore, a faster HR and autonomic recovery in response to the same relative workload indicates that the training program improved post-exercise autonomic function. In conclusion, 16 weeks of brisk walking training reduced resting blood pressure without changes in resting cardiac autonomic function in both obese women with and without T2D. However, training-induced improvements in cardiac autonomic modulation are apparent during the postexercise recovery period suggesting that this obese population of women do gain beneWts in cardiovascular modulation when recovering from acute moderate intensity stress. Acknowledgments This study was founded in part by the New York Sate Diabetes Bridge Grant and by NIH DK063179.

References Albert CM, Mittleman MA, Chae CU, Lee IM, Hennekens CH, Manson JE (2000) Triggering of sudden death from cardiac causes by vigorous exertion. N Engl J Med 343:1355–1361 Alvarez GE, Davy BM, Ballard TP, Beske SD, Davy KP (2005) Weight loss increases cardiovagal baroreXex function in obese young and older men. Am J Physiol Endocrinol Metab 289:E665– 669 Amano M, Kanda T, Ue H, Moritani T (2001) Exercise training and autonomic nervous system activity in obese individuals. Med Sci Sports Exerc 33:1287–1291 Boutcher SH, Stein P (1995) Association between heart rate variability and training response in sedentary middle-aged men. Eur J Appl Physiol Occup Physiol 70:75–80

Eur J Appl Physiol (2007) 100:437–444 Bowman AJ, Clayton RH, Murray A, Reed JW, Subhan MM, Ford GA (1997) EVects of aerobic exercise training and yoga on the baroreXex in healthy elderly persons. Eur J Clin Invest 27:443–449 Burger AJ, Weinrauch LA, D’Elia JA, Aronson D (1999) EVect of glycemic control on heart rate variability in type I diabetic patients with cardiac autonomic neuropathy. Am J Cardiol 84:687–691 Cevese A, Gulli G, Polati E, Gottin L, Grasso R (2001) BaroreXex and oscillation of heart period at 0.1 Hz studied by alpha-blockade and cross-spectral analysis in healthy humans. J Physiol 531:235– 244 Cooke WH, Reynolds BV, Yandl MG, Carter JR, Tahvanainen KU, Kuusela TA (2002) EVects of exercise training on cardiovagal and sympathetic responses to Valsalva’s maneuver. Med Sci Sports Exerc 34:928–935 Davy KP, Willis WL, Seals DR (1997) InXuence of exercise training on heart rate variability in post-menopausal women with elevated arterial blood pressure. Clin Physiol 17:31–40 Gerritsen J, Dekker JM, TenVoorde BJ, Kostense PJ, Heine RJ, Bouter LM, Heethaar RM, Stehouwer CD (2001) Impaired autonomic function is associated with increased mortality, especially in subjects with diabetes, hypertension, or a history of cardiovascular disease: the Hoorn study. Diabetes Care 24:1793–1798 Gulli G, Cevese A, Cappelletto P, Gasparini G, Schena F (2003) Moderate aerobic training improves autonomic cardiovascular control in older women. Clin Auton Res 13:196–202 Hautala AJ, Makikallio TH, Kiviniemi A, Laukkanen RT, Nissila S, Huikuri HV, Tulppo MP (2004) Heart rate dynamics after controlled training followed by a home-based exercise program. Eur J Appl Physiol 92:289–297 Howorka K, Pumprla J, Haber P, Koller-Strametz J, Mondrzyk J, Schabmann A (1997) EVects of physical training on heart rate variability in diabetic patients with various degrees of cardiovascular autonomic neuropathy. Cardiovasc Res 34:206–214 Huggett RJ, Scott EM, Gilbey SG, Bannister J, Mackintosh AF, Mary DA (2005) Disparity of autonomic control in type 2 diabetes mellitus. Diabetologia 48:172–179 Jurca R, Church TS, Morss GM, Jordan AN, Earnest CP (2004) Eight weeks of moderate-intensity exercise training increases heart rate variability in sedentary postmenopausal women. Am Heart J 147:e21 Kanaley JA, Giannopoulou I, Tillapaugh-Fay G, Nappi JS, PloutzSnyder LL (2003) Racial diVerences in subcutaneous and visceral fat distribution in postmenopausal black and white women. Metabolism 52:186–191 La Rovere MT, Bersano C, Gnemmi M, Specchia G, Schwartz PJ (2002) Exercise-induced increase in baroreXex sensitivity predicts improved prognosis after myocardial infarction. Circulation 106:945–949 Lee CM, Wood RH, Welsch MA (2003) InXuence of short-term endurance exercise training on heart rate variability. Med Sci Sports Exerc 35:961–969 Legramante JM, Galante A, Massaro M, Attanasio A, Raimondi G, Pigozzi F, Iellamo F (2002) Hemodynamic and autonomic correlates of postexercise hypotension in patients with mild hypertension. Am J Physiol Regul Integr Comp Physiol 282:R1037– R1043 Levy WC, Cerqueira MD, Harp GD, Johannessen KA, Abrass IB, Schwartz RS, Stratton JR (1998) EVect of endurance exercise training on heart rate variability at rest in healthy young and older men. Am J Cardiol 82:1236–1241 Loimaala A, Huikuri H, Oja P, Pasanen M, Vuori I (2000) Controlled 5-mo aerobic training improves heart rate but not heart rate variability or baroreXex sensitivity. J Appl Physiol 89:1825–1829 Loimaala A, Huikuri HV, Koobi T, Rinne M, Nenonen A, Vuori I (2003) Exercise training improves baroreXex sensitivity in type 2 diabetes. Diabetes 52:1837–1842

443 Malliani A, Pagani M, Lombardi F, Cerutti S (1991) Cardiovascular neural regulation explored in the frequency domain. Circulation 84:482–492 Mari A, Pacini G, Murphy E, Ludvik B, Nolan JJ (2001) A modelbased method for assessing insulin sensitivity from the oral glucose tolerance test. Diabetes Care 24:539–548 Maser RE, Lenhard MJ (2005) Cardiovascular autonomic neuropathy due to diabetes mellitus: clinical manifestations, consequences, and treatment. J Clin Endocrinol Metab 90:5896–5903 Melanson EL, Freedson PS (2001) The eVect of endurance training on resting heart rate variability in sedentary adult males. Eur J Appl Physiol 85:442–449 Monahan KD, Dinenno FA, Tanaka H, Clevenger CM, DeSouza CA, Seals DR (2000) Regular aerobic exercise modulates age-associated declines in cardiovagal baroreXex sensitivity in healthy men. J Physiol 529 Pt 1:263–271 Okazaki K, Iwasaki K, Prasad A, Palmer MD, Martini ER, Fu Q, Arbab-Zadeh A, Zhang R, Levine BD (2005) Dose-response relationship of endurance training for autonomic circulatory control in healthy seniors. J Appl Physiol 99:1041–1049 Pagani M, Lombardi F, Guzzetti S, Rimoldi O, Furlan R, Pizzinelli P, Sandrone G, Malfatto G, Dell’Orto S, Piccaluga E et al (1986) Power spectral analysis of heart rate and arterial pressure variabilities as a marker of sympatho-vagal interaction in man and conscious dog. Circ Res 59:178–193 Pagani M, Somers V, Furlan R, Dell’Orto S, Conway J, Baselli G, Cerutti S, Sleight P, Malliani A (1988) Changes in autonomic regulation induced by physical training in mild hypertension. Hypertension 12:600–610 Perini R, Fisher N, Veicsteinas A, Pendergast DR (2002) Aerobic training and cardiovascular responses at rest and during exercise in older men and women. Med Sci Sports Exerc 34:700–708 Pescatello LS, Kulikowich JM (2001) The aftereVects of dynamic exercise on ambulatory blood pressure. Med Sci Sports Exerc 33:1855–1861 Piepoli M, Coats AJ, Adamopoulos S, Bernardi L, Feng YH, Conway J, Sleight P (1993) Persistent peripheral vasodilation and sympathetic activity in hypotension after maximal exercise. J Appl Physiol 75:1807–1814 Pober DM, Braun B, Freedson PS (2004) EVects of a single bout of exercise on resting heart rate variability. Med Sci Sports Exerc 36:1140–1148 Raczak G, Pinna GD, La Rovere MT, Maestri R, Danilowicz-Szymanowicz L, Ratkowski W, Figura-Chmielewska M, Szwoch M, Ambroch-Dorniak K (2005) Cardiovagal response to acute mild exercise in young healthy subjects. Circ J 69:976–980 Rissanen P, Franssila-Kallunki A, Rissanen A (2001) Cardiac parasympathetic activity is increased by weight loss in healthy obese women. Obes Res 9:637–643 Saeki Y, Atogami F, Takahashi K, Yoshizawa T (1997) ReXex control of autonomic function induced by posture change during the menstrual cycle. J Auton Nerv Syst 66:69–74 Schroeder EB, Chambless LE, Liao D, Prineas RJ, Evans GW, Rosamond WD, Heiss G (2005) Diabetes, glucose, insulin, and heart rate variability: the atherosclerosis risk in communities (ARIC) study. Diabetes Care 28:668–674 Task Force of the European Society of Cardiology the North American Society of Pacing and Electrophysiology (1996) Heart rate variability: standards of measurement, physiological interpretation and clinical use. Circulation 93:1043–1065 Terziotti P, Schena F, Gulli G, Cevese A (2001) Post-exercise recovery of autonomic cardiovascular control: a study by spectrum and cross-spectrum analysis in humans. Eur J Appl Physiol 84:187–194 Ueno LM, Moritani T (2003) EVects of long-term exercise training on cardiac autonomic nervous activities and baroreXex sensitivity. Eur J Appl Physiol 89:109–114

123

444 Uusitalo AL, Laitinen T, Vaisanen SB, Lansimies E, Rauramaa R (2004) Physical training and heart rate and blood pressure variability: a 5-year randomized trial. Am J Physiol Heart Circ Physiol 286:H1821–H1826 Vescovi JD, Zimmerman SL, Miller WC, Hildebrandt L, Hammer RL, Fernhall B (2001) Evaluation of the BOD POD for estimating

123

Eur J Appl Physiol (2007) 100:437–444 percentage body fat in a heterogeneous group of adult humans. Eur J Appl Physiol 85:326–332 Yamamoto K, Miyachi M, Saitoh T, Yoshioka A, Onodera S (2001) EVects of endurance training on resting and post-exercise cardiac autonomic control. Med Sci Sports Exerc 33:1496–1502