Changes in Vascular Hemodynamics in Older Women Following 16 Weeks of Combined Aerobic and Resistance Training

Abstract

The purpose of this study was to determine if combined (aerobic and anaerobic) training decreases blood pressure (BP) and improves vascular properties. Seventy-nine post-menopausal women were randomly assigned to three groups that trained at different frequencies. VO₂max, body composition, BP, and arterial elasticity were evaluated prior to training and after 16 weeks of training. There was a significant time effect (decrease) for resting systolic blood pressure (SBP) and rate pressure product (RPP). Exercise SBP, diastolic blood pressure (DBP), heart rate (HR), and RPP also decreased. Changes in total vascular impedance were related to SBP and changes in systemic vascular resistance were related to changes in DBP independent of body composition changes. Our findings suggest that combined training reduces SBP and improves vascular properties; and, that combined training one day/week decreases BP similar to more frequent combined training. Training induced changes in arterial resistance and impedance may be involved in inducing changes in BP.

Introduction

Hypertension (HTN) is one of the leading risk factors for the development of cardiovascular disease (CVD). High blood pressure (BP) causes acceleration of atherosclerosis, arterial smooth muscle hyperplasia and hypertrophy, and increased collagen synthesis, all of which lead to structural and functional alterations to the arterial wall.¹ High BP is associated with small artery and organ damage.² The treatment and prevention of specific organ damage is not identical and reversibility varies.³

Evidence suggests that performing regular physical activity decreases BP and the risk of CVD.^4-7 A strong, inverse relationship between fitness level and mortality was shown in the Aerobic Center Longitudinal study (ACLS); Individuals who exercised at >4 METS (standard metabolic equivalence) showed a significant reduction in all-cause mortality.⁸

Previous research suggests that both aerobic and resistance training decrease BP. ^4,6,7,9-15 However, few studies have evaluated the effects of combined aerobic and resistance training on BP. Altered vascular integrity as measured by artery elasticity and vascular resistance/impedance possibly contributes to elevated BP.¹ Figueroa et al. suggests that combined training most likely improves the functional adaptations within arterial walls.¹⁶ Endothelial-dependent vasodilation may induce a reduction in vasomotor tone within the peripheral arteries which results in decreased BP.¹⁶ Similarly, Vona et al. found that with combined aerobic and resistance training endothelial dysfunction decreased.¹⁷ These changes may be sufficient enough to improve overall vascular integrity.

Exercise frequency might be particularly important when considering the effects of a combined aerobic and resistance training program. Older women may require more time to recover after exercise training so an increased volume of training could induce an overtraining response. This type of exercise response can counteract the beneficial exercise induced adaptations.¹⁸ Determining an optimal training frequency may decrease the possibility of overtraining.

The objective of this study was to determine what affect 3 different frequencies of combined aerobic and resistance training have on both resting and submaximal exercise BP, artery elasticity, vascular resistance, and vascular impedance.

Methods and Procedures

Study Participants

All participants were healthy, African American and European American, women ≥60 years of age enrolled in a larger study designed to look at metabolic factors in women over the age of 60, across three different training frequencies. Subjects were all sedentary and did not participate in any regular exercise training. Exclusion criteria included clinical evidence of heart disease, abnormal EKG (either at rest or during screening exercise testing), smoking, diabetes mellitus, or medications that affected energy expenditure, insulin levels, thyroid status, or heart rate. All participants were randomized, using Block Randomization stratified by race, to one of three exercise groups: Group 1, one day/week aerobic and one different day/week strength training; Group 2, two days/week aerobic and two days/week strength training; Group 3, three days/week aerobic and three days/week strength training. All subjects adhered to over 95% of their sessions, and there was no significant difference in adherence between groups. Methods and procedures were approved by the appropriate institutional review board, and all subjects signed appropriate informed consent forms.

Study Design and Methods

All participants maintained a stable weight through diet control and maintained dietary records prior to evaluations. Subjects were evaluated for muscle performance, maximal and submaximal VO₂, heart rate, and blood pressure (modified Balke treadmill protocol), resting blood pressure and resting artery elasticity, vascular resistance, and vascular impedance, prior to and after 16 weeks of training.

Exercise Testing

Maximum oxygen uptake (VO₂max) was evaluated with a physician-supervised modified Balke treadmill test protocol. A metabolic cart, calibrated prior to testing (Vmax Spectra29, SonsorMedics, Inc, Yorba Linda, California), was used to evaluate ventilatory expired gases. Monitoring consisted of 12-lead electrocardiogram and BP was measured every two minutes (Omron Blood Pressure Monitor, model HEM-780; Omron Healthcare, Inc 1200 Lakeside Dr. Bannockburn, IL). Subjects began walking at 2mph at a 0% grade. The grade increased 3.5% every two minutes and the speed was increased to 3mph at 12 minutes. All Subjects exercised until voluntary fatigue. Maximum oxygen uptake was defined as the highest 20-second average value during the last stage of the exercise test, a maximal respiratory exchange ratio (RER) ≥ 1.1, and a maximal HR that was ≤ 10 beats/min. of the age-predicted maximum HR (220-age). Two of the three criteria for VO₂max were required. Seven days following the maximal VO₂max test subjects performed a submaximal walk test and their BP response was measured at 0% and 5% grade. They walked at 2mph with a 0% grade for four minutes and four minutes at a 5% grade. Blood pressure was measured by auscultation between 3:30-4:00 time points for both stages. Due to equipment malfunction data for exercise HR, SBP, and DBP data (Table3) analysis was for 62 (HR; group 1 (n=21), group 2 (n=22), group 3 (n=19)), 57 (SBP and RPP; group 1 (n=20), group 2 (n=18), group 3 (n=19)), and 56 (DBP; group 1 (n=20), group 2 (n=18), group 3 (n=19) subjects.

Table3.

Changes in Blood Pressure in Response to Exercise Training

		Group 1	Group 2	Group 3	P
Resting
ΔSBP	Pre-training	124.7 ± 2.8	124.7 ± 3.0	124.1 ± 3.1	T = 0.01
	Post Training	116.4 ± 2.2	123.8 ± 2.6	120.5 ± 3.3	G = 0.55
		(n=27)	(n=30)	(n=22)	T*G = 0.17
ΔDBP	Pre-training	68.2 ± 2.1	69.7 ± 2.1	66.5 ± 2.1	T = 0.02
	Post Training	63.9 ± 1.4	67.3 ± 2.0	66.0 ± 1.7	G = 0.53
		(n=27)	(n=30)	(n=22)	T*G = 0.35
ΔHR	Pre-training	63.9 ± 1.3	63.3 ± 1.3	65.1 ± 1.5	T = 0.02
	Post Training	59.9 ± 1.3	62.3 ± 1.2	64.2 ± 1.7	G = 0.28
		(n=27)	(n=30)	(n=22)	T*G = 0.22
ΔRPP	Pre-training	7977.3 ± 256.3	7888.1 ± 243.4	8093.9 ± 293.1	T < 0.01
	Post Training	6978.2 ± 199.9	7704.1 ± 204.3	7780.4 ± 385.5	G = 0.34
		(n=27)	(n=30)	(n=22)	T*G = 0.08
Exercise
ΔSBP	Pre-training	168.8 ± 5.7	164.9 ± 5.3	164.2 ± 5.3	T < 0.01
	Post Training	153.5 ± 3.4	151.5 ± 5.3	141.7 ± 4.3	G = 0.38
		(n=20)	(n=18)	(n=19)	T*G = 0.43
ΔDBP	Pre-training	73.5 ± 2.9	78.2 ± 2.5	76.6 ± 2.0	T = 0.01
	Post Training	71.8 ± 2.2	73.6 ± 2.9	69.7 ± 2.2	G = 0.47
		(n=20)	(n=17)	(n=19)	T*G = 0.45
ΔHR	Pre-training	113.6 ± 3.0	115.1 ± 2.1	114.4 ± 3.0	T < 0.01
	Post Training	104.8 ± 3.0	112.1 ± 2.6	106.0 ± 2.1	G = 0.39
		(n=21)	(n=22)	(n=19)	T*G = 0.16
ΔRPP	Pre-training	19354.4 ± 1007.5	19181.0 ± 875.5	18967.1 ± 1029.0	T < 0.01
	Post Training	16116.0 ± 577.1	17254.8 ± 994.4	15058.8 ± 642.8	G = 0.54
		(n=20)	(n=18)	(n=19)	T*G = 0.30

Values are reported as the mean ± SE. Group 1 trained 1 day/week; group 2 trained 2 days/week group 2 trained 2 days/week; group 3 trained 3 days/week. (SBP, systolic blood pressure; DBP, diastolic blood pressure; HR, heart rate; RPP, rate pressure product).

Body Composition

Dual-energy X-ray absorptiometry (Lunar DPX-L densitometer; LUNAR Radiation, Madison WI) in the Department of Nutrition Sciences at UAB was used to determine total fat and lean mass. Adult Software, version 1.33, was used to analyze the scans.

Resting Blood Pressure

Resting supine BP was taken on three consecutive days (and the measurement from the second day was reported) with automatic auscultation between 7:00 and 8:00 AM in a fasted state prior to exercise (Omron Blood Pressure Monitor, model HEM-780; Omron Healthcare, Inc 1200 Lakeside Dr. Bannockburn, IL). This was done to ensure that a stable measurement was used. Resting BP was also measured after training.

Arterial Elasticity

Arterial elasticity was measured using non-invasive radial artery pulse wave analysis. Pulse wave analysis was performed in duplicate, and average values were reported. The radial artery waveform was obtained with a sensor positioned over the artery and calibrated using an oscillometric method on the opposite arm. Thirty seconds of analog waveforms were digitized at 200 samples/sec, and a beat marking algorithm determined the beginning of systole, peak systole, onset of diastole, and end diastole for all beats in the 30-sec measurement period. An average beat determination was constructed, and a parameter estimating algorithm (Hypertension Diagnostics, Eagan, MN) was applied to define a third-order equation that replicated the diastolic decay and waveform. The estimates of arterial elasticity are based on the asymptotic behavior of a Windkessel mode (1, 2). Mathematically (CR-2000 operator’s manual), the pulse waveform P(t), the pressure (mmHg) at time t elapsed since the beginning of diastole, is modeled as a decaying exponential function plus a sinusoidal function dampened by a decaying exponential:

P(t) = {a1 * exp(-a2t)} + {a3*exp(-a4t) * cos(a5t + a6)}. The modified Windkessel model then uses the parameters a1 – a6 to estimate:

$$\mathrm{LAE}\ast \mathrm{SVR}=2\mathrm{a}4[(\mathrm{a}2+\mathrm{a}4)2+\mathrm{a}52]/[\mathrm{a}2(2\mathrm{a}4+\mathrm{a}2)(\mathrm{a}42+\mathrm{a}52)]$$

SAE*SVR = 1/(2a4 + a2). SVR is the systemic vascular resistance = mean arterial blood pressure/cardiac output. Cardiac output (L/min) is estimated as HR*(-6.6+(0.25 * (ET-35)-(0.62 * HR))+(40.4 * BSA) - (0.51*Age))/1000, where ET is ejection time in milliseconds, HR is heart rate in beats per minute, and BSA is body surface area in millimeters squared (estimated as 0.007184 * WT 0.425 * HT 0.725). ET in milliseconds is directly observable from the pulse waveform. Information from the pulse waveform only provides estimates of LAE*SVR and SAE*SVR. LAE and SAE are estimated by dividing each of LAE*SVR and SAE*SVR by SVR. Due to equipment malfunction data was only collected for 70 subjects (group 1 (n=20), group 2 (n=27), group 3 (n=21)).

Exercise Training

Training sessions lasted 50 minutes in a facility dedicated to research and under the supervision of exercise physiologists. Each session began with a three to four minute warm-up on a bike ergometer or treadmill and three to four minutes of stretching.

Aerobic Training

During the first week subjects performed 20 minutes of continuous exercise at 67% maximum heart rate. Each week intensity and duration were increased so that at 8 weeks subjects were working at 80% maximum heart rate for 40 minutes. Exercise modalities included bike ergometer and treadmill exercise.

Resistance Training

Strength exercises included leg press, squats, leg extension, leg curl, elbow flexion, lateral pull-down, bench press, military press, lower back extension, and bent leg situps. Each exercise consisted of two sets of 10 repetitions with a two-minute rest between sets. The intensity was gradually increased to 80% of the maximum weight the subject could lift at one time (1RM). Subject 1RM was determined every fifth week to insure that intensity was increased appropriately.

Statistical Approach

One-way anova was used to analyze all descriptive data. One-way anova with repeated measures was used to analyze all main variable outcomes. Pearson product correlations were used to evaluate relationships between changes in variables of interest. Two multiple linear regression models for estimating changes in SBP were developed (first model age, ΔSVR, ΔFM, ΔFFM were independent variables and the second model age, ΔTVI, ΔFM, ΔFFM). DBP was also modeled using the same two sets of independent variables. Due to missing data, analyses for arterial elasticity and exercise BP were performed using a reduced cohort (Sample sizes for each variable are included in tables).

Results

Descriptive statistics are shown in Table 1. At baseline age and height were not significantly different between groups. Body weight and percent body fat were significantly different; however, there was little change in the values after training. Changes in large arterial elasticity (LAE), small arterial elasticity (SAE), systemic vascular resistance (SVR), and total vascular impedance (TVI) from pre-training to post-training are shown in Table 2. There was no significant time effect for any of these variables. A significant group affect as well as time by group interaction was observed for small arterial elasticity.

Table1.

Baseline Characteristics of Participants

		Group 1	Group 2	Group 3	P
Age		65.6 ± 0.7	63.7 ± 0.5	64.8 ± 0.7	0.11
Height		166.5 ± 1.1	165.2 ± 1.0	164.4 ± 0.8	0.33
Δ Body Weight	Pre-training	78.2 ± 2.7	75.0 ± 1.7	68.4 ± 2.0	0.01
	Post-training	77.7 ± 2.4	73.8 ± 1.7	68.2 ± 2.0
Δ Percent Body Fat	Pre-training	44.7 ± 1.2	43.0 ± 0.9	39.5 ± 1.4	0.01
	Post-training	43.6 ± 1.3	41.5 ± 0.8	38.8 ± 1.4

Values are reported as mean ±SE. Group 1 (n=27); Group 2 (n=30); Group 3 (n=22)

Table2.

Changes in Arterial Properties in Response to Exercise Training

		Group 1	Group 2	Group 3	P
ΔLAE	Pre-training	13.3 ± 0.9	13.8 ± 1.2	11.9 ± 0.7	T = 0.33
	Post Training	15.3 ± 1.2	12.8 ± 0.7	13.1 ± 1.0	G = 0.26
		(n=22)	(n=27)	(n=21)	T*G = 0.21
ΔSAE	Pre-training	4.2 ± 0.4	4.3 ± 0.4	3.0 ± 0.3	T = 0.87
	Post Training	4.2 ± 0.3	3.7 ± 0.3	3.7 ± 0.4	G = 0.16
		(n=22)	(n=27)	(n=21)	T*G = 0.01
ΔSVR	Pre-training	1538.6 ± 43.9	1528.9 ± 52.3	1673.3 ± 63.6	T = 0.77
	Post Training	1517.2 ± 57.8	1625.7 ± 65.4	1625.4 ± 57.7	G = 0.28
		(n=22)	(n=27)	(n=21)	T*G = 0.12
ΔTVI	Pre-training	165.4 ± 9.4	161.8 ± 7.1	179.3 ± 10.4	T = 0.55
	Post Training	156.6 ± 10.8	170.0 ± 7.6	167.4 ± 10.2	G = 0.49
		(n=22)	(n=27)	(n=21)	T*G = 0.42

Large artery elasticity (LAE), small artery elasticity (SAE), systemic vascular resistance (SVR), and total vascular impedance (TVI) from pre-training to post training. Values are reported as mean ± SE.

Resting and exercise blood pressure and heart rate for the three groups at baseline and 16 weeks are shown in Table 3. At rest a significant time effect was observed for systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR) and rate pressure product (RPP), showing that after 16 weeks of training older women had significantly reduced resting SBP, DBP, HR, and RPP. There was no significant group effect or time by group effect for any variable at rest.

During exercise there was a significant time effect for all variables, showing a significant reduction in SBP, DBP, HR, and RPP during exercise. There was no significant group effect or time by group interaction for any exercise variable.

Correlations between changes in systolic blood pressure (ΔSBP) and diastolic blood pressure (ΔDBP) with age, changes in fat mass (ΔFM), fat free mass (ΔFFM), systemic vascular resistance (ΔSVR), total vascular impedance (ΔTVI), large artery elasticity (ΔLAE), and small artery elasticity (ΔSAE) are shown in Table 4. There was a positive relationship between ΔDBP and ΔFFM, ΔSVR, and ΔTVI. A negative relationship was seen between ΔDBP and age, ΔFM, ΔLAE. A positive relationship was seen between ΔSBP and ΔTVI.

Table4.

Correlations between Changes in Body Composition, Arterial Properties, and Blood Pressure.

	ΔSBP (P)	ΔDBP (P)
Age	-0.118 (0.193)	-0.221 (0.051)
ΔFFM	0.058 (0.335)	0.211 (0.059)
ΔFM	0.164 (0.113)	-0.133 (0.165)
ΔSVR	0.189 (0.381)	0.269 (0.023)
ΔTVI	0.240 (0.037)	0.348 (0.004)
ΔLAE	-0.122 (0.186)	-0.246 (0.034)
ΔSAE	0.175 (0.292)	0.075 (0.292)

systolic blood pressure (ΔSBP) and diastolic blood pressure (ΔDBP) with age, and changes in dexa total fat mass (ΔFM), dexa fat free mass (ΔFFM), systemic vascular resistance (ΔSVR), total vascular impedance (ΔTVI), large artery elasticity (ΔLAE), and small artery elasticity (ΔSAE).

Four linear regression models for estimating resting ΔSBP and ΔDBP are shown in Table 5. The first model includes age, ΔSVR, ΔFM, ΔFFM, for prediction of ΔSBP. After adjusting for ΔFM and ΔFFM age was the only significant independent correlate. The second model was identical to the first except for the substitution of ΔDBP for ΔSBP. After adjusting for ΔFM and ΔFFM both age and ΔSVR were significant independent correlates. The third model includes age, ΔTVI, ΔFM, ΔFFM, for prediction of ΔSBP. After adjustment for ΔFM and ΔFFM both ΔTVI and ΔFM were significant independent correlates. The fourth model was identical to the third except for the substitution of ΔDBP for ΔSBP. After adjusting for ΔFM and ΔFFM age and ΔTVI were significant correlates.

Table5.

Multiple Regression for Estimating Changes in Blood Pressure.

	Intercept	Slope	Adjusted β	P
Regression for ΔSBP
Adjusted R2 = 0.361	9.47			0.77
Age		-1.26	-0.29	0.01
ΔSVR		0.01	0.09	0.41
ΔFM		0.34	0.05	0.70
ΔFFM		0.20	0.02	0.89
Regression for ΔDBP
Adjusted R2 = 0.124	47.61			0.03
Age		-0.69	-0.28	0.04
ΔSVR		0.01	0.28	0.03
ΔFM		-0.21	-0.05	0.71
ΔFFM		1.42	0.21	0.13
Regression for ΔSBP
Adjusted R2 = 0.083	46.62			0.21
Age		-0.70	-0.16	0.23
ΔTVI		0.08	0.32	0.02
ΔFM		2.01	0.28	0.05
ΔFFM		1.48	0.13	0.37
Regression for ΔDBP
Adjusted R2 = 0.172	50.47			0.02
Age		-0.75	-0.30	0.02
ΔTVI		0.06	0.37	0.01
ΔFM		0.05	0.01	0.93
ΔFFM		1.29	0.19	0.16

systolic blood pressure (ΔSBP) and diastolic blood pressure (ΔDBP), from age and changes in systemic vascular resistance (ΔSVR), total vascular impedance (ΔTVI), dexa total fat mass (ΔFM), and dexa fat free mass (ΔFFM).

Discussion

After 16 weeks of combined aerobic and resistance training, similar decreases in BP and RPP (an indicator of myocardial oxygen demand) were observed in all three training groups both during exercise and at rest. This is particularly important in older adults who may have compromised cardiovascular systems and increased risk of stroke and myocardial infarction while performing routine, daily activities. Similar changes in SVR, BP, and RPP between the 3 groups indicate that exercise training one day/week aerobic and one day/week resistance induces BP and RPP changes similar to training for up to three days/week, provided the one resistance and the one aerobic exercise session take place on nonconsecutive days.

Interestingly, changes in TVI were independently related to changes in resting SBP and changes in resting SVR were significantly related to changes in DBP after adjusting for FFM and FM. Although, causality cannot be directly inferred, it does suggest that BP changes following exercise training may at least be partly induced by changes in vascular resistance and vascular impedance.

Endurance training alone has been known to improve cardiovascular health. ^4-7,13,19,20 Kikkinos and Gregg show that aerobic exercise of moderate to vigorous intensities decreased BP in patients with mild to moderate HTN.^4,6 A study conducted by Tanasescu et al., showed a 42% CVD risk reduction in men who ran for an hour one or more times per week.²¹ Tanaka et al. found that middle aged individuals who performed low to high intensity endurance training had a lower SBP and DBP than there sedentary peers, and Higashi et al. found that moderate intensity aerobic training performed five times per week lowered SBP and DBP.^7,9 Physiological adaptations, such as an increase in parasympathetic tone and increased endothelial function lead to increased vasodilation.^17,22,23 These physiological changes induced by performing regular exercise reduces BP.²⁴ Therefore, we hypothesize that in the present study it is likely endurance training induced changes in parasympathetic tone may have contributed to the reductions in resting and exercising SBP and DBP we observed.

In this study the group that performed aerobic exercise one day per week had similar changes in resting blood pressure (with the exception of SAE) as the groups that performed aerobic and resistance exercise two or three days per week. The observed changes could be in response to the strength training performed on a nonconsecutive day from the aerobic training. Previous research suggests that resistance training is related to decreases in DBP.^10-13 Fagard et al. found that resistance training performed two times per week reduced resting DBP and had no affect on SBP.¹³ Collier et al. reported that women exhibit greater decreases in DBP than SBP following resistance training.¹¹ Casey et al. found that performing resistance training on two nonconsecutive days/week decreased DBP.¹² In addition, Tanasescu et al. showed a 23% cardiovascular risk reduction in individuals who performed 30 minutes of resistance exercise one or more times per week. Taken together, these studies support the view that resistance training can also have a positive effect on BP, particularly DBP. The interpretation of our data is that aerobic and resistance training on non consecutive days at a frequency of as little as one day a week is sufficient to achieve improvements in blood pressure in older healthy women. It is difficult to interpret the time by group interaction. It is probable that the apparent increase in SAE in group three may have been primarily the result of regression toward the mean, a consequence of the abnormally low initial SAE in group three. There was no significant group effect or time by group interaction for large artery elasticity, systemic vascular resistance, or total vascular impedance.

Similar to previous research, we observed decreases in HR, BP, and RPP during submaximal exercise.¹⁵ A 9.0% decrease was seen during exercise and 3.0% decrease at rest for SBP. A 5.0% decrease was seen during exercise and 3.0% decrease at rest for DBP. A 14.7% decrease was seen during exercise and a 5.0% decrease was seen at rest for RPP. Reduction in sympathetic stimulation probably contributed to the reduction of BP observed in the submaximal exercise tasks observed after 16 weeks of training. Stimulation of the sympathetic nervous system and thus the adrenal activity (primarily norepinephrine) is reduced during an absolute submaximal work level (i.e. walk at 2 mph) in trained individuals compared to untrained.¹⁸ Vasodilation in response to decreases in sympathetic stimulation causes a reduction in SVR and thus blood pressure.¹⁸ Decreases in HR and BP contribute to decreases in RPP.¹⁸ A lower RPP during absolute submaximal exercise is indicative of less myocardial stress, making a cardiac event less likely to occur during daily activities.¹⁸

Limitations

The subjects in this study were older women who trained for 16 weeks (as this was the group of interest for our study) so the results of this study are not applicable to other age and/or sex groups. In addition, we had relatively small numbers of subjects in each group, although our study is still larger than most in the literature. We also had no control group. Subjects were randomly assigned throughout the 5 year duration of the study, so it is unlikely a seasonal bias occurred in the evaluations. Also, it is unlikely an aging related increase in HR and BP would have occurred during only a 16 week time span.

In conclusion, the present findings indicate that compared to more frequent combined aerobic and resistance training, in this population of women ≥ 60 years, combined aerobic and resistance training one day a week reduces both resting and exercise SBP and DBP. Our data also suggests that following exercise training alterations in vascular properties may at least partly explain some of the decrease in resting BP.