Swimming is ideal for older adults because it includes minimum weight-bearing stress and decreased heat load. However, there is very little information available concerning the effects of regular swimming exercise on vascular risks. We determined if regular swimming exercise would decrease arterial blood pressure (BP) and improve vascular function. Forty-three otherwise healthy adults >50 years old (60 ± 2) with prehypertension or stage 1 hypertension and not on any medication were randomly assigned to 12 weeks of swimming exercise or attention time controls. Before the intervention period there were no significant differences in any of the variables between groups. Body mass, adiposity, and plasma concentrations of glucose and cholesterol did not change in either group throughout the intervention period. Casual systolic BP decreased significantly from 131 ± 3 to 122 ± 4 mm Hg in the swimming training group. Significant decreases in systolic BP were also observed in ambulatory (daytime) and central (carotid) BP measurements. Swimming exercise produced a 21% increase in carotid artery compliance (p <0.05). Flow-mediated dilation and cardiovagal baroreflex sensitivity improved after the swim training program (p <0.05). There were no significant changes in any measurements in the control group that performed gentle relaxation exercises. In conclusion, swimming exercise elicits hypotensive effects and improvements in vascular function in previously sedentary older adults.
Regular exercise is universally the first-line approach to prevent and treat age-related increases in blood pressure (BP). Most studies to date, however, have employed walking, jogging, or cycling as activity modes. Currently, there is very little information available concerning the BP-lowering effects of regular swimming exercise. Thus far swimming exercise has been widely promoted and prescribed without the underpinning of firm scientific support from clinical studies. This is unfortunate because swimming is an ideal form of physical activity for older adults, particularly those with orthopedic problems, bronchospasm, heat disorders, and/or obesity, because it includes minimum weight-bearing stress, a humid environment, and decreased heat load. In addition, no information is available on whether regular swimming exercise modulates key measurements of vascular function (arterial stiffness and endothelium-dependent vasodilation) and whether they are related to the hypotensive effects of swimming exercise. The primary aim of the present study was to determine the effect of swimming exercise intervention on arterial BP and key measurements of vascular functions in adults >50 years of age with increased BP. To evaluate the effects on BP as comprehensively as possible, measurements of ambulatory, central, and casual BP were performed.
Methods
Men and women 50 to 80 years of age were recruited from Austin, Texas and the surrounding communities. Every subject had a systolic BP at rest from 140 to 159 mm Hg (stage 1 systolic hypertension) or 120 to 139 mm Hg (prehypertension) with a diastolic BP of <99 mm Hg. No subjects had been smoking or taking antihypertensive medications. Subjects were free of overt chronic diseases based on medical history, blood chemistries, physical examination, and at-rest and maximal treadmill exercise electrocardiograms. No subjects had performed regular exercise during the preceding 2 years. They also had no orthopedic complications that would have prohibited them from exercising. The nature, purpose, and risks of the study were explained to each subject before written informed consent was obtained.
After baseline measurements subjects were assigned to swimming exercises or relaxation exercises (attention control). Group assignments were made as randomly as possible, with some regard given to individual preference when a few subjects strongly objected to their group assignment. Elimination of subjects who were not randomized did not affect the overall results. During the course of this investigation subjects in the 2 groups were instructed to maintain their usual lifestyle and dietary habits. This was verified by dietary analyses and maximal oxygen consumption tests.
Subjects in the swimming exercise group participated in a supervised 12-week swimming training program. For the first few weeks subjects were instructed by an instructor and swam 15 to 20 minutes/day, 3 to 4 days/week at a relatively low intensity of exercise (∼60% of maximal heart rate). As their overall level of fitness and exercise skill improved, the intensity and duration of exercise increased to 40 to 45 minutes/day, 3 to 4 days/week at a moderate intensity of 70% to 75% of maximal heart rate. Target heart rate was adjusted based on the observation that maximal heart rate during swimming is approximately 10 to 13 beats/min lower than that during running. Each subject was instructed to swim continuously except during the time needed for checking a target heart rate (by Polar heart rate monitor (Polar Electro, Lake Success, New York) secured on a subject’s chest).
The attention time control group was necessary to control for the possibility of random changes over time and the “attention” that the swimming training subjects received from their frequent interactions with the investigators, which could affect dependent variables independent of the intervention. Subjects in the control group visited the laboratory at the same frequency as subjects in the exercise intervention and underwent general progressive relaxation exercises that included a mixture of progressive relaxation and autogenic relaxation. In addition, gentle static stretching exercises for the entire body were used.
All post-training measurements were performed 24 to 48 hours after the last exercise session to avoid the immediate effects of a single bout of exercise. In addition, measurements before and after intervention periods were obtained at the same time of day for each subject.
Lean body mass and body fat percentage were determined by dual energy x-ray absorptiometry using a Lunar DPX (Lunar, Madison, Wisconsin).
Bilateral brachial and ankle BP and carotid and femoral pulse-wave velocities (PWVs) were measured by an automated vascular testing device (VP-2000, Omron Healthcare, Bannockburn, Illinois). Carotid and femoral artery pulsewaves were recorded by arterial applanation tonometry. Time delay was measured automatically with the foot-to-foot method and the PWV was subsequently calculated. Augmentation index, an index of arterial wave reflection and arterial stiffness, was obtained using arterial tonometry on the carotid artery.
BP recordings over a 24-hour period of normal daily activity were measured using a noninvasive ambulatory monitor (Spacelabs, Redlands, Washington). The night-time period was defined as the time when the subject went to bed at night until rising the following morning.
Graded exercise testing was undertaken using a metabolic cart during a modified Bruce protocol. After a 5-minute warm-up subjects walked or ran while the treadmill slope was gradually increased by 2% every 2 minutes until volitional exhaustion.
Stroke volume and cardiac output were measured using a sector transducer connected to an ultrasound machine (Philips iE33, Philips, Bothel, Washington).
Carotid arterial compliance was measured by a combination of ultrasound imaging on the carotid artery and simultaneous applanation tonometry on the contralateral carotid artery as previously described. Longitudinal images of the common carotid artery were acquired using an ultrasound machine (Philips iE33) and analyzed using image analysis software (Medical Imaging Applications, Coralville, Iowa). The pressure waveform and amplitude were obtained from the contralateral carotid artery using arterial applanation tonometry (VP-2000, Omron Healthcare) and analyzed by the investigator who was blinded to the group assignment using waveform browsing software (Dataq, Akron, Ohio).
Brachial flow-mediated dilation (FMD) was measured using a standard procedure. Brachial diameter and blood flow velocity were acquired from a Doppler ultrasound machine equipped with a high-resolution linear array transducer (Philips iE33). After baseline images were obtained the cuff placed on the forearm was inflated to 100 mm Hg above an individual subject’s systolic BP for 5 minutes. All ultrasound-derived blood flow and diameter data were analyzed by the same investigator who was blinded to the experimental condition using image analysis software.
Cardiovagal baroreflex sensitivity (BRS) was determined using the Valsalva maneuver as previously described. Subjects were asked to exhale forcibly against a closed airway and maintain an expiratory mouth pressure of 40 mm Hg for 10 seconds. The RR interval of the electrocardiogram and beat-by-beat BP (Portapres, Finapres Medical Systems, Amsterdam, The Netherlands) were measured continuously. Data for cardiovagal BRS were recorded and analyzed by waveform browsing software (Windaq 2000, Dataq Instruments, Akron, Ohio) during the phase IV overshoot.
Data were analyzed using analysis of variance with repeated measures. For a significant F value, least significant difference post hoc analysis was used to determine differences. Univariate correlation and regression analyses were used to determine associations between variables of interest.
Results
Twenty-four adults >50 years of age completed the swimming training program and 19 subjects completed the relaxation exercise program. Subjects’ adherence to the supervised exercise session was >99%. Before the intervention period (at baseline) there were no significant differences in any physical characteristic variables between the swimming intervention and attention control groups ( Table 1 ).
| Variable | Attention Control | Swimming Training | ||
|---|---|---|---|---|
| Before | After | Before | After | |
| (n = 19) | (n = 19) | (n = 24) | (n = 24) | |
| Men/women | 4/15 | 4/15 | 7/17 | 7/17 |
| Age (years) | 61 ± 2 | — | 58 ± 2 | — |
| Height (cm) | 165 ± 2 | 165 ± 2 | 168 ± 2 | 167 ± 2 |
| Body mass (kg) | 87 ± 4 | 86 ± 4 | 81 ± 3 | 80 ± 3 |
| Body mass index (kg/m 2 ) | 32 ± 1 | 31 ± 1 | 29 ± 1 | 28 ± 1 |
| Body fat (%) | 42 ± 2 | 43 ± 2 | 39 ± 2 | 38 ± 2 |
| Lean body mass (kg) | 45 ± 2 | 44 ± 2 | 45 ± 2 | 46 ± 2 |
| Physical activity score (unit) | 12 ± 2 | — | 14 ± 2 | — |
| Maximal oxygen consumption (ml/kg/min) | 27 ± 1 | 27 ± 1 | 28 ± 1 | 30 ± 1 |
| Total cholesterol (mg/dl) | 211 ± 10 | 196 ± 9 | 202 ± 8 | 196 ± 9 |
| Low-density lipoprotein cholesterol (mg/dl) | 137 ± 10 | 132 ± 7 | 127 ± 8 | 120 ± 10 |
| High-density lipoprotein cholesterol (mg/dl) | 53 ± 4 | 52 ± 5 | 57 ± 4 | 60 ± 4 |
| Triglyceride (mg/dl) | 128 ± 18 | 125 ± 15 | 120 ± 12 | 121 ± 16 |
| Glucose (mg/dl) | 102 ± 2 | 97 ± 2 | 97 ± 3 | 94 ± 2 |
| Hemoglobin A1c (%) | 4.5 ± 0.1 | 4.7 ± 0.1 | 4.7 ± 0.1 | 4.5 ± 0.1 |
| Interleukin-6 (pg/ml) | 5.2 ± 0.9 | 4.8 ± 1.1 | 5.2 ± 2.0 | 4.8 ± 0.8 |
| Interleukin-7 (pg/ml) | 4.2 ± 0.7 | 2.9 ± 1.0 | 3.4 ± 0.8 | 3.5 ± 0.6 |
| Interleukin-10 (pg/ml) | 20.4 ± 5.5 | 19.8 ± 7.1 | 26.2 ± 10.1 | 29.1 ± 13.3 |
| Tumor necrosis factor-α (pg/ml) | 7.5 ± 0.6 | 7.7 ± 0.9 | 6.2 ± 0.6 | 6.4 ± 0.5 |
| Total caloric intake (kcal/day) | 1,924 ± 177 | 1,855 ± 152 | 1,984 ± 98 | 1,980 ± 87 |
| Protein intake (g) | 75 ± 6 | 89 ± 10 | 86 ± 4 | 81 ± 7 |
| Fat intake (g) | 78 ± 10 | 80 ± 12 | 81 ± 8 | 74 ± 6 |
| Carbohydrate intake (g) | 203 ± 19 | 231 ± 27 | 209 ± 15 | 207 ± 13 |
| Alcohol intake (g) | 5 ± 1 | 9 ± 4 | 8 ± 4 | 10 ± 4 |
Subjects in the swimming intervention group were able to gradually and significantly increase their daily swimming distance from the start of intervention. Daily swim distance was significantly increased from 550 ± 40 m/day in the first week, to 1,005 ± 70 m/day at fourth week, and to 1,417 ± 83 m/day in the final week. Maximal oxygen consumption during treadmill exercise did not change significantly with swimming training ( Table 1 ). Body mass, adiposity, and plasma concentrations of cholesterol, glucose, or inflammatory cytokines did not change in either group throughout the intervention period.
There were no group differences in casual BP at rest and daytime or in night-time ambulatory BP at baseline ( Table 2 ). Casual systolic BP decreased (p <0.05) with swimming training ( Figure 1 ) . Casual diastolic BP was decreased by 4 mm Hg but this change did not reach statistical significance. Daytime systolic BP decreased significantly with the swimming training intervention, whereas night-time BP did not change. There were no significant changes in any casual and ambulatory BP values in the attention control group.
| Variable | Attention Control | Swimming Training | ||
|---|---|---|---|---|
| Before | After | Before | After | |
| (n = 19) | (n = 19) | (n = 24) | (n = 24) | |
| Casual blood pressure | ||||
| Systolic blood pressure (mm Hg) | 129 ± 4 | 129 ± 4 | 131 ± 3 | 122 ± 4 ⁎ |
| Mean blood pressure (mm Hg) | 96 ± 3 | 96 ± 3 | 97 ± 2 | 90 ± 3 |
| Diastolic blood pressure (mm Hg) | 76 ± 2 | 75 ± 2 | 76 ± 2 | 72 ± 2 |
| Pulse pressure (mm Hg) | 53 ± 3 | 54 ± 1 | 55 ± 2 | 51 ± 2 |
| 24-Hour ambulatory blood pressure | ||||
| Daytime systolic blood pressure (mm Hg) | 132 ± 8 | 129 ± 5 | 128 ± 5 | 119 ± 2 ⁎ |
| Daytime mean blood pressure (mm Hg) | 98 ± 4 | 95 ± 2 | 95 ± 3 | 89 ± 2 |
| Daytime diastolic blood pressure (mm Hg) | 79 ± 3 | 80 ± 2 | 78 ± 3 | 73 ± 2 |
| Daytime pulse pressure (mm Hg) | 49 ± 6 | 49 ± 4 | 50 ± 3 | 46 ± 2 |
| Night-time systolic blood pressure (mm Hg) | 110 ± 3 | 108 ± 4 | 109 ± 4 | 104 ± 3 |
| Night-time mean blood pressure (mm Hg) | 82 ± 2 | 78 ± 4 | 81 ± 3 | 78 ± 2 |
| Night-time diastolic blood pressure (mm Hg) | 65 ± 2 | 63 ± 2 | 65 ± 2 | 62 ± 2 |
| Night-time pulse pressure (mm Hg) | 45 ± 7 | 45 ± 4 | 45 ± 3 | 43 ± 3 |
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