Methods

Patients

We examined 30 male subjects: 10 patients with stable CHF, 10 patients with CAD and preserved left ventricular function, and 10 healthy controls (table 1​1).). Patients with heart failure included eight patients with ischaemic heart disease and two patients with idiopathic dilated cardiomyopathy. All patients were taking β‐blockers, whereas the controls were taking no drugs. Patients had to be swimmers and in a stable clinical condition. They were informed about the study procedure and written informed consent was obtained from them. The study protocol was reviewed and accepted by the local ethical committee.

Table 1 Characteristics of the study population

Results

Heart rate

During stepwise water immersion up to the pelvis and chest, heart rate decreased from 69 (11) to 64 (9) beats/min in patients with CHF, from 74 (10) to 66 (10) beats/min in patients with CAD with preserved ventricular function, and from 82 (10) to 74 (14) beats/min in controls (fig 1​1).). During swimming, heart rate increased to 93 (14) beats/min, 93 (16) beats/min and 97 (23) beats/min in patients with CHF, patients with CAD and controls, respectively. Compared with controls and patients with CAD, the decrease in heart rate during water immersion was proportionally lower in patients with CHF, whereas the rate response during water gymnastics and swimming paralleled the other two groups.

Figure 1  Haemodynamic adaptation to water immersion, water gymnastics and swimming in patients with stable chronic heart failure (CHF), patients with coronary artery disease (CAD) with preserved left ventricular systolic function and healthy controls ...

Stroke volume

Water immersion up to the chest led to an increase in stroke volume of 30% in normal subjects and of 41% in the patients with CAD (fig 1​1).). In patients with CHF, stroke volume increased by 17%. During swimming, stroke volume was increased further by 47% in controls, by 30% in patients with CAD and by 35% in patients with CHF. Changes in stroke volume showed a positive correlation with peak V̇o₂ achieved during a maximal cardiopulmonary exercise test (r = 0.57; p = 0.006; fig 2​2).

Figure 2 Relationship between peak oxygen uptake V̇o₂ during maximal cardiopulmonary exercise test and change (▵) in stroke volume between rest and swimming.

Cardiac index

Water immersion up to the chest increased cardiac index by 19% in controls, by 21% in patients with CAD and by 16% in patients with CHF (fig 3​3).). During exercise, cardiac index increased further by 87% in controls, by 77% in patients with CAD and by 53% in patients with CHF. Figure 4​4 shows the individual responses of the patients with heart failure. Although cardiac index decreased in two patients during water immersion up to the chest, all patients were able to increase cardiac output during swimming.

Figure 3  Adaptation of cardiac index and oxygen consumption to water immersion, water gymnastics and swimming in patients with stable chronic heart failure (CHF), in patients with coronary artery disease (CAD) with preserved left ventricular systolic ...

Figure 4  Individual haemodynamic response to water immersion (A) and swimming (B) in patients with heart failure (n = 10). ***p<0.001.

Discussion

During head‐out water immersion, intrathoracic blood volume increases. The reason for this volume shift from the periphery to the central organs is an increase of venous return as a consequence of the effect of hydrostatic pressure on the capacitance vessels, supported by a diminution of gravity dependency of the lower body.

To compensate for decreased myocardial contractility and to maintain an adequate cardiac output in patients with heart failure, the left ventricular end‐diastolic volume increases according to the Frank–Starling mechanism. Furthermore, increased diastolic distensibility leads to increased end‐diastolic volume tolerance in order to avoid end‐diastolic pressure rise, which could lead to pulmonary oedema. Volume shifts, as they occur during water immersion, might potentially overstrain these compensatory mechanisms and as a consequence lead to a decrease in stroke volume, a further rise in the end‐diastolic pressure and the occurrence of pulmonary congestion.

In our study, the cardiac response to water immersion up to the chest was characterised by a decrease in heart rate, an increase in stroke volume, no change in systolic blood pressure but a slight decrease in diastolic blood pressure and a reduction in peripheral vascular resistance (fig 1​1).

The observed response is the result of the following reflex mechanisms, all interfering with each other: a raise in atrial pressure due to the increase in venous return would lead to an increase in heart rate to evacuate the higher circulating volume (Bainbridge reflex). On the other hand, the rise in right atrial pressure and the increase in the circulating volume also initiates the Frank–Starling mechanism, which increases stroke volume and systolic blood pressure. The rise in blood pressure on his part activates the arterial baroreceptor control system located in the wall of the internal carotid arteries, the carotid sinus and the aortic arch. This leads finally, through excitation of the vagal centre, to a decrease in heart rate and venous and arteriolar tone over‐ruling, therefore the Bainbridge reflex.

The patients with heart failure were characterised by the lowest heart rate, stroke volume and blood pressure but the highest peripheral vascular resistance of the three groups. The picture of the haemodynamic response, nevertheless, was similar in all three groups, which means that also in the population with heart failure, the reflex mechanisms were still intact. Despite their severely reduced left ventricular function with a peak V̇o₂ between 15.4 and 24.1 ml/kg/min, they tolerated water immersion, gymnastics and swimming clinically well. Although stroke volume decreased in 4/10 patients and cardiac index decreased in 2/10 patients during water immersion, all patients were able to increase cardiac index during exercise (fig 4​4).

After a 60 s swim in a pool at 32°C, we found a mean V̇o₂ of 9.7 ml/kg/min in patients with heart failure, 12.4 ml/kg/min in patients with CAD with preserved left ventricular function and 13.9 ml/kg/min in controls (fig 3​3).). The differences in V̇o₂ between controls and patients with cardiac problems, for the same physical activity, might result from a slightly different swimming speed and technique or, more likely, from differences in the ΔV̇o₂/Δwatt relationship during exercise (CHF, 8.1 (1.5); CAD, 9.2 (0.4); healthy, 10.0 (0.6); table 1​1),), reflecting a reduced central haemodynamic response to exercise in patients with impaired left ventricular ejection fraction and/or condition after myocardial infarction.

Left ventricular function at rest is a poor predictor of exercise capacity.^12,13 When it comes to recommendations for water sports in patients with heart failure, parameters of exercise capacity rather than echocardiographic measures seem therefore to be of particular importance. Water aerobics, water callisthenics and swimming correspond to a metabolic equivalent (MET) intensity level of 4 or a V̇o₂ of 14 ml/kg/min (1 MET = 3.5 ml/kg/min).¹⁴ The oxygen uptake at the anaerobic threshold in our study was 13.5 (3.2), 19.6 (6.2) and 26.4 (6.7) ml/kg/min for the patients with CHF, CAD and controls, respectively. This shows that swimming in the tested conditions (with a mean V̇o₂ of 9.7 (3.3), 12.4 (3.5) and 13.9 (4.0) ml/kg/min in the patients with CHF, CAD and controls, respectively) corresponds to an intensity level below the anaerobic threshold, even in patients with heart failure.

As V̇o₂ is proportional to stroke volume, peak V̇o₂ can be used to appreciate the behaviour of the stroke volume during water immersion and swimming (fig 4​4).). Thus, in a stable clinical condition, a minimal peak V̇o₂ of at least 15 ml/kg/min and an anaerobic threshold >10 ml/kg/min characterises patients who can participate in water sports in the described conditions without the risk of cardiac decompensation. In patients with a peak V̇o₂ of <15 ml/kg/min or a ΔV̇o₂/Δwatt relationship clearly <8, however, caution has to be raised.

To what extent parameters of cardiopulmonary exercise obtained on land can be compared with exercise in water has been investigated in various studies.^2,15,16 In controls, the central shift of blood volume with head‐out water immersion results in a higher stroke volume at rest and during graded intensities of exercise, compared with values on land in the same posture and at the same metabolic rate.¹⁵ Despite an increased stroke volume in water, there is no proportional decrease in heart rate, at least at submaximal exercise levels, and therefore cardiac output is higher in water. Similarly, mean right atrial and pulmonary arterial pressures were found to remain increased, indicating that preload remains increased during graded exercise up to maximal effort in water.²

In patients with cardiac problems, Hanna et al¹⁶ compared the effect of increased preload during head‐out water immersion on exercise response in men with healed myocardial infarction without signs of congestive heart failure and with an exercise capacity of at least 5 MET. At rest, cardiac output and stroke volume increased during water immersion, whereas heart rate did not change. During exercise, contrary to the studies conducted on healthy individuals,^3,15 these patients did not show a shift of the cardiac output–V̇o₂ curve to the left, which means that cardiac output was not increased in water compared with land‐based exercise. This difference has been explained by a lack of further increase of the stroke volume from rest to exercise in the patient group. This might have been the consequence of a more intense adaptation using the Frank–Starling mechanism to maintain cardiac output during land‐based exercise in patients after myocardial infarction and a rapid exhaustion of this compensatory mechanism in water. Furthermore, controls and patients after myocardial infarction showed a different heart rate response to exercise. In healthy people, heart rate response to exercise on land and in water are similar up to a work load of 40% of peak V̇o₂, but becomes lower at higher work loads in water. By contrast, subjects with a healed myocardial infarction had the same average heart rate in water and at land at all work loads examined up to 75% of peak V̇o₂. It can be concluded that in controls, the haemodynamic response to exercise in water is mainly determined by mechanisms including preload and stroke volume, whereas in patients with a reduced ejection fraction, cardiac output is regulated predominantly by changes in heart rate.

In practice, two important points can be deduced from this fact. (1) Chronotropic response during an exercise stress test is a key parameter in the evaluation of water immersion tolerance in patients with heart failure. In our cohort, mean heart rate increased by 24 beats/min. By generalising these data, one can state that an increase in heart rate during submaximal exercise (eg, up to the anaerobic threshold) of this dimension would be a prerequisite for safe water immersion. (2) The data from Sheldahl et al¹⁵ and Christie et al² show that healthy subjects have a similar heart rate response to exercise on land and in water up to 60% of peak V̇o₂ but a somewhat lower heart rate in water at higher work loads with a difference of approximately 10 beats/min. In patients after a myocardial infarction no difference in heart rate response to exercise on land and at all work loads examined in water (up to 75% of peak V̇o₂) was found.¹⁶ Therefore, there is no need for adaptation of the training heart rate for exercise on land or in water at intensities <60% of peak V̇o₂, especially in patients with reduced left ventricular function.

Distention of the peripheral vessels by thermoneutral water results in several salutary effects, which may be particularly beneficial for patients with heart failure: systemic vascular resistance decreases, whereas arginine, vasopressin, renin and norepinephrine are suppressed.¹⁷ Activation of cardiac mechanoreceptors leads to reflex adjustments of water and electrolyte excretions from the kidney,¹⁸ a mechanism that is preserved in patients with heart failure. Gabrielsen et al⁸ also showed that intravascular and central blood volume expansion in compensated heart failure suppresses the activity of the renin–angiotensin–aldosterone system, increases the release of atrial natriuretic peptide and elicits a natriuresis, which is enhanced when angiotensin II and aldosterone concentrations are suppressed by ACE inhibitor treatment. It can be concluded that water immersion elicits a number of physiological reactions that are similar to those achieved by modern pharmacological treatment. While the impact on the renin–angiotensin–aldosterone system is of rather short duration, patients with difficulties in regulating their fluid status could particularly profit from the enhancement of natriuresis and therefore be ideal candidates for regular treatment in water.

Recently, the effect of 8 weeks of hydrotherapy in 25 elderly (72 (6) years), stable patients with CHF has been reported.¹⁹ These patients with a New York Heart Association (NYHA) functional class II to III and with an exercise capacity that was markedly lower than in our patient group (V̇o₂ 14.3 (2.7) vs 18.8 ml/kg/min) were randomised either to 8 weeks of hydrotherapy with three weekly sessions of 45 min (n = 15) or to a control group (n = 10). Hydrotherapy yielded improvements in exercise capacity and was well tolerated without any adverse events, suggesting that such a treatment can be safely offered to patients with CHF. These results are now supported by our haemodynamic studies and should therefore stimulate a paradigm shift in the recommendations of water gymnastics or swimming in thermoneutral water in patients with stable CHF and an NYHA functional class I to II.

Conclusion

Stable clinical conditions and a minimal peak V̇o₂ of at least 15 ml/kg/min with an anaerobic threshold >10 ml/kg/min during a symptom‐limited exercise stress test characterise patients with severely reduced ejection fraction who can safely participate in water sports in thermoneutral water. Although cardiac index and V̇o₂ are lower in these patients compared with patients with CAD and preserved left ventricular function and controls, such patients are able to adequately increase cardiac index during water gymnastics and swimming in thermoneutral water.

In general practice, the ability of a patient to exercise safely on a cycle ergometer with a workload of 70 W (corresponding to 4 METs) or 110 W (corresponding to 6 METs) is a good indicator that water gymnastics and swimming in thermoneutral water are safe even in the presence of stable CHF. However, an inadequate chronotropic response to exercise might denote patients with impaired tolerance to water sports, given the fact that in patients with a reduced ejection fraction, cardiac output during water immersion and swimming is regulated predominantly by the heart rate.

Abbreviations