There is an increase in pulse pressure as a result of the increased cardiac filling and decreased heart rate during thermoneutral or cooler immersion [10,11].
Central blood volume increases by approximately 0.7 L during immersion to the neck, a 60% increase in central volume, with one-third of this volume taken up by the heart and the remainder by the great vessels of the lungs .
Cardiac volume increases 27%–30% with immersion to the neck . Stroke volume increases as a result of this increased stretch. Although normal resting stroke volume is about 71 mL/beat, the additional 25 mL resulting from immersion equals about 100 mL, which is close to the exercise maximum for a sedentary deconditioned individual on land and produces both an increase in end-diastolic volume and a decrease in end-systolic volume .
Mean stroke volume thus increases 35% on average during neck depth immersion even at rest. As cardiac filling and stroke volume increase with progress in immersion depth from symphysis to xiphoid, the heart rate typically drops and typically at average pool temperatures the rate lowers by 12%–15% [14,15].
This drop is variable, with the amount of decrease dependent on water temperature. In warm water, heart rate generally rises significantly, contributing to yet a further rise in cardiac output at high temperatures [16,17].
During aquatic treadmill running, oxygen consumption (VO2) is 3 times greater at a given speed of ambulation (53 m/min) in water than on land, thus a training effect may be achieved at a significantly slower speed than on land [18-20].
The relationship of heart rate to VO2 during water exercise parallels that of land-based exercise, though water heart rate averages 10 beats/min less, for reasons discussed elsewhere . Metabolic intensity in water, as on land, may be predicted from monitoring heart rate.
Cardiac output increases by about 1,500 mL/min during clavicle depth immersion, of which 50% is directed to increased muscle blood flow . Because immersion to this depth produces a cardiac stroke volume of about 100 mL/ beat, a resting pulse of 86 beats/min produces a cardiac output of 8.6 L/min and is already producing an increased cardiac workload. The increase in cardiac output appears to be somewhat age-dependent, with younger subjects demonstrating greater increases (up 59%) than older subjects (up only 22%) and is also highly temperature-dependent, varying directly with temperature increase, from 30% at 33°C to 121% at 39°C [17,21].
During immersion to the neck, decreased sympathetic vasoconstriction reduces both peripheral venous tone and systemic vascular resistance by 30% at thermoneutral temperatures, dropping during the first hour of immersion and lasting for a period of hours thereafter . This decreases end-diastolic pressures. Systolic blood pressure increases with increasing workload, but generally is approximately 20% less in water than on land .
Most studies show either no change in mean blood pressure or a drop in pressures during immersion in normal pool temperatures. Sodium-sensitive hypertensive patients have been noted to show even greater drops (–18 to –20 mm Hg) than normotensive patients, and sodium-insensitive patients smaller drops (–5 to –14 mm Hg) .
Based on a substantial body of research, aquatic therapy in pool temperatures between 31°– 38°C appears to be a safe and potentially therapeutic environment for both normotensive and hypertensive patients, in contrast to widespread belief as manifested by public signage. Recent research has generally supported the use of aquatic environments in cardiovascular rehabilitation after infarct and ischemic cardiomyopathy.
Japanese investigators studied patients with severe congestive heart failure (mean ejection fractions 25 ± 9%), under the hypothesis that in this clinical problem, the essential pathology was the inability of the heart to overcome peripheral vascular resistance. They reasoned that because exposure to a warm environment causes peripheral vasodilatation, a reduction in vascular resistance and cardiac after load might be therapeutic. During a series of studies, these researchers found that during a single 10-min immersion in a hot water bath (41°C), both pulmonary wedge pressure and right atrial pressure dropped by 25%, whereas cardiac output and stroke volume both increased [23,24]. In a subsequent study of patients using warm water immersion or sauna bath one to 2 times per day, 5 days per week for 4 weeks, they found improvement in ejection fractions of nearly 30% accompanied by reduction in left ventricular end-diastolic dimension, along with subjective improvement in quality of life, sleep quality, and general well-being .
Studies of elderly individuals with systolic congestive heart failure during warm water immersion found that most such individuals demonstrated an increase in cardiac output and ejection fractions during immersion [26,27].
Caution is prudent when working with individuals with severe valvular insufficiency, because cardiac enlargement may mechanically worsen this problem during full immersion.
Swiss researchers have studied individuals with more severe heart failure and concluded that aquatic therapy also is probably not safe for individuals with very severe or uncontrolled failure, or very recent myocardial infarction [28-30].
That said, a recent summary of published research in this areas has concluded that aquatic and thermal therapies may be a very useful rehabilitative technique in individuals with mild to moderate heart failure . It is entirely reasonable however to conclude that uncompensated congestive failure or very recent myocardial infarction should be a contraindication to aquatic therapy, to hot tub exposure and perhaps even to deep bathing. Programs typically used include aerobic exercise at light to moderate levels in a neutral temperature environment. See the clinical decision-making algorithm by Bücking and colleagues .
More on Aquatic Therapy Applications in Rehabilitation
-  Lowman CL. Technique of Underwater Gymnastics: A Study in Practical Application. Los Angeles: American Publications; 1937.
-  Arborelius M, Jr., Balldin UI, Lilja B, Lundgren CE. Hemodynamic changes in man during immersion with the head above water. Aerosp Med 1972;43:592-598.
-  Gabrielsen A, Johansen LB, Norsk P. Central cardiovascular pressures during graded water immersion in humans. J Appl Physiol 1993;75: 581-585.
-  Gabrielsen A, Warberg J, Christensen NJ, et al. Arterial pulse pressure and vasopressin release during graded water immersion in humans. Am J Physiol Regul Integr Comp Physiol 2000;278:R1583-R1588.
-  Risch WD, Koubenec HJ, Gauer OH, Lange S. Time course of cardiac distension with rapid immersion in a thermo- neutral bath. Pflugers Arch 1978;374:119-120.
-  Schlant RC, Sonnenblick EH. Normal physiology of the cardiovascular system. In: Hurst J, ed. The Heart. 6th ed. New York: McGraw-Hill; 1986:51.
-  Risch WD, Koubenec HJ, Beckmann U, Lange S, Gauer OH. The effect of graded immersion on heart volume, central venous pressure, pulmonary blood distribution, and heart rate in man. Pflugers Arch 1978;374:115-118.
-  Haffor AS, Mohler JG, Harrison AC. Effects of water immersion on cardiac output of lean and fat male subjects at rest and during exercise. Aviation Space Environ Med 1991;62:123-127.
-  Dressendorfer RH, Morlock JF, Baker DG, Hong SK. Effects of head out water immersion on cardiorespiratory responses to maximal cycling exercise. Undersea Biomed Res 1976;3:177-187.
-  Weston CF, O’Hare JP, Evans JM, Corrall RJ. Haemodynamic changes in man during immersion in water at different temperatures. Clin Sci 1987;73:613-616.
-  Gleim GW, Nicholas JA. Metabolic costs and heart rate responses to treadmill walking in water at different depths and temperatures. Am J Sports Med 1989;17:248-252.
-  Evans BW, Cureton KJ, Purvis JW. Metabolic and circulatory responses to walking and jogging in water. Res Q 1978;49:442-449.
-  Tajima F, Sagawa S, Iwamoto J, Miki K, Claybaugh JR, Shiraki K. Renal and endocrine responses in the elderly during head-out water immersion. Am J Physiol 1988;254:R977-R983.
-  Coruzzi P, Biggi A, Musiari L, Ravanetti C, Novarini A. Renin-aldosterone system suppression during water immersion in renovascular hypertension. Clin Sci (Colch) 1985;68:609-612.
-  Tei C, Horikiri Y, Park JC, et al. Acute hemodynamic improvement by thermal vasodilation in congestive heart failure. Circulation 1995;91: 2582-2590.
-  Tei C, Tanaka N. Thermal vasodilation as a treatment of congestive heart failure: A novel approach. J Cardiol 1996;27:29-30.
-  Tei C, Tanaka N. Comprehensive therapy for congestive heart failure: A novel approach incorporating thermal vasodilation. Intern Med 1996;35:67-69.
-  Cider A, Sunnerhagen KS, Schaufelberger M, Andersson B. Cardiorespiratory effects of warm water immersion in elderly patients with chronic heart failure. Clin Physiol Funct Imaging 2005;25:313-317.
-  Cider A, Svealv BG, Tang MS, Schaufelberger M, Andersson B. Immersion in warm water induces improvement in cardiac function in patients with chronic heart failure. Eur J Heart Fail 2006;8:308-313.
-  Meyer K. Left ventricular dysfunction and chronic heart failure: Should aqua therapy and swimming be allowed? Br J Sports Med 2006;40:817-818.
-  Meyer K, Leblanc MC. Aquatic therapies in patients with compromised left ventricular function and heart failure. Clin Invest Med 2008;31:E90-E97.
-  Mussivand T, Alshaer H, Haddad H, et al. Thermal therapy: A viable adjunct in the treatment of heart failure? Congest Heart Failure (Greenwich, Conn) 2008;14:180-186.