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Human Physiology in an Aquatic Environment

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 Human Physiology in an Aquatic Environment
David R. Pendergast,*1,2 Richard E. Moon,3 John J. Krasney,2 Heather E. Held,4 and Paola Zamparo5

ABSTRACT
Water covers over 70% of the earth, has varying depths and temperatures and contains much
of the earth’s resources. Head-out water immersion (HOWI) or submersion at various depths (div-
ing) in water of thermoneutral (TN) temperature elicits profound cardiorespiratory, endocrine, and
renal responses. The translocation of blood into the thorax and elevation of plasma volume by
autotransfusion of fluid from cells to the vascular compartment lead to increased cardiac stroke
volume and output and there is a hyperperfusion of some tissues. Pulmonary artery and capillary
hydrostatic pressures increase causing a decline in vital capacity with the potential for pulmonary
edema. Atrial stretch and increased arterial pressure cause reflex autonomic responses which re-
sult in endocrine changes that return plasma volume and arterial pressure to preimmersion levels.
Plasma volume is regulated via a reflex diuresis and natriuresis. Hydrostatic pressure also leads
to elastic loading of the chest, increasing work of breathing, energy cost, and thus blood flow to
respiratory muscles. Decreases in water temperature in HOWI do not affect the cardiac output
compared to TN; however, they influence heart rate and the distribution of muscle and fat blood
flow. The reduced muscle blood flow results in a reduced maximal oxygen consumption. The prop-
erties of water determine the mechanical load and the physiological responses during exercise
in water (e.g. swimming and water based activities). Increased hydrostatic pressure caused by
submersion does not affect stroke volume; however, progressive bradycardia decreases cardiac
output. During submersion, compressed gas must be breathed which introduces the potential for
oxygen toxicity, narcosis due to nitrogen, and tissue and vascular gas bubbles during decompres-
sion and after may cause pain in joints and the nervous system. © 2015 American Physiological
Society. Compr Physiol 5:1705-1750, 2015.

Introduction HOWI in thermoneutral (TN) water (34 or 35◦ C for 3-

Water covers ∼70% of earth’s surface. The aquatic environ-
ment is unique. While it is an environment with spectacular
flora and fauna, geology, and vast resources, the physical char-
acteristics of water impose profound physiological stresses on
humans and animals. The underwater world is far less under-
stood than space or high altitude where extensive exploration
has been carried out for many years. This review offers an
overview of how the major environmental challenges, that
is, increased hydrostatic pressure, cold or warm water tem-
peratures, the unbreathable ambient medium and pressure of
the “Silent World” affect breathing, circulation, fluid and
electrolyte balance, locomotion, and thermal regulation in
humans. In addition, the effects of the depth and time of div-
ing can cause deleterious pharmacological and toxic effects.
6 h) results in a translocation of blood from the depen-
dent limbs to the chest, as well as increased plasma vol-
ume (PV) due to transcapillary autotransfusion of fluid from
the cells (201, 204). These responses augment intrathoracic
blood volume (11, 109, 203) which in turn increases cardiac
end-diastolic volume, stroke volume (SV) and cardiac output
(CO) due to increased end-diastolic cardiac fiber length (237).
Atrial stretch and elevated arterial pulse pressure (PP) elicit
baroreflex neuroendocrine responses that increase urine flow.
* Correspondence to dpenderg@buffalo.edu
1 Center for Research and Education in Special Environments,
University at Buffalo, Buffalo, New York, USA
2 Department of Physiology and Biophysics, University at Buffalo,

As humans are terrestrial, exposure to the aquatic envi-
ronment is often viewed negatively and being problematic for
man. While this is partly true, it must be emphasized that life
evolved in the oceans and aquatic organisms leaving the seas
had to adapt to new terrestrial habitats. Coming out of the sea
required profound circulatory and musculoskeletal adapta-
tions to gravity, marked alterations in the capacity to maintain
fluid and electrolyte balance and of course a switch to lung
versus gill respiration. Failure to maintain homeostasis in the
aquatic environment can result in injury or death.
Buffalo, New York, USA
3 Center for Hyperbaric Medicine and Environmental Physiology,
Duke University, Durham, North Carolina, USA
4 Biomedical Hyperbarics Research Laboratory, Molecular
Pharmacology and Physiology, College of Medicine, University of
South Florida, Tampa, Florida, USA
5 Department of Neurological and Movement Sciences, University of
Verona, Verona, Italy
Published online, October 2015 (comprehensivephysiology.com)
DOI: 10.1002/cphy.c140018
Copyright © American Physiological Society.

Volume 5, October 2015 1705

The Aquatic Environment
Autotransfusion may persist for as long as 24 h (depending
on the level of volume repletion).
As the baseline characteristics of cardio-renal regulation
are altered compared to terrestrial exercise, the CO, SV, and
blood flow to nonmuscle tissues are greater, and HR and total
peripheral resistance (TPR) are lower. However, mean arterial
blood pressure (MAP) responses are similar to those observed
in air (297). In spite of this different baseline cardiovascular
and renal status in water, increased metabolism during exer-
cise results in similar adjustments in TN water and air, at
oxygen consumption (VO2 ) above 1.0 L min−1 , and as high
as 80% of maximal aerobic power (VO2 max ) (297, 309). The
potential for pulmonary edema increases during exercise in
water (352), particularly in cold water (196).
Breath-holding for a short time is possible for air breath-
ing mammals, including man. For longer submersions, the
diver has to use pressure compensating equipment to provide
free access to suitable gas. At shallow depths, a snorkel can be
used; however, its effective depth is limited to just under the
surface due to the inability of the respiratory muscles to over-
come the hydrostatic pressure on the chest wall and of course
water entering the snorkel (23). At greater depths, gear called
Self-Contained Underwater Breathing Apparatus (SCUBA),
or a closed-circuit rebreathing system [using special gas mix-
tures or pure oxygen (O2 ) in combination with a carbon diox-
ide (CO2 ) scrubber] control gas flow from a high pressure
tank via a regulator (172). Breathing underwater is also influ-
enced by the depth-induced hydrostatic pressure differences
across the chest wall (static lung loading, SLL) (368), gas
density and composition, and by exercise hyperpnoea, which
in combination cause increased power of breathing (POB) and
fatigue of the respiratory muscles (14, 321, 322, 425).
Alveolar ventilation in normal conditions is regulated to
maintain arterial PCO2 (PaCO2 ) at ∼40 mmHg with little
variation in normal healthy subjects (167), while matching
O2 delivery to metabolic demands. The translocation of blood
from the periphery to the chest in HOWI results in reduction
in air in the lungs, and thus alters ventilation both at rest and
during exercise. In addition, diving may promote hypercap-
nia (CO2 retention) due to a routine practice by divers of
hypoventilating to conserve gas and extend dive time and/or
the increased respiratory work which cannot be performed
due to weak or fatigued respiratory muscles.
When compared to altitude, hypoxia is not an issue in the
aquatic environment as at the surface air is breathed and during
submersion breathing with SCUBA gear increases total pres-
sure and also increases PO2 . However, hyperoxia can damage
pulmonary (25, 76) and neural (84) tissues. Human adap-
tive responses to hyperoxia appear limited since man is not
normally exposed to high ambient PO2 . In addition to O2 ,
pressures of other gases such as N2 may be increased during
submersion at depth such that the gas is absorbed by tissue
compression to the point of saturation; the unloading of which
during decompression imposes further stress on the diver.
Most swimming and diving occurs where water is colder
than the temperature to which subjects can adjust for long
1706
Comprehensive Physiology
periods (TN = 35◦ at rest and 28-30◦ C during exercise), and,
as water has high thermal conductance and capacity, there is
danger of hypothermia when diving in these waters without
adequate thermal protective gear. HOWI or diving in cold
water temperatures below TN results in greater translocation
of blood into the chest relative to the increase in TN immer-
sion and reductions in intracellular fluid, although there is less
autotransfusion and PV is not increased as much (358) such
that there is a similar increase in CO in both cold and TN
immersion (297). Although there is increased sympathetic
activity, arterial blood pressure is not increased in HOWI
in cold water as the skin, subcutaneous tissues, and muscle
reduced blood flow and increased resistances are likely off-
set by increased blood flow in other areas and TPR remains
unchanged (297). The effects of HOWI in warmer or hot
water, particularly during exercise, are not extensively inves-
tigated and present great challenges to adjustment.
Due to body size and physiological differences there
may be gender differences in the responses to HOWI in TN
(408), cold, and warm water. Age may also affect physio-
logical responses to HOWI, as the increase in CO reported
for younger subjects in HOWI is not as great in older sub-
jects (302). In addition, there may be different physiological
responses to body cooling or warming in the elderly, specifi-
cally regulation of metabolism and vascular control (147).
The stresses and strains resulting from the aquatic envi-
ronment may pose dangers to humans’ exposure to them. On
the other hand, HOWI has potential therapeutic benefits and
this area requires further exploration. The wide variety of
aquatic environments will be further developed in the sec-
tions below. The understanding of the aquatic environment
starts with its physical properties. HOWI is not only a com-
mon aquatic environment, but also a tool to understanding the
interactions between the cardio-renal systems and thus is a
major part of this paper. As most of the waters of the world
are relatively cold, its effect on physiological systems has to
be explored. The aquatic environment involves being on the
water in a water craft, at the water’s surface swimming, as well
as being submersed in the water during diving. Each of these
different aquatic environments has specific requirements.
Physical Properties of Water
The properties of the aquatic environment (69) both individu-
ally and collectively impose critical challenges to physiologi-
cal adjustment. Some of these challenges cannot be compen-
sated for physiologically, and thus devices or equipment have
to be used for humans to function in the aquatic environment.
Density
The density of water is about 1 g cm−3 ; however, it is also
influenced by temperature (69). The density of liquid water
increases with temperature and maximal density is at approx-
imately 4◦ C (39◦ F), which is the water temperature of arctic
water. In addition, there are thermoclines in water, the colder
Volume 5, October 2015
Comprehensive Physiology
the temperature the deeper the water. In fresh water at 4◦ C, the
water closer to the surface and cold air lose heat energy such
that the water at the surface is less than 4◦ C. These thermo-
clines in water have an impact on thermal stress in humans.
Floating in water is made possible because of the den-
sity of water (69). Density of water is also dependent on the
salt content which is high in some bodies of water. However,
the high density of water reduces the ability to function in
water, i.e. there is an increase in the energy cost of locomo-
tion. Dynamic viscosity determines how easily bodies move
through water. Dynamic viscosity divided by density is kine-
matic viscosity. It is easier to float in saltwater as it is denser
than fresh water. It costs less energy to swim in warm water
even though it is harder to float. The body is about 75%
water, but body fat contains less than 75% water so humans
with higher fat may float better and have greater resistance to
heat loss.
Compressibility of water is influenced by both pres-
sure and temperature (69) and impacts performance in the
aquatic environment. Water compressibility ranges from
5.1 × 10−10 to 4.4×10−10 Pa−1 and is dependent on water
temperature (0-45◦ C, respectively). The low compressibility
of water often leads to the erroneous conclusion that water is
incompressible.
Pressure
Sea level pressure is 1 atmosphere absolute (ATA) and ambi-
ent pressure increases by 1 ATA for every additional 10 m of
depth. Air in gas-containing spaces contributes to buoyancy in
water, however since air is compressed with increasing depths
of submersion, buoyancy decreases as depth increases. Gas-
containing spaces in the body are compressed underwater, and
then the volume reexpands when returning to the surface. On
returning to the surface from submersion the increase in vol-
ume may cause problems in air-containing tissues/organs, par-
ticularly during uncontrolled ascents. Other pressure-related
effects during diving include the concomitant increase in gas
partial pressures (e.g., O2 and N2 ), and the higher breathing
gas density.
At depths beyond 100-150 m, there are effects of pres-
sure per se, which include tremors and “microsleep.” This is
termed the high pressure nervous syndrome (HPNS) (22).
Convulsions have been observed in monkeys (22). Other
effects include partial reversal of sedation or general anes-
thesia (382, 383). It is believed that these phenomena occur
due to pressure-related changes in macromolecule conforma-
tion and altered neurotransmitter release (331). Narcotic gases
such as nitrogen can partially offset the effects of HPNS (24).
Heat capacity
The specific heat capacity of water is high (pure liquid water =
4.182 J K−1 g−1 ) and conducts heat effectively based on
temperature gradients (69). The high heat capacity and high
heat conductivity of water can have significant influences on
Volume 5, October 2015
The Aquatic Environment
human function in the aquatic environment. Water is in liq-
uid form at normal temperatures, and holds 80% to 90% of
the earth’s heat. Water has the capacity to cool the human
body nominally 20 times greater than air. Therefore, hypother-
mia or hyperthermia are significant risks in cold and warm
water, respectively. Although the effects of cold water are
most common and well-studied, exposure to warm/hot water
(hyperthermia) is understudied.
Head-Out Water Immersion in
Thermoneutral Water
Humans can be in the aquatic environment either immersed
with the HOWI or head in the water (swimming) or sub-
mersed underwater at various depths (diving). Body posture
during immersion is significant. One may be immersed either
in the head-out vertical posture or supine in the water so that
the profile of external hydrostatic pressure forces on depen-
dent regions differs between vertical and supine. Erect HOWI
has been used as a simple, noninvasive maneuver to increase
central blood volume and has provided useful insights into
the regulation of blood volume. Increased body buoyancy
in HOWI minimizes the influence of gravity and therefore
HOWI has provided important insights into the physiology
of microgravity. In addition to its utility for understanding
effects of microgravity and volume regulation, HOWI is an
obvious useful tool for the study of the physiology of the
aquatic environment. Lastly, HOWI can be a useful nonphar-
macological therapeutic modality for the treatment of fluid
retention disorders. An overview of the physiological status
during immersion is shown in Figure 1, and will be described
in the section on immersion below.
As stated above, since there is a hydrostatic pressure gra-
dient acting upon the body surface, an erect versus supine
posture in water influences the character of the physiological
responses as shown in Figure 2. In this article, the focus will
be primarily upon upright HOWI, unless noted otherwise. In
addition, the TN temperature for humans is considered to be
34 to 35◦ C for water immersions of 3 to 6 h and we will first
discuss responses to TN HOWI, followed by a description
of how varying water temperatures influence the basic TN
response. The physiological responses to HOWI are not sim-
ply due to the removal of gravity because during immersion
there is a unique set of stimuli that are not present in true
microgravity.
The overall physiological responses during water immer-
sion appear to be directed toward the homeostatic main-
tenance of central cardiopulmonary blood volume via car-
diopulmonary and arterial baroreflexes. Normally, there is a
tight coupling between oxygen delivery and metabolic rate
via autoregulation of blood flow (151). By contrast, in water
immersion, there appears to be a unique resetting of vascular
autoregulatory control such that the ratio of oxygen delivery
to metabolism increases in the systemic circuit and in some
regional vascular circuits.
1707
The Aquatic Environment Comprehensive Physiology

Head-out immersion:
thermoneutral water

Hydrostatic compression
of immersed tissues

Cell Venous
volume capacity

Autotransfusion,
potassium, amino acids Blood flow/oxygen
shift uptake

Natriuresis
Diuresis Hypervolaemia Venous return Cardiac output

Diuresis
Major effect

Renal Cardiac volume Stroke volume

sympathetic
nerve activity
Activation of
cardiac receptors
Vasopressin Aortic pulse pressure
secretion
Release of atrial
natriuretic peptide
Renin
aldosterone Activation of
secretion arterial baroreceptors

(?)
(?) Redundancy:
Renal atrial
natriuretic Time-dependent effects
peptide Bipeds versus quadrupeds
sensitivity Resetting of reflexes
Hydration state
Physical training
Adaptation

Figure 1 Summary of the circulatory, renal hormonal and neuro responses to thermoneutral HOWI. Central volume expansion and
elevated CO are caused by compression of the dependent veins and autotransfusion. The rise in CO exceeds the metabolic demand
at rest and during exercise. Activation of cardiovascular mechanoreceptors and increased atrial natriuretic peptide secretion sets into
motion neural and hormonal mechanism that promote sodium and fluid loss, thus minimizing hypervolemia and theoretically readjusting
blood flow to the prevailing oxygen uptake. The most powerful efferent mechanism affecting the kidney appears to be sympathetic nerves.
The associated hormonal responses appear to modulate the primary renal response, with many additional factors modulating the basic
renal neurohumoral responses to immersion. Redrawn from Krasney (201) and reproduced with permission from Elsevier Limited, Oxford,
United Kingdom (204).

Circulatory responses and fluid shifts pressure (184). The major role of the kidney in HOWI is to
blunt the expansion of PV and prevent a further increase in PV
Hydrostatic pressure during HOWI translocates blood
(see Fig. 4) and CO as seen in Figure 5 (201,256,257). Early in
to the thorax by compressing the venous compartment.
immersion PV increases about 7% (Fig. 4). There is a signif-
The translocation of blood to the thorax is shown in Figures 2
icant increase in tissue pressure compared to capillary hydro-
and 3 (186). The fluid translocated into the vascular compart-
static pressure promoting capillary reabsorption. Tissue pres-
ment is derived from the intracellular compartment (see Fig.
sure, capillary pressure and central venous pressure (CVP)
2). This autotransfusion into the plasma compartment origi-
are coupled in a linear fashion. Stepwise levels of immersion
nates primarily from the capillaries of the dependent limbs and
from dependent limbs to abdomen, to mid-thorax and to mid-
both expands PV (see Fig. 4) and decreases plasma oncotic
cervical level cause CVP to increase progressively. Plasma

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Comprehensive Physiology The Aquatic Environment

Upright in air Upright water immersion

Right atrial Right atrial

pressure: Aorta pressure: Aorta
0 kPa (mmHg) 2 kPa (15 mmHg)
Cardiac
output

Central
Venous return

Venous return
volume
expansion

Autotransfusion Hydrostatic
Filtration pressure:
16 kPa (120 mmHg)
Venous
compartment Hydrostatic
compression
of dependent
tissues
Systemic hypervolaemia
due to autotransfusion

Figure 2 While standing in air (A), right atrial pressure is low and gravity-dependent veins are distended
resulting in increased net plasma filtration in the limb capillaries. During HOWI (B), central volume expansion
occurs with increased right atrial pressure and cardiac output. These result from hydrostatic compression of
the dependent tissues and capillary reabsorption, or an autotransfusion in the dependent limbs. Redrawn
from Krasney (201) and reproduced with permission from Elsevier Limited, Oxford, United Kingdom (204).

Lymphatic oncotic pressure is decreased in HOWI resulting in hemodi-

lution, whereas plasma osmolarity is unchanged. Amino acids
Plasma Interstitial Intracellular
and potassium are increased in the plasma suggesting that the
Renal
volume fluid fluid majority of the fluid shifted is out of the intracellular compart-
Capillary Cellular ment (83, 201, 358). In spite of this, interstitial fluid volume
Immersion and lymph flow do not change in HOWI. PV, SV, and CO are
elevated and sustained throughout 6 to 12 h immersions com-
pared to erect in air (348). These data support the contention
that the intracellular reservoir of fluid is not diminished sig-
Fluid change (mL·kg–1 · min–1)

0
nificantly during HOWI (185). CO is increased in HOWI and

Rest Water immersion

–0.05 110

105
PV(% Δc)

–0.10

Lymphatic 100
Renal
–0.15 Cellular
95
Capillary

–40 0 40 80 120 0
Time (min) 0 1 2 3 4 5
Time (h)
Figure 3 There are three major fluid shifts that occur during HOWI
(upper flow diagram): across capillary, across the cell wall and across Figure 4 Human plasma volume (PV) expressed as a percentage
the kidney. The lymphatic fluid shift is minor. These compartmental fluid change during HOWI in TN water (35◦ C) (squares) and sitting in
changes are then illustrated (graph) for the 120-min upright, thermoneu- thermoneutral air (22◦ C) (circles) from their respective control values.
tral HOWI. Redrawn from Krasney (201) and reproduced with permis- The ∗ indicate that HOWI values are significantly higher than the air
sion from Elsevier Limited, Oxford, United Kingdom (204). counterparts.

Volume 5, October 2015 1709

The Aquatic Environment
12 Rest Water immersion
11
Q (1 · min–1)
10
9 during HOWI. By comparison there are immediate, although
8
·
7 continues, blood flow to visceral tissues decline to pre-HOWI
6 levels. At this point, the increased CO is redistributed to non-
5
0 1 2 3
Time (h)
Figure 5 Resting cardiac output (Q, L/m) is plotted as a function
of time for humans resting HOWI in TN water (35◦ C) (squares) and
sitting in TN air (22◦ C)(circles). The ∗ indicate that HOWI values are
significantly higher than the air counterparts.
its level is greater for the erect posture, increasing from leg
only immersion to mid-cervical HOWI. The increased CO is
maintained for many hours. CO is increased 32% to 62% dur-
ing HOWI (Fig. 5) due to an increased SV, even though HR is
decreased. The relative increase in SV exceeds the observed
decline of HR such that there is a net increase in CO as
shown in Figure 5. MAP is not effected by HOWI and there-
fore TPR must be decreased (11, 201, 281). VO2 is unchanged
during HOWI in TN water, thus it is apparent that systemic
O2 delivery quickly exceeds systemic O2 demands in HOWI.
Blood flow to specific tissues is autoregulated to meet their
metabolic demands (151); however, it is blunted in HOWI as
shown in Figure 6 for limb blood flow. The expected autoregu-
latory readjustment of systemic blood flows to match tissue O2
demands does not occur in HOWI but rather sustained hyper-
emia occurs in some tissues (see Fig. 6) (59, 154, 297). Blood
flows to respiratory muscles and cardiac muscle increase as
expected in response to their increased metabolism, secondary
to increased respiratory and cardiac work (154). HOWI-
induced changes in vestibular and proprioceptive inputs
caused by buoyancy-microgravity result in hyperemia of
6 Rest Water immersion
LBF (ml · min–1 · cm–1)
5 increase (314). The overall effect of immersion on ventilation-
4 perfusion (VA /Q) relationships depends on the relationship of
3
2 relationships are preserved. Arterial PO2 is usually increased
1
0 older individuals), immersion is associated with an increase in
0 1 2 3
Time (h)
Figure 6 Resting lower limb blood flow measured by plethysmogra-
phy is plotted as function to time of HOWI. The ∗ indicates a significant
increase above air control.
1710
Comprehensive Physiology
the cerebellum. HOWI in TN or warmer water results in
increased temperature of the integument causing significantly
increased blood flows to skin and subcutaneous fat. Urine out-
put increases, in spite of the absence of increased blood flow
temporary, increases in blood flows (and O2 delivery) to the
gastrointestinal tract, liver, pancreas, and spleen. As HOWI
respiratory skeletal muscles. The elevated blood flow to some
4 5
tissues may counterbalance fluid shifts out of cells in some
tissues. The increase in CO and tissue blood flows promote
total-body nitrogen elimination during oxygen breathing dur-
ing HOWI in TN water compared to nonimmersion (15).
Circulatory and renal responses to HOWI are elicited by
reflex activation due to mechanical loading of cardiovascular
stretch receptors. As stated above in humans, HOWI to the
mid-cervical level is estimated to increase CO from 32% to
62% which is shown in Figure 5. The magnitude of the esti-
mated increases in CO depends upon the method and subjects
used (201). The increased CO is due to a significant increase
in SV since HR decreases. MAP reported by most studies is
not shown to change in HOWI, in spite of the increased CO,
as TPR is proportionally decreased. Arterial PP is increased
in HOWI, due to the increase in SV (281). The magnitude
of the increase in CO is coupled to the depth of immersion.
CO increases in a graded fashion from leg (only) immer-
sion through mid-thorax to mid-cervical immersion and the
increase in CO is sustained for several hours (18, 113). The
elevated CO in immersion is a result of increased cardiopul-
monary blood volume which in turn increases cardiac filling
pressures and preload (11).
Pulmonary artery pressure and pulmonary vascular vol-
ume increase in water immersion and there is a decline of vital
capacity (VC) (364). External water pressure compresses the
chest which in-turn increases elastic loading of the chest wall
and results in negative pressure breathing (171). The resul-
tant increase in energy cost of ventilation, secondary to the
increased POB causes an increases in blood flow to the respi-
ratory muscles (154, 314, 366). Prefaut et al. (314) observed
mild hypoxemia in humans with increased lung closing vol-
Recovery ume (CV). While the apical portions of the lung are less
perfused when upright in air, HOWI causes their flow to
CV to expiratory reserve volume (ERV). When CV is less than
ERV (usually in young individuals), during immersion VA /Q
due to an increase in the ventilation to oxygen consumption
ratio (VE /VO2 ) ratio (87). When CV exceeds ERV (common in
4 5 right-to-left shunt (87) and a widening of the alveolar-arterial
PO2 difference (86).
Von Diringshofen (400) was the first to postulate that fluid
shifts into the plasma compartment during water immersion
(see Fig. 3). This hypothesis was validated in dog studies
Volume 5, October 2015
Comprehensive Physiology
(83, 254-257, 260), with increases of PV on the order of ∼7%
following 100 min of immersion. Interstitial pressure during
HOWI is above the capillary hydrostatic pressure, promot-
ing capillary absorption. There is a linear coupling of tissue
pressure, capillary pressure and CVP and the depth of HOWI.
Plasma osmolarity is not affected by HOWI; however, plasma
oncotic pressure is decreased and leads to hemodilution. Inter-
stitial fluid volume and lymph flow are not effected by HOWI;
however, there is an increase in both amino acids and potas-
sium concentration in plasma. These changes suggest that the
fluid is shifted out of the intracellular compartment (83, 201).
The kidneys act to minimize the rise in PV, since evidence
from immersed, anaesthetized and nephrectomized dogs has
shown PV to increase by 40% instead of the 7% increase
observed in dogs with intact kidneys. Figure 3 indicates the
transcellular, transcapillary, and renal fluid shifts that occur
during water immersion.
Graded immersion studies indicate that blood is shifted
from the legs to the abdomen, then from abdomen to chest as
shown in Figures 2 and 3. The abdominal splanchnic veins
are an important volume reservoir (186). The increase in CO
is graded depending on the depth of HOWI in the erect posi-
tion (113). The initial increase in cardiac preload increases
the change in cardiac chambers and inferior vena cava diam-
eter, but this is followed by the excretion of nominally 1.5 L
(range 1.0-2.0 L, 202) of urine that in turn decreases intratho-
racic blood volume, cardiac preload, SV, and CO (see Fig. 5).
The initial HOWI-induced increase in CO is associated with
peripheral vasodilatation, which is followed later by periph-
eral vasoconstriction so that lower limb blood flow decreases
over time as CO falls toward control levels (35). HOWI to
the mid-cervical level results in greater increases in left atrial
diameter; however, MAP remains unchanged and arterial PP
does not change any further. Although there was a greater
increase of CVP during mid-cervical HOWI, plasma nore-
pinephrine (NE) declined to levels observed during shallower
immersions. The decline of plasma NE reflects attenuation
of sympathetic nerve activity (SNA). Subcutaneous vascular
resistance in the forearm decreased similarly during HOWI
both to the xiphoid level and mid-cervical level, whereas
forearm vascular resistance in muscle declined only during
mid-cervical HOWI. This observation implies that cutaneous
vasodilation in the forearm reaches maximal levels at shal-
lower immersion depths compared to vasodilation in skeletal
muscle (127, 128). CVP increases about 5 mmHg along with
an increase of left atrial diameter during mid-cervical HOWI
and the expansion of cardiac volume is related to decreases of
plasma renin activity (PRA), as well as plasma protein con-
centration. By comparison, when the central translocation of
blood out of the lower limbs during HOWI was prevented by
placing pressure cuffs on the thighs, the increases of atrial
dimensions were similar to those observed in the uncuffed
situation, whereas the degree of plasma hemodilution was
less and the level of suppression of PRA was attenuated. This
observation suggests that mechanisms in addition to input
from low- and high-pressure baroreceptors are responsible
Volume 5, October 2015
The Aquatic Environment
for regulation of neurohumoral activity and circulatory func-
tion in HOWI. The volume of fluid expanding the plasma
compartment via the transcapillary fluid shift appears to inde-
pendently influence the magnitude of suppression of the renin-
angiotensin system (127, 128).
There are several possible mechanisms for the dramatic
fluid shift out of the cellular compartment during immer-
sion (See Figs. 1 and 3). First, a primary movement of iso-
tonic fluid out of the interstitium into the capillaries leaves
behind osmotically active proteins that could in-turn draw
water out of the cells. Second, relative differences in compli-
ances between cells, the interstitial compartment and capil-
laries could promote a decrease of cell volume more than the
interstitial fluid, thus increasing interstitial pressure that could
in turn increase capillary reabsorption. Third, if cells per-
ceive hydrostatic compression as an increase in cell volume,
then this could activate cellular volume regulatory decreases
via solute efflux as cells sense and react to volume changes
of 3% or more. The rise in plasma potassium content dur-
ing water immersion is compatible with cellular regulatory
volume decreases due to loss of potassium chloride perhaps
caused by activation of separate cell membrane potassium
and chloride channels, and potassium-chloride cotransporters
(360). It has been suggested that the fluid shift occurs mainly
from the lower extremities (186). In addition to the increase in
blood flow to the respiratory muscles (diaphragm and inter-
costals), coronary blood flow increases commensurate with
the increase in cardiac work during immersion (153, 154).
Secondary to changes in vestibular and proprioceptive inputs
due to buoyancy and the microgravity state, blood flow to the
cerebellum is also increased. However, total cerebral blood
flow is not changed, implying vasoconstriction in some brain
regions. While core temperature is unchanged, HOWI in TN
water heats up the integument, since there is an 8◦ C to 10◦ C
difference between the temperature of TN air and warmer TN
water. Accordingly, blood flow to skin and subcutaneous fat
rises in the order of several hundred percent. Increased cuta-
neous blood flow could account for the common observation
that the cutaneous veins on the dorsum of the feet and hands
remain distended while standing in water.
The mechanisms for other regional flow adjustments
during water immersion are less certain. While blood flow
to the kidney is unchanged, there are early increases in
flows to the gastrointestinal tract, liver, pancreas, and spleen
(154). These increases are proportional to the change in CO.
After about 30 min of immersion, the increased visceral
flow declines to preimmersion levels, and the increased CO
is redistributed to nonrespiratory skeletal muscles. These
regional hyperemias suggest that HOWI has the potential
to be a treatment of decompression sickness (DCS) and
muscle injury and to increase drug delivery to specific
organs, such as the liver. Perhaps these regional hyperemias
elicit local elevations of capillary hydrostatic pressures that
counterbalance fluid shifts from the cells in selected tissues.
In humans, HOWI in either 8◦ C or 22◦ C water results
in a reductions of femoral artery and cutaneous vascular
1711
The Aquatic Environment
(.10) _ 28
1.6 (a-v)O 1·1–1
2
(.15)
1.2
Qm (1 · min–1)
(.20)
0.8
Air
·
30°
0.4
25°
20°
0 0
0 0.5 1.0 1.5 2.0
· –1
VO2 M’ (1 · min )
Figure 7 Muscle blood flow measured by 133 Xe washout from
quadriceps muscle at rest and during cycling exercise is plotted as a
function of VO2 for air and HOWI in 20◦ C, 25◦ C, and 30◦ C water.
The dashed lines represent a constant (a-v)O2 as a function of VO2 .
conductance immediately upon immersion (30-40%). By
comparison cutaneous vasoconstriction was less in 8◦ C water
than 22◦ C water (150). Other studies have demonstrated that
cutaneous (394) and muscle (see Fig. 7) (297) blood flows
decrease in cold water. Blood flow to skin and subcutaneous
tissues reach minimum levels in cool water (≤30◦ C), whereas
there is a graded temperature-dependent blunting of resting
and exercise hyperemia as seen in Figure 7 (297).
During TN water HOWI in humans, cardiopulmonary vol-
ume is increased (109, 199), which augments CO via the
length-tension response. Since by definition systemic VO2
does not change during TN immersion, an unusual situation
develops where systemic oxygen delivery exceeds systemic
tissue requirements more than usual at rest for sustained peri-
ods. Autoregulation typically matches metabolic demands of
peripheral tissues to blood flow (150). However, this relation-
ship is modified during immersion (Figs. 1, 4, 6) to allow
for increased systemic blood flow (60, 153, 154). Gauer and
Henry (131) postulated that the diuresis by the kidneys during
HOWI results in a net reduction of PV. However, this view was
later modified when it was shown that PV is expanded during
HOWI as a result of the transcapillary fluid shift (see Fig.
3). Therefore, the increased urine flow and sodium excretion
during immersion does not reduce PV below preimmersion
levels, at least during short-term immersions, as previously
postulated (131). Instead, the kidneys act to off-set the PV
expansion due to HOWI, which if not compensated for would
cause a 40% increase in PV (201, 254, 256). The elevation of
PV is sustained during HOWI lasting at least 6 to 12 h (185).
In fact, if the renal response did produce a net reduction in
PV as previously postulated (131) the hypovolemia would
be expected to impair orthostatic adjustments upon emerging
from the water. In fact, a previous study demonstrate that this
1712
Comprehensive Physiology
(.05) (.10)
24
20 H 2O (.20)
Q (1 · min–1)
16
12 Rest Temp Max
·
A
8 35
30
4 25
20
0 1 2 3 4
·
VO2 (1 · min–1)
Figure 8 Cardiac output (Q, L/min) is plotted as a function of oxygen
consumption (L/min) for air and HOWI in 20◦ C to 35◦ C water at rest
(VO2 < 1.0 L/min) and exercise (VO2 > 1.0 L/min).
diuresis-induced hypovolemia does impair orthostatic adjust-
ment (173)
The physiological responses to HOWI are temperature
dependent and this is shown in Figures 7 and 8 (297) and,
therefore, the study of water immersion requires the elimina-
tion of thermal stress. In humans, this is achieved by using
water temperatures of 34 to 35◦ C for exposures up to 6 h. For
measurements of hemodynamics, it is important to determine
the hydrostatic indifference point which is the location in the
vasculature at which pressure is independent of posture. This
is a transition zone at which intravascular pressure remains
constant and as such represents a center of gravity for the
cardiovascular system (132, 332, 333). In humans, this point
is usually considered to be at the level of the right atrium
(332, 333). However, during HOWI it is very likely to shift;
therefore, it is inappropriate in immersion to reference mea-
sured physiological pressures to the surface level of the water.
It is better to insert a reference catheter in the esophagus for
estimation of pleural and transmural pressures across the heart
and great vessels (11, 256, 258).
HOWI is a noninvasive maneuver and therefore it has been
considered to be the investigative tool of choice for studying
physiological mechanisms of PV regulation (131). Never-
theless, HOWI cannot be strictly compared to true volume
expansion, microgravity or head-down tilt, since there are
unique characteristics associated with each maneuver. Com-
pared to true volume expansion, the magnitude of the diuresis
and natriuresis caused by HOWI is equivalent to the infusion
of 2 L of 0.9% saline (sodium chloride) solution (109). In
terms of the coupling of the cardiac and renal responses, the
induction of hypovolemia as a result of the removal of 15% of
the total blood volume does not affect the 22% increase in CO
in HOWI; however, the diuresis and sodium excretion were
previously reported to be significantly decreased suggesting
Volume 5, October 2015
Comprehensive Physiology
Vagal
afferent
activity
Atrial
volume
Central
blood
volume
Blood
volume
Free-water
clearance
Figure 9 An early version of the Gauer-Henry hypothesis. Arrows indicate an increase or stimu-
lation of the variable, darkened arrows indicate a decrease or inhibition of the variable. Redrawn
from Krasney (201) and reproduced with permission from Elsevier Limited, Oxford, United Kingdom
(204).
that the renal responses are quantitatively not well-coupled to
the cardiac response (350).
HOWI has been shown by many authors to reduce HR,
and more so in cold water. Both apnea and immersion of the
face in cold water have demonstrated a biphasic decrease in
HR, with a rapid initial decrease and a later slow phase. These
bradycardia responses are exaggerated in adolescent subjects
and they are associated with a high probability of arrhythmias
(412). The apnea-face immersion bradycardia is partly due
to reduced cardiac SNA and increased vagal tone. Muscle
SNA decreases in TN HOWI (262, 263). The decreased HR
and increased SV are associated with an unchanged MAP
in HOWI. This observation is compatible with the view that
SNA to systemic resistance vessels and heart are suppressed
during HOWI while cardiac vagal activity is enhanced. (263).
In contrast to the suppression of cardiac and vascular SNA
in TN immersion cold water immersion (26-27◦ C) increased
vascular SNA (277).
Renal responses to intrathoracic volume expansion
HOWI in a euhydrated subject causes a diuresis, natriuresis,
kaliuresis, and an increased free water clearance (CH2 O)
(108, 109, 319). In nonvolume replete subjects, the renal
responses gradually return to control levels over a 4 h
period while in subjects that have fluid replacement the
renal responses are sustained for the duration of immersion,
although at somewhat lower level. In subjects that are not
euhydrated the diuresis is reduced and thus osmolar clearance
Volume 5, October 2015
The Aquatic Environment
Neural lobe
of hypophysis
Vassopressin
(antidiuretic hormone)
secretion
Water
reabsorption
is increased (19). The level of physical fitness also affects the
nature of the HOWI renal responses. It has been shown that
the diuresis and natriuresis due to HOWI were significantly
blunted in runners and swimmers compared to control
subjects in spite of larger and more persistent increases in CO
(65). Kidney responses to water immersion are primarily due
to alterations in renal tubular functions because glomerular
filtration rate (GFR) does not change. In spite of the lack of
increase in plasma osmolarity during HOWI, plasma vaso-
pressin (antidiuretic hormone) level was decreased and asso-
ciated with the observed increase in CH2 O (26,110,128,282).
The primary mechanoreceptors regulating vasopressin secre-
tion appear to be the high-pressure arterial baroreceptors
and cardiac volume receptors since plasma osmolarity does
not change (127, 128, 201, 333). It can be concluded that the
depression of PRA and aldosterone levels are more consistent
than changes in plasma vasopressin, and in addition seem to
be less associated with the degree of hydration (111, 201).
It is unlikely that the diuretic and natriuretic responses to
HOWI are caused by suppression of aldosterone secretion as
they appear after 20 min and thus too rapid in onset. It has
been reported that renal responses to immersion were poorly
correlated with right atrial pressure in awake dogs (153, 354).
It is clear that the primary increases in cardiopulmonary
and PV elicited by HOWI are wholly or partly compensated
for by the renal responses. As seen in Figure 9, Gauer and
Henry (130) were the first to demonstrate that stretching the
cardiac atria causes a reflex diuresis (increased renal water
loss). In anesthetized dogs obstruction of the mitral valve
1713
The Aquatic Environment
with a balloon catheter in the left atrium, resulted in reduced
vasopressin secretion and elevated CH2 O. These responses
were abolished by cutting the cervical vagus nerves, indicating
that PV is controlled by intrathoracic stretch receptors by way
of cardiac reflex neurohumoral control of the kidneys as seen
in Figure 9.
After 20 to 40 min of TN HOWI in euhydrated humans
the diuresis, natriuresis, kaliuresis, and increased renal free-
water clearance commence (108). As pointed out above, both
the hydration state and physical training have major quantita-
tive influences on the renal response to HOWI. The kaliuresis
reflects tubular washout of potassium secondary to high urine
flow. In subjects who are well hydrated prior to immersion
but then are not allowed to drink, the renal responses persist
for 2 to 4 h. Euhydrated subjects, on the other hand, maintain
a diuresis for the duration of the HOWI (4 h), although at a
blunted rate. Dehydrated subjects, have less diuresis, but an
increase of osmolar clearance (19). Similar observations have
been made in volume repleted and nonrepleted awake dogs
(354). There have been many studies of the renal response to
HOWI in dogs; however, many of these animals were anes-
thetized which reduces their natriuretic response, so conclu-
sions about kidney regulatory mechanisms from anaesthetized
studies are not valid (201).
Studies in humans confirm that PV increases in TN immer-
sion as reported from conscious animal studies. However, cold
water dramatically changes the pattern of body fluid shifts.
Stocks et al. (358) found that immersions limited to one hour
in 33◦ C versus 18◦ C water both caused reductions of intracel-
lular volume of similar magnitude in humans. PV increased
in 33◦ C water accompanied by hemodilution. By contrast PV
decreased in 18◦ C water. Total body water remained constant
whereas intracellular volume decreased by similar amounts in
both TN and cold immersion. This indicates that, compared
to TN immersion, movement of fluid out of the intracellular
compartment increases interstitial fluid volume during cold
water immersion whereas PV decreases. Therefore, it is likely
that microcirculatory dynamics during one hour periods of
cold water immersion impair the entry of fluid from an ele-
vated interstitial volume into the plasma compartment (358).
Atrial natriuretic peptide (ANP) is increased during cold water
immersion. Since ANP reduces transcapillary fluid exchange
(201, 202), it is possible that ANP contributed to the reduc-
tion in PV in cold water. This study indicated that changes
in PV were not associated with changes in total extracellular
fluid volume at least in immersion (358). A further study by
Stocks et al. (358) established that acclimation to 14 days of
cold water immersion does not qualitatively or quantitatively
alter the fluid shifts during 1 h HOWIs. Intracellular and PVs
were reduced by 5% to 6% while intercellular volume was
increased by ∼ 5% before and after cold acclimation. Thus
during 1 h immersions in cold water intracellular fluid is dis-
placed into the interstitium even after cold acclimation (358).
By contrast to observations of TN versus cold water
immersions for 1 hour periods immersions for longer peri-
ods appear to elicit more pronounced changes in body fluid
1714
Comprehensive Physiology
homeostasis. Jimenez et al. (183) immersed unprotected Navy
swimmers for 6 h periods in 34◦ C, 18◦ C, and 10◦ C. In this
study, immersion in 34◦ C decreased PV by ∼7% after 6 h. Pro-
longed immersion at both colder water temperatures resulted
in a more rapid and greater reductions in PV (14.3%-16.3%).
Plasma osmolarity did not change in TN water whereas
plasma osmolarity increased during the cold water immer-
sions. While GFR did not change at 34◦ C (consistent with
other observations) the plasma hyperosmolar responses in
cold water were associated with increases of GFR corre-
lated with significant renal losses of 1.6-1.7 L of water and
sodium (6-8 g) and increases of osmolar and free water clear-
ances (185). PRA and vasopressin levels were unchanged
while aldosterone decreased similarly at all three temper-
atures. Jimenez et al. (183) studied trained swimmers. As
described above, training can influence the renal responses to
immersion. Nevertheless, comparing studies of one hour vs
six hour immersions suggests that progressive hypovolemia
develops with longer immersions in both TN and cold water
secondary to increasing renal losses of water and sodium. It
might be expected that both hypovolemia and cold exposure
would lead to increases in SNA to peripheral vessels and the
kidneys causing salt and water retention. In this regard, it
is surprising that GFR increased along with a diuresis and
natriuresis in the Jimenez (183) study. Perhaps prolonged
HOWI and/or cold water alters neurohumoral regulation of
renal function. Sramek et al. (357) studied subjects during 1 h
immersions at 32, 20, and 14◦ C. In this study, subjects in 32◦ C
had lower PRA, cortisol, and aldosterone, and the urine flow
was increased by 107%. In the same study (357), in colder
water the cortisol was decreased less, but the aldosterone lev-
els were greater. Metabolic rate increased by 350% at 14◦ C
in this study (357) and it was associated with 530% increase
in NE and 250% for dopamine concentrations. Thus at colder
temperatures, there was an uncoupling of the relation between
PRA and aldosterone, and SNA. Again it is surprising that
urine flow increased significantly more at 14◦ C than at 32◦ C
(163% vs. 107%) despite increases in antinatriuretic influ-
ences from aldosterone and sympathetic activity. Although
strict comparisons of the Sramek (357) and Jimenez (183)
studies are not possible, the data suggest that altered neuro-
humoral control of renal function may be more affected by
water temperature than the duration of immersion. Although
renal responses to immersion are clearly altered by cold water
and vary among studies, the data from basic TN immersion
studies are consistent in demonstrating a diuresis and a natri-
uresis and that these responses are related to a decrease of
PRA, aldosterone, and renal SNA.
Vasopressin
Vasopressin mediates the regulation of the total body fluid and
plasma osmolarity. Since plasma osmolarity is not affected by
HOWI, the control of vasopressin secretion likely depends
upon stimulation of volume receptors. Norsk and Epstein
(282) have indicated that a reduction in plasma vasopressin
Volume 5, October 2015
Comprehensive Physiology
concentration causes increased CH2 O in humans during
immersion. However, vasopressin levels are quite low in
euhydrated subjects and it has been difficult to detect reduc-
tions in circulating vasopressin, although recent studies with
improved vasopressin assays report consistently small but
significant reductions in such subjects (128). By contrast,
vasopressin concentrations are high in dehydrated subjects
and decrease during immersion, but CH2 O does not increase.
However, the kidney is quite sensitive to small changes in
plasma vasopressin (26), and the CH2 O response is abol-
ished when subjects are pretreated with vasopressin (110).
Hammerum et al. (155) investigated plasma vasopressin in
hydrated subjects immersed in TN water with controlled
sodium intake. In this study (155) vasopressin and CH2 O
declined. Plasma vasopressin remained suppressed while
CH2 O rose later in immersion. Collectively, the data indi-
cate that in humans the immersion diuresis can be related
to suppression of vasopressin secretion. The level of hydra-
tion appears to determine whether an increase in CH2 O is
manifest.
In animal studies, Hajduczok et al. (153) found a diure-
sis and natriuresis in awake dogs during water immersion
but no change in either vasopressin or CH2 O, despite large
increments in atrial pressure. By contrast, after total cardiac
denervation, immersion led to a decline of vasopressin con-
centration, with the diuresis due to an increased CH2 O. The
Bainbridge reflex increases HR and CO in the intact dog
during water immersion due to increased venous return and
stimulation of the low-pressure baroreceptors, while arterial
PP does not change. However, after cardiac denervation, the
increase in HR is abolished, since it was driven autonomically,
but CO increased the same as the preload-induced elevation in
SV was similar, and arterial PP was increased. These observa-
tions indicate that, in the dog, the decline in circulating vaso-
pressin was due to increased high-pressure arterial barorecep-
tor loading, unmasked by cardiac denervation. Furthermore,
the natriuresis was dependent upon intact cardiac nerves. It is,
therefore, evident that considerable redundancy exists within
the control systems for body fluid regulation, as is evident
for other regulatory systems. In awake dogs, monkeys, and
humans, the major mechanoreceptors regulating vasopressin
secretion are likely arterial baroreceptors (201,333), although
graded distension of central cardiac receptors modulates vaso-
pressin secretion in humans (128).
Renin-angiotensin II-aldosterone system
The renin-angiotensin-aldosterone system and the renal sym-
pathetic nerves are antinatriuretic, and interact with ANP to
regulate extracellular fluid volume and plasma sodium con-
tent. In immersed humans, the decrease in PRA and aldos-
terone concentrations are more consistent than changes in
plasma vasopressin, and are less associated with the sub-
jects’ hydration (109, 201). Schou et al. (340) demonstrated
using lithium clearance that fractional distal tubular reabsorp-
tion of sodium is reduced during TN immersion. Angiotensin
Volume 5, October 2015
The Aquatic Environment
II (ANGII) levels declined also. The authors then infused
ANGII to keep plasma ANGII levels unchanged from control
levels during immersion. Infusion of ANGII markedly attenu-
ated the immersion natriuresis and reduced lithium clearance
implying increased fractional distal reabsorption of sodium.
Thus reduced formation of ANGII is an important natriuretic
mechanism in humans immersed in water and the natriuresis
is in part due to decreased fractional distal tubular sodium
reabsorption.
However, as emphasized above, the rapid onset of diuretic
and natriuretic responses suggest that they are not due to
suppression of ANGII formation and aldosterone secretion.
Indeed, Hajduczok et al. (153) and Sondeen et al. (354)
reported that renal responses of immersed awake dogs were
poorly correlated with PRA.
Atrial natriuretic peptide
Distension of the atria stimulates ANP release, eliciting
diuresis, natriuresis, and vasodilatation and fluid shifts from
the vascular to extravascular compartment (301). HOWI
increases ANP in plasma without delay in humans, dogs,
and rats (201). However, the relative time courses of the
ANP and renal responses during immersion differ. For exam-
ple, although circulating ANP concentration rises rapidly, the
diuresis and natriuresis are evident at 20 to 40 min. In fact,
it is uncertain whether these renal responses can actually be
elicited by the levels of ANP that are attained during water
immersion (149), and the renal responses are poorly corre-
lated with plasma ANP concentrations (254, 354). The renal
responses to ANP were greatly augmented in hypervolemic
(but not hemodiluted) awake dogs (253). Subsequently, it
was demonstrated that the renal sensitivity to two doses of
ANP was greatly augmented in conscious dogs during volume
replete water immersion (202). These observations indicate
that the renal response to ANP is greatly potentiated when the
PV is expanded. ANP reduces PV and increases hematocrit
by causing a transcapillary shift of fluid out of the plasma
compartment (334). In awake dogs, it has been shown that
ANP infusion caused a hemoconcentration in air (202). Dur-
ing water immersion, there was an expected hemodilution.
However, the immersion hemodilution was attenuated in a
graded fashion by increasing doses of ANP. Thus, ANP mod-
ulates and opposes the autotransfusion during water immer-
sion, possibly by raising capillary hydrostatic pressure (201).
Nitric Oxide
Nitric oxide (NO) is synthesized in the kidney and is natri-
uretic. Djikhorst-Oei et al. (91) reported that there is inhibi-
tion of renal NO synthesis on renal hemodynamics and renal
function during 7 h of TN HOWI. During the timed con-
trol immersion with infusion of placebo, arterial pressure and
renal vascular resistance declined while there was a natriuresis
and diuresis.
1715
The Aquatic Environment
A second immersion study was carried out with infusion of
l-NMMA (N(G)-monomethyl-l-arginine) to inhibit NO syn-
thesis. Prior to immersion l-NMMA decreased the [(15)N-
arginine to [(15)N]-citrulline conversion rate with profound
elevations in arterial pressure and reduction of sodium excre-
tion and urine flow. When the subjects were then immersed
during l-NMMA infusion, there were relative reductions in
arterial pressure and renal vascular resistance and increases in
sodium excretion and urine flow that did not differ from those
induced prior to NO inhibition. The authors concluded that
although NO synthesis was estimated to be reduced to one-
third of control levels, the kidney continues to be sensitive to
volume expansion from HOWI resulting in renal vasodilation
and natriuresis and diuresis. These data support the view that
multiple redundant mechanisms are available to bring about
the renal response to the volume expansion of immersion.
Renal sympathetic nerves
DiBona and Kopp (90) and others have shown that renal SNA
can elicit important modulation of kidney function even with-
out renal hemodynamic changes. For example, renal sympa-
thetic activation at intensities that have no effect on renal
blood flow or glomerular filtration causes antinatriuresis,
whereas suppression of renal neural activity evokes a natri-
uresis. Mechanical stretch of atrial or arterial baroreceptors
results in significantly decreased renal SNA, increasing urine
flow, as well as sodium excretion. In addition to this suppres-
sion, it has been shown that plasma NE concentration declines
by as much as 50% during water immersion (111, 281). Haj-
duczok et al. (153) found in dogs with denervated hearts
that the natriuresis of water immersion was entirely due to
the presence of the cardiac nerves, although a water diuresis
persisted in the cardiac-denervated dogs, due to a decline of
vasopressin levels. Thus, the reflex suppression of adrenergic
systems in water immersion is dependent upon the stimula-
tion of cardiac afferent nerves, and major alterations in vaso-
pressin do not occur in neurally intact animals. The decline
in PRA usually observed in HOWI is, therefore, likely to be
related to a decline in renal SNA. Recording of renal SNA
activity in awake dogs, provided the first direct evidence that
SNA is suppressed during water immersion (257). The magni-
tude of this neural activity suppression was about 50% below
preimmersion levels, and the renal response in these dogs
consisted of diuresis and natriuresis, with no change in renal
CH2 O. After chronic bilateral renal denervation, the diure-
sis and natriuresis in HOWI were eliminated. Subsequently,
strong evidence was reported that immersion elicits a car-
diac reflex neurogenic natriuresis, since this natriuresis was
also abolished by denervation of the heart (257). Later, it was
demonstrated that the decline in renal SNA and increased
sodium excretion during water immersion were greatly atten-
uated in cardiac-denervated awake dogs (258). The dramatic
consequences of renal and cardiac denervation emphasize the
important role of reflex suppression of renal sympathetic acti-
vation in the renal responses to water immersion, and imply
1716
Comprehensive Physiology
that the roles of vasopressin, aldosterone, and ANP are less
important. Neurohumoral control of renal function in water
immersion is mediated by low-pressure cardiopulmonary and
the high-pressure arterial baroreceptors. Since vasopressin
only declines during immersion in awake dogs after cardiac
denervation there may be a shift in neurohumoral regulation
of renal function from the cardiopulmonary baroreceptors and
arterial baroreceptors. Indeed, it has been demonstrated that
in awake dogs water immersion selectively increased central
input from the cardiopulmonary baroreceptors that acts to
simultaneously inhibit arterial baroreceptor control of renal
SNA (260). This indicates that the major reflex input that regu-
lates renal function during TN water immersion in the neurally
intact state is from the low-pressure cardiopulmonary barore-
ceptors. The potential contribution from the arterial barore-
ceptors is unmasked by cardiac denervation. These conclu-
sions are derived from studies in quadruped dogs. Additional
effort is essential to fully understand the relative contributions
of low vs high pressure baroreceptors in biped humans.
Circadian influences and intrarenal starling forces
In addition to the denervation and neural recording studies
in animals, the differential effects of neural versus hormonal
control were clarified further by experiments showing a dra-
matic circadian influence on the renal response to immer-
sion in humans. The renal responses to TN HOWI have been
reported to be attenuated at night (205). Subsequently, these
observations were confirmed and further showed that the ele-
vation of CO and the reduction in PRA, aldosterone, and vaso-
pressin were similar during the day and night was confirmed
(344). Later, it was reported that elevations of ANP during
HOWI at night were similar to those during the day, despite
nocturnal suppression of the diuretic and natriuretic responses
(259). Since the day versus night hormonal responses were
similar, by exclusion, these circadian studies imply that a
reduced reflex suppression of renal SNA at night is respon-
sible for the attenuated diuresis and natriuresis during water
immersion.
It has been well documented that the kidneys respond
to increased arterial pressure with a rise in interstitial pres-
sure, and this causes pressure-induced diuresis and natriuresis
(72). However, it has been demonstrated that the immersion-
induced natriuresis was abolished after cardiac denervation,
despite similar elevations in MAP (153), and that abolition
of the natriuresis and diuresis following renal denervation
occurred despite similar elevations in MAP (257). Thus,
increased renal arterial pressure does not appear to contribute
in a major way to the water immersion natriuresis. Auto-
transfusion during upright immersion causes a hypervolemic
hemodilution and a decline of plasma colloid oncotic pressure.
The latter would diminish the tubular reabsorptive capacity for
sodium, contributing to natriuresis. Using graded immersions
in humans when thigh cuffs were inflated to reduce fluid shifts
from the legs, it has been postulated that the decline in plasma
colloid oncotic pressure could be responsible for a significant
Volume 5, October 2015
Comprehensive Physiology
amount of the elevated sodium excretion observed during
water immersion (187). On the other hand, as indicated above,
the hemodilution response in humans during HOWI revealed
minimal circadian influences, yet the natriuretic responses are
suppressed at night, reinforcing the primary impact of renal
sympathetic nerves in mediating immersion-induced natriure-
sis and diuresis.
Effects of exercise during immersion on renal
function
It is well documented that exercise carried out on land results
in vasoconstriction of blood flow to the kidney and thus blunts
the diuresis and increases sodium reabsorption (333). Dur-
ing HOWI where at rest there are diuretic and natriuretic
responses, exercise attenuates these response and potentiates
the kaliuretic response (326). These exercise-associated alter-
ations are likely the effect of increased SNA blunting the
mechanoreceptor-mediated suppression of renal SNA during
HOWI. In addition, plasma renin and aldosterone remained
unchanged while vasopressin was significantly increased
(326).
Pulmonary adjustments
The HOWI-induced CO induces an increase in pulmonary
blood flow, causing elevation of pulmonary artery blood vol-
ume and pressure. The changes in blood volume result in
increased residual volume and decreased VC (171, 227). The
compression of the chest wall causes elastic loading and nega-
tive pressure breathing (171, 227, 368). The negative pressure
breathing has an effect on pulmonary mechanics, causing ele-
vated pressure difference between the outside of the chest
and the alveolar air pressure (SLL) (227). Increased SLL
results if the source of breathing gas (breathing regulator)
is at a different hydrostatic pressure than the lung centroid
(228, 366, 369). SLL is typically negative during immersion
and submersion due to the negative body attitude, even dur-
ing exercise (228), when the mouth is at lower pressure than
the chest which increases the force required by the inspira-
tory muscles, while assisting expiration. The elevated SLL
has been reported to increase ERV (227, 364, 365), resulting
in the respiratory muscles being stretched to a less functional
length resulting in a reduced force development and mainte-
nance (39,247). The inadequate force may not be sufficient to
accomplish the increased total work of breathing (WOB) and
may lead to respiratory muscle fatigue. The increased total
WOB demands more O2 increasing the demand for blood
flow to the respiratory muscles (154, 162), which may also
reduce blood flow and O2 delivery to other skeletal muscles
(158).
HOWI has been reported to increase lung CV in humans,
and may lead to slight hypoxemia (314). It is widely accepted
that there is increased blood flow to apical regions of the lung
(11). Its effect on VA /Q depends on the relationship between
CV and ERV as discussed earlier (114,298) and can be implied
Volume 5, October 2015
The Aquatic Environment
from studies in air where CO is increased (328). The regula-
tion of blood flow in the lung is likely due to active vascular
responses to HOWI, and not as dependent on gravity as previ-
ously reported. It can be concluded that higher blood flow to
pulmonary capillaries is responsible for increased lung blood
volume, as recruiting additional capillaries does not appear to
occur (114,298,328). The high levels of pulmonary blood flow
and pressure in HOWI may lead to failure of the capillary wall
and, in some cases, result in pulmonary edema and sometimes
hemorrhage, particularly during exercise (see below, under
“Immersion Pulmonary Edema”). During HOWI hydrostatic
pressure compresses the body’s fluid and gas containing com-
partments, thus breath-hold dives can lead to “lung-squeeze”
with hemorrhage and edema due to the compression of the
gas containing compartments (220).
As opposed to the depressing effects of a gradual immer-
sion on HR, a rapid immersion in 0◦ C water results in an
sudden increase in HR, respiratory rate and tidal volume with
an associated decrease in end-tidal CO2 (237). However, pro-
longed exposure to cold water results in decreased ventilation
and breathing frequency (Bf ), and this was the case even if
torso or legs were protected (379). HOWI has been shown to
increase CVs in TN water. On the other hand, ERV decreased
in immersion and the alveolar plateau (Phase III) slope was
less steep (86).
HOWI increases the demands on the respiratory system
due to the hydrostatic pressure differential between the feet
and chest and the translocation of blood to the chest discussed
above. If the person is breathing with a snorkel, or SCUBA,
there is likely an increase in breathing resistance. In addition to
the increased SLL described above, the effects of HOWI cause
increased WOB at both rest and during exercise (162,322). In
addition, during HOWI, there is a translocation of blood from
the dependent limbs to the chest (11, 201, 368), resulting in a
decrease in total lung capacity, residual volume (171,228,363)
and lung compliance (227, 228). The sum total of the HOWI-
induced changes in lung volume increase the elastic WOB.
HOWI causes increased airway resistance (Raw) (162).
The increases in resistance would demand a concurrent
increase in alveolar pressure (PA ) to maintain VE . Airway
resistance has been shown to be modulated by NO (4). It
has been reported that synthesis of, or administration of NO
results in a decreased airway resistance in a dose-dependent
manner (103, 166) and due to the increased airway resistance
in HOWI NO production is blunted during HOWI. Ventilation
in water is also dependent on the water temperature on the face
(82). A recent study proposed that the increased inspiratory
force needed to overcome negative SLL during immersion
resulted in increased breathing cycle, that is, increased Bf
(162).
Immersion results in a decrease in WOB for each breath
that is a result of the decrease in resistance for that individ-
ual breath, and thus WOB ̇ per breath was less. The expira-
̇
tory WOB per breath was unaffected by immersion. Negative
SLL increases the inspiratory effort to overcome the nega-
tive pressure and likely explains the total WOB ̇ changes due
1717
The Aquatic Environment
Regional blood distribution in the lung
400 at various levels of water immersion
Regional lung volume (counts/pixel)
350
300
250
200
150
100
0
0 Air Knee Hip Xyphoid ss
Water immersion level
Figure 10 Regional lung volume determined by radioactive labeling
of red blood cells is plotted as a function of the depth of water immersion
(progressive increasing pulmonary blood flow). The lung was divided
into nine equal layers from the apex to the top of the lung. The slopes of
the increase in lung volume as a function of increasing cardiac output
for the nine layers were not significantly different from each other. In
parallel measurements diffusion capacity (DLCO) was measured and
confirmed the increase in pulmonary blood volume was a result of cap-
illary enlargement, and not capillary recruitment (data not shown).
to immersion where negative SLL is increased (162). Dur-
ing immersion, the energy cost of breathing is increased as a
result of the increased total WOB and a decrease in the net
mechanical efficiency of the respiratory muscles (162, 351).
HOWI results in decreased PaO2 and alveolar-arterial O2
difference and increased CO-transfer factor, due to the redis-
tribution of lung perfusion to the apical lung (223). How-
ever, VE in relation to functional residual volume does not
change in immersion (223). HOWI in 35◦ C water has been
shown to increase VE while shunt, VA /Q, and the perfusion
distribution were unaffected (88). More recent studies using
nuclear techniques and diffusion capacity data have shown
that the increased pulmonary blood flow due to HOWI results
in increased volume of blood in the capillaries (capillary
engorgement), as opposed to the opening of more pulmonary
capillaries at the top of the lung (capillary recruitment) as seen
in Figure 10 (114, 298, 328). Increases in lung blood volume
during HOWI is shown in Figure 10. The capillary engorge-
ment, when combined with increased MAP due to exercise
and the vasoconstrictor effects of cold water may predispose
subjects to pulmonary edema. These studies also show that
the capillary engorgement is sustained for 6 h of HOWI.
Cortical and neuromuscular responses
Sustained HOWI (34◦ C) increases the activity of both sen-
sory and motor areas of the cortex (339), influencing cortical
processing of somatosensory inputs (337). Rapid immersion
in cold (0◦ C) water results in an immediate increase in HR,
respiratory rate, and tidal volume. The hyperventilation leads
1718
Comprehensive Physiology
to decreases in ETCO2 and cerebral vasoconstriction reflected
by a decline of middle cerebral artery velocity and is sufficient
to cause disorientation and loss of consciousness (236).
Cooling and heating during HOWI can affect contractile
properties (force generation) of muscle. However, HOWI does
not result in changes in muscle fascicle, tendon, and aponeu-
Region 1
Region 2 rosis were during passive stretch, and in addition there was no
Region 3
Region 4 change in contractile performance of muscles (206). Another
Region 5 study found that HOWI was associated with a decrease in
Region 6
Region 7 maximal voluntary contraction of plantar flexors and the elec-
Region 8
Region 9 tromyography amplitude, as well as the Hofman and Achilles
tendon reflexes and these data imply that there is a triggering
of inhibitory mechanisms (313).
Modulating factors
Hydration
Various fluid supplementation protocols have been applied
during extended water immersion, with the idea of helping
to sustain the blood volume and are based on the assump-
tion that the PV declines in HOWI (131). Protocols have
included hourly boluses of water and replacement of fluid
losses with saline, resulting in a water diuresis. However, due
to immersion-induced autotransfusion, the assumption that
there is reduced PV is incorrect, and the rationale for partic-
ular hydration protocols has never been entirely clear (201).
Egress from water immersion
Upon exiting the water, the fluid shifts experienced during
immersion are reversed, causing reductions of PV and thus
CO, and favoring orthostatic intolerance (35). Although CO
is elevated during diving at rest and low exercise levels (209)
due to immersion, a decrease in CO due to reduced SV has
been shown after a dive (29, 102). It is unclear how long this
depressed cardiac function lasts, or if it is persistent until the
next dives or accumulates with repeat dives.
A recent study has shown that both decreased SNA and
increased para-SNA followed 6 h in-water immersion when
PV was significantly reduced (117). By contrast, they reported
that aldosterone, ANP, AVP, and NE were unchanged postim-
mersion. Importantly, they also showed that cardiovascular
and autonomic control are not sufficient to prevent orthostatic
intolerance postimmersion (117).
Gender
Cutaneous cold-induced vasodilation has been reported to not
be different between men and women during HOWI (30 min
at 9◦ C) of the hand (148, 378). Cutaneous cold immersion
resulted in increased SNA of the hand and reduced blood flow
in both females and males (176) with equal time courses and
magnitude. In addition, the rates of decreases in deep Ts was
similar between the genders (234). When differences in body
size are considered, the cardiovascular or renal responses to
Volume 5, October 2015
Comprehensive Physiology
TN HOWI are likely similar (408). While short-term ventila-
tion with immersion have not been reported to be different in
men and women, during cold, HOWI females were shown to
have a greater increase in ventilation than males (176). During
HOWI in water below TN temperature, no gender differences
have been reported after correction for body fatness and sur-
face area in either the physiological or metabolic responses
(378). Thus, the above description of responses to water
immersion can most likely be applied to both men and women
(148). However, one study reported that in water of 20◦ C, the
drop in Tc was greater in women than men, but only after cor-
rection of body fat content at rest and low levels of exercise,
while no differences were seen at higher exercise levels (230).
Still another study showed that the time course of changes in
deep Ts are not different between men and women (176).
In TN HOWI, the increases in CO and SV and unchanged
HR and BP, and a decrease in TPR, at rest were not different
in adult men and women (428). No significant difference in
atrial diameter, HR, BP, urine volume, osmolality, endothe-
lium, urodilatin, sodium, and potassium excretion were found
between men and women (408). However, in females urodi-
latin excretion per kilogram was reported to be higher and
there was a delay in the kaliuretic response, while men had a
greater potassium excretion, presumably due to greater body
mass (408).
Thermosensitivity, as judged by limb blood flow, was
shown to not be significantly different between genders
immersed in cold water (20◦ C), and the phase of the men-
strual cycle of the females did not affect limb blood flow
(148). This is supported by the data of a study that reported
in women of high versus low body fat the Ts or total body
insulation were not different; however, the fatter group main-
tained a higher Tc than the thinner group, presumably due to
increased body insulation (315).
Responses of BP, HR, and CO and TPR were similar
during exercise, and there was no significant effect of age
or acclimation (428). In 28◦ C, the drop in Tc was inversely
related to exercise VO2 ; however, this was not the case in 20◦ C
water in either men or women (230). It has been shown that no
gender adjustments are necessary for the metabolic pathways
during shivering or prediction models of cold exposure, as
long as percentage of body fat and the ratio of body surface
area to size are taken into account (378).
Age
It has been reported that the well documented increase in
CO in young subjects during HOWI is blunted in older
subjects (302). In TN HOWI, older subjects had less sensitive
spontaneous baroreflex sensitivity than younger subjects
based on the variation of HR (390). This may be due, in part
to older subjects having less carotid arterial compliance than
young, and increased systolic blood pressure (SBP) (390).
SNA is depressed in all subjects during TN HOWI; however,
there is much less suppression in the older subjects (262).
In fact, there is an inverse relationship between age and the
Volume 5, October 2015
The Aquatic Environment
sympathetic suppression induced by TN HOWI (262). Older
subjects have a blunted increase in SV and CO in TN HOWI
to both the shoulder and neck (302). SBP and TPR decrease
in response to HOWI, however less so in the elderly. Ectopic
arrhythmias occurred regularly in elderly, but not in young
subjects. In elderly subjects, blood pressure is elevated in
HOWI, in spite of the blunted increase in SV and constant
HR suggesting that vasoregulatory mechanisms dependent
on the baroreceptor reflex diminish with age (361).
No difference in thermosensitivity, mean Ts , metabolic
heat production, Tc and slope of Tc and heat production were
observed between old and young during HOWI for 40 min
in 20◦ C (147). Sensory perception determined by cold hand
immersion detection threshold was higher in older subjects
and required a greater noxious stimulation to reach the thresh-
old for pain (407).
Older subjects have been reported to have more shunt
blood flow in the lungs than younger subjects resulting in
lower perfusion areas and perfusion distributions showing
more inequality in VA /Q (88). No temporal changes were
seen in old or young subjects over 30 min. In young subjects,
CV increased 77%; however, it was below the tidal breath-
ing range upper limit. However, in older subjects, CV only
increased 34% and was not different from the tidal breathing
range. While the absolute volume change during HOWI is not
dependent on age, ERV was decreased both groups but was
lower in older.
In spite of a lesser elevation of CO in older subjects, their
natriuretic response to HOWI was augmented, with increased
GFR (361) in spite of a decline in pressure-dependent sodium
and water excretion in older subjects (395). Nocturnal urine
production increases with age after 50 years, with increased
urination frequency being reported during supine position dur-
ing sleep when CO is increased (28). Similarly, the renal
responses to HOWI are attenuated at night in young subjects;
this may not be the case in elderly subjects (205, 344).
Exercise in Head-Out Water Immersion
The modes of exercise in the aquatic environment are man-
ifold and so are their respective physiological responses. In
this section, this topic will be covered by dividing the modes
of exercise in water into two main categories.
1. Water locomotion. The energy requirements of cyclic type
activities such as swimming, rowing, and kayaking can be
appropriately described by measuring their “cost of trans-
port” (C). It will be shown how this parameter depends
on the speed and the mode of locomotion and how C is
affected by “biomechanical” factors such as hydrodynamic
resistance and propelling efficiency; the former is larger,
the higher the speed, and the wetted area of the immersed
body/boat, the latter is larger, the greater the distance cov-
ered per cycle. These forms of exercise in water could
also be defined as “competitive aquatic sports” even if this
1719
The Aquatic Environment Comprehensive Physiology

definition includes other activities (such as water polo and 2.5

synchronized swimming) that will not be considered here.

2. Water-based activities. These are performed in HOWI 2.0

(e.g., water walking, water running, and water fitness).
The main difference between these activities and the other
competitive aquatic sports is in their aim: while the former 1.5

E (kw)
are mainly performed to improve an athlete’s performance,
water-based activities are mainly performed to maintain L

·
and improve health in the general population, and/or as a 1.0 UWF
rehabilitation mode for athletes and patients. These activ- AL
ities can be carried out with or without specific equipment K
and their energy demands depend essentially on two “water 0.5
R
characteristics”: buoyancy and drag. The former is larger
the deeper the immersion level of the body/body parts, the
latter is larger the greater the frequency and the amplitude 0
of the movement of the submerged body parts. 0 1 2 3 4 5 6
υ (m · s–1)

Water Locomotion: Energetic and
Mechanical Determinants
As is the case for land locomotion, locomotion in the aquatic
environment can be sustained with or without locomotory
tools; these tools do not supply additional energy but provide
effective compensation for the limitations in our anatomical
design and for inadequacy in muscle performance (2, 261);
their effects on the energetics and mechanics of water loco-
motion allow to better understand the general principles that
determine the physiological responses in this environment;
for this reason, data referring to some of these tools (i.e., fins,
kayak, and rowing shell) will be presented in the following
paragraphs, along with data referring to the swimming strokes
(the “unaided” cyclic modes of water locomotion).
In Figure 11 (adapted from 308) the metabolic power
expenditure (E′ , kW) of different forms of aquatic locomo-
tion is reported as a function of the locomotion speed (v,
m . s−1 ): surface swimming with leg kick (barefoot) (E′ =
0.91 . v1.75 ), fin swimming below the surface with SCUBA
diving equipment (E′ = 1.08 . v1.39 ), front crawl swimming
(E′ = 0.60 . v1.87 ), kayaking (E′ = 0.098 . v2.76 ), and rowing
(E′ = 0.088 . v2.05 ). The equations listed above are determined
from reanalyzing the original data (92,299,338,431,438) with
power functions over the aerobic speed range. As indicated
by Figure 11, metabolic power increases sharply as a function
of speed and, at similar velocities, it is greater for leg kicking
(both underwater and at the surface), slightly lower for the
front crawl and lower by a significant amount in kayaking
and rowing.
The energy expenditure of cyclic forms of locomotion
such as those indicated above, can be expressed not only as
a function of time (e.g., L O2 . min−1 or kJ . s−1 ) but also as
a function of the distance covered, by calculating the energy
cost per unit distance (C) as:
Figure 11 Net energy expenditure (E′ , kW) is plotted as a function
of the speed (v, m . s−1 ) for different forms of aquatic locomotion (orig-
inal data were interpolated over the aerobic speed range, see text for
details). L: swimming by using the leg kick at the surface; UWF: under-
water swimming with SCUBA diving equipment; AL: swimming the front
crawl; K: kayaking; R: rowing. Taken from Pendergast et al. (308) with
permission.
where E′ is metabolic power expenditure and v is the speed
of progression. Expressing the velocity as m . s−1 and E′ in
kJ . s−1 , C results in kJ . m−1 (94): (it represents the energy
expended to cover a specific distance at a given velocity).
Equation 1 indicates that, for a given metabolic power, the
locomotion speed will depend on the differences in C among
locomotion modes. This is shown in Figure 12 where the
energy cost of the forms of locomotion considered above is
reported. The solid lines are the iso-metabolic power hyper-
bolae of 0.5, 1.0, 1.5, and 2 kW. For the same metabolic
power (e.g., 0.5 kW), the locomotion speed will be larger in
the forms of locomotion with the lower C, that is, from about
0.6 m . s−1 in SCUBA diving to about 2.4 m . s−1 in rowing.
For a swimmer, or a boat, to progress in calm water at a
specific, constant, velocity, the propulsive force must be equal
to the sum of the resistances opposing locomotion. Thus, the
increase in E′ with the speed mirrors the increase in (total)
mechanical power output (Wtot ′ , kW) that the swimmer has
to supply to maintain that velocity (261). Figures 11 and 12
indicate, therefore, that the speed of locomotion is a “mea-
sure” of the intensity of exercise and that, for a given form of
aquatic locomotion, the physiological responses to exercise
depend on (could be graded based on) the locomotion speed.
As for land locomotion, the total mechanical power of
aquatic locomotion (Wtot ′ ) is the sum of two terms (e.g., 50):
the power required to move the limbs with respect to the centre
of mass (the internal power, Wint ′ ) and the power required to
compensate for external forces (the external power, Wext ′ ):

C = E′ v−1 (1) ′
Wtot ′
= Wext ′
+ Wint (2)

1720 Volume 5, October 2015

Comprehensive Physiology The Aquatic Environment

1.5 ηP . Propelling and Froude efficiency refer to the mechanical

partitioning only, whereas the performance and the overall
L
efficiency take into account also the energy expenditure. The
UWF
efficiency with which metabolic power input (E′ ) is trans-
AL
formed into useful mechanical power output (Wd′ ) is termed
1.0 K performance (or drag) efficiency (ηd ) and is given by:
R
C(kJ · m–1)

ηd = Wd′ ∕E′ (6)

The efficiency with which metabolic power input (E′ ) is

0.5 transformed into mechanical power output (Wtot ′ ) is termed

overall (or gross or mechanical) efficiency (ηO ) and is given

by:

′
ηO = Wtot ∕E′ (7)
0
0 1 2 3 4 5 6 It follows that: ηO = ηd /ηP . Combining Eqs. (5) to (7) one
υ (m · s–1) obtains:

Figure 12 Net energy cost (C, kJ . m−1 ) is plotted as a function of the
speed (v, m . s−1 ) for different forms of aquatic locomotion (original data
were interpolated over the aerobic speed range, see text for details).
The continuous lines represent iso-metabolic power hyperbolae of 0.5,
1.0, 1.5, and 2 kW (from bottom to top). L: swimming by using the leg
kick at the surface; UWF: underwater swimming with SCUBA diving
equipment; AL: swimming the front crawl; K: kayaking; R: rowing. Taken
from Pendergast et al. (308) with permission.
E′ = Wd′ ∕(ηP ηO ) (8)
that relates the metabolic power input (E′ ) with the power
needed to overcome hydrodynamic resistance (Wd′ ) and with
propelling (ηP ) and overall (ηO ) efficiency, at a specific veloc-
ity.
Since, for any given speed, C = E′ /v and Wd′ = Wd . v:

For aquatic locomotion Wext ′ is comprised of two factors:

the power to overcome drag, generating thrust (Wd′ ), and that
that does not add to the thrust (Wk′ ):
′
Wext = Wd′ + Wk′
Both Wd′ and Wk′ accelerate water giving it kinetic energy
but only Wd′ contributes to propulsion (e.g., 8, 80). The
efficiency with which the external mechanical power pro-
duced the swimmer/kayaker/rower is transformed into “use-
ful” mechanical power (thrust) is termed Froude (theoretical)
efficiency (ηF ) and is given by:
ηF = Wd′ ∕Wext
′
The efficiency with which the overall mechanical power
produced by the swimmer/kayaker/rower is transformed into
“useful” mechanical power (thrust) is termed propelling effi-
ciency (ηP ) and is given by:
ηP = Wd′ ∕Wtot
′
This parameter (ηP ) is of utmost importance in water
locomotion since it indicates the capability of the swim-
C = Wd ∕(ηP ηO ) (9)
that relates the energy cost of locomotion with the work, per
unit distance, that is necessary to overcome hydrodynamic
(3) resistance (Wd ) and with propelling (ηP ) and overall (ηO ) effi-
ciency, at a specific velocity. For further details, see Zamparo
et al. (433).
Equations (8) and (9) show that differences in E′ (or in
C) among locomotion modes in water, at any given speed and
for a specific ηO , depend on differences in ηP and/or in Wd′
(or Wd ); it also indicates that, for a given locomotion mode,
increasing ηP and/or decreasing Wd′ (or Wd ) would result in
decreased E′ (or in C). The justification for this postulate is
(4) discussed in the following paragraphs.
All cyclic forms of locomotion involve the intermittent
application of forces: the mean velocity (v, m . s−1 ) is indeed
the product of the cycle frequency (f, cycle . s−1 , Hz) and of
the distance covered per cycle (dc , m . cycle−1 ) (e.g., 75). As
shown by Figure 13 (which reports the f vs. v relationship
in the forms of locomotion in water taken as an example)
(5) each mode of locomotion is almost univocally defined by its
dc : surface leg kicking = about 0.5 m . cycle−1 ; underwater
fin swimming with SCUBA diving equipment = about 1 m
. cycle−1 ; front crawl swimming = about 2.5 m . cycle−1 ;

mer/kayaker/rower to transform at best his or her muscular
power into power useful for propulsion. Propelling efficiency
could vary from 0 (none of the power provided by the muscles
is useful for propulsion) to 1 (all power is utilized for propul-
sion); if the internal power (Wint′ ) is nil or negligible η =
F
kayaking = about 4 m . cycle−1 ; and rowing = about 8 m .
cycle−1 . These differences have to be attributed (at least in
part) to the length of the “propelling tool” (i.e., arms, legs,
paddles, or oars) but essentially indicate the capability of the
swimmer/rower/kayaker to exert useful forces in water: the

Volume 5, October 2015 1721

The Aquatic Environment
150
L
UWF
100
AL
ƒ(cycles · min–1)
R
50
0 0
0 1 2 3 4 5 6 0
υ (m · s–1)
Figure 13 Cycle frequency (f, cycles . min−1 ) is plotted as a func-
tion of the speed (v, m . s−1 ) for different forms of aquatic locomotion
(original data were interpolated over the aerobic speed range, see text
for details). The average distance the body/boat travels per cycle (dc ,
m . cycle−1 ) is indicated by the continuous lines irradiating from the
origin. L: swimming by using the leg kick at the surface; UWF: under-
water swimming with SCUBA diving equipment; AL: swimming the front
crawl; K: kayaking; R: rowing. Taken from Pendergast et al. (308) with
permission.
power available for propulsion (Wd′ ) is indeed responsible
for the distance the body/boat travels per cycle, as originally
indicated by Craig and Pendergast (75); dc is thus an index of
propelling efficiency and these two parameters were indeed
found to be related: ηP = 0.46 . dc 0.21 (R = 0.78), as shown by
Pendergast et al. (308) for these forms of water locomotion.
The power to overcome drag (Wd′ , W) is given by:
Wd . v, where v is velocity (m . s−1 ) and Wd is the work
to overcome drag in the unit distance (J . m−1 = N), Wd has
thus the same units and significance of hydrodynamic resis-
tance (D, N). Hydrodynamic resistance increases as a function
of velocity in a similar fashion as E′ and C as seen in Figure
14; at comparable (paired) speeds D is larger in underwater
fin swimming (SCUBA diving, D = 115.7 . v1.57 ), slightly
lower for kicking at the surface (D = 42.9 . v1.55 ) and the
front crawl (D = 49.8 . v1.03 ) and significantly reduced for
boats locomotion A rowing shell (D = 12.8 . v1.33 ) offers a
lower resistance to motion than a kayak (D = 14.5 . v201 ) (see
308).
Taken together, the differences in ηP (or dc ) and D can
thus explain the differences in E′ (and C): as an example: (i)
in SCUBA diving ηP (dc ) is larger than when leg kicking at the
surface but the former demands more energy than the latter
because its D is larger; (ii) the similar values of D between leg
kicking and front crawl swimming indicate that the primary
difference in the metabolic power (E′ ) or in the energy cost
(C) between these two forms of locomotion must be in their
relative propelling efficiencies (in their dc ).
1722
Comprehensive Physiology
150
100
D (N)
L
50 UWF
AL
K
R
1 2 3 4 5 6
υ (m · s–1)
Figure 14 Active/passive drag (D, N) is plotted as a function of
the speed (v, m . s−1 ) for different forms of aquatic locomotion (origi-
nal data were interpolated over the aerobic speed range, see text for
details). L: swimming by using the leg kick at the surface; UWF: under-
water swimming with SCUBA diving equipment; AL: swimming the front
crawl; K: kayaking; R: rowing. Taken from Pendergast et al. (308) with
permission.
To understand the physiological demands of cyclic forms
of aquatic locomotion, it is therefore sufficient to measure the
locomotion speed and to know the E′ versus v (the C vs. v)
relationship of that locomotion mode. A deeper understand-
ing of the energetics of aquatic locomotion can be obtained
by assessing the hydrodynamic resistance and the propelling
(and overall) efficiency of the locomotion at stake. These are
not easy tasks in this environment and in the following sec-
tions a survey of the techniques mostly used to assess these
parameters are reviewed.
Measurement of E ′ , W ′ d , and ηP in the water
environment
Metabolic power (E ′ )
The large majority of aquatic locomotion studies report data of
submaximal energy expenditure after steady state conditions
are attained, a condition for which is not necessary to esti-
mate the role of anaerobic energy sources, the determination
of which, as indicated below, is based on several (and some-
times debated) assumptions. Metabolic power (E′ ) at constant,
submaximal (aerobic) speeds can be calculated by measuring
the oxygen consumption after a steady VO2 is obtained (VO2 ss )
using standard open-circuit techniques. Under this condition,
energy expenditure is based only on “aerobic energy sources”
′
(E′ = EAer = VO2 ss ) (93). Douglas bags, balloons, or portable
metabolimeters can be utilized to measure continuously VO2
during exercise but often this is a challenging task in the water
environment. An alternative way to assess VO2 ss is to use the
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Comprehensive Physiology The Aquatic Environment

“back extrapolation technique” where breath by breath oxy- Table 1 Percentage contribution of aerobic (EAer ), anaerobic lactic
gen consumption is taken during the first 30 to 45 s immedi- (EAl ), and anaerobic alactic (EAnAl ) energy sources to overall energy
expenditure during maximal swimming trials (average for the four
ately postexercise (e.g., 327, 431). From the linear regression strokes) over three distances (adapted from 46) and during maximal
of the logarithm of the VO2 values as a function of recovery trials on the Olympic kayak over four distances (adapted, with permis-
time, VO2 can be backward extrapolated “at time zero” and sion, from 434).
the VO2 ss can be estimated (e.g., 71, 269, 270).
Since VO2 reaches a steady state value (at muscular level) Distance Time Speed EAer EAl EAnAl
with a time constant (τ) of about 30 s (330), the methods (m) (s) (m/s) (%) (%) (%)
indicated above could also be applied to measure the aerobic
contribution to metabolic power (Eaer ′ ) in maximal trials last-
Swimming 45.7 25.9 1.76 19.2 54.8 26.0
ing at least 2 to 3 min (e.g., more than 4-5 τ). In these cases,
Swimming 91.4 57.5 1.59 37.4 44.2 19.4
the anaerobic lactic energy contribution to metabolic power
′ ) plays a significant role, the more so the shorter the exer-
(EAnl Swimming 182.9 126.6 1.45 62.4 25.3 12.3
cise time; in these conditions: E′ = Eaer ′ + E′ . The lactate Kayaking 250 61.9 4.04 40.5 37.3 22.2
Anl
′
contribution to E can be calculated from the net increase of Kayaking 500 134.8 3.71 60.4 26.9 13.4
blood lactate concentration (ΔLab ) determined after exercise: Kayaking 1000 289.0 3.46 83.3 8.8 7.9
′
EAnl = b ΔLab . t−1 , where t is the exercise time and b is
Kayaking 2000 568.2 3.52 89.5 6.1 4.4
the energy equivalent of lactate (e.g., 3 mLO2 . mmol/L−1 .
kg−1 , as proposed by di Prampero (93). As can be evaluated
from the above equation, the role of EAnl′ is reduced for longer

exercise durations, regardless the absolute peak lactate con-

centration in blood. This approach has been validated and
used to determine the energy cost of maximal swimming and
kayaking trials by several authors (e.g., 47, 431, 432).
During all-out tests of shorter duration (less than 2-3 min),
metabolic power (E′ ) can be estimated as the sum of three
terms, as proposed by Wilkie (414) and later applied to land
locomotion (94), to swimming (115,432,437) and to kayaking
(42, 431):
E′ = EAnS t−1 + α VO2 max − αVO2 max τ ⋅ (1 − e−(t∕τ) )t−1 (10)
where α is the energy equivalent of O2 (e.g., 20.9 kJ . lO2 −1
consumed, for a QR of 0.96), τ is the time constant (s) where-
with VO2 max is attained at the onset of exercise at the muscular
level (about 30 s, 328), EAnS is the amount of energy derived
from anaerobic energy utilization, t is the time of performance
(s), and VO2 max is the net maximal oxygen uptake (above rest-
ing values). The third term of Eq. (10) is an estimate of the
oxygen debt incurred at the onset of exercise and, therefore,
the aerobic contribution to metabolic power (EAer ′ ) can be esti-
mated as the sum of the second and third term of Eq. (10). EAer ′
thus increases with the duration of exercise becoming equal
to α VO2 max in maximal exercises of 2 to 3 min or more (e.g.,
more than 4-5 τ). EAnS′ (EAnS . t−1 ) is equal to the sum of the
′ ,
metabolic power derived from lactic acid production (EAnl
see above) plus that derived from phosphocreatine splitting:
′ = PCr (1 − e −t/τ) . t −1 , where PCr is the phosphocre-
EAnAl
atine concentration at rest (in the contracting muscles), t is
the exercise duration, and τ is the time constant of PCr split-
ting at work onset (about 30 s). This analysis assumes that
the time constant of PCr breakdown at the start of exercise
is equal to the time constant of the VO2 -on response at the
muscle level (330). As was the case for EAnl ′ , E′ decreases
AnAl
as the exercise time gets longer, regardless the absolute PCr
concentration at rest.
This approach to estimate E′ [by means of Eq. (10)] is
discussed in detail by di Prampero (95) and Capelli et al.
(47) and is only applicable to “square wave” exercises at
intensities at or above maximal aerobic power where oxygen
uptake does not achieve a steady state, and where other energy
sources play a major role.
The percentage contribution of the aerobic (Eaer ′ ) and
′ ′
anaerobic (EAnl and EAnAl ) energy sources to total metabolic
power is shown in Table 1. The percentage contribution of
′ , E′ , and E′
Eaer is almost independent of gender, skill
Anl AnAl
and mode of aquatic locomotion, but is dependent on the dura-
tion of the exercise (t). As an example, for all out efforts of
the same duration (about 1 min, e.g., over a distance of 100 m
in swimming and 250 m in kayaking) the aerobic and anaero-
bic lactic energy sources supply about 40% and the anaerobic
alactic energy source about 20% of total power expenditure
(47, 432).
Passive and active drag
The hydrodynamic resistance (D) determined by towing a
“passive” subject (or a boat) through the water (when the
subject is not providing propulsion) and is defined as passive
drag (Dp , N). When this resistive force is measured (e.g., by
means of a force transducer) at constant speed (v, m . s−1 ),
the power to overcome drag (Wd′ , W) is simply calculated as:
Dp . v. By repeating these experiments at different speeds,
the Dp versus v relationship can be determined. Data of Dp
reported in the literature are fairly consistent (for a review, see
159, 160). Females and children are characterized by lower
values of Dp compared to adult male swimmer due to their
smaller body dimensions and better floating characteristics
(e.g., 52, 64, 195).

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The Aquatic Environment
In “passive conditions,” no propulsion is provided by
the swimmer/rower/kayaker whereas, in actual swimming (or
paddling) conditions, the arms/paddle/oars movements create
propulsion but also create additional resistance; thus, active
drag (Da ) is expected to be significantly larger than passive
drag (Dp ) (159, 417, 433, 436).
The Da versus v relationship in swimming has been inves-
tigated with a specially designed Measuring Active Drag sys-
tem which measures the push off forces (F) exerted by the
swimmer using only arm strokes at a constant speed. The F is
measured by pads fixed to a solid rod positioned underwater
under the swimmer. Under this condition, for the action reac-
tion principle, it is assumed that Da = F (e.g., 387). According
to these authors Da ≈ Dp , this unexpected finding could be
explained by the fact that it is required that the swimmer does
not use the legs, they are floated by a pull buoy, thus reducing
the swimmer’s wetted area (as discussed below). Therefore,
with this method, the values of Da are probably underesti-
mated. Active drag has also been estimated by the difference
in swimming speed caused by free swimming with various
hydrodynamic bodies attached that create a known additional
resistance (197). This method, however, can be applied only
at maximal speed and thus does not allow to determine the Da
versus v relationship.
Active drag can be inferred from metabolic measures as
originally proposed by di Prampero et al. (96): the hydro-
dynamic resistance of a swimmer/boat moving in water at
constant speed, could be increased or decreased by attaching
to the swimmer/boat known forces (e.g., an added drag, AD)
acting in the direction of progression. Using this method, the
relationship between steady state VO2 and added/subtracted
drag is linear for any given speed. The extrapolation of this
relationship to resting VO2 yields a value of AD that is in abso-
lute terms (and opposite in sign) equal to the average active
drag (Da ), that is, to the propelling force that the person has to
provide to proceed at that velocity (see also 94,300,432,438).
With this method, the active drag of front crawl swimming
and kayaking was investigated; these studies have shown that:
(i) in front crawl swimming active drag is almost twice than
passive drag: Da = 44 . v1.60 and Dp = 24 . v1.99 (in elite
male swimmers) (436), and (ii) not only active drag is larger
than passive drag but the former depends on the technical
skill of the subjects; as an example in kayaking: Dp = 0.90 .
v1.63 whereas Da (elite men) = 1.48 . v2.01 and Da (unskilled
man) = 2.32. v1.75 : the lower the technical skill the larger the
additional resistance to motion “created” by the subject while
moving in water at a given speed (299).
These data indicate that Da > Dp , as expected; they also
indicate that, to understand the effects of hydrodynamic resis-
tance on the physiological responses of exercise in the aquatic
environment Da and Dp are not interchangeable and that
Da should be assessed/estimated instead of Dp . However,
whereas measurements of Dp have been made for a long time
using many methods, the measure of Da is still a controver-
sial issue (e.g., 160, 387, 416, 436). The difficulty measuring
Da prompted some authors to investigate the effects of some
1724
Comprehensive Physiology
determinants of Da that are more easily calculated than Da
itself on energy expenditure.
Hydrodynamic resistance can be considered as the sum of
three simultaneously created drag components: (i) form (pres-
sure) drag, that depends on the wetted area of the immersed
body/boat [see Eq. (11) below]; this component of drag
increases with the speed of movement and prevails at low
to moderate speeds (up to about 1.2 m . s−1 ); (ii) friction drag,
that depends on the surface characteristics of the body/boat
and that is determined by viscosity effects between the water
particles that are carried away in the vicinity of the body/boat;
this component of drag is rather unaffected by the speed of
movement; and (iii) wave drag, that derives from displac-
ing and rising water masses against gravity and thus from
creating waves at the water surface; this component of drag
increases as the speed of movement increases and is prevail-
ing at the highest speeds attained in swimming competitions
(1.8-2.0 m ⋅ s−1 ) and in boat locomotion. For more details,
see (268, 306, 307).
Form, or pressure, drag can be calculated as:
Dpr = 1∕2 ρCd Av2 (11)
where ρ is water density, v is the velocity, Cd is the drag coef-
ficient, and A is the projected frontal area (in the direction
of movement). Cd is a coefficient that takes into account the
shape of the body in motion; smaller values of Cd are asso-
ciated with elongated shapes oriented in the direction of flow
(streamlined objects) (397). For partially submerged bodies,
A is the “wetted” area: the surface exposed to the water, since
that exposed to air has a negligible resistance (ρ of air is about
800 times lower than that of water).
Kayaks and rowing shells float on the surface and have
lower values of Cd compared to human swimming; these
boats are long and narrow (a single scull is about 8 m long
and 0.3 m wide) and their design keeps pressure and wave
drag low. In boat locomotion, the weight of the boat (about
10-15 kg for a single sculls) is the major determinant of the
wetted surface area: an increase in weight has been reported
to increase hydrodynamic resistance by 10% for rowing and
20% for kayaking for a 20% increase in weight (299, 343).
As for boat locomotion, the wetted area of the swimmer
depends on the dimensions of the body (e.g., it is larger in
heavier and taller swimmers) and on the fraction of the body
that is submerged (which is larger the larger the “underwater
weight” of the swimmer) but in swimmers A depends also on
the body incline. Indeed, whereas the “underwater weight”
of the swimmer is determined by Archimedes’ principle as is
the case for boats, in swimmers the “wetted area” depends not
only on the balance between weight (W) and buoyant force
(B) but also on the distance between the points of application
of these two forces. In the human body, these do not coincide
and this induces the body to rotate, the entity of this rotation
(the angular momentum) depending on the values of W and B
and on their lever arms. Particularly at low speeds, swimmers
are not horizontal to the surface of the water and this
increases their projected (wetted) frontal area. As the velocity
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Comprehensive Physiology The Aquatic Environment

of progression increases, the body becomes more horizontal
to the surface and the wetted area decreases (436); in this
condition, the major determinant of D is the underwater
weight of the swimmers, as is the case for boat locomotion.
Due to its importance in determining wetted area, and due
to the difficulties of measuring Da , body incline was inves-
tigated in static or dynamic “conditions” by several authors.
The effect of the underwater static position on the energet-
ics of swimming can be described quantitatively by measuring
(with an underwater balance) the underwater torque (T) which
is a quantitative measure of “the tendency of the legs to sink”:
in kayaks and rowing shells (e.g., 307, 434). Drag efficiency
increases with increasing velocity in both swimming and boat
locomotion, as is the case for ηO (e.g., 308).
Even more controversial than ηd are the methods utilized
to estimate overall and propelling efficiency, and the range of
their values. The values of ηO reported in the literature, for
swimming, range from 0.1 to 0.2 (387, 438) and the values of
ηP range from 0.2 to 0.8 (115, 243, 386, 429, 438). As previ-
ously indicated (441), ηp can be calculated based on values
of drag efficiency provided that overall (gross) efficiency is
known (ηO = ηd /ηp ). In cycling, where Wtot ′ can easily be

the greater T the higher the wetted area (and thus D) and the
greater the C is for a given speed. As men have greater T, they
expend more energy per unit distance than women; at low
swimming speeds (0.9-1.1 m . s−1 ) about 70% of the variabil-
ity of C is explained by the variability of T, regardless of the
gender, age and skill of the swimmer (e.g., 96, 300, 431). At
higher swimming velocities (> 1.2-1.4 m . s−1 ) the hydrody-
namic lift counteracts the T, so that the body is horizontal to
the water surface,; at these speeds no relationship between T
and C could be observed anymore (431), at least in the front
crawl.
In “dynamic conditions” (during actual swimming), the
wetted area depends on the body incline of the swimmer’s
body in respect to the waterline and the latter can be measured
by means of underwater cameras (e.g., 268, 435, 436). The
relationship between the static and dynamic position in water
depends thus on the speed and, at high swimming speeds, A
is essentially determined by body surface and by the fraction
of body that is submerged (the body incline being negligible).
As shown by Zamparo et al. (436) at speeds from 1 to 1.6
m . s−1 the average body incline during (front crawl) swim-
ming is about twice that measured when the same swimmer
is passively towed in water (about 10◦ and 5◦ , respectively);
this supports the hypothesis that Da > Dp and actually these
authors calculated that Da is indeed about twice than Dp (see
above), as previously reported also by other authors (e.g.,
96, 300).
Drag, propelling, and overall efficiency
The determination of ηP and ηO requires the measure of the
total mechanical work (or work rate) of aquatic locomotion
[Wtot or Wtot′ , see Eqs. (5) and (7)]. Given the difficulties in
measured with proper ergometers: ηO = 0.25-0.30. Overall
efficiency in all cyclic forms of locomotion should theoreti-
cally have the same value, as long as elastic energy does not
play a role. In addition, the total power output must be pre-
cisely measured to have a valid calculation. This proposal is
supported by a study (152) that demonstrated that ηO can be
as high as 0.24 (in elite oarsman during a simulated 2000 m
race on a rowing ergometer) and the same value was reported
for “simulated swimming” on a laboratory based ergometer
(441). The values of v, C, Wd′ , and ηp for various forms of
aquatic locomotion are shown in Table 2. Thus, the lower ηO
values for swimming are likely due to the failure to account
for all forms of work or lost energy during free swimming. It
necessarily follows that, for ηO values of about 0.20 to 0.25,
and since ηd = 0.03-0.09, ηp could be as high as 0.36 to 0.45:
for example, only 50% of total power output results in propul-
sion (useful thrust) in subjects while swimming (441). These
estimates appear valid as humans are not ideally designed
physically for locomotion in water, as compared to cetaceans
that have ηp values ranging from 0.75 to 0.90 (116).
In the last decade, a novel approach to determine pro-
pelling efficiency was put forward (243, 429, 435, 437, 441):
instead of attempting to assess ηP based on measures of
Table 2 Values of speed (v) energy cost (C), power to overcome drag
(W′ d ) and propelling efficiency (ηp ) at metabolically equivalent speeds
(E′ tot = 0.5 kW) in different modes of aquatic locomotion. Adapted,
with permission, from Pendergast et al. (308) and from Zamparo et al.
(434).
Mode of Speed range v C W′
d
locomotion (m/s) (m/s) (kJ/m) (W) ηp

just assessing Da it is not a surprise that only few papers UWF 0.4-0.8 0.6 0.88 31 0.58
attempted to estimate these two parameters. Drag efficiency
LK 0.6-1.0 0.7 0.70 17 0.36
(ηd ) only requires measures of drag and energy expenditure
[Eq. (6)] which are easily made and thus ηd values are likely FC 0.9-1.4 0.9 0.55 40 0.45
valid. This is the case even if the methods currently used to PW 1.1-1.3 1.3 0.36 44 0.39
estimate drag (active and/or passive) are controversial, they K 1.0-3.0 1.8 0.28 85 0.70
reliably show that less than 10% of the subject’s metabolic
WB 1.2-2.9 2.3 0.23 73 0.57
power can be transformed into mechanical power output
(ηd = 0.03-0.09) in the aquatic environment (e.g., 169, 300, R 2-5 2.4 0.22 99 0.70
387, 438).
UWF: underwater SCUBA diving with fins; LK: swimming with the leg
In boat locomotion, the values of drag efficiency are higher kick only; FC; front crawl swimming; PW: paddle-wheel boat; K: kayak-
than reported for swimming: for example, about 0.15 to 0.20 ing (slalom kayak); WB: water-bike: R: rowing shell.

Volume 5, October 2015 1725

The Aquatic Environment
force/power (which is quite difficult in the aquatic environ-
ment, as indicated above) the efficiency of leg kicking and arm
stroking were determined by methods designed for analysis
of animal locomotion. In swimmers using the leg kick (with
and without fins), ηp has been determined from values of for-
ward speed and of the speed of the backward wave traveling
along the body (439, 440) as previously applied to the study
of undulating fish (e.g., 8, 80, 217). The technique for the arm
stroke in front crawl swimming is comparable to the tech-
nique used for animals using a “rowing” motion that move
water by producing power strokes, due to the backward move-
ment of their appendages, with the recovery strokes returning
the appendages back to their starting position, moving for-
ward (8, 80). In the front crawl, as a first approximation, the
body can be assumed to move forward at constant velocity
(v) while the upper limbs (the appendages) move forward and
backward with a velocity u relative to the body. The ratio v/u
is proportional to the Froude efficiency in animal locomotion
(8) as well as in fluid machines (pumps, turbines, propellers,
fans, water wheels, and paddle wheels) as it is dependent on
the velocity of the components of the fluid and rotor at the
inlets and outlets (122). The velocity of the appendages (u, the
hand speed for the arm stroke) can be directly measured by
means of underwater kinematic analysis (115) or estimated,
by modeling the upper arms motion as the motion of a pad-
dle wheel (438); the values of ηp calculated in this way were
about 0.45 (in male elite swimmers). This value was expected
on theoretical grounds (441), and was not different between
the two methods (115).
Propelling efficiency in boat locomotion is larger than in
swimming (in the 0.65-0.75 range [e.g., 51,308)], and overall
efficiency was reported to be of about 0.20 to 0.22 (e.g., 92,
308) as previously found for exercise on a rowing ergometer
(where mechanical work can be accurately assessed) (e.g.,
152, see above).
The determinants of the energy cost of locomotion
(C)
Data reported in Figures 1-4 refer to selected aquatic loco-
motion modes and to elite male athletes. Differences in E′ , C,
D, and ηP are however reported in the literature as a function
of age, gender, and skill level; these parameters also differ
among strokes (in swimming) and depend on the specific
locomotor tool utilized to move in water. In the following
sections, more detailed information regarding the energetics
of water locomotion is reported.
The energy cost of swimming, for a given speed, is the
lowest for the front crawl, then backstroke and butterfly, with
breaststroke having the greatest cost (47, 170). For young
elite swimmers, the relationships between C and v for the four
strokes are well described by the following equations (adapted
from Capelli et al. 47): front crawl: C = 0.670 . v1.614 , Back-
stroke: C = 0.799 . v1.624 , Butterfly: C = 0.784 . v1.809 , breast-
stroke: C = 1.275 . v0,878 . Since elite athletes are characterized
by similar values of maximal metabolic power (Emax ′ ) these
1726
Comprehensive Physiology
differences in C should be accompanied for by differences in
maximal swimming speed (vmax ) among strokes. Indeed, this
was reported for male swimmers (US Olympic trials, 1976)
over the 100 m distance, the corresponding vmax are: 1.92,
1.70, 1.78, and 1.48 m . s−1 , respectively (75). Moreover, the
differences in C among strokes should depend on differences
in Da and ηP . Active drag or ηP have not been studied for
swimming strokes other than the front crawl but, as indicated
above, the distance covered per stroke (dc ) is an index of pro-
pelling efficiency. As reported by the same authors for the
same swimmers in the same conditions, dc is of 2.03, 2.24,
1.99, and 1.46 m . cycle−1 for the front crawl, backstroke,
butterfly, and breaststroke, respectively. Thus, as indicated by
Eq. (9), the greater the distance the body travels per stroke
(an index of ηP ) the lower the C; this general rule seems not
to hold for the backstroke which is characterized by a larger
dc than the front crawl but also by a larger C. This state of
affairs is probably due to differences in active drag between
these two strokes.
Compared to other forms of locomotion (e.g., cycling
or running) where minimal differences in C are observed
among subjects with different technical skills (5-10%), tech-
nical ability in swimming has a significant influence on C,
thus improving skill significantly reduces the C. As previ-
ously indicated, a recreational swimmer can spend as much
as twice the energy a good swimmer uses for proceeding in
water at the same speed (its C is 200% larger) and the latter
consumes about 20% to 30% more energy than an elite swim-
mer at comparable speeds (169, 170). Training is expected
to improve technical skills and thus would lead to improved
ηP and reduced C. It has been shown that 4 years of high
velocity training caused a 20% decrease in energy expendi-
ture (E′ ) and a 16% improvement in dc (propelling efficiency
was not calculated in this study) (367). In addition improved
skill would decrease Da by 15% to 35% (308); as shown by
Eq. (9) the reduction of Da is an important factor in reducing
C rafter training.
Both ηP and Da are influenced by the anthropometric char-
acteristics of the swimmer that change with growth, and are
also influenced by concurrent development and training. C
is thus expected to differ between children and adults and
between males and females. Women have indeed a lower C
(10-30%) than men (e.g., 52, 53, 269, 300, 431). The lower C
has been reported to be due to lower hydrodynamic resistance
secondary to smaller body size, and higher body fat (thus
they assume a more horizontal attitude in the water) (e.g.,
300, 430). A few studies have investigated the determinants
of C in children and adolescents. These studies indicate that,
at similar velocities, C is lower (10-50%) in children than in
adults (195, 312, 320, 437), the more so the younger the sub-
jects (437). Master swimmers are characterized by a higher C
compared to younger swimmers and, at comparable speeds,
C increases as a function of age (435); the decrease in maxi-
mal metabolic power (Emax ′ ) that occurs with age forces these
swimmers to reduce their speed; this, in turn, is related to an
unfavorable alignment of the body (and thus with an increase
Volume 5, October 2015
Comprehensive Physiology
in Wd ). More importantly, though, with age a deterioration in
propelling efficiency occurs so that C increases due both to
an increase in Wd and to a decrease in ηP (435).
These examples indicate that differences in C (E′ ) should
be expected based on differences in Wd , ηP , and ηO among
swimmers. The ACSM guideline tables (9) emphasize this
relationship by warning readers that physical activity energy
expenditure (PAEE) “can vary substantially from person to
person during swimming as a result of different strokes and
skill levels.” Thus, whereas it is true that in aquatic locomo-
tion an increase in speed corresponds to an increase in exercise
intensity, care should be taken in selecting the appropriate C
versus v (or E′ vs. v) relationship to estimate the actual values
of C (E′ ) in this environment. This is at variance with land
locomotion where in “healthy young adults” interindividual
differences in C for walking, running, and cycling are negli-
gible allowing for a proper and simpler prescription of PAEE
in “standardized conditions” (e.g., on flat and firm terrain, at
sea level and in the absence of wind).
Compared with swimming, boat locomotion is charac-
terized by far lower values of drag and far larger values of
propelling efficiency; this means that, according to Eq. (9),
C is much lower than in swimming. As is the case for swim-
ming, however, the energy cost of boat locomotion increases
(nonlinearly) as a function of the speed and is determined by
the design of the boat and the skill level of the athlete. As an
example, for sprint flat-water kayaking (K1 scull) C = 0.020
v2.26 (441) and for rowing C = 0.088 v1.05 (92).
By analogy to swimming studies, in kayaking C was found
to be up to 30% to 50% lower (at paired speeds) in elite than in
less experienced paddlers (42, 299). These differences were
attributed to differences in propelling efficiency. As is the
case for swimming, for the same skill level, male kayakers
were found to be less economical than females (299): a 5%
to 12% difference in C, increasing with increasing speed. In
this case, the difference was attributed to differences in Wd (a
lower body mass in female kayakers and hence a lower wetted
area).
As previously indicated for swimming, training decreases
the energy cost of boat locomotion (of about 25-33% in rowing
and 6-10% in kayaking), due to an increase in dc (an index of
ηP ) and a decrease in Da (e.g., after 4 years of training active
drag can be reduced by 18-50% in kayaking) (307).
Water based activities
Water-based activities (WA) are modes of physical exercise
performed in water and in HOWI. This general definition is
useful to distinguish these exercise modes from the cyclic
modes of aquatic locomotion (e.g., swimming, kayaking, and
rowing) and from other sport activities performed in water
(e.g., diving, synchronized swimming, or water polo).
WA (besides the recreational purposes) could be divided
into three major categories: (i) “aquatic fitness” (activities to
maintain and improve physical fitness carried out in water
using different techniques and methods); (ii) “aqua training”
Volume 5, October 2015
The Aquatic Environment
(a combination of water based activities to improve the
athletes’ physical performance); and (iii) “aquatic rehabilita-
tion” (a combination of water based activities aimed to total
or partial orthopedic and neurological rehabilitation). These
activities can be performed without specific equipment (i.e.,
water walking and running, aqua gym, and aqua aerobics),
can utilize small tools to increase water resistance (e.g.,
hand paddles) or to improve buoyancy (e.g., pull buoys and
buoyant jackets) or can be performed with specific equipment
(such as water steps, treadmills, and bikes). The physiological
responses to these forms of exercise (the energy expenditure
of WA) are greatly influenced by: (i) buoyancy and (ii)
hydrodynamic resistance.
Buoyancy
Archimedes’ principle is a law of physics stating that an
immersed body is buoyed up by a force (B) equal to the
weight of the fluid it actually displaces. According to this
principle, the submerged weight of a body in water (UW =
body weight − B) is reduced in proportion to the immersion
level; as a rule of thumb it allows for a 35% reduction in body
weight when the body is submerged up to the thigh, 50% up to
the navel, 75% up to the chest, and 90% up to the neck. In full
immersion, a human body thus weights only few Newtons. A
larger “unloading effect” could be obtained with immersion
in seawater (which has a larger density than fresh water).
Body volume (Vb ), mass (M), and density (Vb ) are related
as: Vb = M/ρb and thus, for a given immersion level, the
buoyant force will be larger the smaller the body density and
the larger the body mass. The density of muscle is about 1
g . cm−3 , of fat about 0.8 g . cm−3 and of bone about 3 g .
cm−3 ; this means that different buoyant forces will charac-
terize subjects with different anthropometric characteristics
(e.g., lean muscular subjects are less buoyant than subjects
with a large percentage of body fat due to their different
values of ρb ; hence differences should be expected between
males and females and between young and elderly people).
Moreover, when the lungs are also submerged, body density
will change with the changes in lung volume since air density
is about 800 times lower than that of water.
Thus, the “unloading effect of water” depends on the
level of immersion, on the density of water, on the volume
of the immersed body, on its density and on the volume of
air filling the lungs (when these are submerged). Therefore,
for a given water depth, different “unloading effects” can be
elicited in different subjects resulting in different physiologi-
cal responses.
The buoyant force has also a deep impact on the “static
equilibrium” (e.g., on the “static position” the body assumes
in water) as well as on the “dynamic equilibrium” (e.g., dur-
ing body movements). Let us consider, as an example, the
condition of a subject standing still (upright) in water up to
the neck: since the points of application of the buoyant force
(B) and body weight (W) do not coincide (the former is more
cranial and closer to the lungs than the latter) if they are not
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The Aquatic Environment
aligned on the vertical line (a condition in which the lever
arms of these two forces are nil) the body will rotate.
In dynamic conditions (e.g., while raising an arm) the
body’s centre of gravity changes and, if the arm is raised out
of the water, the value of B will also change. Furthermore,
inspirations and expirations will change the position of the
centre of buoyancy (and also the value of B); this means that,
in water, energy has to be expended to maintain the desired
body position (e.g., vertical during head out water activities)
and to avoid unwanted (and unbalancing) rotations, the more
so the larger the amplitude of the movements.
Buoyancy helps a body/body part to move toward the
water surface but resists a body/body part moving from the
water surface; buoyancy can be increased “artificially” by
utilizing flotation devices (e.g., pull buoys or buoyancy jack-
ets); since this equipment comes with a variety of size and
shapes this has an obvious influence not only on the value
of B itself but also on the angular momentum (depending on
where these devices are positioned on the body) as well as on
hydrodynamic resistance (see below).
Buoyant force can reduce the effect of the body’s weight
on its joints thus reducing compressive forces (e.g., 100). WA
can thus be a good alternative to land exercise in persons
with low physical fitness, that is, elderly individuals, people
with orthopedic or neurological disabilities, injured athletes,
as well as obese patients (see below).
Hydrodynamic resistance
The resistance to movement in water is the result of an effort
to move aside masses of water coupled with the effort to
overcome its frictional characteristics (density and viscosity).
When the movement in water is slow (or when the body is
still) buoyancy is the principal force acting on the body; as
the speed of motion increases, the resistance to movement
(D, hydrodynamic resistance) increases, becoming the most
important force acting on the body. As indicated previously,
form or pressure drag [Eq. (11)] is the most important compo-
nent of total drag at low to moderate speeds and thus the most
important form of drag for WA. According to Eq. (11), D (and
thus energy expenditure) will be larger the larger the speed
(v) of movement (or its frequency) and the larger the sub-
merged (wetted) area of the body/body segments in motion
(A). Indeed, the energy expenditure of a given WA is larger
the larger the movement frequency (e.g., 6, 7, 48, 246, 317).
In WA, D can be increased “artificially” by utilizing “resis-
tance equipment” (e.g., hand paddles). Since this equipment
comes with a variety of size and shapes this has an obvious
influence on A (and hence on D and on energy expenditure).
Moreover, the “added resistance” depends on how this equip-
ment is used since the value of A depends on the level of
immersion of the equipment and on its orientation along the
direction of movement.
Water immersion has thus two main consequences on the
physiological responses to exercise: (i) it reduces the energy
needed to rise the body/body segments against gravity thus
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Comprehensive Physiology
reducing the overall energy requirements of exercise, the more
so the larger the level of immersion; but (ii) the larger den-
sity of water (compared to air) provides “loading” during
all movements so that hydrodynamic resistance works as a
“confounding factor” increasing the energy requirements of
WA compared to the same movements performed on land,
the more so the larger the speed (frequency) of movement
and the larger the submerged area of the body/body segments
in motion. As an example, in water walking, the “favorable”
effect of buoyancy seems to be offset by the added resistance
of water when the level of water approaches/exceeds waist
level (145).
Since there is no means to assess with accuracy the
intensity of WA on the basis of “standardized biomechanical
parameters” (such as speed in swimming and boat locomo-
tion), the physiological effects of WA are difficult to sum-
marize and, indeed, the energy requirements of WA could
be larger, equal or lower than those of the same exercise
performed on land. The example of water running will be
reported as a reference of this state of affairs.
Deep water running
Deep water running (DWR) is running in place in the deep-
end of a swimming pool, usually wearing a buoyancy vest that
floats the body so the head is out of the water. The standard-
ized technique that must be used is, as an example, described
by Chu and Rhodes (61): “(i) the trunk should be slightly for-
ward in respect to the upright position; (ii) the arms and legs
should follow a “unilateral forward motion,” thereby avoid-
ing the motions of treading water (i.e., circular leg and arm
motions); (iii) the elbows should be at a 90◦ angle with the
trunk; and (iv) the hands should remain completely open in
the sagittal plane or in a closed fist to avoid “dog paddling” in
the water.
In DWR, there is no loading of the skeletal system and
the workload is generally incremented by increasing the fre-
quency of the movement (i.e., the “stride frequency”) by using
a metronome.
DWR could be considered as: (i) an “aquatic fitness” activ-
ity when aimed to maintain and improve physical fitness in
health individuals (e.g., 41,316); (ii) an “aqua-training” activ-
ity when utilized to maintain and improve the athlete physical
performance (43,324,413); or (iii) an “aquatic rehabilitation”
activity when utilized for total or partial orthopedic and neu-
rological rehabilitation (e.g., 125).
Lower values of VO2 max and HRmax are reported for
DWR compared to running on land or on a treadmill) (e.g.,
100, 123, 362). The lower values of HRmax were attributed
to physiological factors (e.g., altered baroreflex response
and increased venous return in water compared to land, see
below) but they were also found to depend on the different
“running techniques” adopted in water that could alter
segment kinematics and muscle activation patterns and could
prevent the runners from attaining the same intensity level
in the two conditions (266, 362). Indeed, Ghering et al. (143)
Volume 5, October 2015
Comprehensive Physiology
showed that competitive runners, familiar with water running,
were capable of achieving similar VO2 max values on land and
in water; however, those who were untrained in water running
showed a larger difference in VO2 max in the two conditions.
Familiarity thus plays an important role in physiological
requirements of DWR as previously shown (27, 124). Thus,
in accordance with what found is for water locomotion,
another parameter that has to be taken into consideration
to explain the energy expenditure of WA is the technical
skill (the efficiency) in performing that specific movement
in water.
When comparing land treadmill running with aquatic
treadmill running (or with running in shallow water) with
a level of immersion up to the xiphoid process, the differ-
ences in the physiological responses at maximal effort dis-
appear (e.g., 349, 388). In this case, however, the running
technique is expected to be more similar in the two condi-
tions (a push off phase on a solid surface is present in both
cases) and the “unloading effect” is lower than in DWR as
lower could be expected to be the difference in the kinematic
pattern between the two conditions, and hence in their energy
expenditure.
WA in “controlled conditions”
A fair comparison between exercise in water and on land can
be performed using cycloergometry in TN water conditions
so that the pattern of movement can be accurately matched
in the two conditions. To match the power output in the two
environments the effect of water resistance on the energy
requirements of exercise has to be taken into consideration.
The oxygen uptake of moving the legs underwater at a fre-
quency of 60 rpm was suggested to be equivalent to about
25 W of external power (e.g., 118, 297). By taking this into
account, it is possible to match also the power output in the
two conditions and thus have a direct comparison of the “spe-
cific” effect of water immersion on the type of exercise. In
these conditions V′O2 increases linearly as a function of exer-
cise intensity, and the slope in water is comparable to that on
land; no differences are observed in the VO2 /VE ratio and in the
slope of the HR versus VO2 relationship between conditions.
However, resting HR is about 10 bpm less in water compared
to land and HR is lower in water (of the same amount) at
low exercise intensities (< 1-1.2 L/min), as well as at VO2 max .
Additionally, no differences in VO2 max between conditions
are observed (309).
As a general rule, in HOWI in TN temperature at rest, tho-
racic blood volume, CVP and CO increase (e.g., 11,113), HR
remains unchanged (11), or decreases slightly (113). In spite
of the increased CO, MAP is unaffected as TPR is reduced,
secondary to increased blood flow to muscles and/or visceral
tissues (e.g., 11, 201). During moderate exercise CO remains
elevated whereas ventilation, VO2 , and HR do not differ from
those on land (e.g., 11,113,188,297). At higher exercise inten-
sities CO becomes more directly dependent on VO2 and the
ventilatory response is similar to that on land (e.g., 297).
Volume 5, October 2015
The Aquatic Environment
WA in “uncontrolled conditions”: General
considerations
Exercising at submaximal levels in TN water HR is simi-
lar (e.g., 11) or slightly reduced (e.g., 305) compared to that
assessed at similar VO2 values in air. The differences in the
HR response between water and land are expected to increase
at lower water temperatures where lower HR are observed for
a given VO2 (e.g., 230, 362). The lower HR has to be con-
sidered in WA exercise that is prescribed based on HR in the
swimming pool (with water temperatures of about 28◦ C) even
if exercise of moderate-high level reduces the temperature of
thermoneutrality (74).
As suggested by Reilly et al. (324), the lower values of
HR at a given VO′ , during submaximal exercise in water
2
compared to land, can be due to the ability of the subject
to exercise in water (as it occurs when comparing trained
and nontrained subjects for exercise on land). Also for this
reason, care should be taken when using HR to grade exercise
intensity in WA. Finally, the difference in maximal HR and
VO2 values observed in some studies (see the example of
DWR above) suggests that care should be taken also when
grading WA exercises based on the HRmax and VO2 max values
assessed on land.
All these considerations suggest that the differences in
the physiological response observed in WA studies between
water and land exercise in “uncontrolled conditions” could
be attributable to: (i) differences in exercise intensity (e.g., in
water mechanical power output is influenced by buoyancy and
drag and HR could not be used to grade WA intensity), (ii) dif-
ferences in the movement pattern (i.e., in neuromuscular and
kinematic responses); (iii) unfamiliarity/unhabituation with
the “new” environment; and (iv) to thermoregulation issues.
WA: The effects of training
Even if it is difficult to estimate with accuracy the inten-
sity/physiological response of a given WA based on some
E′ versus v relationships, as is the case for swimming and
boat locomotion, it is well recognized in the literature that
VO2 increases when the immersion level is reduced and when
the frequency of the movement in increased. This allows the
gradation of any WA in prescribing these exercises in accord
with dose-response principles (e.g., 9) as well as to utilize
these exercises for training purposes in different populations
of subjects.
Water-based physical activities are suitable for persons
who have low physical fitness, that is, elderly people (e.g.,
41, 389), persons with orthopedic or neurological disabilities
(e.g., 61, 81, 99), athletes after surgery or for treatment of
injuries (e.g., 362), and overweight or obese patients (e.g.,
129). Physical activity in water is also beneficial for fitness
for young adults and other healthy persons participating in
recreational activities (67,68,241). In general terms, when the
effect of water exercises is considered, there is general agree-
ment among the studies that water exercises are an effective
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alternative to traditional physical activities to improve health,
physical fitness, aerobic capacity, muscular strength, flexibil-
ity, and balance (e.g., 31, 61, 67, 68, 241, 313, 389, 398).
Respiratory muscle fatigue and training
In comparison to exercise on land at the surface, exercise
both in and under water has been reported to increase the total
WOB and respiratory muscle fatigue. During submersion,
divers have increased airflow resistance (227, 233, 392, 393)
due to breathing resistance and SLL (87, 369). The increased
WOB is exacerbated at deeper depths as the pressure increases
gas density in the lung and SCUBA gear that has to be used
to breathe (227). An additional factor may be increased end
expiratory lung volume (EELV) present both at rest and during
exercise (227, 364). However, it has been reported that EELV
is not elevated under these conditions (364), but negative SLL
may actually decrease EELV at rest and during exercise (227).
Breathing at decreased or increased EELV, changes the respi-
ratory muscle length to a disadvantaged length in reference to
the length-tension relationship and thus the force developed
for the same effort is reduced (39,247). The combination of the
factors described above causes an increase in the WOB, and
when combined with a lower efficiency (162) lead to higher
energy cost of ventilation and likely lead to the increased
respiratory muscle fatigue observed in aquatic exercise. Res-
piratory muscle fatigue has been demonstrated for surface
swimming, and this observation led to a recommendation to
use respiratory muscle training (RMT) to improve swimming
performance.
Until recently, respiratory muscle fatigue was not appre-
ciated as limiting exercise power or endurance. However, this
opinion has evolved recently for both maximal and submaxi-
mal exercise (38,157,158,158,231,356). Due to the increased
total WOB and potential reduced efficiency, the respiratory
system may be more limiting during aquatic exercise, par-
ticularly at depth. Although it was shown some time ago
that training the respiratory muscles could improve respira-
tory muscle strength and endurance (216), it was not until
more recent years that RMT (37) was shown to improve exer-
cise performance, and more importantly that various forms of
respiratory muscles training improved running, cycling, and
rowing performance (141, 168, 175, 198, 199, 214, 219, 238,
248,273,329,356,399,410). Leith and Bradley (216) were the
first to demonstrate that RMT could improve peak mouth pres-
sures (respiratory muscle strength) and the time a high level
of ventilatory work could be endured (endurance) with spe-
cific protocols that improved either strength or endurance, but
not both (216). They (216) demonstrated that high resistance
breathing (100% of maximal voluntary inspiratory and expira-
tory) improved maximal respiratory pressures but not respira-
tory endurance. They also demonstrated that high inspiratory
and expiratory flows, while isocapnic increased respiratory
endurance, but not strength (216). A later study showed that
resistance RMT at nominally 40% individual maximal inspi-
ratory and expiratory pressures increased both inspiratory and
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Comprehensive Physiology
expiratory pressures (321, 322, 425), but not to the extent that
training with 100% did in the previous study (216). In addition
in the latter studies (321,322,425), there was an improvement
in respiratory endurance, which was not reported for the train-
ing that used 100% pressures (216). Some previous studies
used a fixed resistance over the period of RMT (321,322,425).
More recent studies reported greater improvements in strength
and endurance using progressively increasing resistances as
training persisted over 4 weeks (415). It is important to note
that many of these studies failed to show an increase in max-
imal VO2 , or cardiovascular function; most of the improve-
ments were in respiratory function.
Several studies have reported a reduced VE for a given VO2
after resistive RMT during a submaximal constant-work rate
exercise at 70% to 85% of VO2 max exercise test (80% VO2 max )
(214,321,322,425). The reduced V̇ E was secondary to reduced
Bf , even if Vt was either maintained or slightly increased both
for exercise on land (214) and in water (320,321,421). Resis-
tive RMT increased the strength of the respiratory muscles
and was also associated with reduced VO2 for given WOB
(efficiency). In addition, the ventilatory pattern (increase in
VT and a decrease in Bf , i.e. reduced dead space ventilation)
decreased the WOB. The combination of decreased VO2 and
increased VT allowed swimmer to exercise longer times for
the same work rate.
Ventilation is known to be tightly correlated to VCO2 , how-
ever, in the presence of metabolic acidosis caused by anaer-
obic glycolysis and lactic acid accumulation VE is increased
out of proportion to VCO2 (respiratory compensation for a
metabolic acidosis). Tachypnea occurring at voluntary exer-
cise exhaustion pre-RMT is consistent with an increase in
lactic acid and may have induced premature respiratory mus-
cle fatigue (36-38). It has been demonstrated that 4 days of
nominally 80 cmH2 O intermittent inspiratory loading in dogs
increased the expression of the slow myosin heavy chain iso-
form in the costal, crural diaphragm, and intercostal muscles
(134). An increase in the slower myosin heavy chain isoform
is likely the result of increased airflow resistance and thus,
improves respiratory muscle and exercise endurance, espe-
cially under conditions of airflow limitation.
Head-Out Water Immersion in Cold
Water
Heat loss during cold HOWI is reduced by vasoconstriction
of the skin and subcutaneous fat layer that increases tissue
insulation (289-291, 396). Acclimatization also increases the
resistance to heat loss via peripheral vasoconstriction due to
either or both central or local factors (213). In addition, to
reductions in Ts and Tc , muscle blood flow is reduced in a
graded manner to the drop in Ts and Tc and maximal CO is
reduced leading to reduced VO2 max and exercise performance
in the cold (297). If the increased insulation does not prevent
a reduction in Ts and or Tc shivering takes place in a graded
Volume 5, October 2015
Comprehensive Physiology
manner, increasing VO2 and heat production in an attempt to
mediate heat loss (213).
HOWI in TN water does not increase or decrease resting
VO2 ; however, at cooler water temperatures, VO2 increases
in proportion to the drop in Ts and Tc as a function of time
(297). Swimming in water increases the work due to its higher
density than air, and thus the VO2 for a given velocity is
increased (307, 308).
The most dangerous situation in the aquatic environment
is drowning, which is more likely to occur in cold water
immersion. In nonacclimatized individuals, sudden cold water
immersion results in an increase in HR (31 b/min), hyperven-
tilation (both Bf and VT ) with a lowering of PaCO2 , and a
reduction (50%) in cerebral blood flow velocity (235, 236).
These physiological changes can lead to drowning, without
hypothermia. Acute cold water immersion commonly results
in an initial gasp, and is followed by hypertension and hyper-
ventilation that significantly reduce arterial CO2 (hypocap-
nia). Thus, the expected effect of hypocapnia on ventilation is
overridden by the sudden exposure to cold water. (82). It has
been reported that after just 30 min of immersion or swim-
ming in cold water decision making ability is impaired (101).
Furthermore, swimming failure in cold water is not due to
general hypothermia, but more to muscle failure of the arms
or legs as the reduction in core temperature is greater with
movement due to increased convective heat loss (101).
By comparison, instructing subjects about the effects of
sudden immersion in cold water is an effective way to reduce
negative physiological effects and to prevent the reduction
in cerebral blood flow velocity (235). In addition, 5 days of
acclimatization to cold immersion (3 min in 10◦ C water)
results in significant reductions in respiratory frequency,
minute ventilation, and heart rate, and these effects last 7
to 14 months (383). However, sustained immersion in cold
water can lead to hypothermia, which if uncorrected, does
lead to death. The response to cold water is dependent on
both the water temperature and duration of immersion. Many
studies have shown that TN water temperature is 35◦ C in
resting humans. The minimal temperature that can be tol-
erated using physiological adjustments (vasoconstriction of
subcutaneous and muscle blood vessels to maximize tissue
insulation) is the critical water temperature (CWT) and is
nominally 30◦ C at rest, while temperature below this results
in increased metabolism, and over time leads to hypothermia.
CWT is the lowest temperature that can be tolerated at rest
for 2 h without increased VO2 , and is associated with maximal
peripheral vasoconstriction and body insulation (178). The
CWT does not appear to be effected by water depth (178).
Shivering is driven by changes in Tc , as well as body heat
content (376) and may increase resting metabolism by a factor
of 3 to 4. In water below CWT, there is an association between
changes in deep Ts and hyperventilation, however there is no
association with surface Ts (244). Both CWT and the rate
of development of hypothermia are also influenced by the
subject’s subcutaneous fat content (291). The specific time to
hypothermia is dependent on water temperature, that is, the
Volume 5, October 2015
The Aquatic Environment
colder the temperature, the shorter the time to hypothermia.
Shivering endurance is important in thermal protection; the
shivering drive, but not the intensity of shivering, decreases as
a function of time, suggesting fatigue and habituation, which
in turn cause decreased cold sensitivity (377, 378). Blood
glucose levels increase with shivering on land and increase to
higher levels during immersion, but as time progresses there
is increased fat oxidation (378).
Cold water HOWI, relative to TN water immersion,
elicits similar decreases in intracellular fluid volume; how-
ever, the initial increase in PV is reduced during cold water
HOWI (358) compared to TN HOWI. Exercise performance
is impaired by brief exposures to cold water, even in elite ath-
letes, and the impairment is magnified by prolonged exposure
(297, 341). SNA is responsible for the majority of physiolog-
ical changes due immersion in cold water (357).
CO generally increases similarly during both cold and
TN HOWI but there is a bradycardia during cold immersion,
which is compensated for the increased SV in HOWI. How-
ever, studies at depth report an increase in CO (411). MAP
is mostly reported to not be elevated in HOWI because the
reduced blood flow to skin, subcutaneous tissues, and mus-
cle is balanced by increased blood flow to other tissues and
TPR remains unchanged (297). At pressure, however, there is
an elevation of MAP as the thermal-mediated vasoconstric-
tion is not offset by vasodilatation in other areas to offset the
increased CO (411). In water below TN temperature, there
is a reduction in cutaneous blood flow due to the reduction
in Ts . However, if there is also a decrease in Tc , SNA is
increased more causing further reduction in blood flows and
this response is increased by acclimation (283). Cooling the
skin, but not the core, reduces thermal strain during exer-
cise and may improve performance in warm air environments
(189). Cooling the body after exercise may facilitate sub-
sequent exercise performance and assist with tissue repair.
However, it should be noted that jumping in cold water baths
after gym workouts with high Ts and Tc may lead to arrhyth-
mias, cessation of ventilation and exasperate the effects of
pulmonary edema.
Cold HOWI (16.4-24.1◦ C), for up to 10 h, initially
resulted in an increased Tc , presumably due to cutaneous vaso-
constriction; but thereafter Tc dropped exponentially down
to 35◦ C within 1 to 2 h (376). Shivering can be increased
three to four times basal VO2 . Heat debt is peaked after 2 h
of immersion, due to body’s fat, connective tissue, muscle,
and bone components; and Ts and Tc are also reduced (277).
Another phenomenon in cold water is cold-induced vasodi-
lation (CIVD) during cold immersion (30 min at 9◦ C) of the
hand in men and women, increasing hand skin temperature,
but not the upper arm Tc (142). CIVD during prolonged cold
immersion of the hand has been demonstrated in both men and
women, and twitch force, time-to peak tension, and 1 /2 relax-
ation time were increased during CIVD compared to control
and were associated with the finger temperature (142). Impor-
tantly, CIVD is phasic, does not persist, and is not likely to
have a major influence on performance in cold water.
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The Aquatic Environment
HOWI in cold water immersion immediately decreases Ts
to that of water temperature. However the sensory inputs from
Ts and Tc differ when skin temperature changes are uniform
versus nonuniform as the differences in the uniformity of Ts
yield different physiological responses. With a uniform Ts
(WI in 31.4◦ C) changes in mean Ts and Tc were identical;
however, Ts in trunk was higher and the Ts of the limbs was
lower in when Ts changes were nonuniform. Heat production
and overall skin heat flux with cold HOWI were identical
when Ts changes were uniform, but were 25% lower with
nonuniform Ts than with uniform Ts and insulation was higher
due primarily to higher limb insulation. Thermogenesis due
to shivering was lower (62%) with nonuniform Ts than with
uniform Ts . It can be concluded that when Ts of the trunk is
higher there is an attenuation of shivering in cold water, and
this is likely related to higher overall insulation which defends
Tc (58).
Preheating subjects prior to HOWI results in a larger
decrease in Tc and muscle temperature in 14◦ C HOWI in
a time-dependent manner (5-20 min) (296). Another study
showed that increasing Ts by preimmersion in 40◦ C predis-
posed subjects to greater heat loss and greater decrements in
Tc in cold water than without the increased Ts (7◦ C) (342).
When subjects were exposed to 18◦ C, 22◦ C, and 26◦ C
HOWI for up to 90 min, some subjects completed the set
of immersions, others did not. The subjects who completed
the test and those that did not had the same TS and increase
in VO2 ; however, Tc dropped more rapidly in the intolerant
group, presumably due to less metabolic adjustment, as well
as less vasoconstriction of the skin and fat tissues and therefore
lower overall body insulation. This suggests that shivering-
induced thermogenesis can provide enough heat to protect
some individuals but not all (146).
The depth of immersion affects thermal regulation, as is
the case with the cardiovascular responses to graded HOWI. In
cold water (15◦ C), Ts reductions were similar for the shoulder
and hip, but higher for the knee during both rest and exercise
(215). In 25◦ C water, Ts reductions when the level of HOWI
was below neck level were less than mid-cervical HOWI, and
Ts levels during exercise were higher (215).
HOWI for one hour at 32◦ C did not affect VO2 or Tc but
lowered HR (15%) and SBP and diastolic blood pressure
(DBP) (12%) compared to the nonimmersed condition. By
comparison, HOWI at 20◦ C lowered Tc and increased VO2
(93%) and urine flow increased sharply (89%), while levels
of renin, HR, and BP were similar to TN HOWI. In 18◦ C,
there was a further decrease in Tc and a further increase of
VO2 (230%) and HR and MAP (5-8%), while plasma NE rose
(250-530%) and urine flow (163%) increased more. When
both Ts and Tc fall there is a greater effect on thermogenesis
than when Tc alone falls (402). Changes in plasma cortisol
are not temperature dependent, and there is no association
between Tc and other hormonal responses. These data suggest
that in addition to physiological responses to WI per se, cold
WI specifically, increases SNA (357). HOWI for one hour
in 14◦ C water increased SNA, as indicated by a fourfold
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Comprehensive Physiology
increase in plasma NE, but not epinephrine or dopamine
(180, 181).
The thresholds for both shivering and vasoconstriction
may be influenced by the initial Ts , either due to previous
exposure to warm conditions or exercise. Elevated Ts signif-
icantly affects the shivering and vasoconstriction thresholds
(190). When subjects were immersed in 10◦ C water with
limbs protected but the torso exposed, HR decreased along
with ventilation and skin blood flow during the first initial
period of immersion. However, when the torso was protected
ventilation and skin blood flow still decreased but HR did
not. This suggests that the cold stimulus to the limbs is more
important than the cold stimulus to the torso in in regulation
HR during cold HOWI (379), but not for regulating ventilation
or skin blood flow.
Plasma renin-angiotensin activity was decreased to 1 /2 by
cold HOWI, but aldosterone levels did not decrease. SNA
increased but it did not appear to influence HR whereas it was
associated with peripheral vasoconstriction (increased TPR)
and a small increase in MAP (180).
It is well documented that Tc is lower in the morning than
later in the day. In this regard, men immersed in 20◦ C for 2 h
in the morning did not display shivering or vasoconstriction,
while later in the day they did and they were important adap-
tations to maintain Tc . This suggests that there is a greater risk
of hypothermia during cold exposure in the morning (49).
Protection against cold water exposure can be achieved by
insulating suits such as a wet suit, dry suit, or active heating
suit. Wearing thermal protection gear provides insulation but
results in nonuniform and higher skin temperatures. Although
there are apparently no differences in thermal sensation and
shivering thermogenesis when Ts decreases uniformly versus
nonuniformly (wet suit covering trunk upper arms and legs),
tissue insulation (vasoconstriction) was significantly higher
when Ts changes were nonuniform due to augmented cold
sensory input form the periphery (404). It has also been noted
that when Ts were maintained at a higher level during cold
immersion the temperature gradient between body and water
actually increases and this may result in greater heat loss
and decrease in core temperature (16, 267, 305). This may
be an issue with wet suits. Wearing a wet suit in cold water
resulted in a higher esophageal temperature and attenuation
of shivering and thus VO2 did not increase as much due to the
higher insulation (404).
Wearing a wet suit during intermittent exercise in cold
water was superior to continuous thermogenesis in sustaining
body temperatures (402). While wearing a wet suit does not
affect the acute response to cold water immersion, wearing a
dry suit significantly blunts decreases in body temperatures
in cold water (380). Although wet suits significantly increase
body insulation, the higher Ts while wearing a wet suit may
result in greater heat loss. Therefore, wet suits may not provide
sustained thermal protection.
Although wearing a dry suit can provide thermal insula-
tion sufficient to prevent hypothermia, it is only the case if
the suit stays dry; even then it does not adequately protect
Volume 5, October 2015
Comprehensive Physiology
the hands and feet of the subject. Use of a dry suit eliminates
long term core cooling; however, greater cooling (Ts and Tc )
has been observed in the first 10 min of HOWI in cold water
(112). Active heating systems are available and have been
shown to protect the swimmer from hypo- and hyperthermia
(16, 267, 305); however, they require an electric power source
and thus may not be practical. Previous studies have shown
that having divers cool during compression and warm during
decompression is advantageous for N2 washout (less wash-
in and greater washout) and may reduce the incidence of
DCS (140).
Head-Out Water Immersion in Warm
Water
Cold HOWI has been well researched, with most adjustments
known. However, swimming and diving also occurs in warm
water. Immersion in warm water at or under water, when
combined with exercise, results in an uncompensated heat
load which cannot be balanced by heat loss. Moreover, the
reverse thermal gradient (water to body) may lead to hyper-
thermia and even death. There are likely few acclimatizations
in warm water as those factors that show this adjustment
in air cannot function in water (sweating, evaporation, etc.).
Immersion/submersion in warm water results in a temperature
gradient favoring increased body heat stores. The inability to
evaporate sweat causes a fast and high elevation in Ts and
Tc which could quickly reach serious levels. The addition of
exercise leads to significant additional heat production and
thus increases the risk of hyperthermia. Although sweat can-
not be evaporated, sweating continues, and eventually would
result in reduced PV and, when added to the increased blood
flow to the skin, leads to lower CO and skeletal muscle blood
flow, resulting in reduced exercise capacity and hyperthermia.
Although not documented, based on data for subjects accli-
matized to air persons in water could be at a greater risk of
hyperthermia as this may potentiate sweating and vasodilata-
tion, risking reduced PV, and blood flow to working muscle
and brain. Immersion in water at temperatures greater than
TN can cause hyperthermia. This condition is more risky than
hypothermia because there are no defenses against hyperther-
mia in warm water due to the high heat conductivity of water
and elimination of heat loss by evaporation of sweat. This is
an area of underwater physiology that needs additional study.
It has been proposed that intrathoracic blood volume
should be less in warm water due to the peripheral vasodi-
latation (109); however, it was shown to be not lower in 41◦ C
HOWI, compared to 35◦ C and 25◦ C HOWI (279). This is sup-
ported by the demonstration that HOWI in water temperatures
of 32◦ C, 34.5◦ C, or 36◦ C did not affect the net transcapillary
fluid shift into in the face of temperature-dependent increases
or decreases in vascular tone (426). TN HOWI increases SV
and CO and HR is decreased. By comparison, HOWI in warm
water results in an increase in HR of 32%, while CO increased
18% as compared to a 44% increase in TN water and there
Volume 5, October 2015
The Aquatic Environment
was no significant change in CO in cold water compared the
TN water. Both MAP and TPR are increased in cold water,
while they are decreased in warm water (33).
HOWI in 39◦ C causes dehydration, even with fluid
replacement. Hematocrit increases and there is a decline in
mean power and peak power during exercise as well as a
greater level of perceived exertion (200). HOWI in warm
water has been shown to increase total urinary Aquaporin 2
excretion suggesting elevation of plasma vasopressin levels
(391). Forty-five minutes of TN HOWI followed by warm
water immersion at 41◦ C caused an immediate decrease of
plasma fibrinogen and plasminogen activator inhibitor activ-
ity concentration decreased immediately. These observation
suggest that warm HOWI leads to hemoconcentration and
minimal activation of coagulation, implying increased risk of
thrombotic activity (32).
Acclimatization
While acute HOWI in water below TN temperature causes
adaptations, chronic exposure results in acclimation, and may
be a result of central or/and peripheral adaptations. Original
studies of fishermen indicated that they had developed suffi-
cient acclimatization of the circulation of the hand allowing
them to work for long periods while fishing. However, in this
case the cold exposure was confined to the hands, while the
rest of the body was warm. More recent studies in air have
shown that if the body (torso) is warmed, blood flow to the
hands is maintained and the hands remain functional in cold
air (101). However, this has not been shown to be the case
when the total body is immersed or submersed.
One study has shown that 5 days of acclimatization to
cold HOWI (3 min in 10◦ C water) resulted in significant
reductions in Bf , V̇ E , and HR, and these effects last 7 to 14
months (383). However, these changes do not effect overall
thermal resistance which is likely not changed much due to
acclimatization to immersion in water.
Chronic exposure of the hands to 10◦ C water resulted in
reduced HR and ventilatory responses in habituated male sub-
jects, in spite of identical Ts declines, suggesting a more cen-
tral regulation of circulatory and ventilatory responses (382).
This is in agreement with the historic study of the responses of
fishermen to cold hand immersion. It has been suggested that
the vasoconstriction response due to cutaneous cold receptors
in 15◦ C can protect even in colder water (382). These adap-
tations are due to a decrease in the immediate changes in Bf
and VT , and HR to acute HOWI (381, 382). Repeated HOWIs
in 15◦ C for 1 h three times per week for 4 to 6 weeks has
demonstrated that subjects had lower Tc , presumably due to a
delayed metabolic response and subjective shivering in accli-
matized subjects, while they had less sensation to the cold.
These changes suggest a slight increase in insulation due to
acclimatization (180).
While acclimatization has some cardiorespiratory effects
it does not appear to have a major effect on thermal status,
which is also the case for plasma renin-angiotensin activity
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The Aquatic Environment
and aldosterone concentrations (181). Chronic HOWI in
10◦ C to 4◦ C water for three months resulted in decreased
catecholamine response to cold HOWI (174).
Submersion—Diving
Ventilation can be maintained during shallow immersion
while breathing from a snorkel, however during submersion
special equipment is needed to compensate for the hydrostatic
pressure created by the depth of immersion. The required
equipment for breathing underwater (SCUBA) provides com-
pressed gas with a pressure that compensates for the hydro-
static pressure, allowing breathing (23). In theory breathing
from SCUBA has no depth limit; however, physiologically
there are limits. One limit is the potential for oxygen toxicity
while breathing air with the pressure-dependent increase in
partial pressure of O2 (23). Another issue is that the nitrogen
pressure in air nitrogen is a depressant (nitrogen narcosis) at
depths greater than nominally 100 fsw. Still another issue is if
a diver breath-holds during ascent the air in the lungs would
expand with the potential for alveolar rupture (embolism),
even in relatively shallow waters (23). By following proper
procedures, these risks can be minimized; however, there is a
further complication of diving with SCUBA. While the sub-
ject is breathing compressed gas the body takes up inert gas,
usually N2 , and as the diver ascends, this gas has to be elim-
inated. If this is not done following proper decompression
protocols, it can lead to the formation of bubbles which may
form at the joints causing the victim pain. A further compli-
cation is that the bubbles formed during decompression may
occlude blood flow and compress nervous tissues, causing the
victim neurological pain. This condition is called DCS or the
bends. DCS rarely occurs in diving that follows acceptable
decompression procedures.
Cardiovascular and renal responses to diving
Submersion has been shown to increase CO and more in cold
water than TN water (411). Breath-holding during submer-
sion results in greater depression of CO than during immer-
sion with free breathing, as the bradycardia is due to face
immersion related to the diving reflex (218). Subjects who do
not ventilate sufficiently have increased PaCO2 , however, this
does not cause modulation of cardiovascular variables (17).
HR at depth is reduced compared to submersion at the sur-
face resting, as well as at exercise intensities (303), resulting
in lower maximal HR at maximal exercise. In addition, the
reduced maximal CO may account for the reduced maximal
VO2 observed at depth, in spite of the increased PO2 . The
changes in CO are less important at depth than the changes in
pulmonary function. The latter is discussed at depth below.
The cardio-renal responses to dry pressure exposure alone
result in an increased urine flow, but not GFR (289). This
diuresis is accompanied by excretion of potassium, sodium,
calcium, and phosphate (289). Urine osmolality is reduced
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Comprehensive Physiology
due mainly to decreased water reabsorption (289). The renin-
angiotensin II-aldosterone system is activated at depth in dry
conditions secondary to the transient dehydration induced by
the early hyperbaric diuresis (289). Although these responses
are due to pressure alone, when the subject is submersed in
water the effects of the submersion overshadow the pressure
effects and the cardio-renal responses are similar to those
described above for HOWI.
Pulmonary gas exchange during diving
During exercise at 1 ATA V̇ E normally increases in proportion
to metabolic demand, which maintains arterial pH constant.
In untrained individuals exercising at a constant work rate
(nominally 50% VO2 max ) there is a 20% to 25% increase in
VE after 12 to 15 min (425). A similar, more gradual increase
in VE occurs during the same timeframe underwater (321).
This is not due to a change in acid-base status (292), and since
it can be attenuated or abolished by RMT (321, 425), is most
likely due to respiratory muscle fatigue. At extreme levels
of exercise acidemia may occur despite disproportionately
increased V̇ E and hypocapnia.
Compared with the surface, for any given work rate during
a dive V̇ E tends to be lower, resulting in hypercapnia. All but
a few studies examining contributors to hypercapnia in diving
(56, 210, 278, 335-337) have used end-tidal PCO2 (PET CO2 )
as a surrogate for arterial PCO2 (PaCO2 ), which is usually
valid under resting conditions. However, during exercise the
approximation is less satisfactory: during exercise at 1 ATA
PET CO2 exceeds PaCO2 (222); under conditions in which
dead space is increased (e.g., when gas density is increased)
PET CO2 is lower than PaCO2 . Only two studies have directly
correlated the two in diving, in the dry at 2.8 ATA (278) and
submersed at 4.7 ATA (56), both demonstrating a reasonable
correlation, although with significant scatter.
Total ventilation is maintained to result in an alveolar ven-
tilation that is tightly coupled to PaCO2 , typically ∼40 mmHg
in healthy individuals (167), while matching O2 delivery to
metabolic demands (1). Divers have been reported to sponta-
neously or voluntarily hypoventilate leading to CO2 retention
(272). Hypoventilation and thus CO2 retention can also be
due to divers’ inability to meet the force and energy require-
ment of the increased respiratory work secondary to weak or
fatigued respiratory muscles. Hypoventilation and CO2 reten-
tion (see below) may increase the likelihood of CO2 narcosis
(e.g., 17, 212, 406), as well as central nervous system oxygen
toxicity and nitrogen narcosis (44, 212). A study has shown
that CO2 retention in divers may cause convulsions due to
O2 toxicity, in spite of the dive profile being what would be
considered a safe limit for hyperoxic exposure (212).
In resting subjects, VE is increased at depth primarily due
to an increase in VT with submersion depth (162, 280, 406).
It has been hypothesized that the depth-dependent hyperoxic
hyperventilation is due to the effects of high PO2 at depth
on the reduced peripheral chemoreceptor sensitivity (293).
Reactive oxygen species, secondary to the high PO2 at depth
Volume 5, October 2015
Comprehensive Physiology
are proposed to accumulate in the tissues of the brain and
result in stimulation of the central chemoreceptors in the cau-
dal solitary complex (84), resulting in the observed hyperven-
tilation, by dampening the feedback in the respiratory control.
This postulate is supported by data from a study that reported
a similar observation after carotid body denervation in vivo
(73, 133). If hyperventilation occurs by this, or other mech-
anism, it would result in a reduction of arterial PCO2 below
its normal level; however, this is not supported by studies
examining this potential mechanism (120). It is also possible
that the depth-dependent hyperventilation observed at rest at
depth is the “Haldane effect.” This effect suggests that if there
is less O2 released by hemoglobin that CO2 elimination would
be reduced leading to increased PaCO2 which would lead to
a hyperventilation to reduce PaCO2 (227). The hyperventila-
tion many have negative consequences for the brain (208), as
well as stimulating central chemoreceptors. However, even if
these changes occur PaCO2 would be only slightly increased
(nominally by 1 mmHg), and thus not important (272). It
has also been shown, and is the most probable explanation
for the depth-dependent hyperventilation, that dead space
ventilation is increased, as is the dead space and the dead
space-to-tidal volume ratio, as a function of the less effective
gas mixing in the lungs at depth (272). To compensate for the
increased dead space the diver would have to increase V̇ E via
an increase in VT to maintain adequate alveolar ventilation.
The increased VO2 and VCO2 during exercise results in an
increase in VE in a dose-dependent manner. The increase in
VE as a function of VO2 was reported to be greater when sub-
mersed than in the dry condition, but was decreased at depth
when compared to the surface (162). Increased V̇ E has been
suggested to be due to facial immersion when submersed (82);
however, another study does not support this conclusion (56).
The increased SLL at depth likely results in increased respira-
tory muscle activation during inspiration, as well as increased
duty cycle (162). It has been reported that VT is increased
at depth; however, V̇ E was reduced resulting in an increase
in elastic work (162). This breathing pattern could blunt the
effect of the depth-dependent increased airway resistance and
work due to the increased gas density at depth, but it could
maintain alveolar ventilation even though there is increased
dead space. During spontaneous breathing at 1 ATA the bf and
VT are proposed to be regulated to produce the most efficient
duty cycle (251, 286, 287). If the same is true at depth both at
rest and during exercise, bf and VT are likely balanced by the
respiratory drive in response to the increased dead space and
higher PaO2 to optimize V̇ E .
High external breathing resistance may cause severe
hypercapnia without prodromal symptoms (dyspnea)
(212,406). One possible mechanism is inadequate respiratory
muscle performance (e.g., due to fatigue). Interestingly,
RMT can improve respiratory muscle function and exercise
capacity (214, 219, 425). CO2 sensitivity in low responders
tends to increase; in high responders it tends to decrease
(304). Respiratory muscle fatigue and CO2 retention are
both attenuated (321). The principal causes of hypocapnia
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The Aquatic Environment
are the effects of diving on mechanical load, gas mixing and
diffusion, VA /Q matching and respiratory drive (271).
Mechanical Load
During a dive there are three load parameters that change. The
major one is flow resistance due to the higher gas density (10),
which increases linearly with ambient pressure. In turbulent
flow (which occurs in large airways) resistance is density-
dependent. Higher airways resistance caused by increased
gas density occurs during both inspiration and expiration.
During expiration there can also be expiratory flow limitation
due to airway collapse (421). These effects can be detected by
reduced forced expiratory volume in one second (FEV1 ), peak
expiratory flow and maximum voluntary ventilation (MVV)
(70, 209, 233, 355, 401). At any gas density ρ, peak expiratory
flow or MVV can be predicted by the following formula (420,
422):
A = Ao (ρ∕ρo )−k
where A is either MVV or peak expiratory flow at gas density
ρ, A0 is MVV (or peak expiratory flow) at 1 ATA, ρ is gas
density at the ambient pressure of the dive, ρ0 is gas density
at 1 ATA, and k is a constant with the value 0.4 to 0.5. A sim-
ilar equation has been published for the relationship between
airway conductance and gas density (10).
External resistance is present in all underwater breathing
apparatus and adds to the overall respiratory load. Changes in
viscosity could affect gas flow in small airways where there
may be laminar flow. However, within the pressure range to
which humans have been exposed (up to 70 ATA), there is no
measurable change in gas viscosity.
A second component of mechanical load is elastance.
Elastance is the quality of recoiling on removal of pressure
without disruption, or an expression of the measure of the
ability to do so in terms of unit of volume change per unit
of pressure change; it is the reciprocal of compliance. Tho-
racic elastance is composed of the individual elastances of the
lung and chest wall. Chest wall compliance does not change
significantly during immersion; however, lung elastance is
increased, most likely due to vascular engorgement caused
by redistribution of blood from the periphery into the tho-
rax (78).There may also be an effect on elastic load of the
difference in external hydrostatic pressure between the lung
and the mouth due to the position of the diver in the water
column (365, 366). The immersion-related increase in elas-
tic load causes a further decrease in MVV from that due to
increased gas density (424).
The third component of respiratory load is inertance,
which is the tendency to resist acceleration. Inertance is
a function of the combined masses of the chest wall, the
gas flowing within the airways and breathing apparatus,
and to a minor extent the water surrounding a diver’s torso.
Respiratory system inertance at 1 ATA, typically 0.01
cmH2 O⋅L−1 ⋅s2 , increases in direct proportion to gas density
1735
The Aquatic Environment
(250, 310). During cyclic breathing at a frequency lower than
the resonant frequency of the system inertial impedance is
less than elastic impedance. At a higher frequency, inertial
impedance exceeds elastic impedance. Resonant frequency
of the human respiratory system is typically 6 Hz at 1 ATA
breathing air. This decreases to around 2 Hz if breathing gas
density is higher, as is the case at depth. Therefore, since
most divers tend to breathe more slowly at rest and during
exercise underwater (56, 119, 164, 278, 292, 337), inertial
impedance plays only a minor role in overall respiratory
effort. Assuming a reasonable value for peak acceleration of
30 L⋅s−2 , in an exercising diver breathing a gas with density
10 g⋅L−1 , the transrespiratory pressure due to inertance
would be only ∼3 cmH2 O (271). Inertance can actually be
manipulated to a diver’s benefit: if a breathing circuit is
deliberately designed such that the resonant frequency of the
system approximates the normal breathing frequency, elastic
and inertial work offset each other, resulting in a reduction
in peak-to-peak (inspiratory-to-expiratory) pressure. Using
this principle to design a tunable closed circuit breathing
apparatus, Fothergill et al. demonstrated that divers optimize
their breathing pattern by adjusting their respiratory rate to
match the resonant frequency of the system (121).
Work and Energy Cost of Breathing Underwater
Respiratory muscles, like other muscles, perform work to
inspire and in some cases expire (WOB). However, as VE is a
rate it is the POB, along with net mechanical efficiency that
determines the energy cost of ventilation.
Negative SLL causes the inspiratory muscles to work
harder, but may benefit the expiratory muscles. This is also
associated with the increase in thoracic blood volume due to
its translocation from the dependent limbs during submersion
(78), which also results in a decrease in total lung capac-
ity and residual volume (78, 272, 364) and lung compliance
(78). Combined, these factors during submersion cause an
increased POB due to the elastic component. Increased blood
volume in the chest may provide a small increase in the airway
pressure and require less work to generate expiratory pressure
(PE max ) as blood is nearly incompressible.
The effect of water depth on total WOB has been shown
to have a dose response relationship, as have the RMT-
induced improvements in swimming endurance progressively
increased with greater depth, that is, 30% for surface, 50%
for 4’ and 60% for 55’ and 86% for 120’ of water depth
(321, 322, 425). These data strongly suggest that respiratory
muscular adaptations due to RMT were primarily responsible
for increased swimming time, especially when studies using
placebo groups failed to show any performance improvement
(214, 425). Protocols where subjects were studied at the time
of exhaustion, prior to and after RMT, show that the res-
piratory muscles have greater strength and endurance sug-
gesting they were less fatigued post-RMT (321, 322, 425). In
addition, it has been shown that RMT reduced the energy
cost of swimming (351) and these changes were related to
1736
Comprehensive Physiology
reduction in WOB (321, 322), as well as increased efficiency
(351). These data further demonstration that RMT reduced
the energy cost of ventilation (VO2 and La) for iso-workloads,
which has been shown by many authors (356). Prior to RMT,
the increase in V̇ E and fb combined with a decrease in VT at
the end of exercise as well as the reduced ability to generate
maximal expiratory and inspiratory pressure postexercise sug-
gests that reduced respiratory muscle performance may have
been a limiting factor during the swimming endurance test
at depth.
Increased hydrostatic pressure is depth dependent and
causes an increase in the POB. The increase in POB as a func-
tion of depth is mostly a result of the increase in the airway
resistance which is related to gas density, which is increased in
a depth dependent manner (240). Airway resistance recently
has been calculated from measures of esophageal pressure as
an estimate of alveolar pressure (PA ) and air flow (179, 252);
however, a more accurate measure of PA may be made from
the mouth pressure measured during an airway occlusion
accomplished by a shutter placed at the mouthpiece (P.1 tech-
nique) (285, 318). P.1 also measures the level of activation
of the respiratory muscles (161), as well as central nervous
system respiratory drive (419). Airway resistance at sea level
using the P.1 technique are not different from those measured
using the esophageal balloon method (179, 252). In the past
the P.1 was used to estimate PA and to calculate airway resis-
tance in subjects submersed at depths of 45 ATA (63).
Another factor affecting pulmonary mechanics is the role
of NO in pulmonary resistance. Previous studies in animal
models have demonstrated a role of NO in airway resistance,
that is, increased NO reduces airway resistance in a dose-
dependent manner (103, 166). In addition, the effect of depth
on NO production (V̇ NO ) is reduced in the cerebral vascular
as the PO2 increases in a depth-dependent manner (85) to
prevent an increase in PO2 to the brain to maintain normoxia
(30). These studies in the brain suggest a similar effect of NO
on the smooth muscle of the respiratory airways. If this is the
case a reduced VNO would constrict the airways and lead to an
increased airway resistance in a depth-dependent manner. If
there is bronchoconstriction and increased airway resistance
due to depth, the PA would have to be increased to accomplish
the required alveolar ventilation.
Gas mixing and diffusion
There are three processes by which inspired gas mixes with
alveoli gas: convective mixing, Taylor dispersion, and diffu-
sion (107). Convective mixing of inspired and resident gases
occurs predominantly due to turbulent flow in large conduct-
ing airways. Taylor dispersion consists of radial diffusion
along a radial concentration gradient that occurs in laminar
flow due to the parabolic flow distribution, where flow rate at
the center of a tube that at its periphery. Mixing of inspired
and resident gases is further augmented by both Taylor diffu-
sion and cardiogenic oscillations. Diffusion occurs in distal
gas exchange units where flow is extremely low.
Volume 5, October 2015
Comprehensive Physiology
When gas density is increased, turbulent flow occurs in
more distal airways, thus facilitating convective mixing and
improving gas exchange efficiency (271). Increased gas den-
sity is also likely to facilitate cardiogenic mixing (353). On the
other hand, higher gas density should reduce the effect of Tay-
lor dispersion (and thus worsen gas exchange) by reducing the
number of airways with laminar flow. Increased density also
reduces gas phase diffusivity (393). Diffusion depends on gas
diffusivity (related to molecular weight), concentration gradi-
ents, time for diffusion, number of molecules per unit volume,
and the shape of the space in which the gas is contained (393).
While gas phase diffusion is impaired by higher gas den-
sity, convective mixing is enhanced. The net effect of these
processes on pulmonary gas exchange has been illustrated
by measurements of arterial blood gases during hyperbaric
chamber studies (56, 126, 192, 278, 288, 292, 335-337). Over-
all, despite mild or moderate hypercapnia, adequate blood
oxygenation occurs at gas densities up to 17 g/L (337) and
exercise performance is maintained up to 25 g/L (209).
Airway resistance, alveolar pressure, and work of
breathing
Airway resistance (Raw ) increases with increasing gas den-
sity secondary to increased hydrostatic pressure, thus PA has
to increase proportionally to ensure adequote alveolar ven-
tilation (24, 405). Raw increases by the square root of the
increase in density (294). The increase in VE and rate of
flow are increased by exercise resulting in an increase in
Raw which requires and higher PA (163). Reviewing studies
does not suggest that Raw would be affected by submersion
per se (34). However, a recent study has shown inspiratory
resistance (RawI ) and expired airway resistance (RawE ) were
decreased in submersion in resting subjects (162), in spite of
the observation that Bf , VT , VE , PA during expiration, POB
during expiration that effect RawI and RawE were not signifi-
cantly affected by submersion (162). Based on these changes
airway caliber was likely greater during submersion than in
the dry conditions, in contrast to decreased VC (5,162,207) as
decreased lung volume has been reported to affect Raw (40).
The more-negative PA during inspiration recently reported
for submersed subjects is most likely related to SLL and not
submersion, per se, as the latter would increase chest wall
elastic recoil at the start of inspiration (369).
The changes in Raw and PA previously reported (162)
resulted in increased WOB and POB (162). Expectantly then,
POB increases with greater depth, as its components are also
increased with depth (162). The increased PA at depth is
needed to ventilate with the greater density of gas at depth
where there is also increased airway resistance. Submersion
has been reported to decrease inspiratory POB, mainly due
reduced RawI and thus the WOB per breath, at rest; however,
it is increased while exercising (162). During exercise sub-
mersed, bf has been reported to be higher than dry; however,
WOB per breath was unchanged, and thus inspiratory Ẇ I was
greater (162). Although POB during inspiration is increased
Volume 5, October 2015
The Aquatic Environment
while submersed, the SLL in submersion likely assisted expi-
ration and thus Ẇ E was not different during submersed and
dry conditions (162).
NO inhaled or produced results in bronchodilation of the
airways (21, 249), thus should have an impact on breathing
resistance during submersion and could be affected by the
depth of submersion. However, recent data suggest that V̇ NO
during submersion was not significantly different from the
dry condition, both at rest and during exercise (162). The
V̇ NO observed while exercising at 50% of VO2 max at 2.7 ATA
was slightly decreased compared to rest (162). One possibil-
ity for the lack of increase, and decrease, in V̇ NO could be
the depth-related increase in PaO2 (hyperoxia), which was
proposed earlier (85), which may have blunted the increased
VNO that has been reported for similar exercise intensities at 1
ATA (57, 177). In addition to the high variability among sub-
jects due to fitness (57, 177, 239) and body types (284), the
competing effects of exercise, submersion and depth likely
account for the lack of change or decrease reported (162).
The interaction with depth and submersion may account for
the VNO not being elevated during exercise that has typically
been observed (57, 177, 239). The effects of submersion and
depth on V̇ NO during exercise may be due to the PO2 in these
conditions as studies at 1 ATA have shown that NO production
is associate with PO2 in the surrounding tissue thus is likely
responsible for ensuring appropriate tissue PO2 (30, 104). If
the effect of PO2 at the surface is true at depth, the decreased
VNO at depth (i.e., increased PO2 ) previously reported (162)
would be reasonable. In this case NO may be regulated to
ensure PO2 to the tissues does not increase with hydrostatic
pressure and not to minimize airway resistance which may be
the case during exercise.
Energy cost of ventilation
Since the respiratory muscles are comprised primarily of
slow twitch oxidative fibers, the energy required for respi-
ratory muscle contraction is largely from oxidative mecha-
nism (VO2 ). Using a unique protocol to determine the VO2
to breathing two studies have shown an increase in VO2 sec-
ondary to the increase WOB and POB in submersed subjects.
In addition to the increased WOB and POB, calculated net
mechanical efficiency (WOB/VO2 after correction for units)
is reduced slightly during submersion (162, 351). It has been
shown that RMT could reduce WOB (321, 322), and may
improve net mechanical efficiency (162).
Distributions of ventilation, blood flow, VA /Q
Distribution of ventilation depends upon several factors,
including cyclic fluctuations in externally applied pressure
from the respiratory muscles and regional mechanical prop-
erties of the lung and chest wall. Despite the vast range in path
length in the lung from large airways to gas exchange units,
at 1 ATA breathing air ventilatory time constants of different
lung units, and hence ventilation of different lung regions, are
1737
The Aquatic Environment
Human dry, 1 ATA
Human dry, 1-7 ATA
Anesthetized dogs dry, 1 ATA
40
Human immersed, 1 and 19 ATA
30
PAO2 -PaO2 (mmHg)
20
10
0 0.1
0.1 1 10
Breathing gas density (g/L)
Figure 15 Alveolar-arterial PO2 difference versus gas density in four
experiments. From Moon et al. with permission (271).
similar. This is largely due to the geometric properties of the
airways. However, at increased gas density the geometry of
the lung is no longer optimal and heterogeneity of ventilation
is increased. Time constants are more variable and ventilation
of different lung units can become asynchronous (119, 295).
Gas distribution may also depend on other factors. Pleu-
ral pressure variation is not uniform over the entire lung
(107). Even during resting breathing at 1 ATA, regional pres-
sure changes are less in the upper than in the lower chest
(79). When gas density is increased this variation becomes
exaggerated.
If regional ventilatory inequalities are appropriately
matched by changes in perfusion, VA /Q matching would be
preserved. Indeed, despite evidence of impaired CO2 trans-
port (increased physiological dead space) breathing dense gas
actually seems to improve VA /Q matching, as evidenced by a
decrease in alveolar-arterial PO2 difference as seen in Figure
15 (60, 118, 144, 335, 423). Decreased alveolar-arterial PO2
indicates more efficient matching of ventilation and perfu-
sion. Paradoxically, dead space/tidal volume ratio (VD /VT ) is
usually increased (56, 249, 278, 335, 423), implying impaired
pulmonary exchange of CO2 . Immersion effects modify the
effect, as shown by Peacher et al. In their study, the increase
in dead space/tidal volume ratio may not occur during immer-
sion except at extremely high PO2 (1.75 ATA) (292).
A previous study speculated that increased breathing gas
density reduces PAO2 − PaO2 by promoting intraregional
convective mixing and thus reduced VA /Q dispersion (423),
which affects VD /VT to a lesser degree than PAO2 − PaO2 as
shown in Figure 16. They proposed that the increase in VD /VT
is mostly due to impaired molecular diffusion of carbon diox-
ide (Fig. 16). Although oxygen diffusion should be similarly
affected, they suggested this may be insufficient to offset the
convective mixing effect (97, 98).
Another phenomenon is related to the fact that lung
perfusion is not temporally uniform, but varies cyclically
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Comprehensive Physiology
1.00
VD/VT = 0.331+0.138*log10 ρ (R2 = 0.85)
Deadspace/tidal volume ratio
0.75
0.50
0.25
0
10 100 1000
Density (g/L)
Figure 16 Dead space/tidal volume ratio versus gas density. From
Moon et al. with permission (272).
with respiration. It has been predicted that this phenomenon
improves alveolar-pulmonary capillary oxygen exchange
(13). Dense gas breathing leads to greater breath-to-breath
variation in pleural pressure, thus augmenting cyclic vari-
ability in lung perfusion and improving pulmonary oxygen
exchange (reduced alveolar-arterial PO2 , A-aDO2 ) (12).
Pulmonary-blood transfer of oxygen
Increased affinity of hemoglobin for oxygen (decreased P50)
has been observed at high pressures in vitro (139, 193, 194,
323, 359) and in a human in vivo study during a saturation
dive to 49.5 ATA (355). This is probably due to pressure-
related conformational changes in hemoglobin and, to a small
extent, binding by inert gas. The effect of these small changes
in hemoglobin P50 on pulmonary gas exchange or exercise
capacity is probably minor (403).
Ventilatory drive
One mechanism for hypoventilation in divers may be low
ventilatory CO2 sensitivity (hypercapnic ventilatory response,
HCVR) (56,191,211,274-276). Overall, however, while there
is indeed a correlation between low HCVR and hypercapnia
at depth there are many outliers, and this test cannot be used
as a predictor for a particular individual (56, 229, 292): in one
study, only 60% of military divers with hypercapnia at depth
had a low HCVR (211). It has been reported that a subject
with extremely low HCVR (0.10 L⋅min−1 ⋅mmHg−1 ) had an
arterial PCO2 no higher than 43 mmHg during immersed exer-
cise (VO2 2.3 L/min) at 37 m depth with a breathing gas PO2
of 1.75 ATA (292).
As pointed out earlier, HCVR can be influenced by RMT,
which tends to change the HCVR of both low and high respon-
ders toward the mean (304), suggesting that RMT could
reduce the likelihood of hypercapnia in susceptible divers
(CO2 retainers).
Volume 5, October 2015
Comprehensive Physiology
Effect of hyperoxia
It has been speculated that respiratory drive in divers may
be affected by a high partial pressure of oxygen, which for
a fixed O2 fraction as in most diving, increases linearly with
depth. Hyperoxia is therefore a feature of diving even using
a breathing gas that is normoxic at the surface. Still higher
PO2 can occur (up to 1.75 atm) when using enriched oxy-
gen breathing gas mixtures that are intentionally designed
to reduce inert gas partial pressure. Hyperoxia attenuates
the ventilatory response to hypercapnia (77, 135, 265, 293),
and has been observed to decrease VE during exercise
(3, 106, 165, 210, 264, 292, 311, 418). However, even under
extreme hyperoxia (breathing 100% O2 at 2 ATA) the rise
in arterial PCO2 during moderately heavy exercise has been
observed to be modest (PaCO2 = 44 mmHg) (62).
Effect of narcosis
It has been suggested that inert gas narcosis, for example
when breathing nitrogen-oxygen mixtures, could contribute
to hypercapnia during diving. Indeed, HCVR is reduced
at an increased ambient pressure; however, studies using
increased breathing resistance and non-narcotic gases sug-
gest that increased gas density is the predominant mechanism
(56, 136, 229).
Effect of pressure
In one study in normal volunteers breathing gases of differing
densities at rest, it was observed that while increased ambi-
ent pressure was associated with an increase in PaCO2 , gas
density appeared to have only a small effect (335). The mech-
anism of this effect is unclear, but exercise studies have largely
excluded pressure per se as having a significant influence on
ventilation (221).
Pathological Effects of Diving
Impaired gas exchange after saturation dives
During saturation dives, divers often remain in a hyperbaric
environment for several days or weeks. There are reduced
opportunities for normal exercise activity, thus cardiorespi-
ratory fitness is gradually reduced. Furthermore, the ambient
PO2 is higher than normal (typically 0.4-0.5 ATA), thus
exposing the divers to oxygen tensions that could be mildly
toxic to the lung. Additionally, venous gas embolism often
occurs during decompression, often lasting for several days.
Thorsen has observed that after a saturation dive to 37 ATA
divers may experience persistent reduction in VO2 max and
DL CO, and increased respiratory deadspace (372). Decon-
ditioning, the cumulative effect of venous gas embolism on
the lung (372) and mild pulmonary oxygen toxicity may
all contribute. Logistic regression analysis of possible risk
factors after a series of saturation dives implicated both
hyperoxia and venous gas embolism as factors contributing to
Volume 5, October 2015
The Aquatic Environment
impairment in pulmonary gas exchange (374). A major role
for pulmonary oxygen toxicity is supported by results of an
experiment in which volunteers were exposed for 28 days in a
hyperbaric chamber to an ambient pressure of either 2.5 ATA
(atmospheric PO2 0.4 atm) or 1.5 ATA (atmospheric PO2 0.21
atm). Neither exposure produced venous gas emboli during
decompression. Nevertheless, the participants exposed to the
higher PO2 experienced a significant reduction in VO2 max and
carbon monoxide transfer factor, with no change in DL CO
after the lower pressure exposure (373). These data strongly
suggest that hyperoxia is the major contributor to pulmonary
gas impairment after long saturation dives.
Immersion pulmonary edema
Immersion pulmonary edema (IPE, often termed swimming-
induced pulmonary edema, SIPE) causes cough, hemoptysis,
dyspnea, and hypoxemia after surface swimming or diving,
frequently in young, healthy individuals (156, 196, 224, 232,
242,352,416), including exceptionally fit military divers (226,
232, 346, 409). The condition usually resolves spontaneously,
although it can be fatal in some subjects (66, 105, 352). β2
adrenergic agonists or diuretics have been used for treatment.
Risk factors may include cold water (196,416), exertion (156,
346,347,409), fluid loading (409), negative SLL (375), or low
VC (346).
It has been proposed that hydrostatic pulmonary edema
is due to capillary stress failure due to high pulmonary cap-
illary flow and pressure (196, 225). Possible mechanisms for
high pulmonary vascular pressure include the additive effects
of increased afterload, immersion-induced increase in pul-
monary blood volume and pulmonary artery hypertension due
to exertion, and cold water (138, 416).
Many of the published IPE cases have occurred in mil-
itary divers or combat swimmer trainees, in whom no pre-
disposing factors can generally be identified. Pulmonary
artery wedge pressure after an IPE episode has been reported
as normal (156), although pulmonary capillary hyperten-
sion is likely during the acute IPE event. Bronchoalveolar
lavage studies have excluded an inflammatory process. Post
event echocardiography in military cases is usually normal
(156, 196, 224, 352). In nonmilitary cases identifiable pre-
disposing factors have been found, including left ventricular
dysfunction (20, 89) and acute coronary syndrome (137). A
review of published cases and series revealed potential risk
factors in approximately 50% of civilian cases (245). A recent
publication observed acute reversible myocardial dysfunction
in nearly 1 /3 of 54 consecutive civilian cases of IPE (138),
suggesting that during the acute event hypoxemia due to pul-
monary edema may have impaired cardiac function. A number
of the cases reported in previous studies developed hyperten-
sion, consistent with increased afterload and perhaps SNA as
predisposing factors (138, 416).
By contrast, compressed gas in isolated spaces, such as
the middle ears and sinuses, has to be vented during decreases
in pressure as depth is decreased to prevent barotrauma (24).
1739
The Aquatic Environment
Figure 17 Mechanism of pulmonary barotrauma in a diver breathing compressed
gas and ascending while holding his breath. From Vann et al. with permission (394).
A diver breathing from diving breathing gear, breathes gas
provided at essentially the same pressure as the hydrostatic
pressure on the chest. If however, the diver ascends after
inspiration that fills the lung at depth and does not expire
gas to eliminate the expanded volume there is risk of pul-
monary barotrauma and gas embolism (24). Another fac-
tor is that the depth-dependent elevated gas pressure in the
lungs causes an increased partial pressure of the gases and
may introduce the potential for nitrogen narcosis and oxygen
poisoning (24).
Decompression illness
Decompression illness (DCI) consists of a syndrome initiated
by vascular or tissue bubbles. There are two mechanisms for
bubble formation in divers breathing compressed gas. Alve-
oli can hyperexpand and rupture during ascent when gas exit
through the tracheobronchial tree is prevented by breath hold-
ing or bronchial obstruction. In such cases, alveolar gas most
1740
Comprehensive Physiology
commonly tracks through the pulmonary interstitium into the
mediastinum, from where it can enter the neck, subcutaneous
tissue or abdomen. It can also enter the pulmonary capillary
blood, and then arterial tree causing arterial gas embolism
(AGE) as seen in Figure 17. Pleural rupture and pneumotho-
rax are less common. The second mechanism is in situ bubble
formation due to supersaturation of inert gas in tissues. This
occurs with slow tissue inert washout during decompression,
allowing tissue inert gas tension to exceed ambient pressure.
De novo bubble formation can occur in tissues around joints,
in spinal cord, and other tissues. Clinical manifestations due
to the second mechanism are referred to as DCS. AGE and
DCS are collectively referred to as DCI.
Bubbles exert their immediate effects via mechanical dis-
tortion (pain) and vascular occlusion (stroke-like manifesta-
tions). Secondary effects include endothelial disruption caus-
ing extravasation of plasma, hemoconcentration, and shock.
Vasoplegia due to endothelial hyporesponsiveness to vasoac-
tive agents has been reported in vitro. Platelet activation
Volume 5, October 2015
Comprehensive Physiology
and endothelium-leukocyte adhesion have also been reported.
Microparticle generation may also play a role (370,371,427).
Tissues commonly targeted include the joints (pain), spinal
cord, brain, and inner ear, although skin and lung can also
be involved. The most common manifestations include pain
(typically near a joint), hypesthesia/paresthesias, nonspe-
cific malaise, motor weakness, mental status changes, dizzi-
ness/vertigo, and incoordination. Frank paralysis is less com-
mon (394). Symptoms of DCI typically occur within minutes
of surfacing in AGE, while DCS manifestations can also be
delayed, often up to 24 h after surfacing.
Summary
The physical properties of the underwater environment make
it unique, and impose pronounced physiological stresses on
humans. It imposes major stresses due to the unbreathable
ambient medium, water temperatures higher and lower than
TN temperatures, and pressure stress breathing, circulation,
renal-body fluid and electrolyte balance, locomotion, and
thermal balance. These stresses are all unique to the underwa-
ter environment. Even immersion at the surface of the water
poses different challenges vs. being in air, and these chal-
lenges are amplified with submersion and its depth. HOWI
results in fluid shifts from both cell and the vascular compart-
ment, resulting in an expansion of PV and venous return, thus
increasing CO, in spite of the reduced HR as SV is increased
by increased cardiac preload. In spite of the increased CO,
BP is generally believed to be unchanged, secondary to a
reduction in SNA reducing vascular resistance. The reduced
vascular resistance leads to increases in tissue blood flows that
are time-dependently regulated among tissues to prevent sus-
tained overperfusion. The increased venous return and atrial
stretch lead to attenuated secretion of antinatriuretic hormones
and vasopressin which result in a diuresis and natriuresis that
act to return the PV to normal levels. As restoration of PV
evolves, there may be a small overshoot and PV may decrease
an additional 7% as the increased CO is sustained. While the
diuresis peaks at about 2 h and then abates the renal-hormones
remain elevated, indicating the regulation of PV is multifac-
torial.
The translocation of blood effects on pulmonary blood
flow and gas compartments. There is an increase in ventilation
during HOWI. The increased blood volume in the lung results
in engorgement of capillaries which displaces gas volumes
and may increase the risk of pulmonary edema. In spite of
these changes, arterial saturation is not compromised, even
during exercise.
Although resting cardiorespiratory variables are altered in
HOWI, the cardiopulmonary responses to exercise are simi-
lar; however, maximal aerobic power is lower, secondary to a
lower maximal CO. A negative consequence of the increased
pulmonary blood flow and blood pressure that causes
lung capillary engorgement may cause pulmonary edema,
particularly during hard exercise and in cold water. While
Volume 5, October 2015
The Aquatic Environment
experimentally, exercise is carried out on a cycle ergometer,
in practice locomotion in water is typically carried out by
swimming, where the efficiency is lower and the resistance
to movement (drag) is much greater. Drag is comprised of
friction, form and wave forms and all are velocity dependent.
As the drag increases with increasing swimming velocity
with an exponent from 1.7 to 2.0, the increase in the energy
cost of swimming increases exponentially with velocity, as
opposed to land exercise which increases linearly with speed.
Major differences between the sexes in physiological
responses to the aquatic environment have not been reported,
even after correction for body size and fatness. Age does
make a difference in physiological responses to the aquatic
environment. Adolescents appear to have greater sympathetic
neural response that declines with maturation, while older
subjects have blunted cardio-renal and sympathetic responses
to HOWI.
A major modulator of physiological responses to the
aquatic environment is the temperature of the water, as Ts
rapidly equilibrates with ambient temperature. A decrease in
Ts results in a proportional increase in heat flux from the body,
unless it is opposed by increased body insulation. Thermo-
genesis is also triggered by decreases in Ts and Tc , which
can increase VO2 by threefold to fourfold, but in colder tem-
peratures thermogenesis is not sufficient to maintain a phys-
iological Tc . Immersion in water lower the TN temperature
results in increased vascular resistance of subcutaneous tis-
sues, as well as muscle to increase resistance to heat loss.
This vasoconstriction is initiated by a decrease in Ts , but as
Tc decreases the vasoconstriction become more pronounced.
At a CWT, resistance is maximized and Tc is sustained at a
normal level. At temperatures below this the body cools in
a time-dependent manner, and hypothermia can occur. Insu-
lation suits can only partially protect divers in cold water.
Exposure to warm or hot water is even more threatening than
cold water, and occurs in water temperatures above 35◦ C. As
the body takes up heat from the water, and the ability to elim-
inate heat by evaporation is limited, body temperature can
rise rapidly to dangerous levels, particularly during exercise.
In warm water, no apparent protection is known, and active
cooling systems are required to maintain core temperature.
Another major modulator of the physiological responses
to the aquatic environment is the depth of the water, and
the resultant hydrostatic pressure. There are cardio-renal
responses to pressure per se, however, in submersed con-
ditions, the responses are primarily due to the submersion.
There are suggestions that postdive resting cardiac responses
are depressed, but it is unclear for how long and if this has
physiological significance. The major effects of depth are
on the respiratory system. In addition, to the increased fluid
volume and reduced gas volume in the lung due to immer-
sion/submersion, the presence of SLL, increased breathing
gear resistance and hydrostatic pressure on the lung increases
the work (power) of both inspiration and expiration, reduces
mechanical efficiency and thus increases the energy cost of
ventilation.
1741
The Aquatic Environment
Exercising at a moderate to high intensity, especially in
cold water, may lead to pulmonary edema in some individu-
als. Diving is very safe if done properly as there is minimal
risk. However, if performed improperly, there is a risk of
decompression illness, and AGE.
Acknowledgements
The authors wish to acknowledge Journal of Applied Physi-
ology, European Journal of Applied Physiology and Elsevier
Limited, Oxford, United Kingdom for permission to use some
material from previous publications by these authors.
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