77
Chapter four: Pressure regulation
collapse of 225 m for California sea lions (McDonald and Ponganis 2012). Experimental
work showed deeper alveolar collapse depths closer to 170 m for sea lions in a hyperbaric
chamber (Kooyman and Sinnett 1982).
However, experimental studies of the tracheal structure under pressure (using hyperbaric chambers) have shown that the trachea is not incompressible (Kooyman et al. 1970).
There is also considerable interspecific variation in tracheal compliance in the excised conducting airways of several phocid seals and odontocetes (Moore et al. 2014), perhaps related
to variation in life history and diving abilities. Furthermore, the pressure–volume curves
of excised lungs diverged during deflation (i.e., exhalation) versus compression (Denison
et al. 1971; Fahlman et al. 2011; Kooyman and Sinnett 1982; Piscitelli et al. 2010).
Thus, if the trachea were to begin to compress prior to full alveolar collapse, it would
cause alveolar collapse depths to be deeper than initially predicted by Scholander’s balloon-pipe model (Figure 4.2) (Bostrom et al. 2008; Fitz-Clarke 2007). In fact, a model with
a slightly compliant trachea suggested alveolar collapse depths of 110 m for bottlenose
dolphins based on the Ridgway and Howard (1979) study and suggested that peak arterial
N 2 seen at 30 m depth by Falke et al. (1985) might, rather than showing alveolar collapse
depth, correspond to a depth-dependent pulmonary shunt that would affect the diffusion rate, that is, the alveoli might not collapse until greater depths (Bostrom et al. 2008).
That said, theoretical models are highly dependent on appropriate assumptions, and even
though some studies have tested model output against empirical data for dolphins, seals
and sea lions (Fahlman et al. 2009; Hooker et al. 2009), there is scant information about the
physiological responses of most marine mammal species. Thus, model results should be
viewed with care but are useful in defining important areas for further research and providing alternative explanations to earlier experimental work.
Whether breath-hold diving marine mammals experience alveolar collapse is not disputed, but there is probably considerable variability in how gas exchange is managed both
within and between species. This variability would arise from differences in respiratory
anatomy (Fahlman et al. 2014a; Moore et al. 2011; Moore et al. 2014; Piscitelli et al. 2010) and
behavior, for example, shallow versus deep divers. Our current understanding suggests
that the inherent anatomy of each species may limit deep diving. For example, deep divers
seem to have smaller lungs as compared with shallow-diving species (Piscitelli et al. 2010).
Still, there is evidence that there is limited plasticity in altering the structural properties
to help prevent barotrauma (Fahlman et al. 2014a). Interestingly, lung conditioning appears
to help increase vital capacity in humans (Johansson and Schagatay 2012) and recent work
has suggested that lung growth may occur even in adults (Butler et al. 2012). Thus, repeated
atelectasis and alveolar recruitment may be important for healthy lung function. However,
a more important factor on a dive-to-dive basis for determining the depth of alveolar collapse is the diving lung volume, that is, the air volume at the outset of the dive. Different
species also have different tactics in terms of inspired air volume. Although phocid seals
are thought to exhale prior to diving, the important question is to what extent does this
occur, that is, what is the diving lung volume? Studies show that they still dive with as
much as 60% of their inspiratory volume (Kooyman et al. 1971). Fur seals, sea lions and
cetaceans are thought to dive on inhalation (Kerem et al. 1975; Kooyman 1973).
Whatever the depth of alveolar collapse, many marine mammal species will reach depths
sufficient to cause a period of atelectasis followed by recruitment. That they do this repeatedly
and without any apparent side effects as the animal resurfaces is remarkable (Denison and
Kooyman 1973). The lungs produce a pulmonary surfactant that lines the alveolar air–water
interface, and varies the surface tension with lung volume to reduce the work of breathing,
alter compliance, and prevent adhesion of respiratory surfaces. An anti-adhesive surfactant with
Chapter four: Pressure regulation
collapse of 225 m for California sea lions (McDonald and Ponganis 2012). Experimental
work showed deeper alveolar collapse depths closer to 170 m for sea lions in a hyperbaric
chamber (Kooyman and Sinnett 1982).
However, experimental studies of the tracheal structure under pressure (using hyperbaric chambers) have shown that the trachea is not incompressible (Kooyman et al. 1970).
There is also considerable interspecific variation in tracheal compliance in the excised conducting airways of several phocid seals and odontocetes (Moore et al. 2014), perhaps related
to variation in life history and diving abilities. Furthermore, the pressure–volume curves
of excised lungs diverged during deflation (i.e., exhalation) versus compression (Denison
et al. 1971; Fahlman et al. 2011; Kooyman and Sinnett 1982; Piscitelli et al. 2010).
Thus, if the trachea were to begin to compress prior to full alveolar collapse, it would
cause alveolar collapse depths to be deeper than initially predicted by Scholander’s balloon-pipe model (Figure 4.2) (Bostrom et al. 2008; Fitz-Clarke 2007). In fact, a model with
a slightly compliant trachea suggested alveolar collapse depths of 110 m for bottlenose
dolphins based on the Ridgway and Howard (1979) study and suggested that peak arterial
N 2 seen at 30 m depth by Falke et al. (1985) might, rather than showing alveolar collapse
depth, correspond to a depth-dependent pulmonary shunt that would affect the diffusion rate, that is, the alveoli might not collapse until greater depths (Bostrom et al. 2008).
That said, theoretical models are highly dependent on appropriate assumptions, and even
though some studies have tested model output against empirical data for dolphins, seals
and sea lions (Fahlman et al. 2009; Hooker et al. 2009), there is scant information about the
physiological responses of most marine mammal species. Thus, model results should be
viewed with care but are useful in defining important areas for further research and providing alternative explanations to earlier experimental work.
Whether breath-hold diving marine mammals experience alveolar collapse is not disputed, but there is probably considerable variability in how gas exchange is managed both
within and between species. This variability would arise from differences in respiratory
anatomy (Fahlman et al. 2014a; Moore et al. 2011; Moore et al. 2014; Piscitelli et al. 2010) and
behavior, for example, shallow versus deep divers. Our current understanding suggests
that the inherent anatomy of each species may limit deep diving. For example, deep divers
seem to have smaller lungs as compared with shallow-diving species (Piscitelli et al. 2010).
Still, there is evidence that there is limited plasticity in altering the structural properties
to help prevent barotrauma (Fahlman et al. 2014a). Interestingly, lung conditioning appears
to help increase vital capacity in humans (Johansson and Schagatay 2012) and recent work
has suggested that lung growth may occur even in adults (Butler et al. 2012). Thus, repeated
atelectasis and alveolar recruitment may be important for healthy lung function. However,
a more important factor on a dive-to-dive basis for determining the depth of alveolar collapse is the diving lung volume, that is, the air volume at the outset of the dive. Different
species also have different tactics in terms of inspired air volume. Although phocid seals
are thought to exhale prior to diving, the important question is to what extent does this
occur, that is, what is the diving lung volume? Studies show that they still dive with as
much as 60% of their inspiratory volume (Kooyman et al. 1971). Fur seals, sea lions and
cetaceans are thought to dive on inhalation (Kerem et al. 1975; Kooyman 1973).
Whatever the depth of alveolar collapse, many marine mammal species will reach depths
sufficient to cause a period of atelectasis followed by recruitment. That they do this repeatedly
and without any apparent side effects as the animal resurfaces is remarkable (Denison and
Kooyman 1973). The lungs produce a pulmonary surfactant that lines the alveolar air–water
interface, and varies the surface tension with lung volume to reduce the work of breathing,
alter compliance, and prevent adhesion of respiratory surfaces. An anti-adhesive surfactant with