ArticlePDF Available

Aerobic exercise 2 hours before a dive to 30 msw decreases bubble formation after decompression


Abstract and Figures

A single bout of aerobic exercise 24 h before a dive significantly reduces the formation of circulating venous gas emboli (VGE) on decompression. The purpose of this investigation was to determine the effect of aerobic exercise 2 h before a dive. There were 16 trained military divers who were compressed to 30 msw (400 kPa) for 30 min breathing air in a dry hyperbaric chamber at rest, then decompressed at a rate of 10 m x min(-1) with a 9-min stop at 3 msw. Each diver performed two dives 3 d apart, one with and one without exercise that consisted of running for 45 min at 60-80% of maximum heart rate (estimated as 220 - age). VGE were graded according to the Spencer scale using a pulsed Doppler detector on the precordium at 30 min (T30) and 60 min (T60) after surfacing. Mean bubble grades at T60 were 1.25 for control dives and 0.44 for dives preceded by exercise, the difference being highly significant. None of the divers showed an increase in venous bubble grade after exercise. Like exercise 24 h ahead, 45 min of running 2 h before a dive decreases bubble formation after diving, suggesting a protective effect of aerobic exercise against DCS. The threshold of exercise intensity and duration necessary to change venous circulating bubbles is unknown. Mechanisms underlying the protective effect of exercise remain unclear. Rather than altering the nitrogen elimination rate, exercise may affect the population of gaseous nuclei from which bubbles form.
Content may be subject to copyright.
Delivered by Ingenta to: HIA STE ANNE Documentation
IP: On: Wed, 26 Apr 2017 06:04:17
Copyright: Aerospace Medical Association
Aerobic Exercise 2 Hours Before a Dive to 30 msw
Decreases Bubble Formation After Decompression
´ric Blatteau, Emmanuel Gempp,
Franc¸ois-Michel Galland, Jean-Michel Pontier,
Jean-Marie Sainty, and Claude Robinet
ROBINET C. Aerobic exercise 2 hours before a dive to 30 msw decreases
bubble formation after decompression. Aviat Space Environ Med
2005; 76:666–9.
Background: A single bout of aerobic exercise 24 h before a dive
significantly reduces the formation of circulating venous gas emboli
(VGE) on decompression. The purpose of this investigation was to
determine the effect of aerobic exercise 2 h before a dive. Methods:
There were 16 trained military divers who were compressed to 30 msw
(400 kPa) for 30 min breathing air in a dry hyperbaric chamber at rest,
then decompressed at a rate of 10 m min
with a 9-min stop at 3 msw.
Each diver performed two dives 3 d apart, one with and one without
exercise that consisted of running for 45 min at 6080% of maximum
heart rate (estimated as 220 age). VGE were graded according to the
Spencer scale using a pulsed Doppler detector on the precordium at 30
min (T30) and 60 min (T60) after surfacing. Results: Mean bubble grades
at T60 were 1.25 for control dives and 0.44 for dives preceded by
exercise, the difference being highly significant. None of the divers
showed an increase in venous bubble grade after exercise. Conclusion:
Like exercise 24 h ahead, 45 min of running 2 h before a dive decreases
bubble formation after diving, suggesting a protective effect of aerobic
exercise against DCS. The threshold of exercise intensity and duration
necessary to change venous circulating bubbles is unknown. Mecha-
nisms underlying the protective effect of exercise remain unclear. Rather
than altering the nitrogen elimination rate, exercise may affect the
population of gaseous nuclei from which bubbles form.
Keywords: diving, gas nuclei, decompression sickness, heat shock pro-
tein, nitric oxide.
DECOMPRESSION sickness (DCS) is caused by cir-
culating bubbles of inert gas in blood and tissues
resulting from supersaturation during decompression.
At present, Doppler-detected venous gas emboli (VGE)
are widely used as an indicator of decompression
stress. Although bubbles are frequent after symptom-
free dives, the occurrence of many bubbles is clearly
linked to a high risk of DCS (16). Regular activity, like
running, is a common practice in the military diving
community. The objectives are to stay in a good phys-
ical shape and to maintain a high level of cardiovascu-
lar fitness.
Intense physical exercise before diving has long been
considered an additional risk factor for DCS (22). It is
suggested that muscle contraction and tissue movement
produce gas nuclei leading to bubble formation and a
corresponding increase in the risk of DCS (10). Re-
cently, several studies indicate this notion needs updat-
It has been reported that exercise training weeks be-
fore dives could reduce the incidence of neurological
DCS in pigs (3) and rats (19). Similarly in humans, data
about aerobic fitness as a DCS protective factor are
described. It has been demonstrated that aerobically
trained runners appeared to be at lower risk for venous
bubbling than sedentary subjects (1,6). Moreover, recent
studies in rats have shown that a single bout of high-
intensity aerobic exercise 20 h before the dive sup-
pressed bubble formation and prevented death with no
effect at any other time (48, 10, 5, and 0.5 h prior to the
dive) (23,25). In a study of 12 divers, a single bout of
aerobic exercise 24 h before a dive significantly reduced
venous gas emboli and consequently could have a pre-
ventive effect on occurrence of DCS (8). It was also
observed that the incidence of VGE decreased when the
rest interval from an anaerobic exercise (150 deep knee
squats over a 10-min period) to altitude depressuriza-
tion lengthened and was performed 1–2 h before expo-
sure (7). Thus, it appeared relevant to determine the
effect of a single bout of aerobic exercise 2 h before a
dive on VGE formation in human volunteers.
We recruited 16 trained military divers, ages 24 41
yr (mean: 33.4), who were medically fit for diving. The
subjects were all experienced divers with 300–3000
dives (mean: 970). Their body mass index varied be-
tween 20.4 and 28 kg m
(mean: 24). None of them
had experienced DCS in the past. The protocol was
conformed to the principles of the declaration of Hel-
sinki and all subjects gave written, informed consent.
Subjects were asked to avoid physical exertion during
the 2 d that preceded the dive.
Each subject performed a single bout of submaximal
exercise consisting of endurance running at an intensity
From CEMPP, Toulon Arme´es, France (J-E
´. Blatteau); GPD me´di-
terrane´e, Toulon Arme´es, France (E. Gempp); IMNSSA, Toulon
Arme´es, France (F-M. Galland, J-M. Pontier, C. Robinet); and the
Hoˆpital Sainte-Marguerite, Marseille, France (J-M. Sainty).
This manuscript was received for review in January 2005. It was
accepted for publication in March 2005.
Address reprint requests to: Jean-E
´ric Blatteau, M.D., CEMPP, BP
84, 83800 Toulon Arme´es, France;
Reprint & Copyright © by Aerospace Medical Association, Alexan-
dria, VA.
666 Aviation, Space, and Environmental Medicine Vol. 76, No. 7, Section I July 2005
Delivered by Ingenta to: HIA STE ANNE Documentation
IP: On: Wed, 26 Apr 2017 06:04:17
Copyright: Aerospace Medical Association
of 60 80% of maximum theoretical heart rate (220
age) for a total exercise session of 45 min. Heart rate was
recorded continuously during the test using a HR mon-
itor (Polar Vantage, Kempele, Finland). The divers were
then compressed in a hyperbaric chamber (Sainte-Anne
hospital, Toulon, France) to 30 msw (400 kPa) at a rate
, breathing air and remaining at rest at
pressure for 30 min. They were decompressed at a rate
of 10 m min
to 3 msw, where they remained for 9
min before they were decompressed to the surface at
the same rate (French Navy MN90 procedure). Each
diver performed two dives 3 d apart, one with and one
without exercise 2 h before the dive. The order of the
two dives was randomly allocated.
VGE detection on the precordial area was performed
with a pulsed Doppler 2 Mhz by an experienced oper-
ator. We have previously shown that pulsed Doppler is
more sensitive and less operator dependant than con-
tinuous Doppler (2). Moreover, it is suggested that
there is a good correlation between different pulsed
Doppler methods, with and without image-assisted de-
tection (4).
During bubble detection, divers were supine for 3
min at rest, then, in order to improve the detection, two
successive lower limbs flexions were performed. The
Spencer scale was used to evaluate the signals of bub-
bles and the determination of the bubble grade was
carried out at 30 and 60 min after surfacing (21). A
persistent and stable bubble score during at least 10
systoles after 2 successive lower limbs flexions was
considered a consistent finding. Differences in bubble
grade (at peak) between groups were determined using
the non-parametric Wilcoxon test with p 0.05 as the
level of significance.
None of the divers suffered from DCS after the dives.
For all the dives, the maximum bubble count (bubble
peak) was observed 60 min after surfacing. Mean bub-
ble grade was 1.25 at rest and 0.44 after exercise (p
0.0062). None of the divers showed an increase in ve-
nous bubble grade after performing the exercise (Fig. 1).
The present study puts forward a previously unre-
ported finding that a single bout of an aerobic exercise
2 h before a dive results in lower bubble scores in
human volunteers following decompression. The mech-
anisms underlying the protective effect of exercise re-
main unclear and numerous parameters should be eval-
uated. Rather than altering nitrogen elimination,
exercise may alter the population of gaseous nuclei
from which bubbles form (23). It has been generally
postulated that these preformed gaseous nuclei must be
present for bubbles to develop at the modest gas super-
saturations encountered by divers, aviators, and astro-
nauts (10,27). These nuclei are not stable in blood and
two major stabilizing factors are suggested: 1) the exis-
tence of intercellular hydrophobic crevices on the en-
dothelial surface that trap gas nuclei (10,12); and 2) the
concept of surface-active molecules like surfactant,
platelets, or proteins that coat gas nuclei (27). The half-
life and the faculty for nuclei to initiate bubble forma-
tion during decompression depend on these stabilizing
factors. Previous studies have hypothesized the lifetime
of those bubbles could be on the order of minutes to a
few hours (7), and it took about 10–100 h to regenerate
the nuclei population (27).
It has been suggested that the protection from bubble
formation by appropriately timed exercise could be
related to biochemical processes. A large number of
studies have shown that in normal control animals (20)
and healthy subjects (11), exercise training improves
endothelial function and protection against cardiovas-
cular diseases (11). The likely mechanism by which
aerobic exercise activates endothelial function is an in-
crease in vascular shear stress resulting from increased
blood flow. This beneficial effect seems essentially re-
lated to an increase in vascular endothelial nitric oxide
(NO) bioavailability (increase in NO production and/or
decrease in NO inactivation) (11). Aside from effects on
vascular tone, it has been established that NO inhibits
leukocyte and platelet adhesion under low and high
shear conditions (17) and could reduce hydrophobicity
of the endothelial wall, reducing the number of nuclei
adhering to the surface (23). It is speculated that phys-
ical activity may trigger synthesis of a molecular species
that is expressed in the endothelium about 20 h later,
leading to an increase in endothelial NO synthase
(eNOS) activity through activation of several signal
transduction pathways (25). However, it has been
shown that bubble production is increased by NO
Fig. 1. Individual Spencer scores
for venous gas emboli 60 min after
simulated dives to 30 msw for 30
min. Black bars represent control
dives and gray bars represent dives
preceded by exercise.
667Aviation, Space, and Environmental Medicine Vol. 76, No. 7, Section I July 2005
Delivered by Ingenta to: HIA STE ANNE Documentation
IP: On: Wed, 26 Apr 2017 06:04:17
Copyright: Aerospace Medical Association
blockade in sedentary but not in exercised rats (24). This
indicates that the exercise effect may be mediated by
factors other than nitric oxide.
A few studies have focused on other endothelial pro-
tective mechanisms induced by exercise. In vitro appli-
cation of laminar shear stress to cultured endothelial
cells involves changes to the architecture of the vascular
wall that decrease the turbulence of blood flow, up-
regulate antioxidant defenses, and increase mediators
of anticoagulant pathways such as protacyclin (15).
Heat shock proteins (HSP), present in most cells, in-
cluding endothelial cells, play a key role in normal
cellular homeostasis and protection from cell damage in
response to stress stimuli. However, the precise func-
tions of these proteins have not been completely delin-
eated (14).
It is well documented that endurance exercise is a
stressor that increases the HSP expression (26). Human
studies have shown that HSP 70 mRNA concentration
in muscle cells was significantly increased 30 min and
3 h after the end of a single exercise bout (18). HSP 70
levels were also increased in peripheral blood leuko-
cytes 0, 3, and 24 h after running (9). It has also been
demonstrated that heat shock pretreatment before div-
ing enhanced the expression of HSP70 and protected
rats from air-embolism-induced lung injury (13). More-
over, several investigators have focused on the interac-
tion of eNOS with HSP90, emphasizing a possible close
link between HSP and the endogenous NO pathway
(11). However, a recent study on heat shock precondi-
tioning before diving supports the findings that HSP90
is less heat induced than HSP70 and that HSP90 and
eNOS are probably less important for the protective
mechanism against bubble formation (5). Thus, it is
conceivable that exercise-induced HSP70 production af-
fects bubble formation after diving by a different mech-
anism than the NO pathway. The real bioprotective
mechanism of HSP70 against DCS has not yet been
described and requires further research.
Regarding the limitations of our study, we did not
use a precise calibration for the physical exertion pro-
tocol. In the future, it would be interesting to determine
each subject’s aerobic fitness (maximal oxygen uptake;
max) by a maximal exercise test before the experi-
mental procedure. Moreover, our findings may be con-
sidered limited because of the small sample size. It
would also be useful to perform a longer air dive in
order to produce a significant and a reproducible
amount of bubbles.
To date, the threshold of exercise intensity and dura-
tion of exercise necessary for changes in venous circu-
lating bubbles is unknown. Further investigations are
needed to determine the real pre-dive/exercise protec-
tive latency in divers.
This study demonstrates that a single bout of aerobic
exercise 2 h predive decreases venous gas bubble for-
mation in man. These results could have considerable
implications for DCS prevention. Further work is
needed to elucidate the mechanisms underlying this
exercise-induced reduction in bubble formation.
This paper represents the views of the authors and does not nec-
essarily reflect the official opinion of the French Navy.
1. Behnke AR. Investigations concerned with problems of high alti-
tude flying and deep diving; application of certain findings
pertaining to physical fitness to the general military service.
Milit Surg 1942; 90:9–28.
2. Blatteau JE, Hugon M, Galland FM. Etude des bulles veineuses
circulantes chez l’homme. Comparaison doppler pulse´/dopp-
ler continu en de´tection pre´cordiale (Study of circulating ve-
nous bubbles in man. Comparison between pulsed and con-
tinuous precordial Doppler detection). Bull Med Sub Hyp
2004; In press.
3. Broome JR, Dutka AJ, McNamee GA. Exercise conditioning re-
duces the risk of neurologic decompression illness in swine.
Undersea Hyperb Med 1995; 22:73–85.
4. Brubakk AO, Eftedal O. Comparison of three different ultrasonic
methods for quantification of intravascular gas bubbles. Un-
dersea Hyperb Med 2001; 28:131–6.
5. Bye A, Medbye C, Brubbak AO. Heat shock treatment prior to
dive increases survival in rats. In: Grandjean B, Meliet J-L, eds.
Proceedings of the 30
annual scientific meeting of the EUBS;
2004 sept 15–19; Ajaccio, Corsica. Ajaccio, France: EUBS; 2004:
6. Carturan D, Boussuges A, Vanuxem P, et al. Ascent rate, age,
maximal oxygen uptake, adiposity, and circulating venous
bubbles after diving. J Appl Physiol 2002; 93:1349–56.
7. Dervay JP, Powell MR, Butler B, et al. The effect of exercise and
rest duration on the generation of venous gas bubbles at alti-
tude. Aviat Space Environ Med 2002; 73:22–7.
8. Dujic Z, Duplancic D, Marinovic-Terzic I, et al. Aerobic exercise
before diving reduces venous gas bubble formation in humans.
J Physiol (London) 2004; 555(Part 3):637–42.
9. Fehrenbach E, Passek F, Niess AM, et al. HSP expression in
human leukocytes is modulated by endurance exercise. Med
Sci Sports Exerc 2000; 32:592–600.
10. Harvey EN, Whiteley AH, McElroy WD, et al. Bubble forma-
tion in animals. I. Physical factors. II. Gas nuclei and their
distribution in blood and tissues. J Cell Comp Physiol 1944;
11. Higashi Y, Yoshizumi M. Exercise and endothelial function: role
of endothelium-derived nitric oxide and oxidative stress in
healthy subjects and hypertensive patients. Pharmacol Ther
2004; 102:87–96.
12. Hills BA. A hydrophobic oligolamellar lining to the vascular
lumen in some organs. Undersea Biomed Res 1992; 19:107–20.
13. Huang KL, Wu CP, Chen YL, et al. Heat stress attenuates air
bubble-induced acute lung injury: a novel mechanism of div-
ing acclimatization. J Appl Physiol 2003; 94:1485–90.
14. Kregel KC. Invited review: heat shock proteins: modifying factors
in physiological stress responses and acquired thermotoler-
ance. J Appl Physiol 2002; 92:2177–86.
15. Marsh SA, Coombes JS. Exercise and the endothelial cell. Int
J Cardiol 2005; 99:165–9.
16. Nishi RY. Doppler evaluation of decompression tables. In: Lin
YC, Shida KK, eds. Man in the sea 1990. San Pedre: Best
Publishing Company; 1990:297–316.
17. Provost P, Merhi Y. Endogenous nitric oxide release modulates
mural platelet thrombosis and neutrophil-endothelium inter-
actions under low and high shear conditions. Thromb Res
1997; 85:315–26.
18. Puntschart A, Vogt M, Widmer HR, et al. HSP 70 expression in
human skeletal muscle after exercise. Acta Physiol Scand 1996;
19. Rattner BA, Gruenau SP, Altland PD. Cross-adaptive effects of
cold, hypoxia, or physical training on decompression sickness
in mice. J Appl Physiol 1979; 47:412–7.
20. Sessa WC, Pritchard K, Seyedi N, et al. Chronic exercise in dogs
increases coronary vascular nitric oxide production and endo-
thelial cell nitric oxide synthase gene expression. Circ Res 1994;
21. Spencer MP. Decompression limits for compressed air deter-
mined by ultrasonically detected blood bubbles. J Appl Physiol
1976; 40:229–35.
668 Aviation, Space, and Environmental Medicine Vol. 76, No. 7, Section I July 2005
Delivered by Ingenta to: HIA STE ANNE Documentation
IP: On: Wed, 26 Apr 2017 06:04:17
Copyright: Aerospace Medical Association
22. Vann RD. Mechanisms and risks of decompression. In: Bove AA,
Davis JC, eds. Diving medicine. Philadelphia: Saunders; 1990:
23. Wisloff U, Brubakk AO. Aerobic endurance training reduces bub-
ble formation and increases survival in rats exposed to hyper-
baric pressure. J Physiol (London) 2001; 537(Part 2):607–11.
24. Wisloff U, Richardson RS, Brubakk AO. NOS inhibition increases
bubbles formation and reduces survival in sedentary but not
exercised rats. J Physiol (London) 2003; 546(Part 2):577–82.
25. Wisloff U, Richardson RS, Brubakk AO. Exercise and nitric oxide
prevent bubble formation: a novel approach to the prevention
of decompression sickness? J Physiol (London) 2004; 555(Part
26. Xu Q. Role of heat shock proteins in atherosclerosis. Arterioscler
Thromb Vasc Biol 2002; 22:1547–59.
27. Yount D, Strauss R. On the evolution, generation and regener-
ation of gas cavitation nuclei. J Acoust Soc Am 1982; 65:
669Aviation, Space, and Environmental Medicine Vol. 76, No. 7, Section I July 2005
... Indeed, since several years, field research focuses on "preconditioning" methods that might attenuate bubble formation post-dive. Several practical, simple and feasible pre-dive measures have been studied such as endurance exercise (Blatteau et al., 2005;Castagna et al., 2011), pre-dive exposition to a warm environment (Blatteau et al., 2008), oral hydration or ingestion of dark chocolate (Theunissen et al., 2015). Others have tested the benefit of predive oxygenation (Castagna et al., 2009;Bosco et al., 2010), or whole-body vibration (Germonpré et al., 2009). ...
... Participants were instructed not to dive 72 h prior to the experimental dive. They were also were asked to refrain from strenuous exercise and nitrate-rich food for 48 h before the tests (Blatteau et al., 2005). ...
Full-text available
Purpose: Since non-provocative dive profiles are no guarantor of protection against decompression sickness, novel means including pre-dive “preconditioning” interventions, are proposed for its prevention. This study investigated and compared the effect of pre-dive oxygenation, pre-dive whole body vibration or a combination of both on post-dive bubble formation. Methods: Six healthy volunteers performed 6 no-decompression dives each, to a depth of 33 mfw for 20 min (3 control dives without preconditioning and 1 of each preconditioning protocol) with a minimum interval of 1 week between each dive. Post-dive bubbles were counted in the precordium by two-dimensional echocardiography, 30 and 90 min after the dive, with and without knee flexing. Each diver served as his own control. Results: Vascular gas emboli (VGE) were systematically observed before and after knee flexing at each post-dive measurement. Compared to the control dives, we observed a decrease in VGE count of 23.8 ± 7.4% after oxygen breathing (p < 0.05), 84.1 ± 5.6% after vibration (p < 0.001), and 55.1 ± 9.6% after vibration combined with oxygen (p < 0.001). The difference between all preconditioning methods was statistically significant. Conclusions: The precise mechanism that induces the decrease in post-dive VGE and thus makes the diver more resistant to decompression stress is still not known. However, it seems that a pre-dive mechanical reduction of existing gas nuclei might best explain the beneficial effects of this strategy. The apparent non-synergic effect of oxygen and vibration has probably to be understood because of different mechanisms involved.
... Likewise, several studies have demonstrated that physical activity or sauna exposure, some hours before the dive, could have a cardiovascular-mediated preventive effect on VGE formation [17][18][19][20]. An animal model with rats demonstrated that a single bout of exercise 20 h pre-dive reduces VGE post-dive and also DCS occurrence and related mortality [21]. ...
Full-text available
Background: Despite evolution in decompression algorithms, decompression illness is still an issue nowadays. Reducing vascular gas emboli (VGE) production or preserving endothelial function by other means such as diving preconditioning is of great interest. Several methods have been tried, either mechanical, cardiovascular, desaturation aimed or biochemical, with encouraging results. In this study, we tested mini trampoline (MT) as a preconditioning strategy. Methods: In total, eight (five females, three males; mean age 36 ± 16 years; body mass index 27.5 ± 7.1 kg/m2) healthy, non-smoking, divers participated. Each diver performed two standardized air dives 1 week apart with and without preconditioning, which consisted of ±2 min of MT jumping. All dives were carried out in a pool (NEMO 33, Brussels, Belgium) at a depth of 25 m for 25 min. VGE counting 30 and 60 min post-dive was recorded by echocardiography together with an assessment of endothelial function by flow-mediated dilation (FMD). Results: VGE were significantly reduced after MT (control: 3.1 ± 4.9 VGE per heartbeat vs. MT: 0.6 ± 1.1 VGE per heartbeat, p = 0.031). Post-dive FMD exhibited a significant decrease in the absence of preconditioning (92.9% ± 7.4 of pre-dive values, p = 0.03), as already described. MT preconditioning prevented this FMD decrease (103.3% ± 7.1 of pre-dive values, p = 0.30). FMD difference is significant (p = 0.03). Conclusions: In our experience, MT seems to be a very good preconditioning method to reduce VGE and endothelial changes. It may become the easiest, cheapest and more efficient preconditioning for SCUBA diving.
... Further studies investigated the effect of exercise taken closer to the dive time. Recent work in humans involving both medium and high intensity running exercise commencing 2 h prior to a dive, was found to reduce VGE formation (Blatteau et al., 2005. Similarly, medium or high-intensity cycling exercise commencing 2 h before an open water dive also reduced VGE grades . ...
Full-text available
Human extravehicular activity (EVA) is essential to space exploration and involves risk of decompression sickness (DCS). On Earth, the effect of microgravity on physiological systems is simulated in an experimental model where subjects are confined to a 6° head-down bed rest (HDBR). This model was used to investigate various resting and exercise regimen on the formation of venous gas emboli (VGE), an indicator of decompression stress, post-hyperbaric exposure. Eight healthy male subjects participating in a bed rest regimen also took part in this study, which incorporated five different hyperbaric exposure (HE) interventions made before, during and after the HDBR. Interventions i–iv were all made with the subjects lying in 6° HD position. They included (C1) resting control, (C2) knee-bend exercise immediately prior to HE, (T1) HE during the fifth week of the 35-day HDBR period, (C3) supine cycling exercise during the HE. In intervention (C4), subjects remained upright and ambulatory. The HE protocol followed the Royal Navy Table 11 with 100 min spent at 18 m (280 kPa), with decompression stops at 6 m for 5 min, and at 3 m for 15 min. Post-HE, regular precordial Doppler audio measurements were made to evaluate any VGE produced post-dive. VGE were graded according to the Kisman Masurel scale. The number of bubbles produced was low in comparison to previous studies using this profile [Kisman integrated severity score (KISS) ranging from 0–1], and may be because subjects were young, and lay supine during both the HE and the 2 h measurement period post-HE for interventions i–iv. However, the HE during the end of HDBR produced significantly higher maximum bubble grades and KISS score than the supine control conditions (p < 0.01). In contrast to the protective effect of pre-dive exercise on bubble production, a prolonged period of bed rest prior to a HE appears to promote the formation of post-decompression VGE. This is in contrast to the absence of DCS observed during EVA. Whether this is due to a difference between hypo- and hyperbaric decompression stress, or that the HDBR model is a not a good model for decompression sensitivity during microgravity conditions will have to be elucidated in future studies.
... El ejercicio en profundidad ha sido siempre considerado un factor de riesgo, porque aumenta el consumo de oxígeno muscular, acelera el ritmo cardíaco, aumenta el gasto cardíaco, acelera el ritmo respiratorio y, como consecuencia de todo ello, aumenta el volumen de gas inerte fijado en los tejidos. No obstante, recientemente se ha comprobado que un ejercicio moderado previo y/o posterior a la inmersión disminuye los índices de embolismo gaseoso subclínico 31,32 . La baja temperatura y el frío provocan vasoconstricción periférica, lentifican el ritmo circulatorio y obstaculizan la difusión y la eliminación del gas inerte desde los tejidos saturados. ...
Full-text available
... Venous gas emboli are often used as a surrogate marker for decompression stress following exercise; however, the data on VGE and exercise are limited to a few conflicting field studies (Blatteau et al., 2005;Castagna et al., 2011;Madden et al., 2014) and simulated dives (Dujic et al., 2004;Gennser et al., 2012). MPs and endothelial function show promise as other markers to assess decompression stress and these may contribute to DCS or other forms of illness with mechanisms separate from circulating gas emboli. ...
AimSCUBA diving frequently involves repetitive exposures. The goal of this study was to see how exercise impacts microparticles (MPs), endothelial function and venous gas emboli (VGE) throughout multiple dives.Methods Sixteen divers in two groups (G1 and G2) each completed six dives, three preceded by exercise (EX) and three as controls (CON). Blood for MP analysis was collected before and after each dive. VGE were monitored via transthoracic echocardiography 30, 60 and 90 min after surfacing. Exercise before diving consisted of 60-min running including eight, 3-min intervals at 90% VO2max.ResultsExercise did not have a significant impact on VGE. There was no significant difference in MP counts between EX and CON. Both groups experienced a significant decrease in MP counts in the last three dives compared to the first three (G1 P = 0·0008, G2 P = 0001). Other indices of neutrophil/platelet interaction (dual-positive CD63/41 and CD62/41) show a significant increase (P = 0·004 and 0·0001) in G2.Conclusion Both groups experienced a significant decrease in MPs at all measurements in the second series of dives compared to the first, regardless of the placement of exercise. Whether this is related to an effect of suppression of MPs or exercise timing is not clear.
Risk in SCUBA diving is often associated with the presence of gas bubbles in the venous circulation formed during decompression. Although it has been demonstrated time-after-time that, while venous gas emboli (VGE) often accompany decompression sickness (DCS), they are also frequently observed in high quantities in asymptomatic divers following even mild recreational dive profiles. Despite this VGE are commonly utilized as a quantifiable marker of the potential for an individual to develop DCS. Certain interventions such as exercise, antioxidant supplements, vibration, and hydration appear to impact VGE production and the decompression process. However promising these procedures may seem, the data are not yet conclusive enough to warrant changes in decompression procedure, possibly suggesting a component of individual response. We hypothesize that the impact of exercise varies widely in individuals and once tested, recommendations can be made that will reduce individual decompression stress and possibly the incidence of DCS. The understanding of physiological adaptations to diving stress can be applied in different diseases that include endothelial dysfunction and microparticle (MP) production.
This study aims to investigate the relationship of self-reported pre-dive behaviours of Canadian Forces (CF) divers and detected venous gas emboli (VGE) post-experimental dive. A retrospective chart review of pre-dive questionnaires and matching post-dive venous Doppler bubble scores of 1,092 CF experimental dives was completed. Non-parametric categorical statistics were used to measure the effect of independent variables of age, exercise, alcohol, medication, smoking, food, fluid, fatigue, and infectious symptoms on maximum bubble grades (BG) measured precordially and at any site. Dives were analyzed as a single group and stratified into high-, moderate-, and low-stress dives, as well as exercise / no exercise during the dive subsets. Results: 12.6% of precordial BG and 26.1% of maximum any-site BG recorded as ≥ 3. Within 48 hours of diving, 45% exercised, 16.7% used oral medications, 38.25% consumed alcohol, 15.4% smoked, and 9.7% experienced infectious symptoms. Prior to the dive, 88.1% consumed food, 91.8% consumed liquids, and 26.3% felt fatigued. There was a statistically significant difference in BG among divers based on age (p = 0.043, binary logistic regression All Dives, MaxBG) and smoking (p = 0.045, Fisher's exact test, All Dives MaxBG). These differences did not continue in the other diving subsets, and no statistically significant effects attributed to the other variables were noted in any dive subset. CF experimental divers do report exposure to potential pre-dive risk factors for VGE. Significant association is detected between age, smoking status, and BG in one subset (all dives, MaxBG any site). No significant effect attributed to the remaining risk factors and BG is found. This study suggests that these factors may not affect VGE formation and its attendant risk of decompression sickness (DCS) in this military experimental diver population. However, as the result of study limitations, future studies are required to evaluate each risk factor prospectively to determine its impact on VGE formation during diving.
Recently a new cavitation model was proposed in which bubble formation in aqueous media is initiated by spherical gas nuclei stabilized by surface-active membranes of varying gas permeability. By tracking the changes in nuclear radius that are caused by increases or decreases in ambient pressure, the varying-permeability model has provided precise quantitative descriptions of several bubble counting experiments carried out with supersaturated gelatin. The model has also been used to calculate diving tables and to predict levels of incidence for decompression sickness in a variety of animal species. The model equations, in their present form, are essentially static and can be derived by requiring mechanical or chemical equilibrium at each setting in a rudimentary pressure schedule. The time dependence of the evolution of an individual nucleus from one equilibrium state to another is examined, and a statistical process by which the equilibrium size distribution of an entire population of nuclei may be generated or regenerated is then investigated.
The effects of adaptation to cold, hypoxia, or exercise on hyperbaric decompression tolerance were investigated in two factorial experiments. For either 14 or 28 days, groups of mice were handled (control); exposed discontinuously for 4 h to cold (4 degrees C) or hypoxia (P approximately 379 or 320 Torr); or exercised by swimming (15 min at 31 degrees C) or treadmill excursion (8.1 m/min for 1 or 1.5 h). The animals were divided into subgroups, exposed to one of three hydrostatic pressures (7.6--11.1 ATA) for 30 min, decompressed, and observed to determine survival rate or bends incidence (type II decompression sickness). Decompression sickness was significantly reduced (P less than 0.05) in the treadmill-trained animals, was unchanged in cold-exposed and swim-exercised mice, and tended to increase in animals adapted to hypoxia. Enhanced tolerance by treadmill training is presumably due to lean body conformation, which could reduce nitrogen saturation of tissues, and greater muscle capillarization and cardiovascular fitness, which may improve nitrogen elimination. Reduced tolerance with adaptation to hypoxia may be attributed to rheological changes associated with polycythemia, which facilitate bubble production.
The direct decompression limits for a group of divers over a range of pressure-time air exposures was determined using ultrasonic detection of venous gas emboli (VGE). In addition to dry chamber exposures, ranging from 233 ft for 7 min to 25 ft for 720 min, we exposed six divers to open ocean dives at 165 ft for 10 min. Findings demonstrated a strong individual propensity to form VGE, correlating with susceptibility to bends. No bends developed without the prior detection of precordial VGE. The present concept of no problems after any period of time at 30 fsw was not confirmed. Isopleths of equal percentage occurrence of VGE were computed between 10 and 60%. Open ocean exposures increased the percentage of VGE and bends, when compared to dry chamber exposures. Limiting tissue half times computed from the 20% VGE isopleth suggested that saturation exposures are controlled by a greater sensitivity of the short-half-time tissues than previously appreciated, rather than by additionally extended half times.
Various endothelial surfaces from sheep and humans have been studied for their hydrophobicity using a standard method based on the angle of contact (theta) of the surface with a droplet of saline placed on it. Most surfaces were relatively hydrophilic (theta less than 25 degrees) but some were distinctly hydrophobic with theta exceeding 65 degrees for sheep pulmonary vein, left ventricle, and aorta, and human umbilical vein. These results are discussed as compatible with the theory that surface-active phospholipid (surfactant) migrates from lung tissue into the pulmonary circulation or reaches intravascular sites from other sources. Transmission electron microscopy of cerebral vessels demonstrated an oligolamellar lining of surfactant on many endothelial surfaces, bridging the "tight" junctions between endothelial cells in many cases. Lamellar bodies were found adjacent to the endothelium. The oligolamellar surfactant lining and lamellar bodies are discussed as potentially very important factors in influencing bubble formation on vessel walls. It is believed to impart hydrophobicity while it could also determine the microgeometry of any crevices vital for bubble formation or retention.
Recently, we have shown that chronic exercise increases endothelium-derived relaxing factor (EDRF)/nitric oxide (NO)-mediated epicardial coronary artery dilation in response to brief occlusion and acetylcholine. This finding suggests that exercise can provide a stimulus for the enhanced production of EDRF/NO, thus possibly contributing to the beneficial effects of exercise on the cardiovascular system. Therefore, the purpose of the present study was to examine whether chronic exercise could influence the production of NO (measured as the stable degradation product, nitrite) and endothelial cell NO synthase (ECNOS) gene expression in vessels from dogs after chronic exercise. To this end, dogs were exercised by running on a treadmill (9.5 km/h for 1 hour, twice daily) for 10 days, and nitrite production in large coronary vessels and microvessels and ECNOS gene expression in aortic endothelial extracts were assessed. Acetylcholine (10(-7) to 10(-5) mol/L) dose-dependently increased the release of nitrite (inhibited by nitro-L-arginine) from coronary arteries and microvessels in control and exercised dogs. Moreover, acetylcholine-stimulated nitrite production was markedly enhanced in large coronary arteries and microvessels prepared from hearts of dogs after chronic exercise compared with hearts from control dogs. One potential mechanism that may contribute to the enhanced production of nitrite in vessels from exercised dogs may be the induction of the calcium-dependent ECNOS gene. Steady-state mRNA levels for ECNOS were significantly higher than mRNA levels for von Willebrand's factor (vWF, a specific endothelial cell marker) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH, a constitutively expressed gene) in exercised dogs.(ABSTRACT TRUNCATED AT 250 WORDS)
During development of a pig model of neurologic decompression illness (DCI) we noted that treadmill-trained pigs seemed less likely to develop DCI than sedentary pigs. The phenomenon was formally investigated. Twenty-four immature, male, castrated, pure-bred Yorkshire swine were conditioned by treadmill running, while 34 control pigs remained sedentary. All pigs (weight 18.75-21.90 kg) were dived on air to 200 feet of seawater (fsw) in a dry chamber. Bottom time was 24 min. Decompression rate was 60 fsw/min. Pigs that developed neurologic DCI were treated by recompression. Pigs without neurologic signs were considered neurologically normal if they ran on the treadmill without gait disturbance at 1 and 24 h postdive. Of the 24 exercise-conditioned pigs, only 10 (41.7%) developed neurologic DCI, compared to 25 of 34 (73.5%) sedentary pigs (X2 = 5.97; P = < 0.015). Neither mean carcass density (adiposity) nor mean age were significantly different between groups. No patent foramen ovale was detected at necropsy. An additional control group of 24 pigs was dived to clarify the influence of weight. The results suggest that the risk of neurologic DCI is reduced by physical conditioning, and the effect is independent of differences in age, adiposity, and weight.
Prolonged exercise of a sufficiently high intensity is thought to create physiological stress and to disturb cellular homeostasis, ultimately inducing cellular adaptations which enable the organism to better deal with any future exercise challenge. Heat shock proteins (hsp) are expressed when cells are exposed to different types of stress. In this study, we have investigated whether the expression of the heat inducible form of hsp70 is increased in human skeletal muscle cells after a single bout of exercise. Five untrained subjects performed an exercise bout at their individual anaerobic threshold for 30 min on a treadmill. Hsp70 mRNA concentration was significantly increased by a factor of four at 4 min post-exercise. Similarly high levels were also observed 30 min and 3 h after the end of exercise. Hsp70 protein concentration, on the contrary, did not change within 3 h after cessation of exercise. Thus, a single exercise bout in humans is able to increase the steady state concentration of hsp70 mRNA, but is probably not sufficient to have an effect on the already high basal level of its protein. The analysis of hsp70 mRNA is potentially useful as a method to detect stress in tissues with a high basal level of heat shock proteins.