Spleen and cardiovascular function during short apneas in divers

Palada, Ivan; Eterović, Davor; Obad, Ante; Baković, Darija; Valić, Zoran; Ivančev, Vladimir; Lojpur, Mihajlo; Shoemaker, J. Kevin; Dujić, Željko

doi:10.1152/japplphysiol.00182.2007

Cited by 50 publications

(62 citation statements)

References 22 publications

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“…At the beginning of apnoea, the immediate response consisted of a rapid fall of SBP and DBP, as previously observed at rest (Andersson and Schagatay, 1998;Palada et al, 2007;Perini et al, 2008) and at exercise (Sivieri et al, 2015). This fall was associated with a reduction of SV, supporting the notion that the fall of SBP may be due to an acute reduction of venous return related to the act of holding the breath at elevated lung volumes (Andersson and Schagatay, 1998).…”

Section: The Characteristics Ofsupporting

confidence: 68%

Cardiovascular responses to dry resting apnoeas in elite divers while breathing pure oxygen

Fagoni

Sivieri

Antonutto

et al. 2015

Respiratory Physiology & Neurobiology

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a b s t r a c tPurpose: We hypothesized that the third dynamic phase ( 3) of the cardiovascular response to apnoea requires attainment of the physiological breaking point, so that the duration of the second steady phase ( 2) of the classical cardiovascular response to apnoea, though appearing in both air and oxygen, is longer in oxygen. Methods: Nineteen divers performed maximal apnoeas in air and oxygen. We measured beat-by-beat arterial pressure, heart rate (f H ), stroke volume (SV), cardiac output (Q ). Results: The f H , SV andQ changes during apnoea followed the same patterns in oxygen as in air. Duration of steady 2 was 105 ± 37 and 185 ± 36 s, in air and oxygen (p < 0.05), respectively. At end of apnoea, arterial oxygen saturation was 1.00 ± 0.00 in oxygen and 0.75 ± 0.10 in air. Conclusions:The results support the tested hypothesis. Lack of hypoxaemia during oxygen apnoeas suggests that, if chemoreflexes determine 3, the increase in CO 2 stores might play a central role in eliciting their activation.

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Section: The Characteristics Ofsupporting

confidence: 68%

Cardiovascular responses to dry resting apnoeas in elite divers while breathing pure oxygen

Fagoni

Sivieri

Antonutto

et al. 2015

Respiratory Physiology & Neurobiology

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“…Then SBP returned to control values within the end of phase I, whereas DBP increased by about 8 mmHg above pre-apnoea values. Transient hypotension at the beginning of dry apnoea was previously reported Palada et al 2007), and was attributed to the reduction of venous return due to holding the breath. The Wnal result of the BP changes was an increase in MBP by about 8-10% at the end of phase I, comparable to previous data obtained during dry apnoeas lasting 30 s (Leuenberger et al 2001) and 60 s (Andersson et al 2000).…”

Section: Discussionmentioning

confidence: 68%

“…Blood Xow is likely redistributed toward vital organs, whereas peripheral tissues may be unperfused so that lactate is accumulated in them. Spleen contraction may also occur (Bakovic et al 2003;Palada et al 2007). The ensemble of these changes, generally referred to as diving response, is interpreted as an O 2 -conserving mechanism (Ferretti 2001;Foster and Sheel 2005).…”

Section: Introductionmentioning

confidence: 99%

“…Observations during 30 s apnoeas in air (Palada et al 2007) as well as at the beginning of apnoeas with face immersion Andersson et al 2000) have shown that transient hypotension and tachycardia may precede the increase in BP and the decrease in HR. In apnoeas prolonged to the volitional breaking point, there is a continuous increase in BP without associated decrease in HR both with and without face immersion Andersson et al 2000).…”

Section: Introductionmentioning

confidence: 99%

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Heart rate and blood pressure time courses during prolonged dry apnoea in breath-hold divers

et al. 2008

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To define the dynamics of cardiovascular adjustments to apnoea, beat-to-beat heart rate (HR) and blood pressure and arterial oxygen saturation (SaO(2)) were recorded during prolonged breath-holding in air in 20 divers. Apnoea had a mean duration of 210 +/- 70 s. In all subjects, HR attained a value 14 beats min(-1) lower than control within the initial 30 s (phase I). HR did not change for the following 2-2.5 min (phase II). Then, nine subjects interrupted the apnoea (group A), whereas 11 subjects (group B) could prolong the breath-holding for about 100 s, during which HR continuously decreased (phase III). In both groups, mean blood pressure was 8 mmHg above control at the end of phase I; it then further increased by additional 12 mmHg at the end of the apnoea. In both groups, SaO(2) did not change in the initial 100-140 s of apnoea; then, it decreased to 95% at the end of phase II. In group B, SaO(2) further diminished to 84% at the end of phase III. A typical pattern of cardiovascular readjustments was identified during dry apnoea. This pattern was not compatible with a role for baroreflexes in phase I and phase II. Further readjustment in group B may imply a role for both baroreflexes and chemoreflexes. Hypothesis has been made that the end of phase II corresponds to physiological breakpoint.

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“…However, larger heart rate during dynamic apnea when compared to static apnea indicates larger sympathetic activity. In addition, we and others have suggested that splenic contraction is also a part of diving response [14,21] and that it occurs even with very short breath-holds lasting only 15 s, without the presence of chemical stimuli like hypoxia and/or hypercapnia [22].…”

Section: Physiological Diving Responsementioning

confidence: 84%

Breath-hold diving as a brain survival response

Dujić

Brešković

Baković

2013

Translational Neuroscience

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Apnea disciplines and current records BREATH HOLD DIVING AS A BRAIN SURVIVAL RESPONSE AbstractElite breath-hold divers are unique athletes challenged with compression induced by hydrostatic pressure and extreme hypoxia/hypercapnia during maximal field dives. The current world records for men are 214 meters for depth (Herbert Nitsch, No-Limits Apnea discipline), 11:35 minutes for duration (Stephane Mifsud, Static Apnea discipline), and 281 meters for distance (Goran Čolak, Dynamic Apnea with Fins discipline). The major physiological adaptations that allow breath-hold divers to achieve such depths and duration are called the "diving response" that is comprised of peripheral vasoconstriction and increased blood pressure, bradycardia, decreased cardiac output, increased cerebral and myocardial blood flow, splenic contraction, and preserved O 2 delivery to the brain and heart. This complex of physiological adaptations is not unique to humans, but can be found in all diving mammals. Despite these profound physiological adaptations, divers may frequently show hypoxic loss of consciousness. The breath-hold starts with an easy-going phase in which respiratory muscles are inactive, whereas during the second so-called "struggle" phase, involuntary breathing movements start. These contractions increase cerebral blood flow by facilitating left stroke volume, cardiac output, and arterial pressure. The analysis of the compensatory mechanisms involved in maximal breath-holds can improve brain survival during conditions involving profound brain hypoperfusion and deoxygenation.

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Spleen and cardiovascular function during short apneas in divers

Cited by 50 publications

References 22 publications

Cardiovascular responses to dry resting apnoeas in elite divers while breathing pure oxygen

Cardiovascular responses to dry resting apnoeas in elite divers while breathing pure oxygen

Heart rate and blood pressure time courses during prolonged dry apnoea in breath-hold divers

Breath-hold diving as a brain survival response

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