Maximum effort breath-hold times for males and females of similar pulmonary capacities during sudden face-only immersion at water temperatures from 0 to 33 °C

2006 ◽  
Vol 31 (5) ◽  
pp. 549-556 ◽  
Author(s):  
Ollie Jay ◽  
Matthew D. White
Keyword(s):  
Water Temperature ◽  
Hold Time ◽  
Breath Holding ◽  
Breath Hold ◽  
Main Effect ◽  
Before And After ◽  
Maximum Effort ◽  
Males And Females ◽  
End Tidal ◽  
Air Control

For non breath-hold-trained males and females matched for pulmonary capacity and body size, the effects of sex, water temperature, and end-tidal gas tensions were studied for their potential influences on breath-holding ability. Maximum breath-hold time (BHTmax) was measured a total of 546 times in 13 males and 13 females, each repeating 3 trials of sudden face immersion (i.e., no prior hyperventilation) in water at 0, 5, 10, 15, 20, and 33 °C and in an air control condition (AIR). End-tidal carbon dioxide (PETCO2) and oxygen (PETO2) gas tensions were measured before and after breath-holding in a subset of 11 males and 11 females. For BHTmax there was no main effect of sex (p = 0.20), but there was a main effect of immersion condition (p < 0.001). Relative to pre-immersion rest values, end-tidal gas tensions were significantly higher in males than in females (p ≤ 0.05) and significantly lower at decreased water temperatures relative to AIR (p ≤ 0.05). In conclusion, for these matched groups (i) sex did not influence BHTmax; (ii) irrespective of sex, decreases in water temperature at 0, 5, 10, and 15 °C gave proportionate decreases of BHTmax; (iii) significantly greater deviations in both PETCO2 and PETO2 following breath-holding were evident in males relative to females; and (iv) irrespective of sex, there were significantly smaller changes in both PETCO2 and PETO2 at lower water temperatures relative to AIR, with or without removing the variance due to breath holding.

Effect of lung volume on breath holding

1987 ◽  
Vol 62 (5) ◽  
pp. 1962-1969 ◽  
Author(s):  
W. A. Whitelaw ◽  
B. McBride ◽  
G. T. Ford
Keyword(s):  
Lung Volume ◽  
Hold Time ◽  
Esophageal Pressure ◽  
Breath Holding ◽  
Breath Hold ◽  
Pressure Waves ◽  
Expiratory Muscle ◽  
Inspiratory Muscles ◽  
Consistent Change ◽  
Rhythmic Contractions

The mechanism by which large lung volume lessens the discomfort of breath holding and prolongs breath-hold time was studied by analyzing the pressure waves made by diaphragm contractions during breath holds at various lung volumes. Subjects rebreathed a mixture of 8% CO2–92% O2 and commenced breath holding after reaching an alveolar plateau. At all volumes, regular rhythmic contractions of inspiratory muscles, followed by means of gastric and pleural pressures, increased in amplitude and frequency until the breakpoint. Expiratory muscle activity was more prominent in some subjects than others, and increased through each breath hold. Increasing lung volume caused a delay in onset and a decrease in frequency of contractions with no consistent change in duty cycle and a decline in magnitude of esophageal pressure swings that could be accounted for by force-length and geometric properties. The effect of lung volume on the timing of contractions most resembled that of a chest wall reflex and is consistent with the hypothesis that the contractions are a major source of dyspnea in breath holding.

scholarly journals Effect of gravity on aerosol dispersion and deposition in the human lung after periods of breath holding

2000 ◽  
Vol 89 (5) ◽  
pp. 1787-1792 ◽  
Author(s):  
Chantal Darquenne ◽  
Manuel Paiva ◽  
G. Kim Prisk
Keyword(s):  
Flow Rate ◽  
Turbulent Mixing ◽  
Direct Evidence ◽  
Human Lung ◽  
Hold Time ◽  
Aerosol Deposition ◽  
Breath Holding ◽  
Breath Hold ◽  
Constant Flow Rate ◽  
Aerosol Dispersion

To determine the extent of the role that gravity plays in dispersion and deposition during breath holds, we performed aerosol bolus inhalations of 1-μm-diameter particles followed by breath holds of various lengths on four subjects on the ground (1G) and during short periods of microgravity (μG). Boluses of ∼70 ml were inhaled to penetration volumes (Vp) of 150 and 500 ml, at a constant flow rate of ∼0.45 l/s. Aerosol concentration and flow rate were continuously measured at the mouth. Aerosol deposition and dispersion were calculated from these data. Deposition was independent of breath-hold time at both Vp in μG, whereas, in 1G, deposition increased with increasing breath hold time. At Vp = 150 ml, dispersion was similar at both gravity levels and increased with breath hold time. At Vp = 500 ml, dispersion in 1G was always significantly higher than in μG. The data provide direct evidence that gravitational sedimentation is the main mechanism of deposition and dispersion during breath holds. The data also suggest that cardiogenic mixing and turbulent mixing contribute to deposition and dispersion at shallow Vp.

Measurement of temporal changes in DLSBCO-3EQ from small alveolar samples in normal subjects

1994 ◽  
Vol 76 (4) ◽  
pp. 1494-1501 ◽  
Author(s):  
G. R. Soparkar ◽  
J. T. Mink ◽  
B. L. Graham ◽  
D. J. Cotton
Keyword(s):  
Hold Time ◽  
Normal Subjects ◽  
Gas Diffusion ◽  
Phase Iii ◽  
Mixing Efficiency ◽  
Breath Holding ◽  
Breath Hold ◽  
Inspiratory Capacity ◽  
Ventilation Inhomogeneity ◽  
Single Breath

The dynamic changes in CO concentration [CO] during a single breath could be influenced by topographic inhomogeneity in the lung or by peripheral inhomogeneity due to a gas mixing resistance in the gas phase of the lung or to serial gradients in gas diffusion. Ten healthy subjects performed single-breath maneuvers by slowly inhaling test gas from functional residual capacity to one-half inspiratory capacity and slowly exhaling to residual volume with target breath-hold times of 0, 1.5, 3, 6, and 9 s. We calculated the three-equation single-breath diffusing capacity of the lung for CO (DLSBCO-3EQ) from the mean [CO] in both the entire alveolar gas sample and in four successive equal alveolar gas samples. DLSBCO-3EQ from the entire alveolar gas sample was independent of breath-hold time. However, with 0 s of breath holding, from early alveolar gas samples DLSBCO-3EQ was reduced and from late alveolar gas samples it was increased. With increasing breath-hold time, DLSBCO-3EQ from the earliest alveolar gas sample rapidly increased, whereas from the last alveolar gas sample it rapidly decreased such that all values from the small alveolar gas samples approached DLSBCO-3EQ from the entire alveolar sample. These changes correlated with ventilation inhomogeneity, as measured by the phase III He concentration slope and the mixing efficiency, and were larger for maneuvers with inspired volumes to one-half inspiratory capacity vs. total lung capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

An increase in breath-hold time appearing after breath-holding

1968 ◽  
Vol 4 (1) ◽  
pp. 73-77 ◽  
Author(s):  
J.R. Heath ◽  
C.J. Irwin
Keyword(s):  
Hold Time ◽  
Breath Holding ◽  
Breath Hold

Single-breath breath-holding estimate of pulmonary blood flow in man: comparison with direct Fick cardiac output

1989 ◽  
Vol 76 (6) ◽  
pp. 673-676 ◽  
Author(s):  
A. H. Kendrick ◽  
A. Rozkovec ◽  
M. Papouchado ◽  
J. West ◽  
G. Laszlo
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Pulmonary Blood Flow ◽  
Hold Time ◽  
Normal Subjects ◽  
Breath Holding ◽  
Breath Hold ◽  
Single Breath ◽  
Significant Difference ◽  
Cardiac Disorders

1. Resting pulmonary blood flow (Q.), using the uptake of the soluble inert gas Freon-22 and an indirect estimate of lung tissue volume, has been estimated during breath-holding (Q.c) and compared with direct Fick cardiac output (Q.f) in 16 patients with various cardiac disorders. 2. The effect of breath-hold time was investigated by comparing Q.c estimated using 6 and 10 s of breath-holding in 17 patients. Repeatability was assessed by duplicate measurements of Q.c in the patients and in six normal subjects. 3. Q.c tended to overestimate Q.f, the bias and error being 0.09 l/min and 0.59, respectively. The coefficient of repeatability for Q.c in the patients was 0.75 l/min and in the normal subjects was 0.66 1/min. For Q.f it was 0.72 l/min. There was no significant difference in Q.c measured at the two breath-hold times. 4. The technique is simple to perform, and provides a rapid estimate of Q., monitoring acute and chronic changes in cardiac output in normal subjects and patients with cardiac disease.

Alveolar gas composition and exchange during deep breath-hold diving and dry breath holds in elite divers

1991 ◽  
Vol 70 (2) ◽  
pp. 794-802 ◽  
Author(s):  
G. Ferretti ◽  
M. Costa ◽  
M. Ferrigno ◽  
B. Grassi ◽  
C. Marconi ◽  
...  
Keyword(s):  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Breath Hold ◽  
O2 Consumption ◽  
Gas Composition ◽  
Arterial Blood ◽  
Co2 Output ◽  
Before And After ◽  
Volume Blood ◽  
End Tidal

End tidal O2 and CO2 (PETCO2) pressures, expired volume, blood lactate concentration ([Lab]), and arterial blood O2 saturation [dry breath holds (BHs) only] were assessed in three elite breath-hold divers (ED) before and after deep dives and BH and in nine control subjects (C; BH only). After the dives (depth 40-70 m, duration 88-151 s), end-tidal O2 pressure decreased from approximately 140 Torr to a minimum of 30.6 Torr, PETCO2 increased from approximately 25 Torr to a maximum of 47.0 Torr, and expired volume (BTPS) ranged from 1.32 to 2.86 liters. Pulmonary O2 exchange was 455-1,006 ml. CO2 output approached zero. [Lab] increased from approximately 1.2 mM to at most 6.46 mM. Estimated power output during dives was 513-929 ml O2/min, i.e. approximately 20-30% of maximal O2 consumption. During BH, alveolar PO2 decreased from approximately 130 to less than 30 Torr in ED and from 125 to 45 Torr in C. PETCO2 increased from approximately 30 to approximately 50 Torr in both ED and C. Contrary to C, pulmonary O2 exchange in ED was less than resting O2 consumption, whereas CO2 output approached zero in both groups. [Lab] was unchanged. Arterial blood O2 saturation decreased more in ED than in C. ED are characterized by increased anaerobic metabolism likely due to the existence of a diving reflex.

Temperature effect on the human dive response in relation to cold water near-drowning

1984 ◽  
Vol 56 (1) ◽  
pp. 202-206 ◽  
Author(s):  
J. S. Hayward ◽  
C. Hay ◽  
B. R. Matthews ◽  
C. H. Overweel ◽  
D. D. Radford
Keyword(s):  
Heart Rate ◽  
Water Temperature ◽  
Cold Water ◽  
Breath Holding ◽  
Breath Hold ◽  
Cold Stimulation ◽  
Near Drowning ◽  
Voluntary Hyperventilation ◽  
Dive Response ◽  
Breath Hold Duration

To facilitate analysis of mechanisms involved in cold water near-drowning, maximum breath-hold duration (BHD) and diving bradycardia were measured in 160 humans who were submerged in water temperatures from 0 to 35 degrees C at 5 degrees C intervals. For sudden submersion BHD was dependent on water temperature (Tw) according to the equation BHD = 15.01 + 0.92Tw. In cold water (0–15 degrees C), BHD was greatly reduced, being 25–50% of the presubmersion duration. BHD after brief habituation to water temperature and mild, voluntary hyperventilation was more than double that of sudden submersion and was also dependent on water temperature according to the equation BHD = 38.90 + 1.70Tw. Minimum heart rate during both types of submersions (diving bradycardia) was independent of water temperature. The results are pertinent to accidental submersion in cold water and show that decreased breath-holding capacity caused by peripheral cold stimulation reduces the effectiveness of the dive response and facilitates drowning. These findings do not support the postulate that the dive response has an important role in the enhanced resuscitatibility associated with cold water near-drowning, thereby shifting emphasis to hypothermia as the mechanism for this phenomenon.

Vascular dysfunction following breath-hold diving

2020 ◽  
Vol 98 (2) ◽  
pp. 124-130 ◽  
Author(s):  
Otto F. Barak ◽  
Nebojsa Janjic ◽  
Ivan Drvis ◽  
Tanja Mijacika ◽  
Ivana Mudnic ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Potential Role ◽  
Decompression Sickness ◽  
Vascular Dysfunction ◽  
Scuba Diving ◽  
Breath Hold ◽  
Flow Mediated Dilation ◽  
Significant Difference ◽  
Main Effect ◽  
Before And After

The pathogenesis of predominantly neurological decompression sickness (DCS) is multifactorial. In SCUBA diving, besides gas bubbles, DCS has been linked to microparticle release, impaired endothelial function, and platelet activation. This study focused on vascular damage and its potential role in the genesis of DCS in breath-hold diving. Eleven breath-hold divers participated in a field study comprising eight deep breath-hold dives with short surface periods and repetitive breath-hold dives lasting for 6 h. Endothelium-dependent vasodilation of the brachial artery, via flow-mediated dilation (FMD), and the number of microparticles (MPs) were assessed before and after each protocol. All measures were analyzed by two-way within-subject ANOVA (2 × 2 ANOVA; factors: time and protocol). Absolute FMD was reduced following both diving protocols (p < 0.001), with no interaction (p = 0.288) or main effect of protocol (p = 0.151). There was a significant difference in the total number of circulating MPs between protocols (p = 0.007), where both increased post-dive (p = 0.012). The number of CD31+/CD41– and CD66b+ MP subtypes, although different between protocols (p < 0.001), also increased by 41.0% ± 56.6% (p = 0.050) and 60.0% ± 53.2% (p = 0.045) following deep and repetitive breath-hold dives, respectively. Both deep and repetitive breath-hold diving lead to endothelial dysfunction that may play an important role in the genesis of neurological DCS.

scholarly journals Panic disorder in a breath-holding challenge test: a simple tool for a better diagnosis

2003 ◽  
Vol 61 (3B) ◽  
pp. 718-722 ◽  
Author(s):  
Antonio E. Nardi ◽  
Isabella Nascimento ◽  
Alexandre M. Valença ◽  
Fabiana L. Lopes ◽  
Marco A. Mezzasalma ◽  
...  
Keyword(s):  
Anxiety Disorder ◽  
Panic Disorder ◽  
Challenge Test ◽  
Test Method ◽  
Panic Attacks ◽  
Breath Holding ◽  
Breath Hold ◽  
Test Results ◽  
Before And After ◽  
Minute Interval

OBJECTIVE: Our aim was to observe if anxiety disorder patients - DSM-IV - respond in a similar way to the induction of panic attacks by a breath-holding challenge test. METHOD: We randomly selected 29 panic disorder (PD) patients, 27 social anxiety disorder (SAD) patients, 21 generalized anxiety disorder (GAD) patients. They were induced to breath-hold for as long as possible four times with two-minute interval between them. Anxiety scales were applied before and after the test. RESULTS: A total of 44.8% (n=13) PD patients, 14.8% (n=4) SAD patients, 9.5% (n=2) GAD patients had a panic attack after the test (c²= 21.44, df= 2, p=0.001). There was no heart rate or anxiety levels difference among the groups before and after the test. CONCLUSION: In this breath-holding challenge test the panic disorder patients were more sensitive than other anxiety disorder patients.

Central chemoreflex sensitivity and sympathetic neural outflow in elite breath-hold divers

2008 ◽  
Vol 104 (1) ◽  
pp. 205-211 ◽  
Author(s):  
Zeljko Dujic ◽  
Vladimir Ivancev ◽  
Karsten Heusser ◽  
Gordan Dzamonja ◽  
Ivan Palada ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Hypertension ◽  
Sympathetic Activity ◽  
Arterial Oxygen ◽  
System Response ◽  
Breath Holding ◽  
Breath Hold ◽  
Control Subjects ◽  
Obstructive Sleep ◽  
End Tidal

Repeated hypoxemia in obstructive sleep apnea patients increases sympathetic activity, thereby promoting arterial hypertension. Elite breath-holding divers are exposed to similar apneic episodes and hypoxemia. We hypothesized that trained divers would have increased resting sympathetic activity and blood pressure, as well as an excessive sympathetic nervous system response to hypercapnia. We recruited 11 experienced divers and 9 control subjects. During the diving season preceding the study, divers participated in 7.3 ± 1.2 diving fish-catching competitions and 76.4 ± 14.6 apnea training sessions with the last apnea 3–5 days before testing. We monitored beat-by-beat blood pressure, heart rate, femoral artery blood flow, respiration, end-tidal CO2, and muscle sympathetic nerve activity (MSNA). After a baseline period, subjects began to rebreathe a hyperoxic gas mixture to raise end-tidal CO2 to 60 Torr. Baseline MSNA frequency was 31 ± 11 bursts/min in divers and 33 ± 13 bursts/min in control subjects. Total MSNA activity was 1.8 ± 1.5 AU/min in divers and 1.8 ± 1.3 AU/min in control subjects. Arterial oxygen saturation did not change during rebreathing, whereas end-tidal CO2 increased continuously. The slope of the hypercapnic ventilatory and MSNA response was similar in both groups. We conclude that repeated bouts of hypoxemia in elite, healthy breath-holding divers do not lead to sustained sympathetic activation or arterial hypertension. Repeated episodes of hypoxemia may not be sufficient to drive an increase in resting sympathetic activity in the absence of additional comorbidities.

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