The Restrictive Effect of Short-term hyperbaric exposure on Ventilation

The Restrictive Effect of Short-term hyperbaric exposure on Ventilation

A Control Study of 12m-depth Single No-decompression Dive Experiment

Cheng Hua

Sports Science School, Lingnan Normal University

1. Introduction

Both immersion and the increasing of pressure/depth in diving environment have

likely increase the demand for the respiratory system [1-3]. Because static lung loading grows as immersion and breathing gas density increases with depth, the ventilation system is more important in the environment of SCUBA diving than the terrestrial environment [4]. As is well known for all, blood flow to the contracting skeletal muscles during exercise provided oxygen consumption came from the air through respiratory movement [5]. Hyperbaric circumstances are underwater, with intrathoracic pressures fluctuate drastically and exercise-induced fatigue of respiratory muscle can limit cardiac output and therewith the leg blood flow [6]. Meanwhile, reduction in ventilation volumes further brings down the arterial oxygen content and greatly increased the work of the respiratory muscular[7-9].Weiterhin, constrictive effect exert on the heart since expansion of lung volume and chest squeeze can quickly change in systolic and diastolic of cardiac function and affect the heart rate and stroke volume as well[10]. This is a complex result formed by numerous molecular interaction effects of stacking based on the adjustability of respiratory reflex and ultimately caused tissue hypoxia [11]. The above mentioned all together will further intensify the occurrence of exercise-induced fatigue and endurance performance obstacles [12].

Ventilation limitation induced exertion dyspnea and exercise intolerance is an important clinical problem unsolved in exercise as far as today is concerned [13]. Even as the diving technology improves and apparatus upgrades，SCUBA Diving still face the challenge of ventilation limitation. High pressure effects impose on thoracic,

pleura or respiratory tract tissue leads to limitation of pulmonary alveoli expansion

underwater. And the lung capacity reduction increased the external respiratory

work and insufficient in ventilation and/or hypoxemia. Ventilation restriction varies greatly resting with the pattern and time-histories of hyperbaric exposure. But the identifiable parameters for reference that indicated relationships between level of ventilation restriction and depth of the underwater are still rare.

Taking healthy diving trainees as subjects for observation, we carried out a series of experiments grouping on the basis of controlling of depth and speed of decompression in water and in a hyperbaric chamber. Relevant parameters of pulmonary ventilation were observed before and after hyperbaric exposure, to aim at the respiratory physiology for diving pressure to provide experimental data for further research.

2. Method

2.1 Volunteer

Healthy diving trainees enrolled were grouped as diving and chamber diving matched for Age, Gender, Body Mass Index (BMI) and Forced Vital Capacity (FVC) respectively. Subjects require physically healthy, proficiency in SCUBA diving techniques, 1 year or more in diving experience and diving depth at least 20 m/5 min. Rule out those dont agree with the Informed Consent of experimental protocol, and those were abnormal in ECG, suffering from an acute respiratory infection, besides, reject those not manage to complete the whole process . All volunteers were informed the purpose and progress of the experiment before started and must sign the informed consent knowing they had a right to quit at any time . Basic

information and respiratory function index detected were perceived.

2.2 Experimental protocols

Experiment is phased in three temporal durations, namely pre-hyperbaric exposure, 1 h and 24h post-hyperbaric exposure. Subjects』 baseline of pulmonary ventilation detection completed before high pressure exposed. Parameters of pulmonary ventilation at 1 h and 24h post-hyperbaric exposure detection should proceed

with group by group.

Volunteers were required low-fat, high-protein diet a week before experiment and pulmonary ventilation detection finished 2 days before experiment and pulmonary ventilation detection finished 2 days before exposure. For more accurate and stable data of pulmonary ventilation ,one subject measuring need to repeat two more times at one time on the same one experimental condition. Take any necessary average as the experimental data. Similarly here & after.

Acting in accordance with Age, Gender, BMI, FVC of team members, subjects were divided into diving and chamber diving group. The pulmonary function of ventilation testing accomplished in 1 h and 24h after hyperbaric exposure.

Field experimentation for diving group was in a 12-meter deep diving tower where the bottom temperature is 17 degrees centigrade and surface temperature is 23 degrees centigrade. Put on diving suits，with flippers and self-contained breathing apparatus, divers to submergence to the bottom within 2 minutes and ascend to surface in 2 minutes of every single dive bottom time is 20 minutes without doing strenuous exercises. Acquired data of parameters of pulmonary ventilation function by Spirometer at 1 h and 24 h after surfacing.

Through pressurizing atmospheric pressure (100 kPa) to 220kPa within 2 min in a hyperbaric oxygen chamber, chamber diving group stay under pressure of 220kPa for 20 min. Then reduced pressure to atmospheric pressure at full speed, imitates the no-decompression diving process. Experimental chambers temperature controlled in the range of 24 to 28±2 degrees centigrade. Data acquisition of pulmonary ventilation functions in 1 h and 24 h after descending.

2.3 Measuring instrument, parameters and procedure

Pulmonary function of ventilation （VC，FVC，MV& MVV）was measured by Spirometer（MINATO，AS-505）. The accuracy of capacity for the instrument is ±3% or ±50 mL. Flow range is 0~14L/S，and the precision of flow is ±3% of quantitative

value or ±0.01 L/S. It can analysis and diagnosis normal, restrictive, obstructive, combined disturbance of ventilation and make diagnosis of small airway function according to the velocity of flow capacity of the loop curve.

Plug in the filter and mouthpiece before the test. Instruct every participant to take a standing position, clamp the nose with a nose clip and ensure that it wont leak. Teach them hold their coughing while testing and breathe only through the mouth. After input their basic information （Gender，Age，Height & Weight）of the volunteers, setting the pattern of Baldwin, run the tests by pressing the button respectively and asked them to inhale or exhale in sequence in strict accordance with operating instructions. Print results and repeat test procedure 1 ~ 2 times and take the average of the test results. Value variation of MVV should be lower than 8% in continuous testing. The maximum value should be recognized as the test results.

2.4 Data statistics

Differences comparing between the two groups of normal distribution measurement index applied as independent samples t test. Pulmonary ventilation indicators of pre-

& post- hyperbaric exposure at different time were analysis of variance for repeated data. Run normality test and homogeneity test of variance t test apply for the normal

distribution data, and nonparametric test is for non-normal distribution, small sample or unequal variances. Apply repeated measurement data for Mauchlys Test of Sphericity if the results』 concomitant probability p > 0.05, then the assumption is satisfied and no need to correction. But if p acuities were 0.05, the degree of freedom has to be corrected by ε correction coefficient and accept the Greenhouse

- Geisser correction results in this experiment. A p value of< 0.05 was regarded as statistically significant. Data was analysis by IBM SPSS 20.0 for statistics.

3. Results

3.1 Overall situation

Overall subjects average Age was 22.07±1.13 years, average Weight 63.5±7.78Kg, an average of Height 172±6 cm, average BMI at21.4±2.00. There were 12 divers in diving group (Experiment Group, EG, the same below) and 17 divers in chamber diving group (Control Group, CG, the same below) completed the respiratory function test for baseline reference. Two-independent sample K-S test 2 groups of Weight, Height, BMI and FVC variables for the normality. Results demonstrate that Z value is 0.701 ~ 0.937and p is higher than 0.05, significant level. Therefore believe that the variables in the two groups are approximately normal distribution.

Equal variances assumed of p higher than the significance level of 0.05 in a test of homogeneity of variances of Age, Weight, Height, BMI and FVC in two groups. And t test results suggest the variables above are no significant differences because of p higher than the significance level of 0.05.

The mean values of Static lung volume (namely TV, IRV, ERV, IC and VC) and time-related lung volume (FVC, FEV1.0,FEV1.0/FVE%, FEV1.0/VC%, PEF, FEF25-75, MEF75,

MEF50, MEF25, and MV) analyzed as shown in Tab.1.

3.2 Grouping situation

3.2.1 Static lung volume

Although the variation range of TV before and after hyperbaric exposure is not significance(F=0.258，p=0.0.773). Variables of TV raised in 1 h (t=-0.831，p=0.413) and 24 h (t=-0.040，p=0.969) post-hyperbaric exposure. Yet there was no significant difference between two groups (t=0.390，p=0.698), such as Tab.2 & Fig.1-A.

IRV is depending on the integrative action of thoracic elastic resistance and inspiratory muscle strength. Significant differences were found in IRV different time pre- & post- hyperbaric exposure (F=3.787，p=0.029).It suggested antagonism of high pressure exposure to thoracic elastic resistance and inspiratory muscle strength is still strong in 1 h (t=-3.356，p=0.002),much less in 24 h after exposure（t=0.773，p=0.446）. There was no significant difference between two groups （t=0.318，p=0.751）, such as Tab.3 & Fig.1-B.

ERV reflects gas reserve capacity of lung. It is decided by the rises of diaphragm, thoracic elastic resistance and bronchioles obstruction as exhale forcefully. ERV declines in 1 h （t=2.298，p=0.029） and 24 h （t=0.829，p=0.414）after hyperbaric exposure. And the founding indicates gas reserve capacity of lung is shrinking after hyperbaric exposure（F=4.910，p=0.011）. There was no significant

difference between two groups（F=0.825，p=0.444）, such as Tab.4 & Fig.1-C.

Influenced by the IRV and TV, a significant difference present in IC in different times being after hyperbaric exposure（F=8.085，p=0.000）. Similar to IRV, IC significantly increased because of high-pressure effect last for a short term of 1h （t=-3.589，p=0.001）and decline in 24 h （t=0.821，p=0.419）after exposure. There was no significant difference between two groups（F=1.979，p=0.148）, such as Tab.5 & Fig.1-D.

VC is the sum of the TV, IRV and ERV. Under the comprehensive function of many factors, VC change significantly （F=4.078，p=0.022）because of high-pressure

effect, while increased（t=-2.638，p=0.013） in 1 h and declined in 24 h （t=2.759，p=0.010）significantly post-hyperbaric exposure. There was no significant difference between two groups（F=1.003，p=0.373）, such as Tab.6 & Fig.1-E.

3.2.2 Time-related lung volume

Made comparison between EG & CG and found no significant difference in FVC before or after high pressure exposure（t=0.000，p=0.998）. FEV1.0 （t=-1.579，p=0.118）and FEV1.0 %（t=-1.771，p=0.080）in EG is higher than in the CG but there was no statistically significant difference between them, as in Fig.2-A、Fig.2-B、Fig.2C. And FEV1.0 / VC in CG is significantly higher than EG（t=-2.189，p=0.033）, as in Tab.7 & Fig 2-D.

Fluctuating value of PEF in two groups before and after hyperbaric exposure is not significant（F=0.069，p=0.933）, which indicated that large bronchus obstruct by high pressure effect was not significant, as in Fig.2-F. Similarly in the same way with FEF25-75（F=0.185，p=0.832）, MEF75（F=0.012，p=0.988）, MEF50（F=0.240，p=0.787）、MEF25（F=0.502，p=0.608）, suggested that bronchioles obstruct were not significant as well, as in Fig.2-E、2-F.

The experimental results suggest that similar changes happened in FVC,

FEV1.0 and FEV1.0/ FVC % between 2 groups, which proved the blockage effect of high-pressure exposed in two groups were not significant. And FEV1.0/VC is considerably greater in CG than in EG, because of VC is far lower in CG than the EG. Under pressure of 2.2 ATA，all values of PEF, FEF25-75, MEF75, MEF50, MEF25

are higher in CG, which indicated the degree of restricting effect for the airway in EG is higher.

MVV declined in EG members while a rise in the CG after exposure (t = 0.327, p = 0.746). But the change is not statistically significant. It can be thought of no statistical significance of MVV before and after hyperbaric exposure, such as in Fig.2-H.

The value of MV is influenced by TV, RR. It is normally less when resting, but increases while exercise. It rises to 40 ~ 60L during moderate-intensity exercise. Both

MV and RR decline after exposure, but the differences are not statistical significance because of concomitant probability less than 0.05. The results indicated that MV and RR do not change significantly in a 12 m/2.2 ATA high pressure exposure, such as in Fig.2-G.

4. Discussion

When submerging down underwater, the ambient pressure of surroundings raised, the breathing gas density and partial pressure, external respiratory work and pulmonary physiological dead space are likewise increased[3, 14]. These factors might likely have an effect on the respiratory function. Such as gas density and partial pressure caused respiratory resistance increased, extra respiratory work motivated respiratory muscle fatigue and low ventilation perfusion ( ) ratio, all leading to hypoventilation and CO2 retention [15, 16]. There is supposed to be very large amounts of gas bubbles generated after no-decompression air dives even if divers obey standardized diving protocols. High bubble loads have closely relationship with the VGE travelling to the circulation. Even so, there is still no acute

decompression-related pathology was observed [17]. Because it is believed that no considerable impacts on ratio after dives of within the no-decompression-stop limits [18]. So our study only concentrates on ventilation of external respiration and irrespective of gas exchange or internal respiration regulation in this section.

Lung structure and pulmonary function change significantly along with the age

increase. With the degenerate of lung elastic elements, loss of the parenchymal

tissue, dilation of alveolar ducts and bronchioles, decreases of chest wall compliance, reduction of the intercostal muscle mass and force, ventilation volume

expands and gas exchange surface lessens [19]. In addition to age, ventilation is correlated with type of exercise, gender, height, weight, and BMI, as well [20]. In the study, we couldn』t observe too much fluctuation on TV before or after hyperbaric

exposure, because the study design settings are multi-index matching was concerned, such as the Age, Sex, Weight, Height and FVC. Increasing inspiratory muscles』 strength overcomes the resistance from the thoracic with the pressure from the hydrostatic pressure/hyperbaric air environment and to complete respiratory movement. The reason why IRV increased in 1h after exposure because the greater inertia produced by the negative pressure increasing inside the lung through the thoracic expansion and the elastic load of chest wall augment which caused by forced air inhalation. As higher gas density and pressure increased airways resistance, exhalation gas flow also reduced. Meantime tissue elastic load of lung increase, so as negative pressure within lungs, which contribute to the decline of involuntary movements of air-breathing. The increase of pulmonary elastic load is responsible for the reduction in transmural pressure, and result in the occurrence of decreasing of ERV. This result is consistent with previous cognition on EVR during immersion, which is the subject breathing harder trying to increase the diameter of the airway and reducing the airways resistance [21-23].

In addition, vascular contraction due to the drops in ambient temperature results

in reduction in pulmonary perfusion. While diving underwater, higher pulmonary

artery pressure and bigger vascular volume during exercise make residual volume

(RV) increase and VC decreased [24]. The stress of increased static lung load affects the lung volume at the end of the expiratory [25]. In that case, the length of respiratory muscle couldnt reach the optimum length and couldnt maintain enough power to increase the ability of breathing [26, 27][3].

When airflow obstruct, forced expiratory prolong, the FEV1.0 and FEV1.0/FVC % reduced. When ventilation is restricted, the compliance of the lung and thorax reduced. Therefore VC decreases. The vast majority of VC exhales in a very short time lead to the increase of FEV1.0 /VC [28-31]. FEV1.0/ VC increased in EG after hyperbaric exposure suggested there is more restrictive effect of thoracic activity in EG is higher individual than CG. Because even though the equivalence of pressure underwater or in the hyperbaric chamber , the higher medium density of water produce higher hydrostatic pressure than the air in the chamber, plus the close-fitting diving suit, and the weight of breathing apparatus itself has strain on the respiratory system.

Peak expiratory flow（PEF）is resting with the respiratory muscle strength of

individuals and the presence of airway obstruction[32]. Reduced in FEF25-75, MEF50 or MEF25 has been noted as a symbol of obstruction in small airways. Studies had proved that respiratory system inertia is usually proportional to the gas density increases under standard atmospheric pressure (1ATA). Respiratory resistance originates in inside is mainly the increasing gas density and quality, which add up systematic inertia of respiratory.

Minute ventilation volume (MV) didn』t change much pre- or post- hyperbaric exposure between 2 groups. But we discovered the value of MVV is far lower than the predicted value. That is due to the fact that not only the gas density makes the airway resistance rise underwater, but also the lung elastic load increase due to the pulmonary blood volume and oxygen partial pressure rose triggered by immersion. That submerged generate additional mechanical load to the chest wall, making static pressure load across the chest wall as well as lung compliance lower. Therefore the airway resistance and lung elastic load can lead to the reduction of ventilation

underwater. Moreover, more physiological dead space and die cavity/tidal volume ratio（Vd /Vt）affected the gas diffusion and ventilation distribution in lungs[21].

5. Conclusion

Ventilation restricted during hyperbaric exposure, whether in 12m-depth underwater or 2.2ATA hyperbaric chamber. Forced expiratory increase and inspiratory decrease to physiologically rectify ventilation in a short term, like 1h after high pressure effect removed. Ventilation basically comes close to normal within 24 h. Restrictions of high pressure mainly retard exhalation, enlarge residual volume and lessen the pulmonary elasticity, which result in increased of small airway』s resistance. Extent of restriction of underwater is larger than dry air hyperbaric chamber. It may be attributable to the higher water medium density, submerged compressing blood volume of lower limbs and raising inertia added by portable underwater breathing apparatus.

6. References

[1] Peter B. A report on 2014 data on diving fatalities, injuries, and incidents

[Internet][M]. 2016. Durham，NC: Divers Alert Network, 2016.

[2] Pendergast D R, Moon R E, Krasney J J, et al. Human Physiology in an Aquatic Environment[M]//John Wiley & Sons, Inc., 2011.

[3] Doolette D J, Mitchell S J. Hyperbaric Conditions[M]//John Wiley & Sons, Inc., 2010.

[4] Held H E, Pendergast D R. Relative effects of submersion and increased pressure on respiratory mechanics, work, and energy cost of breathing[J]. J Appl Physiol (1985), 2013,114(5):578-591.

[5] Joyner M J, Casey D P. Regulation of Increased Blood Flow (Hyperemia) to Muscles During Exercise: A Hierarchy of Competing Physiological Needs[J]. Physiol Rev, 2015,95(2):549-601.

[6] ODonnell D E, Elbehairy A F, Berton D C, et al. Advances in the Evaluation of Respiratory Pathophysiology during Exercise in Chronic Lung Diseases[J]. Front Physiol, 2017,8:82.

[7] Amann M. Pulmonary system limitations to endurance exercise performance in humans[J]. Exp Physiol, 2011,97(3):311-318.

[8] Guenette J A, Sheel A W. Physiological consequences of a high work of breathing during heavy exercise in humans[J]. J Sci Med Sport, 2007,10(6):341-350.

[9] Dempsey J A, Romer L, Rodman J, et al. Consequences of exercise-induced respiratory muscle work[J]. Respir Physiol Neurobiol, 2006,151(2–3):242-250.

[10] Marabotti C, Scalzini A, Cialoni D, et al. Effects of depth and chest volume on cardiac function during breath-hold diving[J]. Eur J Appl Physiol, 2009,106(5):683-689.

[11] Pamenter M E, Powell F L. Time Domains of the Hypoxic Ventilatory Response and Their Molecular Basis[J]. Compr Physiol, 2016,6(3):1345-1385.

[12] Amann M. Pulmonary system limitations to endurance exercise performance in humans[J]. Exp Physiol, 2012,97(3):311-318.

[13] Babb T G. Exercise Ventilatory Limitation: The Role Of Expiratory Flow Limitation[J]. Exerc Sport Sci Rev, 2013,41(1):11-18.

[14] Balestra C, Theunissen S, Papadopoulou V, et al. Pre-dive Whole-Body Vibration Better Reduces Decompression-Induced Vascular Gas Emboli than Oxygenation or a Combination of Both[J]. Front Physiol, 2016,7:586.

[15] Maio D A, Farhi L E. Effect of gas density on mechanics of breathing.[J]. J Appl Physiol, 1967,23(5):687.

[16] Teculescu D B, Manicatide M A, Racoveanu C L. Transfer factor for the lung, airway obstruction and hyperinflation in chronic bronchitis and emphysema[J]. Med Interne, 1976,14(2):125-131.

[17] LJUBKOVIC M, DUJIC Z, M?LLERL?KKEN A, et al. Venous and Arterial Bubbles at Rest after No-Decompression Air Dives[J]. Med Sci Sports Exerc, 2011,43(6).

[18] Moore G S, Wong S C, Darquenne C, et al. Ventilation-perfusion inequality in the human lung is not increased following no-decompression-stop hyperbaric exposure[J]. Eur J Appl Physiol, 2009,107(5):545-552.

[19] Lalley P M. The aging respiratory system-Pulmonary structure, function and neural control[J]. Respir Physiol Neurobiol, 2013,187(3):199-210.

[20] Rong C, Bei H, Yun M, et al. Lung Function and Cytokine Levels in Professional Athletes[J]. J Asthma, 2008,45(4):343-348.

[21] Moon R E, Cherry A D, Stolp B W, et al. Pulmonary gas exchange in diving[J]. J Appl Physiol (1985), 2009,106(2):668-677.

[22] Hesser C M, Linnarsson D, Fagraeus L. Pulmonary mechanisms and work of breathing at maximal ventilation and raised air pressure[J]. J Appl Physiol Respir Environ Exerc Physiol., 1981,50(4):747.

[23] Taylor N A S, Morrison J B. Static respiratory muscle work during immersion with positive and negative respiratory loading[J]. J Appl Physiol (1985), 1999,87(4):1397.

[24] Lundgren C E. Respiratory function during simulated wet dives.[J]. Undersea Biomedical Research, 1984,11(2):139-147.

[25] Taylor N A S, Morrison J B. Lung volume changes in response to altered breathing gas pressure during upright immersion[J]. Eur J Appl Physiol Occup Physiol, 1991,62(2):122-129.

[26] Pendergast D R, Lundgren C E G. The underwater environment: cardiopulmonary, thermal, and energetic demands[J]. J Appl Physiol (1985), 2009,106(1):276-283.

[27] McCully K K, Faulkner J A. Length-tension relationship of mammalian diaphragm muscles[J]. J Appl Physiol Respir Environ Exerc Physiol, 1983,54(6):1681.

[28] Park H, Han D. The effect of the correlation between the contraction of the pelvic floor muscles and diaphragmatic motion during breathing[J]. J Phys Ther Sci,

2015,27(7):2113-2115.

[29] Pellegrino R, Viegi G, Brusasco V, et al. Interpretative strategies for lung function tests[J]. Eur Respir J, 2005,26(5):948.

[30] Vasilopoulos T, Grant M D, Franz C E, et al. Shared and Distinct Genetic Influences Among Different Measures of Pulmonary Function[J]. Behav Genet, 2013,43(2):141-150.

[31] Mohamed Hoesein F A A, Zanen P, Lammers J J. Lower limit of normal or FEV1/FVC <0.70 in diagnosing COPD: An evidence-based review[J]. Respir Med, 2011,105(6):907-915.

[32] Güder G, Brenner S, St?rk S, et al. Diagnostic and prognostic utility of mid-expiratory flow rate in older community-dwelling persons with respiratory symptoms, but without chronic obstructive pulmonary disease[J]. BMC Pulm Med, 2015,15:83.

推薦閱讀：