Hold your breath : peripheral and cerebral oxygenation during dry static apnea

Acute breath-holding deprives the human body from oxygen. In an effort to protect the brain, the diving response is initiated, coupling several physiological responses. The aim of this study was to describe the physiological responses to voluntary breath-holding at the cardi-ac, peripheral and cerebral level in order to obtain insight into the protective mechanisms for the brain.METHODS:31 physically active subjects (17 male, 14 female, 23.3 ±1.8 years old) performed a maximal static breath-hold in a seated position. Heart rate (HR) and muscle (M. Vastus Lateralis) and cerebral (prefrontal cortex) oxygenation (by means of near-infrared spectroscopy) were continuously measured. RM MANOVA’s were used to identify changes in HR, cerebral (cTOI) and peripheral tissue oxygenation (mTOI) and oxygenated (O2Hb) and deoxygenated (HHb) hemoglobin at different time points during apnea.RESULTS:Subjects held their breath for 157 ±41 s on average (range: 96-244 s). HR started decreasing 15 s after the onset of apnea (p=0.003) reach-ing minimal values after 83 ±58 s. HR dropped on average by 27 ±14 bpm (30 ±13%) from baseline (p<0.001). mTOI started decreasing 10 s after apnea (p<0.001) and continued to decrease until 10 s post apnea, reaching baseline only 30 s post apnea (p=0.369). mTOI fell on average by 8.6 ±4% (p<0.001). Following an immediate drop after 5 s (p<0.01), cTOI increased continuously, reaching a maximal increase of 4.6 ±3% (p<0.001) after 100 ±49 s, followed by a steady decrease until the end of apnea. cTOI fell on average 6.5 ±7.6% below baseline (p<0.001) with individual decreases up to 25%. cTOI increased immediately after apnea, already reaching baseline 10 s post apnea (p=0.811). One subject fainted during testing after only 65 s of apnea. Visual analysis revealed a similar pattern for HR. Examination of mTOI, mO2Hb and mHHb suggested impaired peripheral vasoconstriction, while cTOI showed a very strong immediate drop, followed by incomplete recovery resulting in a second fast drop in cTOI until the subject passed out.CONCLUSION:During apnea, the human body elicits several protective mechanisms in order to protect itself against the deprivation of oxygen. HR slows down decreasing oxygen demand of the cardiac muscle. The decrease in mTOI and increase in cTOI imply a redistribution of blood flow prioritizing the brain. However, data from one participant suggests that syncope can be induced by impaired redistribution, observed as a less pronounced peripheral vasoconstriction deducted from muscle oxygenation responses and a disturbed cerebral oxygen

Hold your breath : peripheral and cerebral oxygenation during dry static apnea

Purpose Acute breath-holding deprives the human body from oxygen. In an effort to protect the brain, the diving response is initiated, coupling several physiological responses. The aim of this study was to describe the physiological responses to apnea at the cardiac, peripheral and cerebral level. Methods 31 physically active subjects (17 male, 14 female, 23.3 +/- 1.8 years old) performed a maximal static breath-hold in a seated position. Heart rate (HR), muscle and cerebral oxygenation (by means of near-infrared spectroscopy, NIRS) were continuously measured. RM MANOVA's were used to identify changes in HR, peripheral (mTOI) and cerebral (cTOI) tissue oxygenation and oxygenated (O(2)Hb) and deoxygenated (HHb) hemoglobin during apnea. Results Average apnea duration was 157 +/- 41 s. HR started decreasing after 10 s (p < 0.001) and dropped on average by 27 +/- 14 bpm from baseline (p < 0.001). mTOI started decreasing 10 s after apnea (p < 0.001) and fell by 8.6 +/- 4.0% (p < 0.001). Following an immediate drop after 5 s (p < 0.001), cTOI increased continuously, reaching a maximal increase of 3.7 +/- 2.4% followed by a steady decrease until the end of apnea. cTOI fell on average 5.4 +/- 8.3% below baseline (p < 0.001). Conclusion During apnea, the human body elicits several protective mechanisms to protect itself against the deprivation of oxygen. HR slows down, decreasing O(2)demand of the cardiac muscle. The decrease in mTOI and increase in cTOI imply a redistribution of blood flow prioritizing the brain. However, this mechanism is not sufficient to maintain cTOI until the end of apnea

What parameters define maximal apnea duration?

Purpose: The current world record of static breath-holding is set at an astonishing 11 min 35 s in male and 9 min 2 s in female. In order to accomplish such apnea performances, individuals must be able to store large amounts of oxygen and conserve this oxygen efficiently during apnea. Additionally, they should be able to withstand hypoxia (low oxygen levels) and hypercapnia (high carbon dioxide levels) in blood and tissues. Previous research has already gained some insights in the fascinating physiological responses to breath-holding, but a lot of pieces are still missing to the puzzle. The aim of this study is therefore to explore the determining physiological parameters in order to perform longer apneas and to investigate why men can perform longer apneas than women. Methods: 28 physically active individuals (23 ± 3 years old), 16 males (180 ± 6 cm; 73.2 ± 7.5 kg) and 12 females (168 ± 8 cm; 64.3 ± 5.8 kg), naïve to apnea participated in this study. All subjects were medically screened for contra-indications. Lung function tests were performed and hemoglobin mass (Hb mass) was determined using the optimized CO-rebreathing method. ANOVA was used to compare differences in apnea duration, Hb mass and vital capacity (VC) between male and female subjects. Linear regressions were used to examine the relation between apnea duration, Hb mass and VC. Results: Male subjects had an average breath-hold time of 199 s ± 46 s while female subjects could hold their breath on average for 148 s ± 53 s (p = 0.011). Hb mass was on average 853.9 ± 106.6 g in men and 618.2 ± 69.1 g in women (p < 0.001). Also VC was higher in men with a mean value of 6.1 ± 0.7 L versus a mean value of 4.7 ± 0.6 L in women (p < 0.001). Both Hb mass (p = 0.011; R² = 0.186) and VC (p = 0.001; R² = 0.336) showed a significant positive correlation with maximal apnea duration. Conclusion: A higher Hb mass and greater lung volume seems to lead to longer apnea durations. Since men exhibit a higher Hb mass and VC, we expect men to have higher oxygen (O2) storage and carbon dioxide (CO2) buffer capacity which contribute to a longer apnea duration

What parameters define maximal apnea duration?

Purpose: The current world record of static breath-holding is set at an astonishing 11 min 35 s in male and 9 min 2 s in female. Apnea duration is dependent on three main factors: oxygen storage, oxygen consumption and CO2 tolerance. The aim of this study is to explore the determinants of apnea duration and to investigate sex differences. Methods: 28 healthy individuals, 16 males (180 ± 6 cm; 73.2 ± 7.5 kg) and 12 females (168 ± 8 cm; 64.3 ± 5.8 kg), naïve to apnea participated in this study. Vital capacity (VC) and hemoglobin mass (Hb mass) were measured. Subjects performed a series of six maximal static apneas interspersed with 2 min rest intervals. Peripheral oxygenation (muscle tissue oxygenation index, mTOI) was measured continuously. End-tidal CO2 (EtCO2) was measured pre and post apnea. ANOVA was used to compare sex differences. Linear regressions were used to examine the relation between apnea duration, Hb mass, VC, mTOI and EtCO2. Results: Maximal breath-hold time was higher in males (199 ± 46 s) compared to females (148 ± 53 s, p=0.011). Hb mass (853.9 ± 106.6 g versus 618.2 ± 69.1 g, p<0.001) and VC (6.1 ± 0.7 L versus 4.7 ± 0.6 L, p<0.001) were higher in men. mTOI decreased more in men (-11 ± 5% versus -4 ± 5%, p<0.001). Both Hb mass (p=0.011; R²=0.186), VC (p=0.001; R²=0.336), ΔEtCO2 (p=0.002; R²=0.312) and ΔmTOI (p<0.001; R²=0.495) were correlated with maximal apnea duration. Conclusion: A greater Hb mass, lung volume, EtCO2 increase and mTOI decrease seem to lead to longer apnea durations. Since men exhibit a higher Hb mass and VC, we expect men to have higher O2-storage and CO2-buffer capacity which, in combination with a lower oxygen consumption (mTOI) and a better tolerance to hypercapnia (EtCO2), contribute to longer apnea durations

Case studies in physiology: is blackout in breath-hold diving related to cardiac arrhythmias?

Syncope or "blackout" (BO) in breath-hold diving (freediving) is generally considered to be caused by hypoxia. However, it has been suggested that cardiac arrhythmias affecting the pumping effectivity could contribute to BO. BO is fairly common in competitive freediving, where athletes aim for maximal performance. We recorded heart rate (HR) during a static apnea (STA) competition, to reveal if arrhythmias occur. Four male freedivers with STA personal best (PB) of 349±43s, volunteered during national championships, where they performed STA floating face down in a shallow indoor pool. A non-coded Polar T31 chest strap recorded R-R intervals and a water- and pressure proof pulse oximeter arterial oxygen saturation. Three divers produced STA near their PB without problems, while one diver ended with BO at 5min17s, which was 12s beyond his PB. He was immediately brought up by safety divers and resumed breathing within 10s. All divers attained similar lowest diving HR (47±4bpm), but HR recordings displayed a different pattern for the diver ending with BO. After a short tachycardia the three successful divers developed bradycardia which became more pronounced during the second half of the apnea. The fourth diver developed pronounced bradycardia earlier, and at 2.5min into the apnea HR started alternating between approximately 50 and 140 bpm, until the diver lost consciousness. At resumed breathing, HR returned to baseline. Nadir oxygen saturation was similar for all divers. We speculate that arrhythmia could have contributed to BO, by lowering stroke volume leading to a systolic blood pressure drop, affecting brain perfusion. </jats:p

Acute apnea does not improve 3-km cycling time trial performance

Purpose Intense exercise evokes a spleen contraction releasing red blood cells into blood circulation. The same mechanism is found after acute apnea, increasing hemoglobin concentration ([Hb]) by 2% to 5%. The aim of this study was twofold: [1] to identify the optimal apnea modalities to acutely increase [Hb] and [2] use these modalities to examine whether prerace apnea can improve a 3-km time trial (TT). Methods In part 1, 11 male subjects performed 12 different apnea protocols based on three modalities: mode, frequency, and intensity. Venous blood samples for [Hb] were collected before, immediately, and 5 min after each protocol. In part 2, 12 recreationally active subjects performed 3-km cycling TT in three different conditions: apnea, control, and placebo, after a 10-min warm-up. Power output, HR, and oxygen uptake (V & x2d9;O-2) were continuously measured. Venous [Hb] was sampled at baseline, after warm-up, and before TT. Additionally, these subjects performed constant cycling at Delta 25 (25% between gas exchange threshold and V & x2d9;O-2 max) in two conditions (control and apnea) to determine V & x2d9;O-2 kinetics. Results Although including one single apnea in the warming up evoked a positive change in [Hb] pattern (P = 0.049) and one single apnea seemed to improve V & x2d9;O-2 kinetics in constant submaximal cycling (tau: P = 0.060, mean response time: P = 0.064), performance during the 3-km TT did not differ between conditions (P = 0.840; apnea, 264.8 +/- 14.1 s; control, 263.9 +/- 12.9 s, placebo, 264.0 +/- 15.8 s). Average normalized power output (P = 0.584) and V & x2d9;O-2, HR, and lactate did not differ either (P > 0.05). Conclusions These results suggest that potential effects of apnea, that is, speeding of V & x2d9;O-2 kinetics through a transient increase in [Hb], are overruled by a warming-up protocol