Role of the ventilatory chemoreflex as respiratory adaptation mechanism in competitive level swimmers: Rol del quimiorreflejo ventilatorio como mecanismo de adaptación respiratoria en nadadores de nivel competitivo

This doctoral thesis is based on the publication of 4 studies that aim to analyze the role of the peripheral chemoreflex on apnea time in competitive swimming athletes, for which experiments were carried out on a population ranging from animal models, physically active humans and competitive swimmers.
The objective of Research 1 was to determine the acute effects of high-intensity interval training (HIIT) exercise and endurance exercise (EE) on lung function, sympathetic/parasympathetic balance, and cardiorespiratory coupling (CRC) in healthy subjects. Eight physically active subjects (recreational runners; four men and four women) participated: height: 1.7 ± 0.1 m; body mass: 63.3 ± 5.7 kg; body mass index: 22.0 ± 2.4 kg/m2; age: 23.9 ± 3.1 years). Using a repeated measures crossover design, participants were exposed to EE (20 min at 80% of maximal heart rate (HR), HIIT (1 min of exercise at 90% of maximal HR for 1 min of rest, 10 times) or control condition (rest). Pulmonary function was assessed by spirometry (VC, PEF, PIF, FEV1, FEV1/VC, FEF 25, FEF 50, and FEF75), Electrocardiogram (ECG), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean blood pressure (MAPB), oxygen saturation, CRC, and heart rate variability (LFHRV, HFHRV, LF/HFHRV) before and after the interventions. At baseline, there were no significant differences between EE, HIIT, and control in cardiovascular and respiratory parameters. EE and HIIT significantly increased SBP, MABP, and HR (p < 0.05, pre vs post). Resistance exercise and HIIT sessions did not induce changes in FEV1, FEV1/CV, FEF 25, FEF, or FEF 75 (p>0.05; pre vs post). Furthermore, no significant differences in lung function were found between EE, HIIT and control (pre vs post). An isolated EE session failed to induce significant changes in the LFHRV, HFHRV and LF/HFHRV ratio (p<0.05; pre vs. post) (Figure 3). However, total spectral power was significantly reduced after EE (p<0.05; pre vs. post). In contrast, HIIT induces significant changes in HRV spectral data. In fact, LFHRV increased while HFHRV decreased with HIIT (all p<0.05; pre vs post). Consequently, the LF/HFHRV ratio increased after the HIIT protocol (p<0.05; pre vs. post). Furthermore, the total spectral power of HRV was reduced with HIIT. Resistance exercise and HIIT showed a significant decrease in time domain variables (SDNN; RMSSD, NN50, pNN50, p<.05; pre vs. post). Furthermore, SD1 and SD2 were significantly reduced after EE and HIIT. Directionality analysis showed that the coupling between respiration and heart rate (B → H) was greater than that between heart rate and respiration (H → B) under control conditions. B → H but not H → B coupling increased significantly after EE (0.14 ± 0.03 vs. 0.16 ± 0.03 Hz, pre vs. post, respectively, p<0.05). No effect of HIIT on B→H coupling or H→B coupling was found. The main findings were: (a) neither EE nor HIIT changed lung function; (b) HIIT and no EE produced acute HRV changes evidenced by a decrease in HFHRV and an increase in LFHRV after exercise; (c) HIIT but not EE has a detrimental effect on normal cardiovascular autonomic adjustment to an incline challenge; and (d) EE but not HIIT induced an acute increase in CRC. Overall, our findings suggest that acute cardiorespiratory responses to EE and HIIT may differ between these two exercise modalities, which could have some implications for chronic adaptations to exercise.

The aim of research 2 was to determine the effect of acute high-altitude exposure on sympathetic/parasympathetic modulation of baroreflex control (BR)in normal rats. Twelve male Sprague Dawley rats were randomly assigned to sea level (n = 7) and high altitude (n = 5) groups (3270 m above sea level). The rats were randomly distributed into the Sea Level group (n = 7) and the High-Altitude group (n = 5). Sea-level rats underwent catheterization surgery and baseline blood pressure (BP) recording for one hour. Subsequently, the BR experiment was performed as follows: 8 boluses of phenylephrine were injected to increase BP (i.v.) and after 30 min of recovery, 8 boluses of sodium nitroprusside were injected to decrease BP (i.v.). The second series of rats (High Altitude group) ascended to 3,270 m above sea level (Caspana, Antofagasta, Chile) in a mobile laboratory and after 24 h, catheterization surgery was performed. Similar to the first series of animals (Sea-Level group), 8h after the surgical procedure, baseline recordings of BP (1 hour) and the BR experiment were performed. Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MABP), pulse pressure (PP), heart rate (HR) was measured. Autonomic control was estimated using an indirect measurement by calculating heart rate variability (HRV). Basally there were no significant differences between sea level and high-altitude exposure in body weight DBP, SBP, MABP, PP and HR. After acute exposure to high altitude, rats showed increased sympathetic drive and decreased parasympathetic modulation of the heart. The LFHRV component increased significantly (p<0.05) from sea level (42.12 ± 7.44 nu) to high altitude (60.55 ± 4.47 nu), while the HFHRV component decreased significantly (p<0.05) from sea level (39.37 ± 4.44 nu) to high altitude (57.82 ± 7.43 nu). Consequently, the LF/HFHRV ratio increased significantly (p<0.05) at high altitude compared to sea level (1.66 ± 0.27 vs. 0.85 ± 0.23, respectively). After acute exposure to high altitude and after Phe administration, bradycardic responses were significantly decreased (p<0.05). The sigmoidal curve of the BR analysis showed diminished BR vagal bradycardia. In addition, curvature (0.04 ± 0.01 vs. 0.07 ± 0.01 mmHg/beats/min) and maximal bradycardia (50.70 ± 0.28 vs. 58.01 ± 0.81 beats/ min) was significantly (p<0.05) reduced after acute exposure at high altitude compared to sea level. Peak tachycardia response to SNP, range, slope, BP midpoint, lower plateau, and upper plateau of BR analysis were not significantly different between groups at sea level and high altitude. The main findings of the present study were: (i) after acute exposure to high altitude there is impaired cardiac autonomic control; (ii) High Altitude exposure produces impaired cardiac baroreflex control in normal rats; and (iii) there is reduced parasympathetic drive activation during acute high-altitude exposure in normal rats. The present results suggest that acute exposure to high altitudes leads to impaired autonomic control and impaired baroreflex function, mainly characterized by decreased parasympathetic activity after 24 h of exposure to high altitudes.

The aim of research 3 was to determine hypoxic ventilatory response (HVR), hypoxic cardiac response (HCR), and cardiovascular adjustments during maximal voluntary apnea in highly trained young swimmers. Fifteen swimmers participated in the research (eight men and seven women; age, 20.93 ± 5.18 years; height, 169.53 ± 10.44 cm; body mass, 71.5 ± 12.77 kg; mass index (BMI), 24.7 ± 2.05 kg/m2), with 5-12 years of swimming training and a mean weekly training volume of 4h per day, five times per week and twenty-seven controls (twenty-two men and five women, age, 17.22 ± 2.42 years, height, 169.52 ± 8.12 cm, body mass, 63.85 ± 10.3 kg, BMI, 22.12 ± 2.49 kg/m2). A descriptive cross-sectional study was conducted to determine HVR and autonomic response to hypoxia and maximal voluntary apnea in highly trained young swimmers compared to controls. Hypoxic ventilatory response was assessed by transient hypoxic challenge. Participants underwent three consecutive tests consisting of five breaths of 100% N2. Subsequently, subjects changed from a supine to a sitting position and were asked to hold maximal voluntary apnea. To determine CHR, 1 min of rest in normoxia and 1 min of maximal HR response in hypoxia were used for analysis. Heart rate variability (HRV) was assessed as an indirect measure of the autonomic balance of the heart. From the ECG recording, time series of the R-R interval were obtained, and a time-varying spectrogram was used to obtain the spectral density (PSD) of HRV. In addition to cardiovascular parameters, respiratory function was measured by spirometry and TD, PEF, PIF, FEV1, FEV1/VC, FEF 25, FEF 50 and FEF 75 were recorded. At baseline, demographic, respiratory, cardiovascular and metabolic variables were not different between swimmers and controls. The maximum duration of voluntary apnea was longer in swimmers than in controls (83.18 ± 41.43 vs. 55.77 ± 23.71 s, respectively). HR response during apnea was higher in swimmers compared to controls (HR: 71.99 ± 7.67 vs. 63.20 ± 10.07 beats/min). Furthermore, the maximal HR response to voluntary apnea was greater in swimmers compared to controls (∆HR: 2.94 ± 7.88 vs. 2.20 ± 7.86 1 beats/min). During a maximal voluntary apnea, the LFHRV in the swimmers increased compared to the resting condition, however, the control group participants did not show significant changes in LFHRV between the rest and the apnea test. ∆LFHRV was higher in swimmers than controls (999.2 ± 1368 vs. 140.4 ± 1194 ∆AUC; p = 0.033). Regarding HFHRV during apnea, both groups showed decreased parasympathetic drive. Both groups showed an increase in LF/HF from rest to apnea (swimmers: 0.23 ± 0.18 to 0.54 ± 0.44, p<0.001; control: 0.23 ± 0.22 to 0, 37 ± 0.41, p=0.037). Regarding the ventilatory and cardiac response to hypoxia, normoxic swimmers showed a smaller increase in VE (0.11 ± 0.04 v/s to 0.19 ± 0.04 L*min*kg-1) from normoxic to hypoxic condition than controls (0.14 ± 0.04 v/s at 0.27 ± 0.06 a L/min/kg). HVR, expressed as ∆VE/∆SpO2, was significantly lower in swimmers compared to control participants (0.007 ± 0.001 vs. 0.016 ± 0.002 ∆VE/∆SpO2). HCR was similar between swimmers (0.27 ± 0.51 ∆HR/∆SpO2) and controls (0.52 ± 1.04 ∆HR/∆SpO2). Swimmers showed with respect to controls: (i) longest maximum duration of voluntary apnea; (ii) marked decrease in HVR; (iii) increased cardiac response during maximal voluntary apnea testing characterized by a general autonomic imbalance. Our results strongly suggest that the lower ventilatory response to hypoxia (determined through a hypoxic challenge) could contribute to a longer duration of apnea in swimmers.

The aim of research 4 was to summarize the available evidence related to chemoreflex control in immersion water sports. Immersion water sports involve long-term apneas; therefore, athletes must physiologically adapt to maintain muscle oxygenation, despite not performing pulmonary ventilation. Breath-holding (ie, apnea) is common in water sports and involves a decrease and increase in PaO2 and PaCO2, respectively, as the main signals that trigger the end of apnea. The main physiological sensors of O2 are the carotid bodies, which are capable of detecting arterial gases and metabolic alterations before reaching the brain, which helps to adjust the cardiorespiratory system. Furthermore, the main H+/CO2 sensor is the retrotrapezoidal nucleus (RTN), which is located at the level of the brainstem; this mechanism helps detect respiratory and metabolic acidosis. Although these sensors have been characterized in pathophysiological conditions, current evidence shows a possible role for these mechanisms as physiological sensors during voluntary apnea. Diving and swimming athletes have been found to show longer apnea times than land-sport athletes, as well as decreased chemoreflex control of peripheral O2 and central CO2. However, although resting chemosensitivity might decrease, we recently found marked sympathoexcitation during maximal voluntary apnea in young swimmers, which might activate the spleen (which is a reservoir organ for oxygenated blood). Therefore, it is possible that the chemoreflex, autonomic function, and oxygen storage/supply organs are related to apnea in immersive water sports. Based on the summarized information we propose a possible physiological mechanistic model that could contribute to providing new ways to understand the respiratory physiology of aquatic sports.