Hot water immersion: Maintaining core body temperature above 38.5°C mitigates muscle fatigue.

PURPOSE: Hot water immersion (HWI) has gained popularity to promote muscle recovery, despite limited data on the optimal heat dose. The purpose of this study was to compare the responses of two exogenous heat strains on core body temperature, hemodynamic adjustments, and key functional markers of muscle recovery following exercise-induced muscle damage (EIMD). METHODS: Twenty-eight physically active males completed an individually tailored EIMD protocol immediately followed by one of the following recovery interventions: HWI (40°C, HWI40 ), HWI (41°C, HWI41 ) or warm water immersion (36°C, CON36 ). Gastrointestinal temperature (Tgi ), hemodynamic adjustments (cardiac output [CO], mean arterial pressure [MAP], and systemic vascular resistance [SVR]), pre-frontal cortex deoxyhemoglobin (HHb), ECG-derived respiratory frequency, and subjective perceptual measures were tracked throughout immersion. In addition, functional markers of muscle fatigue (maximal concentric peak torque [Tpeak ]) and muscle damage (late-phase rate of force development [RFD100-200 ]) were measured prior to EIMD (pre-), 24 h (post-24 h), and 48 h (post-48 h) post-EIMD. RESULTS: By the end of immersion, HWI41 led to significantly higher Tgi values than HWI40 (38.8 ± 0.1 vs. 38.0°C ± 0.6°C, p < 0.001). While MAP was well maintained throughout immersion, only HWI41 led to increased (HHb) (+4.2 ± 1.47 µM; p = 0.005) and respiratory frequency (+4.0 ± 1.21 breath.min-1 ; p = 0.032). Only HWI41 mitigated the decline in RFD100-200 at post-24 h (-7.1 ± 31.8%; p = 0.63) and Tpeak at post-48 h (-3.1 ± 4.3%, p = 1). CONCLUSION: In physically active males, maintaining a core body temperature of ~25 min within the range of 38.5°C-39°C has been found to be effective in improving muscle recovery, while minimizing the risk of excessive physiological heat strain.

Intermittent normobaric hypoxia alters substrate partitioning and muscle oxygenation in individuals with obesity: implications for fat burning.

This single-blind, crossover study aimed to measure and evaluate the short-term metabolic responses to continuous and intermittent hypoxic patterns in individuals with obesity. Indirect calorimetry was used to quantify changes in resting metabolic rate (RMR), carbohydrate (CHOox, %CHO), and fat oxidation (FATox, %FAT) in nine individuals with obesity pre and post: 1) breathing normoxic air [normoxic sham control (NS-control)], 2) breathing continuous hypoxia (CH), or 3) breathing intermittent hypoxia (IH). A mean peripheral oxygen saturation ([Formula: see text]) of 80-85% was achieved over a total of 45 min of hypoxia. Throughout each intervention, pulmonary gas exchanges, oxygen consumption (V̇o2) carbon dioxide production (V̇co2), and deoxyhemoglobin concentration (Δ[HHb]) in the vastus lateralis were measured. Both RMR and CHOox measured pre- and postinterventions were unchanged following each treatment: NS-control, CH, or IH (all P > 0.05). Conversely, a significant increase in FATox was evident between pre- and post-IH (+44%, P = 0.048). Although the mean Δ[HHb] values significantly increased during both IH and CH (P < 0.05), the greatest zenith of Δ[HHb] was achieved in IH compared with CH (P = 0.002). Furthermore, there was a positive correlation between Δ[HHb] and the shift in FATox measured pre- and postintervention. It is suggested that during IH, the increased bouts of muscle hypoxia, revealed by elevated Δ[HHb], coupled with cyclic periods of excess posthypoxia oxygen consumption (EPHOC, inherent to the intermittent pattern) played a significant role in driving the increase in FATox post-IH.

Possible causes of narcosis-like symptoms in freedivers.

During deep-sea freediving, many freedivers describe symptoms fairly similar to what has been related to inert gas narcosis in scuba divers. This manuscript aims to present the potential mechanisms underlying these symptoms. First, known mechanisms of narcosis are summarized while scuba diving. Then, potential underlying mechanisms involving the toxicity of gases (nitrogen, carbon dioxide and oxygen) are presented in freedivers. As the symptoms are felt during ascent, nitrogen is likely not the only gas involved. Since freedivers are frequently exposed to hypercapnic hypoxia toward the end of the dive, it is proposed that carbon dioxide and oxygen gases both play a major role. Finally, a new "hemodynamic hypothesis" based on the diving reflex is proposed in freedivers. The underlying mechanisms are undoubtedly multifactorial and therefore require further research and a new descriptive name. We propose a new term for these types of symptoms: freediving transient cognitive impairment.

Pre-acclimation to altitude in young adults: choosing a hypoxic pattern at sea level which provokes significant haematological adaptations.

PURPOSE: This single-blind, repeated measures study evaluated adaptive and maladaptive responses to continuous and intermittent hypoxic patterns in young adults. METHODS: Changes in haematological profile, stress and cardiac damage were measured in ten healthy young participants during three phases: (1) breathing normoxic air (baseline); (2) breathing normoxic air via a mask (Sham-controls); (3) breathing intermittent hypoxia (IH) via a mask, mean peripheral oxygen saturation (SpO2) of 85% ~ 70 min of hypoxia. After a 5-month washout period, participants repeated this three-phase protocol with phase, (4) consisting of continuous hypoxia (CH), mean SpO2 = 85%, ~ 70 min of hypoxia. Measures of the red blood cell count (RBCc), haemoglobin concentration ([Hb]), haematocrit (Hct), percentage of reticulocytes (% Retics), secretory immunoglobulin A (S-IgA), cortisol, cardiac troponin T (cTnT) and the erythropoietic stimulation index (calculated OFF-score) were compared across treatments. RESULTS: Despite identical hypoxic durations at the same fixed SpO2, no significant effects were observed in either CH or Sham-CH control, compared to baseline. While IH and Sham-IH controls demonstrated significant increases in: RBCc; [Hb]; Hct; and the erythropoietic stimulation index. Notably, the % Retics decreased significantly in response to IH (-31.9%) or Sham-IH control (-23.6%), highlighting the importance of including Sham-controls. No difference was observed in S-IgA, cortisol or cTnT. CONCLUSION: The IH but not CH pattern significantly increased key adaptive haematological responses, without maladaptive increases in S-IgA, cortisol or cTnT, indicating that the IH hypoxic pattern would be the best method to boost haematological profiles prior to ascent to altitude.

Post-exercise Heart Rate Variability: Whole-body Cryotherapy vs. Contrast Water Therapy.

High-intensity training sessions are known to alter cardiac autonomic modulation. The purpose of this study was to compare the effects of whole-body cryotherapy, contrast water therapy and passive recovery on the time course of cardiac autonomic markers following a standardized HIT session. Eleven runners completed a high intensity session followed by one of the following recovery interventions: whole-body cryotherapy, contrast water therapy or passive recovery. Changes in cardiac autonomic modulation were assessed in supine and standing positions during an active tilt test at pre-, post-14 h and post-38 h. In supine, high-frequency power increased from pre- to post-14 h following whole-body cryotherapy (1661.1±914.5 vs. 2799.0±948.4 ms2, respectively; p=0.023) and contrast water therapy (1906.1±1327.9 vs. 4174.3±2762.9 ms2, respectively; p=0.004) whereas high frequency power decreased in response to passive recovery (p=0.009). In standing, low-frequency power increased from pre-to post-38 h (1784.3 ± 953.7 vs. 3339.8±1862.7 ms2, respectively; p=0.017) leading to an increase in total power from pre- to post-38 h (1990.8 ± 1089.4 vs. 3606.1±1992.0 ms2, respectively; p=0.017). Spectral analysis revealed that contrast water therapy appears to be a more efficient recovery strategy than whole-body cryotherapy in restoring cardiac autonomic homeostasis.

Autonomic regulation of the heart and arrhythmogenesis in trained breath-hold divers.

AbstractBreath-hold divers are known to develop cardiac autonomic changes and brady-arrthymias during prolonged breath-holding (BH). The effects of BH-induced hypoxemia were investigated upon both cardiac autonomic status and arrhythmogenesis by comparing breath-hold divers (BHDs) to non-divers (NDs). Eighteen participants (9 BHDs, 9 NDs) performed a maximal voluntary BH with face immersion. BHDs were asked to perform an additional BH at water surface to increase the degree of hypoxemia. Beat-to-beat changes in heart rate (HR), short-term fractal scaling exponent (DFAα1), the number of arrhythmic events [premature ventricular contractions (PVCs), premature atrial contractions (PACs)] and peripheral oxygen saturation (SpO2) were recorded during and immediately following BH. The corrected QT-intervals (QTc) were analyzed pre- and post-acute BH. A regression-based model was used to split BH into a normoxic (NX) and a hypoxemic phase (HX). During the HX phase of BH, BHDs showed a progressive decrease in DFAα1 during BH with face immersion (p < 0.01) and BH with whole-body immersion (p < 0.01) whereas NDs did not (p > 0.05). In addition, BHDs had more arrhythmic events during the HX of BH with whole-body immersion when compared to the corresponding NX phase (5.9 ± 6.7 vs 0.4 ± 1.3; p < 0.05; respectively). The number of PVCs was negatively correlated with SpO2 during BH with whole-body immersion (r = -0.72; p < 0.05). The hypoxemic stage of voluntary BH is concomitant with significant cardiac autonomic changes toward a synergistic sympathetic and parasympathetic stimulation. Co-activation led ultimately to increased bradycardic response and cardiac electrophysiological disturbances.

Intermittent not continuous hypoxia provoked haematological adaptations in healthy seniors: hypoxic pattern may hold the key.

PURPOSE: The purpose of this single-blind, repeated measures study was to investigate the effect of two hypoxic patterns, continuous or intermittent on key markers of haematological adaptation, stress and cardiac damage in healthy senior participants. METHODS: Fifteen healthy senior participants each followed a three-phase protocol over 3 consecutive weeks: (1) 5 consecutive days of breathing room air without a mask (2) 5 days of normoxic mask breathing (sham, FiO2 = 21%) (3) 5 days of intermittent hypoxia (IH) tailored to achieve a mean peripheral oxygen saturation (SpO2) of 85% during ~ 70 min of cumulative exposure to hypoxia. After a 5-month washout period, participants were recalled to undertake continuous hypoxia (CH, SpO2 = 85%, ~ 70 min). The red blood cell count (RBCc), haemoglobin concentration ([Hb]), haematocrit (Hct), percentage of reticulocytes (% Retics), secretory immunoglobulin A (S-IgA), cortisol, cardiac troponin T (cTnT) and the OFF-score (i.e. [Formula: see text]) were measured. RESULTS: RBCc only increased by day 5 of IH treatment compared to day 5 baseline values (+ 7.7%, p < 0.01) and day 5 Sham values (+ 12.9%, p < 0.01). [Hb] only increased by day 5 of IH treatment compared to day 5 baseline values (+ 14.7%, p < 0.01) and day 5 Sham values (+ 14.3%, p < 0.01). Hct (+ 12.7%, p < 0.01) and the OFF-score (p < 0.05) increased only during the final day of IH treatment. No difference was observed in S-IgA, cortisol or cTnT following IH or CH. CONCLUSION: These results revealed that inherent differences in the IH and CH hypoxic patterns could provide crucial components required to trigger hematological changes in senior individuals, without eliciting immunological stress responses or damaging the myocardium.

Intermittent hypoxia revisited: a promising non-pharmaceutical strategy to reduce cardio-metabolic risk factors?

PURPOSE: The study aims to investigate the effects of moderate intermittent hypoxia (IH) on key cardio-metabolic risk factors in overweight and obese subjects. METHODS: Six subjects were exposed to 10 sessions of moderate IH over 2 weeks (based on [Formula: see text]; ~70 min per session). Measures were made of blood glucose (GLU) and lactate (La-); high (HDLc) and low-density lipoproteins (LDLc); triglycerides (TRG), systolic (SBP), and diastolic blood pressure (DBP); and cardiac autonomic indices [root mean square of successive R-R interval differences (RMSSD) and short-term fractal scaling exponent (DFAα1)]. RESULTS: GLU decreased and La- increased following a single IH session (6.21 ± 1.62 vs. 5.32 ± 1.03 mmol L-1; p < 0.05; 1.14 ± 0.21 vs. 1.47 ± 0.22 mmol L-1), but no sustained change after 10 sessions of IH occurred (p > 0.05). Conversely, LDLc (3.00 ± 0.68 vs. 2.51 ± 0.60 mmol L-1; p < 0.05), LDLc/HDLc ratio (2.52 ± 0.66 vs. 2.26 ± 0.70 mmol L-1; p < 0.05), and SBP (118.6 ± 13.3 vs. 109.6 ± 11.3 mmHg; p < 0.05) were all significantly decreased after 10 sessions. CONCLUSION: A short course of recurrent IH appears to be a safe and effective non-pharmacological method of reducing key cardiovascular risk factors associated with metabolic disorders.

Do elite breath-hold divers suffer from mild short-term memory impairments?

Repeated apneas are associated with severe hypoxemia that may ultimately lead to loss of consciousness in some breath-hold divers. Despite increasing number of practitioners, the relationship between apnea-induced hypoxia and neurocognitive functions is still poorly understood in the sport of free diving. To shed light onto this phenomenon, we examined the impact of long-term breath-hold diving training on attentional processing, short-term memory, and long-term mnesic and executive functions. Thirty-six men matched for age, height, and weight were separated into the following 3 groups: (i) 12 elite breath-hold divers (EBHD), mean static apnea best time 371 s, 105 months mean apnea experience; (ii) 12 novice breath-hold divers, mean best time 243 s, 8.75 months mean apnea experience; and (iii) 12 physical education students with no breath-hold diving experience; all of these participants performed varied written and computerized neuropsychological tasks. Compared with the 2 other groups, the EBHD group was slower to complete the interference card during a Stroop test (F[1,33] = 4.70, p < 0.05), and presented more errors on the interference card (F[1,33] = 2.96, p < 0.05) and a lower total interference score (F[1,33] = 5.64, p < 0.05). The time to complete the interference card test was positively correlated with maximal static apnea duration (r = 0.73, p < 0.05) and the number of years of breath-hold diving training (r = 0.79, p < 0.001). These findings suggest that breath-hold diving training over several years may cause mild, but persistent, short-term memory impairments.

The oxygen-conserving potential of the diving response: A kinetic-based analysis.

We investigated the oxygen-conserving potential of the human diving response by comparing trained breath-hold divers (BHDs) to non-divers (NDs) during simulated dynamic breath-holding (BH). Changes in haemodynamics [heart rate (HR), stroke volume (SV), cardiac output (CO)] and peripheral muscle oxygenation [oxyhaemoglobin ([HbO2]), deoxyhaemoglobin ([HHb]), total haemoglobin ([tHb]), tissue saturation index (TSI)] and peripheral oxygen saturation (SpO2) were continuously recorded during simulated dynamic BH. BHDs showed a breaking point in HR kinetics at mid-BH immediately preceding a more pronounced drop in HR (-0.86 bpm.%-1) while HR kinetics in NDs steadily decreased throughout BH (-0.47 bpm.%-1). By contrast, SV remained unchanged during BH in both groups (all P > 0.05). Near-infrared spectroscopy (NIRS) results (mean ± SD) expressed as percentage changes from the initial values showed a lower [HHb] increase for BHDs than for NDs at the cessation of BH (+24.0 ± 10.1 vs. +39.2 ± 9.6%, respectively; P < 0.05). As a result, BHDs showed a [tHb] drop that NDs did not at the end of BH (-7.3 ± 3.2 vs. -3.0 ± 4.7%, respectively; P < 0.05). The most striking finding of the present study was that BHDs presented an increase in oxygen-conserving efficiency due to substantial shifts in both cardiac and peripheral haemodynamics during simulated BH. In addition, the kinetic-based approach we used provides further credence to the concept of an "oxygen-conserving breaking point" in the human diving response.

Ischaemia-modified albumin during experimental apnoea.

Ischaemia-modified albumin (IMA) is a marker of the release of reactive oxygen species (ROS) during hypoxaemia. In elite divers, breath-hold induces ROS production. Our aim was to evaluate the kinetics of IMA serum levels during apnea. Twenty breath-hold divers were instructed to perform a submaximal static breath-hold. Twenty non-diver subjects served as controls. Blood samples were collected at rest, every minute, at the end of breath-hold, and 10 min after recovery. The IMA level increased after 1 min of breath-hold (p < 0.003) and remained high until recovery. Divers were separated into 2 groups: subjects who held their breath for less than 4 min (G-4) and those who held it for more than 4 min (G+4). After 3 min of apnoea, the increase of IMA was higher in the G-4 group than in the G+4 group (p < 0.008). However, at the end of apnoea, the IMA level did not differ between groups. If IMA level was globally correlated with the apnoea duration, it is interesting to note that the higher IMA level was not found in the best divers. Similarly, if arterial blood oxygen saturation (SpO2) was globally inversely correlated with apnoea duration, the lowest SpO2 at the end of breath-hold was not found in the divers that performed the best apnoea. We concluded that these divers save their oxygen. The IMA level provides a useful measure of resistance to hypoxaemia.

Modeling the diving bradycardia: Toward an "oxygen-conserving breaking point"?

PURPOSE: Although it has been demonstrated that the exponential decay model fits the heart rate (HR) kinetics in short static breath holding (BH), this model might be inaccurate when BH is maintained for several minutes. The aim of this study was to build a new meaningful model to quantify HR kinetics during prolonged static BH. METHODS: Nonlinear regression analysis was used to build a model able to quantify the beat-to-beat HR reduction kinetics observed in prolonged static BH performed both in air and in immersed condition by 11 trained breath-hold divers. Dynamic changes in cardiac autonomic regulation through heart rate variability indices [root mean square of successive difference of R-R intervals (RMSSD); short-term fractal scaling exponent: (DFAα1)] and peripheral oxygen saturation (SpO2) were also analyzed to strengthen the model. RESULTS: The tri-phasic model showed a sharp exponential drop in HR immediately followed by a slight linear rise up until a breaking point preceding a linear drop in HR. The breaking points had similar level of SpO2 whether in air or in immersed condition (95.1 ± 2.1 vs. 95.2 ± 3.0 %, respectively; P = 0.49), and the subsequent linear drop in HR was concomitant with a shift in cardiac autonomic regulation in air (RMSSD: +109.0 ± 47.8 %; P < 0.001; DFAα1: -18.0 ± 17.4 %; P < 0.05) and in immersion (RMSSD: +112.6 ± 55.8 %; P < 0.001; DFAα1: -26.0 ± 12 %; P < 0.001). CONCLUSION: In addition to accurately fitting the HR kinetics, the most striking finding is an "oxygen-conserving breaking point" highlighted by the model, which might be interpreted as unique adaptive feature against hypoxic damages in the human diving bradycardia.

Doppler detection in Ama divers of Japan.

OBJECTIVE: Symptoms consistent with neurological decompression sickness (DCS) in commercial breath-hold (Ama) divers has been reported from a few districts of Japan. The aim of this study was to detect circulating intravascular bubbles after repetitive breath-hold diving in a local area where DCS has been reported in Ama divers. METHODS: The participants were 12 partially assisted (descent using weights) male Ama divers. The equipment (AQUALAB system) consisted of continuous-wave Doppler with a 5-MHz frequency, and the Doppler probe was placed in the precordial site with the ultrasonic wave directed into the pulmonary infundibulum. We carried out continuous monitoring for 10 minutes at the end of the series of repetitive dives, and the recordings were made on numerical tracks and graded in a blind manner by 2 experienced investigators, according to the Spencer Doppler code. RESULTS: Depths and number of dives were 8 to 20 m and 75 to 131 times. Mean diving duration and surface interval were 64 ± 12 seconds and 48 ± 8 seconds, respectively (mean ± SD). We detected the lowest grade of intravascular bubbles (Spencer's grade I) in an Ama diver whose mean surface interval was only 35.2 ± 6.2 seconds. His mean descending, bottom, and ascending times were 10.4 ± 1.6 seconds, 39.2 ± 8 seconds, and 18.2 ± 3.0 seconds, respectively, over the course of 99 dives. CONCLUSIONS: Intravascular bubbles may be formed after repetitive breath-hold dives with short surface intervals or after a long breath-holding session in Ama divers. Symptoms consistent with neurological accidents in repetitive breath-hold diving may be caused in part by the intravascular presence of bubbles, indicating the need for safety procedures.

Cardio-ventilatory responses to poikilocapnic hypoxia and hypercapnia in trained breath-hold divers.

Trained breath-hold divers (BHDs) are exposed to repeated bouts of intermittent hypoxia and hypercapnia during prolonged breath-holding. It has thus been hypothesized that their specific training may develop enhanced chemo-responsiveness to hypoxia associated with reduced ventilatory response to hypercapnia. Hypercapnic ventilatory responses (HCVR) and hypoxic ventilatory responses at rest (HVRr) and exercise (HVRe) were assessed in BHDs (n=7) and a control group of non-divers (NDs=7). Cardiac output (CO), stroke volume (SV) and heart rate (HR) were also recorded. BHDs presented carbon dioxide sensitivity similar to that of NDs (2.85±1.41 vs. 1.85±0.93Lmin(-1)mmHg(-1), p>0.05, respectively). However, both HVRr (+68%) and HVRe (+31%) were increased in BHDs. CO and HR reached lower values in BHDs than NDs during the hypoxic exercise test. These results suggest that the exposure to repeated bouts of hypoxia/hypercapnia frequently experienced by trained breath-hold divers only enhances their chemo-responsiveness to poikilocapnic hypoxia, without altering HCVR.

Hemodynamic adjustments during breath-holding in trained divers.

PURPOSE: Voluntary breath-holding (BH) elicits several hemodynamic changes, but little is known about maximal static immersed-body BH. We hypothesized that the diving reflex would be strengthened with body immersion and would spare more oxygen than maximal dry static BH, resulting in a longer BH duration. METHODS: Eleven trained breath-hold divers (BHDs) performed a maximal dry-body BH and a maximal immersed-body BH. Cardiac output (CO), stroke volume (SV), heart rate (HR), left ventricular end-diastolic volume (LVEDV), contractility index (CTI), and ventricular ejection time (VET) were continuously recorded by bio-impedancemetry (PhysioFlow PF-05). Arterial oxygen saturation (SaO2) was assessed with a finger probe oximeter. RESULTS: In both conditions, BHDs presented a bi-phasic kinetic for CO and a tri-phasic kinetic for SV and HR. In the first phase of immersed-body BH and dry-body BH, results (mean ± SD) expressed as percentage changes from starting values showed decreased CO (55.9 ± 10.4 vs. 39.3 ± 16.8 %, respectively; p < 0.01 between conditions), due to drops in both SV (24.9 ± 16.2 vs. 9.0 ± 8.5 %, respectively; p < 0.05 between conditions) and HR (39.7 ± 16.7 vs. 33.6 ± 17.0 %, respectively; p < 0.01 between conditions). The second phase was marked by an overall stabilization of hemodynamic variables. In the third one, CO kept stabilizing due to increased SV (17.0 ± 20.2 vs. 10.9 ± 13.8 %, respectively; p < 0.05 between conditions) associated with a second HR drop (14.0 ± 10.0 vs. 12.7 ± 8.9 %, respectively; p < 0.01 between conditions). CONCLUSION: This study highlights similar time-course patterns for cardiodynamic variables during dry-body and immersed-body BH, although the phenomenon was more pronounced in the latter condition.

Effect of additional respiratory muscle endurance training in young well-trained swimmers.

While some studies have demonstrated that respiratory muscle endurance training (RMET) improves performances during various exercise modalities, controversy continues about the transfer of RMET effects to swimming performance. The objective of this study was to analyze the added effects of respiratory muscle endurance training (RMET; normocapnic hyperpnea) on the respiratory muscle function and swimming performance of young well-trained swimmers. Two homogenous groups were recruited: ten swimmers performed RMET (RMET group) and ten swimmers performed no RMET (control group). During the 8-week RMET period, all swimmers followed the same training sessions 5-6 times/week. Respiratory muscle strength and endurance, performances on 50- and 200-m trials, effort perception, and dyspnea were assessed before and after the intervention program. The results showed that ventilatory function parameters, chest expansion, respiratory muscle strength and endurance, and performances were improved only in the RMET group. Moreover, perceived exertion and dyspnea were lower in the RMET group in both trials (i.e., 50- and 200-m). Consequently, the swim training associated with RMET was more effective than swim training alone in improving swimming performances. RMET can therefore be considered as a worthwhile ergogenic aid for young competitive swimmers. Key PointsRespiratory muscle endurance training improves the performance.Respiratory muscle endurance training improves the ventilatory function parameters, chest expansion, respiratory muscle strength and endurance.Respiratory muscle endurance training decreases the perceived exertion and dyspnea.Respiratory muscle endurance training can be considered as a worthwhile ergogenic aid for young competitive swimmers.