THE INFLUENCE OF REDUCED BREATHING DURING SWIMMING ON SOME RESPIRATORY AND METABOLIC VALUES IN BLOOD VPLIVI ZMANJŠANE FREKVENCE DIHANJA MED PLAVANJEM NA DIHALNE IN METABOLNE KAZALCE V KRVI Jernej Kapus Anton Ušaj Venceslav Kapus Boro Štrumbelj 14 Kapus, J., Ušaj, A., Kapus, V., & Štrumbelj, B. (2002). The influence of reduced breathing during swimming … KinSI 8(1), 14–18 Abstract The purpose of the present study was to ascertain the influence of reduced pulmonary ventilation on blood acid-base balance during swimming. Five trained swimmers (age 21±2 years, height 187±5 cm and weight 83±6 kg) volunteered to participa- te in this study. They had to swim 400 m front crawl at velocity V OBLA two times. Firstly, they were ta- king breath every two strokes (B2). During the se- cond trial they swam the same distance at a similar velocity, however with reduced breathing fre- quency, taking breath every four strokes (B4). Mea- sures included lactate concentration ([LA]) and pa- rameters of blood acid-base status (pH, Po 2 , Pco 2 ) before and during the third minute after the exer- cise. Only Pco 2 significantly increased after B4 than after B2 (p<0.05). After the exercise other parame- ters ([LA], pH, HCO 3 and Po 2 ) did not change sig- nificantly in response to reduced breathing fre- quency during swimming. It may be concluded that the reduced breathing frequency during front crawl swimming at V OBLA velocity did not cause hypoxia nor increased [LA]. However, it increased the Pco 2 to the range of hypercapnia. Keywords: swimming, reduced breathing frequency, blood acid base status, blood lactate Contact address Jernej Kapus University of Ljubljana – Faculty of Sport Gortanova 22 SI-1000 Ljubljana Slovenia Tel:: +386 1 520-77-00 Fax.: +386 1 520-77-50 E-mail: Jernej.Kapus@sp.uni-lj.si Izvleček Namen raziskave je bil ugotoviti učinke zmanjšane frekvence dihanja na kazalce acidobaznega statu- sa krvi med plavanjem s hitrostjo, ki jo določa kri- terij Onset of Blood Lactat Accumulation (V OBLA ). V raziskavo je bilo vključenih pet zdravih plavalcev, starih od 18 do 23 let (višina 187 ± 6 cm in teža 83 kg ± 9 kg), ki so odplavali 400 m kravl z dihanjem na vsak drugi zavesljaj (D2) in 400 m kravl z diha- njem na vsak četrti zavesljaj (D4). Pri tem smo me- rili: vsebnost laktata ([LA]) in kazalce acido-bazne- ga statusa v krvi (pH, Po 2 , Pco 2 ). Vzorce smo jemali pred naporom in v tretji minuti po naporu. Le vred- nosti Pco 2 po D4 so značilno višje od vrednosti Pco 2 po D2 (p<0.05). Preostale vrednosti drugih kazalcev acido-baznega statusa po D4 so podob- ne vrednostim po D2. Na osnovi teh rezultatov smo zaključili, da zmanjšana frekvenca dihanja med pla- vanjem pri hitrosti V OBLA ne vpliva na znižanje Po 2 ali povečanje [LA], temveč zviša Pco 2 v področje hiperkapnije. Ključne besede: plavanje, zmanjšana frekvenca di- hanja, acido-bazni status krvi, krvni laktat (Received: 25. 02. 2002 – Accepted: 05. 09. 2002) INTRODUCTION Pulmonary ventilation is limited by the swimming technique. Breathing frequency has to be in accor- dance with the stroke frequency. It may be assu- med that the front crawl swimming velocity should also be regulated in a way, which ensures maintai- ning needs of increased pulmonary ventilation. If the breathing pattern is changed at a similar velo- city, this may dramatically influence blood oxyge- nation and acid-base status and the swimmer’s per- formance. Hypoxia and/or hypercapnia with additional respiratory acidosis may hypothetically be effects of reduced pulmonary ventilation. Du- ring front crawl swimming with restricted breathing (a breath every four, six or eight strokes), the swim- ming technique may not permit an adequate in- crease of pulmonary ventilation to match it’s needs. It may have a significant influence on the swim- mer’s exertion (Dicker, Lofthus, Thorton, & Brooks, 1980; Town, & Vanness, 1990). Swimmers, throughout their training learn to main- tain the highest swimming velocity (»critical« velo- city) where ventilation generally still matches its needs. However, it may be expected that swim- ming velocity may exceed this »critical« velocity for a while, especially during shorter swimming distan- ces. On the other hand, the similar phenomenon may be caused during swimming with reduced breathing frequency or during swimming of certain distances with breath holding. This training techni- que is often referred to as »hypoxic training« (Ma- glischo, 1990). It has been thought that reduced breathing frequency can be used to induce arterial hypoxemia, and to enhance lactate production in working muscles (Counsilman, 1977). It is believed that reduced breathing frequency during swim- ming permits swimmers to derive both »aerobic« and »anaerobic« conditioning from exercise of sub maximal intensity (Dicker et al., 1980). Some previous studies focused on reduced breat- hing frequency during swimming, running and cy- cling. Swimmers restricted the breathing frequency (a breath every four, six and eight strokes) during tethered flume swimming (Dicker et al., 1980; Town et al., 1990) and during interval training (Holmer, & Gulstrand, 1980). Studies on the bicycle ergometer used cycling bouts at different intensities and diffe- rent breathing patterns: normal breathing, breat- hing every 4 s, breathing every 8 s and reduced fre- quency as low as possible. Subjects held their breath at functional residual capacity (Yamamoto, Mutoh, Kobayashi, & Miyashita, 1987; Yamamoto, Takei, Mutoh, & Miyashita, 1988) and at total lung capacity (Lee, Cordain, Sockler, & Tucker, 1990). Runners performed intervals at 125% Vo2max with breath holding (Matheson, & Mckenzie, 1988). Although reduced breathing frequency during swimming was associated with reduced ventilation (VE), increased alveolar partial pressure of CO 2 (P A co 2 ) and in decreased alveolar partial pressure of O 2 (P A o 2 ) (Town et al., 1990), compensatory res- ponses resulted in increased tidal volume (VT). But this reduction of P A o 2 was insufficient to cause a marked reduction in arterial oxygen saturation (Dic- ker et al., 1980). The arterial oxygen desaturation during exercise with reduced breathing frequency appears to depend on lung volume at which breath holding occurs. Alveolar hypoxia was accentuated more during breath holding at functional residual capacity than at total lung capacity (Yamamoto et al., 1987; Lee et al., 1990). Reduced breathing fre- quency during exercise increased lactate concen- tration (Lee et al., 1990) or did not influence it (Ya- mamoto et al., 1987; Matheson et al., 1988; Town et al., 1990). Holmer et al. (1980) noted a signifi- cantly lower Vo 2 during swimming with reduced breathing frequency and a slight decrease in blood lactate concentration. This seemed contradictory because reduced oxidative metabolism should be compensated for by an increased anaerobic yield. Reduced breathing frequency during swimming could also impede stroke rate. Especially when the need to breathe becomes critical, swimmers have to increase their stroke rate, which helps to increa- se ventilation (Town et al., 1990). It has been assumed that maximal lactate steady state occurs during swimming at constant velocity, which corresponded to Onset of blood lactate ac- cumulation (OBLA) (Sjodin, Schele, Karlsson, Li- narsson, & Care, 1982). Therefore the volume of CO 2 , which comes from the bicarbonate buffer sys- tem, should be also constant together with additio- nal volume of CO 2 from the aerobic metabolism. Oxygen delivery to muscles seems not to be limi- ted due to constant Po 2 . If pulmonary ventilation is reduced substantially during this velocity, then it may be expected that lower volume of CO 2 will be expired by the lungs, which may cause hypercap- nia and respiratory acidosis. According to data of Yamamoto et al. (1986) an influence on increased Pco 2 and no effect on [LA] may be expected. Un- fortunately, these data were not obtained at velo- city V OBLA and/or during swimming. It may be 15 Kapus, J., Ušaj, A., Kapus, V., & Štrumbelj, B. (2002). The influence of reduced breathing during swimming … KinSI 8(1), 14–18 hypothesised that V OBLA is the lowest velocity, which can be swum for a longer distance (400 m) also with restricted breathing. This fact is necessary for studying phenomena related to restricted breat- hing. The purpose of the present study was there- fore to ascertain the influence of reduced breat- hing frequency on the blood acid-base status during swimming at Onset of Blood Lactate Accu- mulation velocity (V OBLA ). METHODS Subjects Five trained swimmers (age 22 ± 2 years, height 184 ± 8 cm and weight 80 ± 6 kg) volunteered to participate in this study. Procedures Swimmers swam a 5 × 200 m front crawl progres- sive step test. The swimming velocity of the first step was 1.09 m/s. From step to step the swimming velocity was increased by 0.1 m/s. Breaks between each exercise step were 3 minutes. After the progressive step test swimmers had to swim 400 m front crawl at V OBLA twice: first, by ta- king breath every two strokes (B2) and the second, by taking breath every four strokes (B4). Velocity and stroke rate of 400 m front craw with B4 were defined with 400 m front crawl with B2, since we knew that swimmers reduced swimming velocity and/or increased stroke rate, when the need to breathe become critical during swimming with re- duced breathing frequency (Town et al., 1990). Blood collection and breathing measurements During the break between each exercise in the front crawl progressive step test a blood sample (10 µl) is taken in order to determine the lactate con- centration ([LA]). [LA] was analysed with the use of MINI8 (dr. LANGE, Germany) photometer. Measures before and after 400 m front crawl with different breathing frequency included parameters of blood acid-base status (pH, Po 2 , Pco 2 , [HCO 3 – ]) and [LA]. Capillary blood samples (60 – 80 µl) were collected in the third minute after each swim from a hyperemied ear lobe for pH, Po 2 , Pco 2 , [HCO 3 – ] analysis using an ABL5 (Radiometer Copenhagen) instrument. Stroke rate, inspiratory time (T I ), expi- ratory time (T E ), number of breaths per 25 meters (Ni) and breathing frequency during swimming (BF) were obtained by analysing film shots. Data processing and analysis OBLA (Onset of Blood Lactate Accumulation) is defined by [LA] 4 mmol/l (Maglischo, 1990) and it is one of the possible criteria for anaerobic thres- hold (Ušaj, & Starc, 1990). It was evaluated on the basis of lactate concentration in dependence to swimming velocity curves. Statistics The values were presented as means ± standard de- viations (SD). The paired t-test was used to compa- re the data between swimming in two different conditions. All statistical parameters were calcula- ted using the graphical statistics package Sigma Plot (Jandel, Germany). RESULTS 16 Kapus, J., Ušaj, A., Kapus, V., & Štrumbelj, B. (2002). The influence of reduced breathing during swimming … KinSI 8(1), 14–18 Table 1: OBLA velocity, measured B2 and B4 velocity and measured B2 and B4 stroke frequency. SUBJECT V OBLA (m/s) V B2 (m/s) SF B2 (min -1 )V B4 (m/s) SF B4 (min -1 ) 1. 1.21 1.19 29 1.20 29 2. 1.46 1.44 31 1.44 31 3. 1.20 1.21 24 1.21 24 4. 1.34 1.33 31 1.33 32 5. 1.43 1.43 32 1.43 31 MV1.33 1.32 / 1.32 / SD 0.12 0.12 / 0.11 / Legend: V OBLA – OBLA velocity; V B2 – measured B2 velocity SF B2 – measured B2 stroke frequency V B4 – measured B4 velocity SF B4 – measured B4 stroke frequency MV – mean values; SD – standard deviation Table 3 shows that Pco2 was significantly higher af- ter B4 than after B2 (p<0.05). Other parameters ([LA], pH, Po2) did not change significantly in res- ponse to reduced breathing frequency during swimming. DISCUSSION The results of this study indicate that reduced breat- hing frequency during swimming 400 meters front crawl at velocity V OBLA increased Pco 2 in capillary blood (Figure 1), which was different than during non-restricted breathing. The average Pco 2 (5.4 kPa) measured 3 min after the swimming under B4 conditions (B4 (reduced pulmonary ventilation) was within the upper limit of 17 Kapus, J., Ušaj, A., Kapus, V., & Štrumbelj, B. (2002). The influence of reduced breathing during swimming … KinSI 8(1), 14–18 Table 2: Respiratory parameters of swimming with two different breathing conditions (B2 and B4). B2 B4 MVSD MVSD T I (s) 0.72 0.1 0.72 0.1 T E (s) 1.29 0.2 3.30 0.5 Nb (per whole distance) 124 9 74 9 BF (min -1 ) 24 2.7 15 2 Legend: T I – inspiratory time; T E – expiratory time; Nb – number of breaths per whole distance; BF – breathing frequency As expected, swimming speeds and stroke frequencies did not change between two different breathing conditions (Table 1). Only one subject could not finish the 400 m front crawl taking breath every four stro- kes. Because of fatigue he could swim only 300 m. Reduced Nb and breathing frequency during swimming (BF) was accompanied by almost the same inspi- ratory time (T i ) in both breathing conditions. Table 3: Comparisons [LA], pH, Po 2 , Pco 2 values before and after swimming between two different breat- hing conditions (B2 and B4). B2 B4 Before After Before After MVSD MVSD MVSD MVSD [LA] (mmol/l) 1.2 0.4 7.9 1.1 1.6 0.3 8.1 1.9 pH 7.42 0.01 7.27 0.03 7.41 0.001 7.26 0.05 Pco2 (kPa) 4.8 0.3 4.8* 0.3 5 0.2 5.4* 0.2 Po2 (kPa) 11.4 1.3 12.4 1 10.5 0.5 11.3 0.4 [HCO3 – ] (mmol/l) 23 1 17 2 23 1 18 3 Legend: Paired t-test (* - p<0.05) Figure 1: Comparisons the Pco2 values before and after swim- ming between two different breathing conditions. Pco 2 in the resting healthy subjects. However it was still significantly higher than Pco 2 after the B2 (nor- mal breathing during front crawl swimming). So- meone may assume that such differences within re- sting interval may not lead to a conclusion that B4 breathing influences hypercapnia. However, when fast exchange of CO 2 between blood and alveolar air was taken into account and resting interval of 3 minutes is also considered, then it may be conclu- ded that the actual Pco 2 at the end of swimming is higher then measured Pco 2 after 3 minutes of rest. The inadequate pulmonary ventilation could also cause respiratory acidosis. Using trained female runners, Matheson et al. (1988) determined that breath holding during intermittent intense (125% Vo 2 max) exercise induced a measurable rapidly re- versible respiratory acidosis. The reduced breathing frequency during swimming did not influence pH in the present study. It might be presumed that res- piratory acidosis did not occur at all, or it occurs at swimming and during very early recovery phase as an effect of hypercapnia. However it may rapidly di- sappear during later phase of recovery. Yamamoto et al. (1988) and Matheson et al. (1988) reported that blood lactate did not rise during exercise with reduced breathing frequency, but there were grea- ter levels of blood lactate during recovery. They concluded that respiratory acidosis due to reduced pulmonary ventilation inhibited lactate transport from working muscles during activity. Our results did not show any change of [LA] and pH due to decreased ventilation at the third minute after the exercise. Therefore, the presented conclusions can- not be verified by present data and the problem re- mains to be solved in the future. There was no statistical difference in Po 2 after swimming between B2 in B4 in the present study. According to Dicker et al. (1980) P A o 2 in B2 de- creased by 14% in comparison with B4. But esti- mated arterial oxygen saturation was essentially un- diminished during swimming with reduced breathing frequency. Results of their study and our findings argue against the hypothesis of systemic hypoxia during sub maximal swimming with redu- ced breathing frequency. Different studies ascer- tained the hypothesis of systemic hypoxia during cycling exercise or running with reduced breathing frequency. Lee et al. (1990) concluded that the ar- terial oxygen desaturation during exercise with re- duced breathing frequency appears to depend on: lung volume at which breath holding occurs, the barometric pressure of O 2 and exercise intensity. Alveolar hypoxia was accentuated more during breath holding at functional residual capacity than at total lung capacity at sea level and at low altitu- des (Yamamoto et al., 1987). Breath holding at to- tal lung capacity during sub maximal cycling exer- cise at moderate altitude (1520 m) caused arterial hypoxemia, tissue hypoxia, systemic hypercapnia and acidosis (Lee et al., 1990). 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