The Effect of an Olympic Distance Triathlon on Pulmonary Diffusing Capacity and its Recovery 24 Hours Later.

The Olympic distance triathlon includes maximal exercise bouts with transitions between the activities. This study investigated the effect of an Olympic distance triathlon (1.5-km swim, 40-km bike, 10-km run) on pulmonary diffusion capacity (DLCO). In nine male triathletes (age: 24 ± 4.7 years), we measured DLCO and calculated the DLCO to alveolar volume ratio (DLCO/VA) and performed spirometry testing before a triathlon (pre-T), 2 hours after the race (post-T), and the day following the race (post-T-24 h). DLCO was measured using the 9-s breath-holding method. We found that (1) DLCO decreased significantly between pre- and post-T values (38.52 ± 5.44 vs. 35.92 ± 6.63 ml∙min-1∙mmHg-1) (p < 0.01) and returned to baseline at post-T-24 h (38.52 ± 5.44 vs. 37.24 ± 6.76 ml∙min-1∙mmHg-1, p > 0.05); (2) DLCO/VA was similar at the pre-, post- and post-T-24 h DLCO comparisons; and (3) forced expiratory volume in the first second (FEV1) and mean forced expiratory flow during the middle half of vital capacity (FEF25-75%) significantly decreased between pre- and post-T and between pre- and post-T-24-h (p < 0.02). In conclusion, a significant reduction in DLCO and DLCO/VA 2 hours after the triathlon suggests the presence of pulmonary interstitial oedema. Both values returned to baseline 24 hours after the race, which reflects possible mild and transient pulmonary oedema with minimal physiological significance.

The effect of an Olympic distance triathlon on the respiratory muscle strength and endurance in triathletes.

High-intensity exercise, marathons, and long distances triathlons have been shown to induce the fatigue of respiratory muscles (RMs). Never-theless, fatigue and the recovery period have not been studied in re-sponse of an Olympic distance triathlon (1.5-km swim, 40-km bike, 10-km run: short-distance triathlon). The aim of this study was to evaluate the RM fatigue induced by an Olympic distance triathlon. Nine male triath-letes (24±1.1 years) underwent spirometric testing and the assessment of RM performance. Respiratory function tests were conducted in sit-ting position. Spirometric parameters, maximal inspiratory and expirato-ry pressures, and RM endurance assessed by measuring the time limit were evaluated before (pre-T), after (post-T), and the day following the triathlon (post-T-24 hr). Residual volume increased: pre-T vs. post-T (P<0.002), maximal inspiratory pressure significantly decreased from 127.4±17.2 (pre-T) to 121.6±18.5 cmH2O (post-T) (P<0.001) and returned to the pre-T value 24 hr after the race (125.0±18.6). RM endurance sig-nificantly decreased from 4:51±0:8 (pre-T) to 3:13±0:7 min (post-T, P< 0.001) and then remained decreased for 24 hr after the race from 4:51± 0:8 (pre-T) to 3:39±0:4 min 24 hr after (P<0.002). Both, strength and en-durance of inspiratory muscles decrease after Olympic distance triath-lon. Furthermore, the impaired of inspiratory muscle endurance 24 hr after the race suggested a slow recovery and persistence of inspiratory muscle fatigue.

Aggravation of pulmonary diffusing capacity in highly trained athletes by 6 weeks of low-volume, low-intensity training.

PURPOSE: Postexercise alveolar-capillary membrane-diffusing capacity (DLco) often decreases in highly trained endurance athletes and seems linked to their training status. To test the hypothesis that training status influences postexercise DLco, 13 male and 2 female triathletes (20.2 ± 4.4 y old, 175.2 ± 6.7 cm tall; weight in a range of 66.6 ± 7.4 kg to 67.4 ± 7.8 kg during the 1-y study) were randomized into experimental (n = 7) and control (n = 8) groups and performed VO(2max) cycle tests and simulated cycle-run successions (CR) of 30 min + 20 min after 3 periods in the competitive season. METHODS: Both groups were tested before (pre- HTP) and after a 30-wk high-training period (HTP) with high training volume, intensity, and frequency. The experimental group was then also tested after a 6-wk low-training period (LTP) with low training volume, intensity, and frequency, while the control group continued training according to the HTP schedule for these 6 wk. Ventilatory data were collected continuously. DLco testing was performed before and 30, 60, and 120 min after the CR trials. RESULTS: Whatever the period or group, DLco was significantly decreased 30 min after CR, with a significantly greater decrease in the experimental group than the control group in LTP (-15.7% and -9.3% of DLco, respectively). CONCLUSIONS: Six weeks of low training volume and intensity were sufficient to reverse the effects of high training volume and intensity on the alveolar-capillary membrane after a CR succession in competitive triathletes.

Cycling performance following adaptation to two protocols of acutely intermittent hypoxia.

PURPOSE: Adaptation to acutely intermittent hypoxic exposure appears to produce worthwhile enhancements in endurance performance, but the current 5-min duration of hypoxia and recovery intervals may not be optimal. METHODS: Eighteen male competitive cyclists and triathletes were randomized to one of two intermittent-hypoxia groups, and nine similar athletes represented a control group. Athletes in the hypoxia groups were exposed to 60 min per day of intermittent hypoxia consisting of alternating intervals of hypoxia and normoxia lasting either 3 or 5 min. Exposures were performed at rest for 5 consecutive days per week for 3 wk. Oxygen saturation, monitored with pulse oximetry, was reduced progressively from 90% (day 1) to 76% (day 15). All athletes maintained their usual competitive-season training throughout the study. Incremental and repeated-sprint tests were performed pre, 3 d post, and 14 d postintervention. Venous blood at rest was sampled pre, mid-, and postintervention. RESULTS: There were no clear differences between effects of the two hypoxic treatments on performance or various measures of oxygen transport, hematopoiesis, and inflammation. Compared with control, the combined hypoxic groups showed clear enhancements in peak power (4.7%; 90% confidence limits, +/-3.1%), lactate-profile power (4.4%; +/-3.0%), and heart-rate profile power (6.5%; +/-5.3%) at 3 d postintervention, but at 14 d the effects were unclear. Changes in other measures at 3 and 14 d postintervention were either unclear or unremarkable. CONCLUSION: Acutely intermittent hypoxia produced substantial enhancement in endurance performance, but the relative benefit of 3- vs 5-min exposure intervals remains unclear.

Influence of performance level on exercise-induced arterial hypoxemia during prolonged and successive exercise in triathletes.

PURPOSE: To study the relationship between performance and exercise-induced arterial hypoxemia (EIAH), 5 internationally ranked (INT) and 8 regionally ranked (REG) triathletes performed cycle-run successions (CR) and control runs (R) in competition-like conditions: at approximately 75% VO2max. METHODS: Ventilatory parameters and oxyhemoglobin saturation (SpO2) data were collected continuously. Arteriolized partial pressure in O2 (PaO2) and alveolar ventilation (VA) were measured before and after cycling (CRcycle), the successive run (CRrun), and R. Pulmonary diffusing capacity (DLco) was measured at rest and 10 minutes post-CR. Training and short-distance triathlon data were collected. RESULTS: INT showed significantly greater experience than REG in competition years (P>.05), training regimen (P>.05), and swimming (P>.05), and cycling (P>.05) volumes; running showed a trend (P<.06). Cycling, running, and total triathlon performances were significantly higher in INT than REG (P>.01). SpO2 during CR dropped significantly more in INT than in REG. Both groups showed significant inverse correlations between the magnitude of the SpO2 change from CRcycle to CRrun and the triathlon running time (r=-0.784; P<.05 and r=-0.699; P<.05; respectively). When compared with CRcycle, PaO2 significantly decreased and VA significantly increased after CRrun and R in both groups (P<.01). DLco significantly dropped between pre- and postexercise in CR and R with no between-group difference (P<.05). CONCLUSIONS: EIAH was aggravated in higher performers during simulated cycle-run segments, related to longer experience and heavier training regimens. Possibly, relative hypoventilation caused this aggravated EIAH in INT, although pulmonary diffusion limitation was observed in both groups. Beyond EIAH severity, the magnitude of SpO2 variations during the cycle-run transition may affect triathlon running performance.

Effects of the order of running and cycling of similar intensity and duration on pulmonary diffusing capacity in triathletes.

To study the pathophysiological mechanisms involved in the decrease of post-triathlon diffusing capacity (DLco), blood rheologic properties (blood viscosity: eta(b); changes in plasma volume: deltaPV) and atrial natriuretic factor (ANF) were assessed in ten triathletes during cycle-run (CR) and run-cycle (RC) trials at a metabolic intensity of 75% of maximal oxygen consumption ( VO(2max)). The DLco was measured before and 10 min after trials. ANF and deltaPV were measured at rest, after the cycle and run of CR and RC trials, and at the end of and 10 min after exercise. RC led to a greater deltaDLco decrease, a lower ANF concentration and a lower deltaPV than did CR, whereas for both CR and RC eta(b) was increased throughout exercise and 10 min after. In addition, after CR the deltaDLco decrease was inversely correlated ( r=-0.764; P<0.01) with deltaPV. The association of decreased plasma volume, increased eta(b), and lower ANF concentrations after RC suggested that lower blood pulmonary volume may have caused the greater decrease in Dlco as compared with CR. The inverse correlation between deltaPV and deltaDLco reinforces the hypothesis that fluid shifts limit the post-exercise DLco decrease after the CR succession in triathletes. Lastly, cycling in the crouched position might increase intra-thoracic pressure, decrease thorax volume due to the forearm position on the handlebars, and weaken peripheral muscular pump efficacy, all of which would limit venous return to the heart, and thus result in low pulmonary blood volume. Compared with cycling, running appeared to induce the opposite effects.