Evidence for an inadequate hyperventilation inducing arterial hypoxemia at submaximal exercise in all highly trained endurance athletes

PURPOSE: The majority of highly trained endurance athletes with a maximal oxygen uptake greater than 60 mL x min(-1) x kg(-1) develop exercise-induced hypoxemia (EIH). Yet some of them apparently do not. The pathophysiology of EIH seems to be multifactorial, and one explanatory hypothesis is a relative hypoventilation. Nevertheless, conflicting results have been reported concerning its contribution to EIH. The aim of this study was to compare the cardiorespiratory responses to maximal exercise of highly trained endurance athletes demonstrating the same aerobic capacity without EIH (N athletes) and with EIH (H athletes). METHODS: Ten N athletes and twelve H athletes performed an incremental exercise test. Measurements of arterial blood gases and cardiorespiratory parameters were performed at rest and during exercise. RESULTS: All athletes presented a significant decrease in PaO2 (P < 0.05) from rest up to 80% VO2max associated with an increase in PaCO2, both findings consistent with a relative hypoventilation. Then the H athletes, who had a greater training volume per week and a higher second ventilatory threshold than the N athletes (respectively, 17 +/- 1.1 vs 13.1 +/- 0.7 h x wk(-1); 91.8 +/- 1.7 vs 86.1 +/- 1.8% VO2max), presented a continuous PaO2 decrease up to VO2max. This was associated with a widening (Ai-a)DO2. CONCLUSION: This study showed that a relative hypoventilation, probably induced by a high level of endurance training, induced hypoxemia in all athletes. However, a nonventilatory mechanism, perhaps related to the volume of training, seemed to affect gas exchanges beyond the second ventilatory threshold in the H athletes, thereby enhancing EIH.     

Interleukins 1-beta, -8, and histamine increases in highly trained, exercising athletes

PURPOSE: Exercise-induced hypoxemia (EIH) in highly trained athletes is associated with an increase in histamine release (%H) during exercise. Certain cytokines, known as histamine-releasing factors, are capable of interacting with basophils and/or mast cells to cause the release of histamine. The aim of this study was to determine whether the increased histamine release in highly trained athletes is related to a high plasma level in interleukin-1 beta (IL-1beta), IL-3, or IL-8 in arterial blood. METHODS: These parameters were measured in 11 endurance athletes (23.2 +/- 1.2 yr (mean +/- SEM)) known to develop exercise-induced hypoxemia and 11 control subjects (25.0 +/- 1.1 yr) at rest, during an incremental exhaustive exercise test, and at the fifth minute of recovery. RESULTS: Histamine release increased between rest and maximal exercise in the athletes (P < 0.01), showing a strong correlation with EIH (r = 0.76, P < 0.01) and was unchanged in the controls. IL-3 plasma concentration was not altered with training and/or with exercise. Circulating IL-8 levels were not different between trained and untrained subjects at any testing level and increased at maximal exercise in both groups (P < 0.01). IL-1beta plasma levels were higher in athletes than in controls (P < 0.05) at each testing level and increased during exercise only in the athletes (P < 0.05). CONCLUSION: An elevated concentration of IL-1beta in plasma and its association with increased IL-8 levels during exercise may partly explain the increase in %H associated with EIH in highly trained athletes. Histamine, IL-8, and IL-1beta releases during exercise reflect an inflammatory reaction, which is probably involved in EIH.     

Degree of arterial desaturation in normoxia influences VO2max decline in mild hypoxia.

PURPOSE: Elite endurance athletes display varying degrees of pulmonary gas exchange limitations during maximal normoxic exercise and many demonstrate reduced arterial O2 saturations (SaO2) at VO2max--a condition referred to as exercise induced arterial hypoxemia (EIH). We asked whether mild hypoxia would cause significant declines in SaO2 and VO2max in EIH athletes while non-EIH athletes would be unaffected. METHODS: Nineteen highly trained males were divided into EIH (N = 8) or Non-EIH (N = 6) groups based on SaO2 at VO2max (EIH <90%, Non-EIH >92%). Athletes with intermediate SaO2 values (N = 5) were only included in correlational analyses. Two randomized incremental treadmill tests to exhaustion were completed--one in normoxia, one in mild hypoxia (FIO2 = 0.187; approximately 1,000 m). RESULTS: EIH subjects demonstrated a significant decline in VO2max from normoxia to mild hypoxia (71.1+/-5.3 vs. 68.1+/-5.0 mL x kg(-1) min(-1), P<0.01), whereas the non-EIH group did not show a significant deltaVO2max (67.2+/-7.6 vs. 66.2+/-8.4 mL x kg(-1) x min(-1)). For all 19 athletes, SaO2 during maximal exercise in normoxia correlated with the change in VO2max from normoxia to mild hypoxia (r = -0.54, P<0.05). However, the change in SaO2 and arterial O2 content from normoxia to mild hypoxia was equal for both EIH and Non-EIH (deltaSaO2 = 5.2% for both groups), bringing into question the mechanism by which changes in SaO2 affect VO2max in mild hypoxia. CONCLUSIONS: We conclude that athletes who display reduced measures of SaO2 during maximal exercise in normoxia are more susceptible to declines in VO2max in mild hypoxia compared with normoxemic athletes.     

Effet d'un interval-training supra-maximal sur l'apparition d'une hypoxémie d'exercice chez des sportifs non-spécialistes de l'endurance

Highly trained sportsmen and sportswomen in endurance may present exercise-induced hypoxemia (EIH). The aim of this investigation was to determine whether a 8 week interval training period may induced EIH in low trained athletes.Results – After training, in a population of 24 subjects, 7 presented a mild or moderate EIH, 7 presented a light EIH and 10 did not present EIH during a progressive and maximal running test.Conclusion – It seems that after a relative short period of training, EIH may appear in athletes in spite of moderate maximal O₂ consumption.     

Effect of prolonged exercise on arterial oxygen saturation in athletes susceptible to exercise-induced hypoxemia

This study examined the effect of prolonged endurance exercise on the development of exercise-induced hypoxemia (EIH) in athletes who had previously displayed EIH during an incremental maximal exercise test. Five male and three female endurance-trained athletes participated. Susceptibility to EIH was confirmed through a maximal incremental exercise test and defined as a reduction in the saturation of arterial oxygen (SpO(2)) of >/=4% from rest. Sixty minutes of running was conducted, on a separate day, at an oxygen consumption corresponding to 95% of ventilatory threshold. Immediately following the 60 min exercise bout, athletes commenced a time trial to exhaustion at 95% maximal oxygen consumption (VO(2max)). The reduction in SpO(2) was significantly greater during the maximal incremental test, than during the 60 min, or time trial to exhaustion (-8.8+/-1.4%, -3.3+/-1.1%, and -4.1+/-2.3%, P<0.05, respectively). The degree of desaturation during the 60 min was significantly related to the relative intensity of exercise at 95% ventilatory threshold (adjusted r(2)=0.54, P=0.02). In conclusion, athletes who did not exercise at greater than 73% VO(2max) during 60 min of endurance exercise did not display EIH, despite being previously susceptible during an incremental maximal test.     

Effects of successive running and cycling on the release of atrial natriuretic factor in highly trained triathletes

AIM: To evaluate the influence of successive running and cycling on both exercise-induced arterial hypoxemia (EIAH) and atrial natriuretic factor (ANF) release, 5 triathletes performed 2 separate exercise trials. METHODS: One trial consisted of a 20-min+20-min successive cycle-run exercise (C(1)-R(2)) and the other consisted of a 20-min+20-min successive run-cycle exercise (R(1)-C(2)). Arterial oxygenation (PaO(2)) and ANF were determined at pre-exercise, at the end of each 20-min segment of exercise and after 10 min of recovery. RESULTS: EIAH was noted during C(1)-R(2) and R(1)-C(2) trials. A higher EIAH was observed during running compared with cycling performed in the 1(st) position (R(1) vs C(1)) in the succession. In contrast, no difference was observed between successive running and successive cycling (R(2) vs C(2)), (-10.6+/-7.0 vs -15.6+/-4.0 mmHg for C(1)-R(2) and -20.9+/-6.0 vs -16.2+/-2.4 mmHg for R(1)-C(2)). ANF showed no difference between cycling and running performed in first position, whereas a significantly lower ANF was observed during successive cycling compared with successive running (C(2) vs R(2)) (19.9+/-3.72 vs 36.2+/-6.4 pmol.L(-1)). During recovery, neither PaO(2) nor ANF plasma returned to baseline level after either trial. CONCLUSION: This study provides new information on some of the physiological modifications that occur during multi-sports. Specifically, the impact of the modality of the successive exercise on ANF release and body fluid regulation was observed. Cycling as the successive exercise seems to cause lower ANF release than does running.     

Training status (endurance or sprint) and catecholamine response to the Wingate-test in women

The aim of this study was to verify if, as for men, training status induces different catecholamine responses to exercise. To do this, we investigated the effect of training status (sprint or endurance) on plasma catecholamine response to a supramaximal exercise in women. Nineteen subjects took part in our study: six untrained subjects (UT), seven endurance trained subjects (ET) and six sprint trained ones (ST). The trained subjects (ET and ST) were all competing at a high national level. The maximal power (W max ) and the mean power (W) were determined from the Wingate-test. Blood lactate, adrenaline (A) and noradrenaline (NA) were analysed at rest (La 0, A 0 and NA 0 ), immediately at the end of the exercise (A max and NA max ) and after 5 min recovery (La max [3 min in arterialized blood], A 5 and NA 5 ). The disappearance of A and NA was judged by the ratio (A max -A 5 )/A max and (NA max -NA 5 )/NA 5. The ratio A max /NA max was considered as an index of the adrenal medulla responsiveness to the sympathetic nervous activity. As expected, during the Wingate-test ST exhibited significantly higher performances compared to UT and ET. But in contrast to the men's data no difference was observed between the three groups both for La max (13.1 +/- 0.8 mmol x L (-1); 14.8 +/- 1.0 mmol x L (-1) and 11.2 +/- 0.5 mmol x L (-1) respectively for ET, ST and UT), NA max (22.1 +/- 1.2 nmol x L (-1); 13.1 +/- 2.4 nmol x L (-1) and 20.2 +/- 7 nmol x L (-1)respectively for ET, ST and UT) and A max (4.1 +/- 0.8 nmol x L (-1); 2.6 +/- 0.6 nmol x L (-1); 13.1 +/- 0.6 nmol x L (-1) respectively for ET, ST and UT). Consequently the ratio A max /NA max was similar in UT, ET and ST (respectively 0.2 +/- 0.03; 0.2 +/- 0.04; 0.17 +/- 0.04), These results indicated, in contrast to the men's data, that the catecholamine response to the Wingate-test did not differ between female subjects of different status of training. In conclusion this study did not find any significant effect of training status on the catecholamine response to supramaximal exercise and so argues in favour of sex differences in response to training.     

O2 arterial desaturation in endurance athletes increases muscle deoxygenation

PURPOSE: The aim of this study was to compare the muscle deoxygenation measured by near infrared spectroscopy in endurance athletes who presented or not with exercise-induced hypoxemia (EIH) during a maximal incremental test in normoxic conditions. METHODS: Nineteen male endurance sportsmen performed an incremental test on a cycle ergometer to determine maximal oxygen consumption (VO2max) and the corresponding power output (P(max)). Arterial O2 saturation (SaO2) was measured noninvasively with a pulse oxymeter at the earlobe to detect EIH, which was defined as a drop in SaO2 > 4% between rest and the end of the exercise. Muscle deoxygenation of the right vastus lateralis was monitored by near infrared spectroscopy and was expressed in percentage according to the ischemia-hyperemia scale. RESULTS: Ten athletes exhibited arterial hypoxemia (EIH group) and the nine others were nonhypoxemic (NEIH group). Training volume, competition level, VO2max, Pmax, and lactate concentration were similar in the two groups. Nevertheless, muscle deoxygenation at the end of the exercise was significantly greater in the EIH group (P < 0.05). CONCLUSION: Greater muscle deoxygenation at maximal exercise in hypoxemic athletes seems to be due, at least in part, to reduced oxygen delivery--that is, exercise-induced hypoxemia--to working muscle added to the metabolic demand. In addition, our finding is also consistent with the hypothesis of greater muscle oxygen extraction in order to counteract reduced O2 availability.     

Rectal temperature correction overestimates the frequency of exercise-induced hypoxemia

INTRODUCTION: Exercise-induced hypoxemia (EIH) occurs in an uncertain proportion of endurance trained athletes. Whereas blood gas measurements must be corrected for core temperature at the time of sampling, the commonly used rectal temperature readings may not be the most appropriate. METHODS: Ten males [mean peak oxygen uptake, (.-)VO(2peak), 65.4 +/- 7.0 mL x kg x min] performed incremental treadmill exercise from rest to exhaustion with radial artery blood samples collected at the end of each 2-min workload for gas analysis. The thermogenic effect of exercise was monitored with rectal, arterial blood, and esophageal temperature probes, and the values obtained at all three sites, simultaneous with blood sampling, were used to correct the standard blood gas measurements made at 37 +/- C. RESULTS: The mean increase in rectal temperature across exercise (1.4 +/- 0.4 +/- C) was approximately half that recorded in radial arterial blood (2.3 +/- 0.5+/- C) and the esophagus (2.4 +/- 0.5 degrees C). In consequence, the uncorrected fall in PaO2 across exercise of 15.4 +/- 8.2 mm Hg was reduced to 8.4 +/- 7.7 mm Hg when corrected for rectal temperature, and to 2.9 +/- 7.4 and 2.1 +/- 8.8 mm Hg when corrected for arterial blood and esophageal temperatures. Using a fall of > or = 10 mm Hg as the index of EIH, the proportion in the 10 subjects in the present study fell from 80% (uncorrected) through 50% (rectal correction) to 20% (arterial blood and esophageal corrections). CONCLUSION: When correcting arterial blood gas values for the thermogenic effects of exercise, the proportion of athletes meeting the definition of EIH depends on the site of core temperature measurement.     

Is hemoglobin desaturation related to blood viscosity in athletes during exercise?

Several studies have suggested that athletes with low hemoglobin saturation during exercise may experience impaired pulmonary blood gas exchange during maximal exercise. Blood viscosity may be implicated in exercise-induced pulmonary hemorrhage in race horses. We hypothesized that blood rheology may contribute to impaired gas exchange and reduced hemoglobin saturation during exercise in humans. A group of 20 highly trained endurance athletes participated in this study, 9 with low hemoglobin saturation during exercise (Low-SpO (2) group) and 11 with normal hemoglobin saturation (High-SpO (2) group). All subjects performed a progressive exercise test conducted to V.O (2max). Venous blood was sampled at rest, 50 % V.O (2max) and maximal exercise. Blood viscosity (etab) was measured at very high shear rate (1000 s (-1)) and 37 degrees C with a falling ball viscometer. The erythrocyte rigidity coefficient, "Tk", was calculated using the Dintenfass equation. At rest, no significant difference in etab was observed between the two groups (3.00 +/- 0.08 mPa . s vs. 3.01 +/- 0.04 mPa . s for the Low-SpO (2) and High-SpO (2) group, respectively). At 50 % V.O (2max) and maximal exercise, etab was higher in Low-SpO (2) (p < 0.01). Tk decreased in High-SpO (2) (p < 0.01) but remained unchanged in the other group during testing. The greater increase in etab in the Low-SpO (2) group during exercise may therefore have been due to the lack of reduction in Tk. As suggested by previous studies, the greater increase in blood viscosity in athletes with low hemoglobin saturation may lead to vascular shear stress. Whether this could impair the blood gas barrier and result in exercise-induced hypoxemia requires further study.     

Evidence of exercise-induced O2 arterial desaturation in non-elite sportsmen and sportswomen following high-intensity interval-training

The aim of this study was to investigate the development of exercise-induced hypoxemia (EIH defined as an exercise decrease > 4 % in oxygen arterial saturation, i. e. SaO (2) measured with a portable pulse oximeter) in twelve sportsmen and ten sportswomen (18.5 +/- 0.5 years) who were non-elite and not initially engaged in endurance sport or training. They followed a high-intensity interval-training program to improve V.O (2)max for eight weeks. The training running speeds were set at approximately 140 % V.O (2)max running speed up to 100 % 20-m maximal running speed. Pre- and post-training pulmonary gas exchanges and SaO (2) were measured during an incremental running field-test. After the training period, men and women increased their V.O (2)max (p < 0.001) by 10.0 % and 7.8 %, respectively. Nine subjects (seven men and two women) developed EIH. This phenomenon appeared even in sportsmen with low V.O (2)max from 45 ml x min (-1) x kg (-1) and seemed to be associated with inadequate hyperventilation induced by training: because only this hypoxemic group showed 1) a decrease in maximal ventilatory equivalent in O (2) (V.E/V.O (2), p < 0.01) although maximal ventilation increased (p < 0.01) with training, i. e. in EIH-subjects the ventilatory response increased less than the metabolic demand after the training program; 2) a significant relationship between SaO (2) at maximal workload and the matched V.E/V.O (2) (p < 0.05, r = 0.67) which strengthened a relative hypoventilation implication in EIH. In conclusion, in this field investigation the significant decrease in the minimum SaO (2) inducing the development of EIH after high-intensity interval-training indicates that changes in training conditions could be accompanied in approximately 40 % non-endurance sportive subjects by alterations in the degree of arterial oxyhemoglobin desaturation developing during exercise.     

Basophil releasability in young highly trained and older athletes

PURPOSE: Exercise-induced hypoxemia in highly trained athletes is associated with an increase in histamine release during exercise. The cells most implicated in blood histamine release are basophils. The aim of this study was to determine whether high-level endurance training induces modifications in histamine releasability from human basophils. METHODS: Seven young highly trained athletes (YA) [aged 26.1+/-1.3 yr (mean +/- SEM)] and seven master athletes (MA) (64.4+/-4.1 yr), all known to develop exercise-induced hypoxemia, were respectively compared with seven young untrained men (YC) (23.0+/-1.5 yr) and seven older untrained men (OC) (61.6+/-1.3 yr). During an incremental exhaustive exercise, blood samples for measurement of anti-IgE-induced histamine release from leukocytes were drawn at rest, VO2max, and recovery. RESULTS: Basophils from "leukocyte-rich" supernatant in YA and MA showed significantly higher histamine release induced by anti-IgE (1 microg x mL(-1) than, respectively, YC (P<0.01) and OC (P<0.05) at rest, VO2ax (P<0.01), and recovery (P<0.01). Basophils in YA and MA also showed a histamine release induced by anti-IgE that was higher at VO2max than at rest (respectively. P<0.01 and P<0.05), but this change was not found in the control groups. CONCLUSION: In conclusion, the basophils in highly trained endurance athletes, both young and older, showed higher anti-IgE-induced histamine release than those of untrained men. This effect of high-level training seemed to be potentiated by exercise.     

Chronic L-arginine supplementation enhances endurance exercise tolerance in heart failure patients

The purpose of the study was to determine the potential beneficial effect of six weeks oral L-arginine supplementation (LAS) on endurance exercise, an important determinant of daily-life activity in patients with chronic stable heart failure (CHF). After an initial incremental maximal exercise test, CHF patients performed an identical thirty-minute interval endurance exercise test before and after six weeks with (L-arginine group; ARG) or without LAS (control group; CTL). Hemodynamic, respiratory, and metabolic parameters were determined at rest, during exercise, and during recovery. Mean heart rate decreased throughout exercise and recovery after LAS (- 8.2 +/- 1.4 b x min(-1); p = 0.003 and - 6.7 +/- 1.6 b x min(-1); p < 0.001, respectively), systemic blood pressure and respiratory parameters remaining unchanged. Resting L-argininaemia increased from 102 +/- 11 to 181 +/- 37 micromol x l(-1) (p < 0.004) and exercise-induced peak increase in plasma lactate was blunted after LAS (4.13 +/- 0.75 vs. 3.13 +/- 0.39 mmol x l(-1); p = 0.02). No significant change was observed in the control group. In heart failure patients, six weeks oral LAS enhances endurance exercise tolerance, reducing both heart rate and circulating lactates. This suggests that chronic LAS might be useful as a therapeutic adjuvant in order to improve the patient's physical fitness.     

N-acetylcysteine attenuates oxidative burst by neutrophils in response to ergometer rowing with no effect on pulmonary gas exchange.

This study evaluated whether the reduction of the neutrophil oxidative burst by N-acetylcysteine improves pulmonary gas exchange during a six minute maximal ergometer row. Healthy trained oarsmen were double-blinded randomized to either N-acetylcysteine (6 g daily for three days) or placebo groups. As determined by the relative changes of the zymosan-stimulated luminol-enhanced chemiluminescence response, N-acetylcysteine suppressed the exercise-induced enhanced neutrophil oxidative burst response to rowing (-7 +/- 6% vs. 17 +/- 8%; P < 0.05). This was the case although the concentration of neutrophils remained similarly elevated above the pre-exercise level in both trials (to 5.4+/-0.5 vs. 5.9+/-0.6 x 10(9) cells x l(-1), respectively, P>0.05). In the placebo and N-acetylcysteine groups, pulmonary ventilation increased and the arterial CO2 partial pressure decreased to the same extent during exercise. Also, at the end of exercise the arterial O2 partial pressure (77 1 vs. 78+/-1 mmHg), haemoglobin O2 saturation (92 +/- 1% vs. 93 +/- 1%) and O2 uptake (5.0 +/- 0.2 vs. 4.9 +/- 0.21 x min(-1)) were not significantly affected by N-acetylcysteine. Equally, two hours after exercise, the pulmonary diffusion capacity was reduced by 7 +/- 2% below the pre-exercise with no significant influence of N-acetylcysteine. We conclude that the neutrophil oxidative burst to exercise does not influence pulmonary gas exchange during and after maximal rowing.     

Exercise-induced arterial hypoxemia is not different during cycling and running in triathletes

This study examined the effect of running and cycling on exercise-induced arterial hypoxemia (EIAH) in individuals well trained in each modality. Thirteen male triathletes (X+/-SD: age=36+/-5 years, mass=69+/-8 kg, body fat=12+/-1%) performed progressive exercise to exhaustion during cycle ergometry and treadmill running. Gas exchange was determined, while oxyhemoglobin saturation (SaO(2)) was measured with an ear oximeter. At maximal exercise, the respiratory exchange ratio (1.15+/-0.06 vs. 1.10+/-0.05) and the ventilatory equivalent for oxygen uptake (37.6+/-3.8 vs. 34.2+/-2.7) were greater during cycling vs. running (P<0.05). However, there were no differences at maximal exercise in oxygen uptake (64.4+/-3.2 vs. 67.0+/-4.6 mL kg(-1) min(-1)), SaO(2) (93.4+/-2.8% vs. 92.6+/-2.2%), or the ventilatory equivalent for carbon dioxide (V(E)/VCO(2); 33.1+/-3.1 vs. 31.0+/-3.1), during cycling vs. running, respectively. During submaximal exercise, the V(E)/VCO(2) was less for cycling (26.0+/-1.0) compared with running (29.1+/-0.4; P<0.05), but this had no apparent effect on the SaO(2) response. In conclusion, EIAH was not significantly different during cycling and running in athletes who were well trained in both exercise modalities.     

Individual differences in self-reported heat tolerance. Is there a link to the cardiocirculatory, thermoregulatory and hormonal response to endurance exercise in heat?

AIM: Tolerance to exercise in heat exhibits great interindividual variability. We questioned whether individual differences in self-reported heat tolerance within a group of endurance trained athletes are linked to the cardiocirculatory, thermoregulatory and hormonal response to endurance exercise in heat. METHODS: Using a rating scale to assess the individual degree of tolerance to exercise in heat we allocated 12 non-heat-acclimated trained runners into two groups of 5 highly heat tolerant (HHT) and 7 less heat tolerant (LHT) athletes. Both groups performed a 60-min treadmill run (velocity 90% of individual anaerobic threshold, room temperature and humidity 28 inverted exclamation mark C and 50%, respectively). RESULTS: Sweating rate did not differ between HHT (mean +/- SEM: 0.44+/-0.02) and LHT (0.40+/-0.02 ml x kg(-1) x min(-1)). Compared to LHT, exercise-induced rises in core temperature (39.3+/-0.2/40.0+/-0.2 inverted exclamation mark C), heart rate, plasma norepinephrine and cortisol were significantly lower in HHT, while epinephrine did not exhibit differences between the groups. In contrast, response of human growth hormone (hGH) was significantly more pronounced in HHT. CONCLUSION: Our initial results, obtained in a small group of endurance-trained runners, show that self-reported tolerance to exercise in heat is associated with an attenuated rise in body core temperature during prolonged exercise under elevated ambient temperatures. This finding in heat tolerant athletes is paralleled by a lower stress response as reflected by lower rises in heart rate and stress hormones such as norepinephrine and cortisol. The functional significance (i.e. with respect to sweating function) of the more pronounced response of hGH in heat tolerant athletes warrants further research.     

Does exercise training alter myocardial creatine kinase MB isoenzyme content?

Skeletal muscle biopsies from highly trained endurance athletes have been shown to contain an increased percentage of the creatine kinase MB (CK-MB) isoenzyme, which has been attributed to continuous regeneration of the skeletal muscle fibers in response to exercise-induced injury. The purpose of this study was to determine whether myocardium undergoes a similar degenerative-regenerative process as a result of exercise training. Fifteen mongrel dogs underwent a 12-wk period of training (N = 8) or cage confinement (N = 7). The animals were then sacrificed, and samples of left and right ventricular myocardium were analyzed for total CK activity and CK-MB isoenzyme content. Percentages of CK-MB were slightly but insignificantly higher from both ventricles of exercise-trained as compared with cage-confined dogs: left ventricle, 4.6 +/- 0.6% vs 3.3 +/- 0.6%, respectively (P = 0.15); right ventricle, 4.0 +/- 0.4% vs 3.0 +/- 0.8%, respectively (P = 0.29). We conclude that chronic exercise training does not induce physiologically important degenerative changes in myocardium.     

Exercise-induced arterial hypoxaemia in athletes: a review

During exercise, healthy individuals are able to maintain arterial oxygenation, whereas highly-trained endurance athletes may exhibit an exercise-induced arterial hypoxaemia (EIAH) that seems to reflect a gas exchange abnormality. The effects of EIAH are currently debated, and different hypotheses have been proposed to explain its pathophysiology. For moderate exercise, it appears that a relative hypoventilation induced by endurance training is involved. For high-intensity exercise, ventilation/perfusion (V(A)/Q) mismatching and/or diffusion limitation are thought to occur. The causes of this diffusion limitation are still under debate, with hypotheses being capillary blood volume changes and interstitial pulmonary oedema. Moreover, histamine is released during exercise in individuals exhibiting EIAH, and questions persist as to its relationship with EIAH and its contribution to interstitial pulmonary oedema. Further investigations are needed to better understand the mechanisms involved and to determine the long term consequences of repetitive hypoxaemia in highly trained endurance athletes.     

Expiratory flow limitation confounds ventilatory response during exercise in athletes

INTRODUCTION: A significant number of highly trained endurance runners have been observed to display an inadequate hyperventilatory response to intense exercise. Two potential mechanisms include low ventilatory responsiveness to hypoxia and ventilatory limitation as a result of maximum expiratory flow rates being achieved. PURPOSE: To test the hypothesis that expiratory flow limitation can complicate determination of ventilatory responsiveness during exercise the following study was performed. METHODS/MATERIALS: Sixteen elite male runners were categorized based on expiratory flow limitation observed in flow volume loops collected during the final minute of progressive exercise to exhaustion. Eight flow limited (FL) (VO2max, 75.9+/-2.4 mL x kg(-1) x min(-1); expiratory flow limitation, 47.3+/-20.4%) and eight non-flow limited subjects (NFL) (VO2max, 75.6+/-4.8 mL x kg(-1) x min(-1); expiratory flow limitation, 0.3+/-0.8%) were tested for hypoxic ventilatory responsiveness (HVR). RESULTS: Independent groups ANOVA revealed no significant differences between FL and NFL for VO2max, VE max (136.2+/-16.0 vs 137.5+/-21.6 L x min(-1)), VE/VO2, (28.4+/-3.2 vs 27.6+/-2.9 L x lO2(-1)), VE/VCO2 (24.8+/-3.1 vs 24.4+/-2.0 L x lCO2(-1)), HVR (0.2+/-0.2 vs 0.3+/-0.1 L x %SaO2(-1)), or SaO2 at max (89.1+/-2.4 vs 86.6+/-4.1%). A significant relationship was observed between HVR and SaO2 (r = 0.92, P < or = 0.001) in NFL that was not present in FL. Conversely, a significant relationship between VE/VO2 and SaO2 (r = 0.79, P < or = 0.019) was observed in FL but not NFL. Regression analysis indicated that the HVR-SaO2 and SaO2-VE/VO2 relationships differed between groups. DISCUSSION: When flow limitation is controlled for, HVR plays a more significant role in determining SaO2 in highly trained athletes than has been previously suggested.     

Erythropoiesis and performance after two weeks of living high and training low in well trained triathletes

The purpose of our study was to evaluate hematologic acclimatization during 2 weeks of intensive normoxic training with regeneration at moderate altitude (living high-training low, LHTL) and its effects on sea-level performance in well trained athletes compared to another group of equally trained athletes under control conditions (living low - training low, CONTROL). Twenty-one triathletes were ascribed either to LHTL (n = 11; age: 23.0 +/- 4.3 yrs; VO 2 max: 62.5 +/- 9.7 [ml x min -1 x kg -1]) living at 1956 m of altitude or to CONTROL (n = 10; age: 18.7 +/- 5.6 yrs; VO 2 max: 60.5 +/- 6.7 ml x min -1 x kg -1) living at 800 m. Both groups performed an equal training schedule at 800 m. VO 2 max, endurance performance, erythropoietin in serum, hemoglobin mass (Hb tot, CO-rebreathing method) and hematological quantities were measured. A tendency to improved performance in LHTL after the camp was not significant (p < 0.07). Erythropoietin concentration increased temporarily in LHTL (Delta 14.3 +/- 8.7 mU x ml -1; p < 0.012). Hb tot remained unchanged in LHTL whereas was slightly decreased from 12.5 +/- 1.3 to 11.9 +/- 1.3g x kg -1 in CONTROL (p < 0.01). As the reticulocyte number tended to higher values in LHTL than in CONTROL, it seems that a moderate stimulation of erythropoiesis during regeneration at altitude served as a compensation for an exercise-induced destruction of red cells.