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.     

Cardiac responses to exercise in competitive child cyclists

PURPOSE: Cardiovascular responses to exercise in highly trained child endurance athletes have not been well-defined. This study compared hemodynamic responses with progressive cycle exercise in seven competitive child cyclists (mean age 11.9 yr) compared with 39 age-matched untrained boys. METHODS: Doppler echocardiography and gas exchange variables were utilized to assess cardiovascular changes during submaximal and maximal exercise. RESULTS: Mean VO2max was 60.0 (+/-6.0) and 47.0 (+/-5.8) mL x kg(-1) x min(-1) in the cyclists and nonathletes, respectively. At rest and maximal exercise, the cyclists demonstrated greater stroke index than the untrained subjects (resting mean 59 (+/-6) vs 44 (+/-9) mL x m(-2); maximal mean 76 (+/-6) vs 60 (+/-11) mL x m(-2)), but the ratio of maximal:rest stroke index was similar in both groups (1.31 for cyclists, 1.41 for nonathletes). Both groups showed a plateau in stroke volume beyond low-intensity work levels. No significant difference was observed in maximal arteriovenous oxygen difference. CONCLUSIONS: These findings indicate that 1) maximal stroke volume is the critical determinant of the high VO2max in child cyclists and 2) factors that influence resting stroke volume are important in defining VO2max differences between child endurance athletes and untrained boys.     

Accuracy of pulse oximetry during exercise stress testing.

Pulse oximetry is used extensively during exercise stress-testing in the clinical and sports medicine settings. There are few validation studies to assess the appropriateness of using pulse oximetry under conditions of potentially compromised peripheral blood flow. To study the accuracy of pulse oximetry during severe exercise stress, 10 athletes undertook 3 bouts of exhaustive exercise; once at an intensity requiring VO2max (max), once at 115% of VO2max (Smax), and once at Smax while FIO2 was increased to 0.30. The results indicate relatively large underestimations occur when pulse oximetry is used to estimate %SaO2 during exercise, when compared to the criterion samples of gas analysis in arterial blood. These differences were exacerbated as the exercise intensity increased from a mean(+/- SE) difference of 2.9 +/- 0.7 %SaO2 at max to 4.6 +/- 0.7 %SaO2 at Smax. Breathing a higher FIO2 reversed the hypoxemia that occurred during the normoxic exercise, however, pulse oximetry measurements failed to detect this alteration in %SaO2. Estimates of oxygen saturation during severe exercise using pulse oximetry should be viewed with caution, as potentially large errors may occur.     

Prevalence of exercise-induced arterial hypoxemia in healthy women

PURPOSE: Exercise-induced arterial hypoxemia (EIAH) is reported to occur in approximately 50% of highly trained male endurance athletes. Few studies have examined EIAH in women and the prevalence remains unclear. It has been reported that some female subjects who develop EIAH possess maximal oxygen consumption (VO2max) values that are within 15% of their predicted value. This is unique to women, where EIAH has generally been reported in men who have a high VO2max. The primary objective of this investigation was to determine the prevalence of EIAH in a large female population with a wide range of VO2max values. It was hypothesized that EIAH would occur with a greater prevalence and at relatively lower predicted VO2max than that previously reported in males. METHODS: Young women (N = 52; 26.5 +/- 4.9 yr) performed a cycle test to exhaustion to determine VO2max, and oxyhemoglobin saturation (SaO2) was monitored via pulse oximetry. All subjects were tested during the early follicular phase of their menstrual cycle. A >/= 4% drop in SaO2 represented EIAH. RESULTS: Values for VO2max were variable (VO2max range: 28.0-61.3 mL x kg(-1) x min(-1)). EIAH was present in 67% of the women with N = 19 displaying mild EIAH (92-94%SaO2) and N = 16 displaying moderate EIAH (87-91%SaO2). CONCLUSION: It appears that the prevalence of EIAH in women is slightly greater than the 50% prevalence value that is typically reported for highly fit men.     

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.     

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.     

Specific inspiratory muscle training in well-trained endurance athletes

PURPOSE: It has been reported that arterial O2 desaturation occurs during maximal aerobic exercise in elite endurance athletes and that it might be associated with respiratory muscle fatigue and relative hypoventilation. We hypothesized that specific inspiratory muscle training (SIMT) will result in improvement in respiratory muscle function and thereupon in aerobic capacity in well-trained endurance athletes. METHODS: Twenty well-trained endurance athletes volunteered to the study and were randomized into two groups: 10 athletes comprised the training group and received SIMT, and 10 athletes were assigned to a control group and received sham training. Inspiratory training was performed using a threshold inspiratory muscle trainer, for 0.5 h x d(-1) six times a week for 10 wk. Subjects in the control group received sham training with the same device, but with no resistance. RESULTS: Inspiratory muscle strength (PImax) increased significantly from 142.2 +/- 24.8 to 177.2 +/- 32.9 cm H2O (P < 0.005) in the training but remained unchanged in the control group. Inspiratory muscle endurance (PmPeak) also increased significantly, from 121.6 +/- 13.7 to 154.4 +/- 22.1 cm H2O (P < 0.005), in the training group, but not in the control group. The improvement in the inspiratory muscle performance in the training group was not associated with improvement in peak VEmax, VO2max breathing reserve (BR). or arterial O2 saturation (%SaO2), measured during or at the peak of the exercise test. CONCLUSIONS: It may be concluded that 10 wk of SIMT can increase the inspiratory muscle performance in well-trained athletes. However, this increase was not associated with improvement in aerobic capacity, as determined by VO2max, or in arterial O2 desaturation during maximal graded exercise challenge. The significance of such results is uncertain and further studies are needed to elucidate the role of respiratory muscle training in the improvement of aerobic-type exercise capacity.     

Whole‐body fat oxidation determined by graded exercise and indirect calorimetry: a role for muscle oxidative capacity?

During whole-body exercise, peak fat oxidation occurs at a moderate intensity. This study investigated whole-body peak fat oxidation in untrained and trained subjects, and the presence of a relation between skeletal muscle oxidative enzyme activity and whole-body peak fat oxidation. Healthy male subjects were recruited and categorized into an untrained (N=8, VO(2max) 3.5+/-0.1 L/min) and a trained (N=8, VO(2max) 4.6+/-0.2 L/min) group. Subjects performed a graded exercise test commencing at 60 W for 8 min followed by 35 W increments every 3 min. On a separate day, muscle biopsies were obtained from vastus lateralis and a 3 h bicycle exercise test was performed at 58% of VO(2max). Whole-body fat oxidation was calculated during prolonged and graded exercise from the respiratory exchange ratio using standard indirect calorimetry equations. Based on the graded exercise test, whole-body peak fat oxidation was determined. The body composition was determined by DEXA. Whole-body peak fat oxidation (250+/-25 and 462+/-33 mg/min) was higher (P<0.05) and occurred at a higher (P<0.05) relative workload (43.5+/-1.8% and 49.9+/-1.2% VO(2max)) in trained compared with untrained subjects, respectively. Muscle citrate synthase activity and beta-hydroxy-acyl-CoA-dehydrogenase activity were higher (49% and 35%, respectively, P<0.05) in trained compared with untrained subjects. Both lean body mass and maximal oxygen uptake were significantly correlated to whole-body peak fat oxidation (r(2)=0.57, P<0.001), but leg muscle oxidative capacity was not correlated to whole-body peak fat oxidation. In conclusion, whole-body peak fat oxidation occurred at a higher relative exercise load in trained compared with untrained subjects. Whole-body peak fat oxidation was not significantly related to leg muscle oxidative capacity, but was related to lean body mass and maximal oxygen uptake. This may suggest that leg muscle oxidative activity is not the main determinant of whole-body peak fat oxidation.     

Ventilatory threshold and work efficiency on a bicycle and paddling ergometer in top canoeists.

The purpose of this investigation was to determine the effect of increasing specific (paddling ergometer) and non-specific (bicycle ergometer) work load on the parameters at the ventilatory threshold (VT) and on work efficiency (WE) during increasing exercise ergometry. When highly trained male canoeists were given an unspecific exercise load, the values of %VO2max at VT were close to the values characteristic for an untrained population (72.3 +/- 5.3% VO2max). When the same subjects were given a specific work load, they produced values typical for highly trained athletes (83.4 +/- 2.5% VO2max). Non-specific exercise produced WE values close to those of untrained subjects on the bicycle ergometer (23.3 +/- 2.1%), and when loading is specific, the groups of working muscles are smaller, producing lower WE values (14.7 +/- 3.5%). It was concluded that the responses to submaximal exercise intensities in the case of nonspecific loading suggests caution in the interpretation of physiological variables which may be sensitive to training status. The assessment of VT and WE as supplementary characteristics during laboratory measurements, enables us, along with other parameters, to ascertain not only the effectiveness of the training process used, but also the specificity of a loading apparatus.     

Circulating white blood cells affect red cell pulmonary transit times in endurance athletes during intense exercise

PURPOSE: The aim of this study was to determine the relationship between the right-to-left ventricular red cell pulmonary transit times (PTT) during intense exercise and circulating white blood cell (WBC) counts in highly trained endurance athletes. We postulated that high levels of WBCs preexercise would slow PTT. Eleven endurance-trained athletes (VO2max = 69.6 +/- 7.7 mL.kg-1.min-1; weight = 75.0 +/- 6.2 kg; height = 181.0 +/- 7.1 cm) performed 6.5 min constant-load, near-maximal cycling exercise (approximately 92% VO2max) on two different days. Preexercise WBC counts were measured in arterial blood drawn from the radial artery 30 min before exercise. PTT was measured during the 3rd min of exercise by first-pass radionuclide cardiography using centroid and deconvolution analysis, whereas cardiac output (Q) was measured during the last 2.5 min of exercise via a count-based ratio method from the MUGA technique. RESULTS: Combined mean PTT from both deconvolution and centroid analysis at minute three of exercise was 2.45 +/- 0.21 s, whereas the preexercise WBC count was 5.3 +/- 1.6 x 109.L-1. Cardiopulmonary blood volume at minute three of exercise was 1.22 +/- 0.13 L, VO2 was 4.58 +/- 0.44 L.min-1, and Q was 30.2 +/- 4.2 L.min-1. We found that PTT was negatively correlated with circulating WBC (r = -0.61; adjusted r2 = 0.30; P = 0.04; N = 11) but not with the dispersion (spread) of transit times around the mean (r = 0.19; P = 0.57). CONCLUSION: This suggests that athletes with higher circulating numbers of WBCs preexercise have faster (shorter) red cell transit times through the lung during intense exercise.     

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.     

Beta-endorphin time course response to intensity of exercise: effect of training status

The concentration of beta-endorphin (B-EP) was measured in 6 trained and 6 untrained cyclists during three intensities of exercise to determine the time course changes of B-EP. B-EP was determined by radioimmunoassay with less than 5% cross reactivity with beta-lipotrophin. A counter-balanced design was used to avoid an order effect from exercise intensity. Resting B-EP values were similar across visits. There were no differences in resting B-EP values comparing the trained (4.61 +/- 0.25 pmol.l-1) to the untrained (4.03 +/- 0.23 pmol.l-1) group. Cycling at 60% VO2max did not increase B-EP in either group at any time measured. Cycling at 70% VO2max increased B-EP by 10 min in both groups p less than 0.05. The rate and magnitude of increase of B-EP were similar for both groups. B-EP changes at 80% VO2max were significantly greater that at 70% VO2max and were identical for the two groups. Both groups demonstrated increases by 5 min and further increases at 30 min of exercise p less than 0.01. These changes occurred despite the fact that lactate levels were lower in the trained group at both 70 and 80% VO2max intensities. It is concluded that the time course change for B-EP is similar for trained and untrained individuals working at the same relative intensity of exercise and does not seem to be related to plasma lactate concentrations.     

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.     

Re-examination of the incidence of exercise-induced hypoxaemia in highly trained subjects.

The purpose of this study was to examine the occurrence of exercise-induced hypoxaemia (EIH) during maximal exercise in highly trained athletes. Eleven trained cyclists (mean(s.d.) age 23(3.5) years; mean(s.d.) VO2max 66.9(4.8) ml kg-1min-1) performed a continuous, multistage (270 kpm min-1) cycle ergometer test to exhaustion. Measurements of arterial oxygen-haemoglobin saturation (%HbO2) were obtained simultaneously at rest, every 2 min during exercise, and at maximum exercise capacity from arterial blood sampling (%SaO2) and ear oximetry (%SpO2). Exercise induced hypoxaemia (%HbO2 < or = 91%) was present in 64% of the athletes examined when EIH was determined using pulse oximetry, whereas none of the subjects exhibited EIH when %HbO2 was determined using arterial blood. At rest the values for %HbO2 were similar with mean(s.d.) %SaO2 being 97.3(0.6)% and mean(s.d.) %SpO2 being 96.5(1.6)%. During exercise, statistically significant differences were found for %HbO2 between arterial blood and ear oximetry at the 6-min, 8-min, and maximal exercise sampling times (repeated measures analysis of variance, P < 0.05). The results indicate that ear oximetry overestimates the incidence of EIH and underestimates the oxyhaemoglobin saturation in highly trained cyclists during exercise in comparison with those measurements made from arterial blood.     

Effects of a proposed challenge on effort sense and cardiorespiratory responses during exercise.

PURPOSE: Highly trained endurance athletes train and race at relatively high intensities and are often confronted with challenges throughout a running event. The purpose of this study was to examine the effects of the anticipation of a proposed challenge on effort sense, heart rate (HR), ventilation ([dotVE), and ventilatory equivalent VE/VO2), a measure of ventilatory efficiency. METHODS: Highly trained endurance athletes (VO2max = 68.46 +/- 1.47 mL x kg(-1) x min(-1) ran two sessions at approximately 75% of VO2max for 35 min in a control condition and a proposed challenge condition. During the control condition, the subjects ran on a treadmill while simultaneously viewing a video depicting a runner exercising at 75% of VO2max and were told the run would continue at a speed that elicited 75% of VO2max. During the proposed challenge condition, subjects completed the same exercise protocol but viewed a video of a struggling runner and were told that the treadmill speed would be increased to "an extremely difficult" 95% of VO2max matching the intensity of the runner on the video. However, after data assessment at 17 min, subjects were told that the treadmill was malfunctioning and the treadmill speed could not be altered. The same intensity was maintained in both conditions. RPE, HR, VE, and VE/VO2 were assessed during the treadmill runs at 10, 17, 25, and 35 min. RESULTS: The effects of the manipulation were represented by a significant increase in state anxiety immediately following the video proposing the 95% challenge. RPE, HR, and VE increased similarly under both conditions, while VE/VO2 did not change. CONCLUSION: These findings suggest that for highly trained endurance athletes, anticipation of proposed challenge during running does not influence cardiorespiratory responses; thus these athletes demonstrate a "physiologically toughened" response.     

Exercise-induced hypoxaemia in highly trained athletes

Traditionally, the pulmonary system has not been considered the limiting factor in determining maximal oxygen uptake (VO2max) in healthy individuals since arterial oxygen-haemoglobin saturation is thought to remain high during intense exercise. However, there appears to be a major exception to this rule. Recent evidence suggests that arterial hypoxaemia results during heavy exercise in well trained individuals with a high VO2max. Further, the degree of arterial desaturation is inversely related to VO2max. This exercise-induced hypoxaemia does not appear to be due to hypoventilation although athletes who have limited hyperventilation seem to exhibit the lowest arterial oxygen-haemoglobin saturation. A significant venoarterial shunt has been ruled out as a primary cause of the hypoxaemia based on both experimental and theoretical considerations. Therefore, it appears that the exercise-induced hypoxaemia seen in highly trained athletes during heavy exercise is primarily due to diffusion limitations and ventillation-perfusion inequality. It is postulated that incomplete diffusion in the healthy lung may be due to a rapid red blood cell transit time through the pulmonary capillary. In summary, recent findings suggest that the limits of the human pulmonary system may be reached or even exceeded during intense exercise in some individuals. In light of these findings the role of the pulmonary system as a limiting factor during maximal exercise in the highly trained endurance athlete warrants further investigation.     

Physiological profile of handball players

BACKGROUND: The purpose of this study was to determine the physiological profile of handball players compared to sprinters, endurance trained and untrained subjects. METHODS: Forty-six subjects aged between 19 and 28 years took part in this study: 10 were national handball players (NHB); 7 were international handball players (IHB), 11 were sprint trained subjects (ST); 8 were endurance trained subjects (ET); and 10 were untrained subjects (UT). They performed an incremental treadmill test to determine the maximal oxygen uptake (VO2max), and a Wingate anaerobic test (WanT) to determine maximal power (Wmax). Plasma lactate (La) concentration was measured 5 minutes after the end of the Wingate-test. RESULTS: The VO2max of NHB was similar to that of the IHB and ST athletes but higher than that of the untrained and lower than the endurance trained athletes. Values for Wmax were similar in the IHB and NHB groups and very close to the sprinters. When normalized for body mass or to lean body mass, Wmax was greater in handball players when compared to untrained or endurance trained subjects. Lactate values were in the same range in the NHB, IHB and ST groups and were statistically higher in the NHB and IHB groups than in the UT or ET groups. CONCLUSIONS: The results suggest that the anaerobic metabolism seems to be important for the handball players similarly to sprinters. Since handball is known as a sport with typically short exercise periods of high intensity alternating with rests, anaerobic metabolism appears then to be higbly relevant to performance.     

Reevaluation of contribution of physical fitness, body weight, and different sports activity to resting blood pressure in young men

The purposes of the present study were to evaluate the relationship between resting blood pressure and maximal oxygen uptake (VO2max) and to elucidate the association of different types of sports activity on the resting blood pressure in Japanese young men with a wide range of VO2max. The subjects (n = 46) consisted of untrained subjects (n = 24), judo athletes (n = 11), and triathletes (n = 11) aged 21 to 35 years. Systolic (SBP) and diastolic (DBP) blood pressures were measured in the sitting position after 5 min of resting, and VO2max was directly measured by the Douglas bag method. SBP, DBP, and mean blood pressure (MBP) were negatively correlated with VO2max and positively correlated with body weight. A stepwise selective multiple regression analysis for SBP resulted in two significantly correlating variables: VO2max and body weight. For DBP and MBP, the analysis resulted in two explaining variables: VO2max and body weight. Two independent variables explained 37% of the variation of the SBP, 43% of that of DBP, and 54% of that of MBP. These results indicate that variance in resting blood pressure is partly accounted for by the variance in endurance capacity (i.e., VO2max). However, SBP, DBP, and MBP were significantly higher in judo athletes compared with untrained men (P less than 0.05) when it was compared with the same range of VO2max. These results indicate that resting blood pressure is probably influenced with VO2max, while the relationship is influenced by the type and intensity of training and other factors.     

Improved insulin sensitivity in carbohydrate and lipid metabolism after physical training

To estimate physical training effects quantitatively, the relationship between tissue sensitivity to exogenous insulin (glucose metabolism determined by euglycemic insulin-clamp technique) and maximal oxygen uptake (VO2 max) was defined in 9 well-trained athletes and 14 untrained subjects with normal glucose tolerance. Tissue sensitivity to exogenous insulin in the athletes was significantly higher than in the controls (P less than 0.001). Seven untrained subjects continued the physical exercise program. After physical training for 1 month, glucose metabolism increased from 40.3 +/- 3.9 mumol/kg/min to 42.2 +/- 4.4 mumol/kg/min (P less than 0.05) and VO2 max also increased significantly (P less than 0.05). During euglycemic hyperinsulinemia, both plasma FFA (P less than 0.001) and glycerol (P less than 0.05) decreased rapidly after physical training. Glucose metabolism directly correlated with VO2 max (P less than 0.001). These results suggest that the euglycemic insulin-clamp technique provides a reliable estimate of training effects, tissue sensitivity to physiologic hyperinsulinemia is 46% higher in trained athletes, and physical training improves insulin sensitivity not only in glucose metabolism but also in lipid metabolism.     

Effect of exercise-induced arterial O2 desaturation on VO2max in women

PURPOSE: We have recently reported that many healthy habitually active women experience exercise induced arterial hypoxemia (EIAH). We questioned whether EIAH affected VO2max in this population and whether the effect was similar to that reported in men. METHODS: Twenty-five healthy young women with widely varying fitness levels (VO2max, 56.7 +/- 1.5 mL x kg(-1) x min(-1); range: 41-70 mL x kg(-1) x min(-1)) and normal resting lung function performed two randomized incremental treadmill tests to VO2max (FIO2: 0.21 or 0.26) during the follicular phase of their menstrual cycle. Arterial blood samples were taken at rest and near the end of each workload during the normoxic test. RESULTS: During room air breathing at VO2max, SaO2 decreased to 91.8 +/- 0.4% (range 87-95%). With 0.26 FIO2, SaO2, at VO2max remained near resting levels and averaged 96.8 +/- 0.1% (range 96-98%). When arterial O2 desaturation was prevented via increased FIO2, VO2max increased in 22 of the 25 subjects and in proportion to the degree of arterial O2 desaturation experienced in normoxia (r = 0.88). The improvement in VO2max when systemic normoxia was maintained averaged 6.3 +/- 0.3% (range 0 to +15%) and the slope of the relationship was approximately 2% increase in VO2max for every 1% decrement in the arterial oxygen saturation below resting values. About 75% of the increase in VO2max resulted from an increase in VO2 at a fixed maximal work rate and exercise duration, and the remainder resulted from an increase in maximal work rate. CONCLUSIONS: These data demonstrate that even small amounts of EIAH (i.e., >3% delta SaO2 below rest) have a significant detrimental effect on VO2max in habitually active women with a wide range of VO2max. In combination with our previous findings documenting EIAH in females, we propose that inadequate pulmonary structure/function in many habitually active women serves as a primary limiting factor in maximal O2 transport and utilization during maximal exercise.