Oxidative stress in athletes during extreme endurance exercise

Despite the many known health benefits of exercise, there is a body of evidence suggesting that endurance exercise is associated with oxidative stress. To determine whether extreme endurance exercise induces lipid peroxidation, 11 athletes (3 females, 8 males) were studied during a 50 km ultramarathon (trial 1) and during a sedentary protocol (trial 2) 1 month later. The evening before each trial, with dinner, subjects consumed 75 mg each d(3)-RRR and d(6)-all rac-alpha-tocopheryl acetates. Blood was obtained at baseline, 30 min pre-race, mid-race, post-race, 1 h post-race, 24 h post-race, and at corresponding times during trial 2. All 11 subjects completed the race; average run time was 391 +/- 23 min. Plasma F(2)-isoprostanes increased from 75 +/- 7 pg/ml at pre-race to 131 +/- 17 (p <.02) at post-race, then returned to baseline at 24 h post-race; F(2)-isoprostanes were unchanged during trial 2. Deuterated alpha-tocopherol disappearance rates were faster (2.8 x 10(-4) +/- 0.2 x 10(-4)) during the race compared to the sedentary trial (2.3 x 10(-4) +/- 0.2 x 10(-4); p <.03). These data suggest that extreme endurance exercise results in the generation of lipid peroxidation with a concomitant increase in vitamin E disappearance.     

Validity of pulse oximetry during exercise in elite endurance athletes.

Eleven highly trained male cyclists [maximal aerobic power (VO2max) = 70.6 +/- 4.2 ml.kg-1.min-1] performed both high intensity constant load (90-95% VO2max) and incremental cycle exercise tests with arterial blood sampling to evaluate the accuracy of pulse oximeter estimates (%SpO2) of arterial oxyhemoglobin fraction of total hemoglobin (%HbO2). Three subjects also performed an incremental exercise test in hypoxic conditions (inspired partial pressure of O2 = 89, 93, or 100 Torr). Arterial %HbO2 was determined via CO-oximetry and ranged from 72 to 99%. Three Ohmeda 3740 pulse oximeters were used to estimate %HbO2, one on each ear lobe and a finger probe. The finger probe tended to provide the best estimate of %HbO2 during exercise: the mean %SpO2 - %HbO2 difference for 232 exercise observations was 0.52 +/- 1.36% (SD). Finger probe %SpO2 and %HbO2 were highly correlated [r = 0.98, standard error of the estimate (SEE) = 1.32%, P less than 0.0001]. The accuracy of pulse oximeters has been questioned during high-intensity exercise. When aerobic power was greater than 81% of VO2max (n = 75), the finger probe's mean error was -0.01 +/- 1.40%. Finger probe %SpO2 and %HbO2 were highly correlated (r = 0.97, SEE = 1.32%, P less than 0.0001). These results indicate that this pulse oximeter is a valid predictor of %HbO2 in elite athletes during cycle exercise.     

A hemodynamic comparison of young and older endurance athletes during exercise

This study assessed the hemodynamic responses to exercise of master athletes (56 +/- 5 yr of age) who placed in the top 10% of their age groups in local 10-km competitive events, competitive young runners (26 +/- 3 yr), young runners matched in training and performance to the master athletes (25 +/- 3 yr), and healthy older sedentary subjects (58 +/- 5 yr). The maximal O2 consumption (VO2max) of the master athletes was 9 and 19% lower than that of the matched young and competitive young runners, respectively. When compared at the same relative submaximal work rates, these three groups had similar stroke volumes and arteriovenous O2 (aVO2) differences, though the master athletes had lower VO2, cardiac output, and heart rate, and higher vascular resistance. The older sedentary group had a lower stroke volume, aVO2 difference, and higher vascular resistance than the master athletes. Maximal stroke volume and estimated aVO2 difference were the same in the three groups of athletes; the lower maximal heart rate of the master athletes appears to account for their lower VO2max. The older sedentary subjects' VO2max was 47% lower than that of the master athletes; this difference was almost equally the result of a lower stroke volume and a lower a-VO2 difference. Thus these older athletes did not exhibit the decline in maximum stroke volume and aVO2 difference that occurs with aging in sedentary individuals; they also appear to have retained a greater peripheral vasodilatory response than their sedentary peers.     

Sustained maximal ventilation after endurance exercise in athletes

Although impaired respiratory muscle performance that persists up to 5 min after exercise is stopped has been demonstrated during exhaustive exercise in normal young men, it is not known whether impaired respiratory muscle function follows endurance exercise to exhaustion in highly trained athletes. To study the effects of exercise on sustained maximal voluntary ventilation immediately after exercise, eight elite cross-country skiers performed a 4-min maximal sustained ventilation (MSV) test before and immediately after exhaustive exercise. Subjects were encouraged to maintain maximal ventilation (VE) throughout the MSV test. To encourage greater effort, rapid visual feedback of VE was provided on a computer terminal along with a target VE based on their 12-s maximum voluntary ventilation (MVV). The subjects (7 males, 1 female) were 18.5 +/- 0.9 yr old (mean +/- SD) and exercised for 62.5 +/- 16.7 min at 77 +/- 5% of their maximum oxygen consumption during which average VE was 106.7 +/- 24.2 l/min BTPS. The mean MVV was 196.0 +/- 29.9 l/min or 107% of their age- and height-predicted MVV. Before exercise the MSV was 86% of the MVV or 176.7 +/- 30.5 l/min, whereas after exercise the MSV was 90% of the MVV or 180.3 +/- 28.9 l/min (P = NS). The total volume of gas expired during the 4-min MSV was 706.7 +/- 121.9 liters before and 721.2 +/- 115.5 liters after exercise (P = NS). In this group of athletes, exhaustive exercise produced no deleterious effects on the ability to perform a 4-min MSV test immediately after exercise.     

Expiratory threshold loading impairs cardiovascular function in health and chronic heart failure during submaximal exercise.

We determined the effects of augmented expiratory intrathoracic pressure (P(ITP)) production on cardiac output (Q(TOT)) and blood flow distribution in healthy dogs and dogs with chronic heart failure (CHF). From a control expiratory P(ITP) excursion of 7 +/- 2 cmH2O, the application of 5, 10, or 15 cmH2O expiratory threshold loads increased the expiratory P(ITP) excursion by 47 +/- 23, 67 +/- 32, and 118 +/- 18% (P < 0.05 for all). Stroke volume (SV) rapidly decreased (onset <10 s) with increases in the expiratory P(ITP) excursion (-2.1 +/- 0.5%, -2.4 +/- 0.9%, and -3.6 +/- 0.7%, P < 0.05), with slightly smaller reductions in Q(TOT) (0.8 +/- 0.6, 1.0 +/- 1.1, and 1.8 +/- 0.8%, P < 0.05) owing to small increases in heart rate. Both Q(TOT) and SV were restored to control levels when the inspiratory P(ITP) excursion was augmented by the addition of an inspiratory resistive load during 15 cmH2O expiratory threshold loading. The highest level of expiratory loading significantly reduced hindlimb blood flow by -5 +/- 2% owing to significant reductions in vascular conductance (-7 +/- 2%). After the induction of CHF by 6 wk of rapid cardiac pacing at 210 beats/min, the expiratory P(ITP) excursions during nonloaded breathing were not significantly changed (8 +/- 2 cmH2O), and the application of 5, 10, and 15 cmH2O expiratory threshold loads increased the expiratory P(ITP) excursion by 15 +/- 7, 23 +/- 7, and 31 +/- 7%, respectively (P < 0.05 for all). Both 10 and 15 cmH2O expiratory threshold loads significantly reduced SV (-3.5 +/- 0.7 and -4.2 +/- 0.7%, respectively) and Q(TOT) (-1.7 +/- 0.4 and -2.5 +/- 0.4%, P < 0.05) after the induction of CHF, with the reductions in SV predominantly occurring during inspiration. However, the augmentation of the inspiratory P(ITP) excursion now elicited further decreases in SV and Q(TOT). Only the highest level of expiratory loading significantly reduced hindlimb blood flow (-4 +/- 2%) as a result of significant reductions in vascular conductance (-5 +/- 2%). We conclude that increases in expiratory P(ITP) production-similar to those observed during severe expiratory flow limitation-reduce cardiac output and hindlimb blood flow during submaximal exercise in health and CHF.     

Mechanical constraints on exercise hyperpnea in endurance athletes.

We determined how close highly trained athletes [n = 8; maximal oxygen consumption (VO2max) = 73 +/- 1 ml.kg-1.min-1] came to their mechanical limits for generating expiratory airflow and inspiratory pleural pressure during maximal short-term exercise. Mechanical limits to expiratory flow were assessed at rest by measuring, over a range of lung volumes, the pleural pressures beyond which no further increases in flow rate are observed (Pmaxe). The capacity to generate inspiratory pressure (Pcapi) was also measured at rest over a range of lung volumes and flow rates. During progressive exercise, tidal pleural pressure-volume loops were measured and plotted relative to Pmaxe and Pcapi at the measured end-expiratory lung volume. During maximal exercise, expiratory flow limitation was reached over 27-76% of tidal volume, peak tidal inspiratory pressure reached an average of 89% of Pcapi, and end-inspiratory lung volume averaged 86% of total lung capacity. Mechanical limits to ventilation (VE) were generally reached coincident with the achievement of VO2max; the greater the ventilatory response, the greater was the degree of mechanical limitation. Mean arterial blood gases measured during maximal exercise showed a moderate hyperventilation (arterial PCO2 = 35.8 Torr, alveolar PO2 = 110 Torr), a widened alveolar-to-arterial gas pressure difference (32 Torr), and variable degrees of hypoxemia (arterial PO2 = 78 Torr, range 65-83 Torr). Increasing the stimulus to breathe during maximal exercise by inducing either hypercapnia (end-tidal PCO2 = 65 Torr) or hypoxemia (saturation = 75%) failed to increase VE, inspiratory pressure, or expiratory pressure. We conclude that during maximal exercise, highly trained individuals often reach the mechanical limits of the lung and respiratory muscle for producing alveolar ventilation. This level of ventilation is achieved at a considerable metabolic cost but with a mechanically optimal pattern of breathing and respiratory muscle recruitment and without sacrifice of a significant alveolar hyperventilation.     

Carbon dioxide storage capacity of endurance and sprint-trained athletes in exercise

The purpose of this study was to compare CO2 storage capacity of endurance and sprint-trained athletes during steady state exercise. Ten subjects, five sprinters and five distance runners, performed a submaximal treadmill exercise at two different work rates, 45% and 65% of VO2max. CO2 storage capacity was determined by measuring the excess CO2 washout associated with hyperventilation, normalized for body weight and expressed per unit change in mixed venous PCO2 (ml kg-1 Torr-1). Mixed venous PCO2 (PvCO2) was measured by rebreathing equilibration. It was found that CO2 storage capacities of the runners were significantly (P less than 0.05) greater than the sprinters at the two work rates. The sprinters CO2 storage capacities were 2.69 and 2.14 ml kg-1 Torr-1 at low and high work rates, respectively. The corresponding mean values for the runners were 4.56 and 3.92 ml kg-1 Torr-1, respectively. These results may be explained by the metabolic differences between the sprinters and runners. The sprinters' musculature depends more heavily on the glycolytic metabolic pathway, which is associated with an increased lactate production and hence a reduction in the combining power of the blood for CO2 during exercise. At the low work rate, the body's storage capacity for CO2 was significantly (P less than 0.05) greater than the higher work rate for both groups. Obviously, at the higher work level more blood would be presented to the lungs per unit time allowing an increase in CO2 clearance from the body stores.     

Protein metabolism during endurance exercise

After reviewing all the available results from our laboratory and numerous reports in the literature concerning changes that have occurred in various aspects of protein metabolism during exercise, a number of conclusions can be drawn with some degree of confidence. During exercise, protein synthesis is depressed and this change leaves amino acids available for catabolic processes. The rate of leucine oxidation appears to be increased during exercise, and there is a movement of amino acids, mostly in the form of alanine, from muscle to liver where the rate of gluconeogenesis is increased as a result of exercise. These changes in protein metabolism are probably physiologically significant in at least three ways: amino acid conversion to citric acid cycle intermediates enhances the rate of oxidation of acetyl-CoA generated from glucose and fatty acid oxidation; increased conversion of amino acids to glucose helps to prevent hypoglycemia; oxidation of some amino acids may provide energy for muscular contraction.     

Hypohydration impairs endurance exercise performance in temperate but not cold air.

This study compared the effects of hypohydration (HYP) on endurance exercise performance in temperate and cold air environments. On four occasions, six men and two women (age = 24 +/- 6 yr, height = 170 +/- 6 cm, weight = 72.9 +/- 11.1 kg, peak O2 consumption = 48 +/- 9 ml.kg(-1).min(-1)) were exposed to 3 h of passive heat stress (45 degrees C) in the early morning with [euhydration (EUH)] or without (HYP; 3% body mass) fluid replacement. Later in the day, subjects sat in a cold (2 degrees C) or temperate (20 degrees C) environment with minimal clothing for 1 h before performing 30 min of cycle ergometry at 50% peak O2 consumption followed immediately by a 30-min performance time trial. Rectal and mean skin temperatures, heart rate, and ratings of perceived exertion measurements were made at regular intervals. Performance was assessed by the total amount of work (kJ) completed in the 30-min time trial. Skin temperature was significantly lower in the cold compared with the temperate trial, but there was no independent effect of hydration. Rectal temperature in both HYP trials was higher than EUH after 60 min of exercise, but the difference was only significant within the temperate trials (P < 0.05). Heart rate was significantly higher at 30 min within the temperate trial (HYP > EUH) and at 60 min within the cold trial (HYP > EUH) (P < 0.05). Ratings of perceived exertion increased over time with no differences among trials. Total work performed during the 30-min time trial was not influenced by environment but was less (P < 0.05) for HYP than EUH in the temperate trials. The corresponding change in performance (EUH-HYP) was greater for temperate (-8%) than for cold (-3%) (P < 0.05). These data demonstrate that 1) HYP impairs endurance exercise performance in temperate but not cold air but 2) cold stress per se does not.     

Incidence of exercise induced hypoxemia in elite endurance athletes at sea level

Recent evidence suggests that exercise-induced hypoxemia (EIH) may occur in healthy trained endurance athletes. However, at present, no data exist to describe the regularity of EIH in athletes or non-athletes. Therefore, the purpose of the present investigation was to determine the incidence of EIH during exercise in healthy subjects varying in physical fitness. Subjects (N = 68) performed an incremental cycle ergometer test to volitional fatigue with percent arterial oxyhemoglobin saturation (%SaO2) measured min-by-min. For the purpose of data analysis subjects were divided into three groups according to their level of physical training: 1) untrained (N = 16), 2) moderately trained (N = 27), and 3) elite highly trained endurance athletes (N = 25). EIH was defined as a %SaO2 of less than or equal to 91% during exercise. EIH did not occur in any of the untrained subjects or the moderately trained subjects. However, EIH occurred in 52% of the highly trained endurance athletes tested and was highly reproducible (r = 0.95; P less than 0.05). These findings further confirm the existence of EIH in healthy highly trained endurance athletes and suggests a rather high incidence of EIH in this healthy population. Hence, it is important that the clinician or physiologist performing exercise testing in elite endurance athletes recognize that EIH can and does occur in the elite endurance athlete in the absence of lung disease.     

The effects of progressive exercise on cardiovascular function in elite athletes: focus on oxidative stress

Some side-effects of excessive physical training are ascribed to reactive oxygen species production. In this work we investigated the effects of progressively imposed maximal physical effort (levels I to V), using progressive maximal exercise test, on peripheral blood lactate, NO (through NO2-), superoxide anion (O2-) and methemoglobin (MetHb) in a group of 19 elite soccer players. Blood lactate (mmol/L) was increased (4.55, level V vs. resting level, 1.95). The basal production of NO2- was in the direct relation with O2 consumption. Significant increase (p<0.05) in O2- values at effort level I (4.18) as compared to the resting value (4.01), and the significant increase (p<0.01 or p<0.05) in the MetHb (%) was found between II (18.79) and III (19.63) or between II and IV (19.24) effort levels, respectively. The regression lines of NO2- and O2- crossed at the level of the respiratory compensation point (RC), suggesting that RC could be of a crucial importance not only in the anaerobic and aerobic metabolism but in mechanisms of signal transductions as well. The results could be of the theoretical interest and also useful in designing an athlete training strategy.     

Force-velocity relationship and stretch-shortening cycle function in sprint and endurance athletes

This study examined the torque-velocity and power-velocity relationships of quadriceps muscle function, stretch shortening cycle function, and leg-spring stiffness in sprint and endurance athletes. Isokinetic maximal knee extension torque was obtained from 7 sprinters and 7 endurance athletes using a Con-trex isokinetic dynamometer. Torque and power measures were corrected for lean-thigh cross-sectional area and lean-thigh volume, respectively. Stretch-shortening cycle function and muscle stiffness measurements were obtained while subjects performed single-legged squat, countermovement, and drop-rebound jumps on an inclined sledge and force-plate apparatus. The results indicated that sprinters generated, on average, 0.15 +/- 0.05 N.m.cm(-2) more torque across all velocities compared with endurance athletes. Significant differences were also found in the power-velocity relationships between the 2 groups. The sprinters performed significantly better than the endurance athletes on all jumps, but there were no differences in prestretch augmentation between the groups. The average vertical leg stiffness during drop jumps was significantly higher for sprinters (5.86 N.m(-1)) compared with endurance runners (3.38 N.m(-1)). The findings reinforce the need for power training to be carried out at fast contraction speeds but also show that SSC function remains important in endurance running.     

Effects of exhaustive submaximal exercise on cardiovascular function during sleep

The influence of an afternoon bout of exhaustive submaximal exercise on cardiovascular function and catecholamine excretion during sleep was examined in five female and four male subjects. Subjects walked on a treadmill for successive 50-min periods at 50, 60, and 70% maximal O2 consumption, separated by 10-min rest periods. Exercise terminated with volitional exhaustion. Following an adaptation night, electroencephalographic and impedance cardiographic measures were obtained during three successive nights of sleep, with exercise preceding night 3. Relative to the base-line night (night 2), exhaustive exercise resulted in a sustained elevation of heart rate and cardiac output throughout the entire night's sleep. The magnitude of these elevations was unaffected by sleep stage but decreased over the night. The typical pattern of circadian decline in cardiac output was unaltered. However, the decline in heart rate with sleep onset was greater on the exercise night. Changes in impedance dZ/dt and R-Z interval suggested an enhanced myocardial contractility during the first 3 h of sleep postexercise. Analysis of morning urine samples revealed that in seven of nine subjects norepinephrine excretion increased, epinephrine excretion decreased, and dopamine excretion was unchanged during sleep on the exercise night. It is suggested that these cardiac changes reflect a sustained increase in myocardial beta-receptor activity.     

Substrate utilization during endurance exercise in men and women after endurance training

We investigated the effect of endurance training on whole body substrate, glucose, and glycerol utilization during 90 min of exercise at 60% peak O2 consumption (VO2(peak)) in males and females. Substrate oxidation was determined before and after 7 wk of endurance training on a cycle ergometer, with posttesting performed at the same absolute (ABS, W) and relative (REL, VO2(peak)) intensities. [6,6-2H]glucose and [1,1,2,3,3-2H]glycerol tracers were used to calculate the respective substrate tracee flux. Endurance training resulted in an increase in VO2(peak) for both males and females of 17 and 22%, respectively (P < 0.001). Females demonstrated a lower respiratory exchange ratio (RER) both pretraining and posttraining compared with males during exercise (P < 0.001). Glucose rate of appearance (R(a)) and rate of disappearance (R(d)) were not different between males and females. Glucose metabolic clearance rate (MCR) was lower at 75 and 90 min of exercise for females compared with males (P < 0.05). Glucose R(a) and R(d) were lower during exercise at both ABS and REL posttraining exercise intensities compared with pretraining (P < 0.001). Females had a higher exercise glycerol R(a) and R(d) compared with males both pre- and posttraining (P < 0.001). Glycerol R(a) was not different at either the ABS or REL posttraining exercise intensities compared with pretraining. We concluded that females oxidize proportionately more lipid and less carbohydrate during exercise compared with males both pre- and posttraining, which was cotemporal with a higher glycerol R(a) in females. Furthermore, endurance training resulted in a decrease in glucose flux at both ABS and REL exercise intensities after endurance exercise training.     

Determinants of time trial performance and maximal incremental exercise in highly trained endurance athletes

Human endurance performance can be predicted from maximal oxygen consumption (Vo(2max)), lactate threshold, and exercise efficiency. These physiological parameters, however, are not wholly exclusive from one another, and their interplay is complex. Accordingly, we sought to identify more specific measurements explaining the range of performance among athletes. Out of 150 separate variables we identified 10 principal factors responsible for hematological, cardiovascular, respiratory, musculoskeletal, and neurological variation in 16 highly trained cyclists. These principal factors were then correlated with a 26-km time trial and test of maximal incremental power output. Average power output during the 26-km time trial was attributed to, in order of importance, oxidative phosphorylation capacity of the vastus lateralis muscle (P = 0.0005), steady-state submaximal blood lactate concentrations (P = 0.0017), and maximal leg oxygenation (sO(2LEG)) (P = 0.0295), accounting for 78% of the variation in time trial performance. Variability in maximal power output, on the other hand, was attributed to total body hemoglobin mass (Hb(mass); P = 0.0038), Vo(2max) (P = 0.0213), and sO(2LEG) (P = 0.0463). In conclusion, 1) skeletal muscle oxidative capacity is the primary predictor of time trial performance in highly trained cyclists; 2) the strongest predictor for maximal incremental power output is Hb(mass); and 3) overall exercise performance (time trial performance + maximal incremental power output) correlates most strongly to measures regarding the capability for oxygen transport, high Vo(2max) and Hb(mass), in addition to measures of oxygen utilization, maximal oxidative phosphorylation, and electron transport system capacities in the skeletal muscle.     

Reproductive function in male endurance athletes: sperm analysis and hormonal profile

Lucía, Alejandro, José L. Chicharro, MargaritaPérez, Luis Serratosa, Fernando Bandrés, and Julio C. Legido. Reproductive function in male endurance athletes: spermanalysis and hormonal profile. J. Appl.Physiol. 81(6): 2627-2636, 1996.The purpose ofthis investigation was to study the effects of endurance exercise onmale reproductive function (sex hormones and seminograms). Professionalcyclists [n = 12; mean age 24 ± 2 (SD) yr], elite triathletes(n = 9; 26 ± 3 yr),recreational marathon runners (n = 10;32 ± 6 yr), and sedentary subjects (control group;n = 9; 30 ± 4 yr) were selected assubjects. For each group, the following parameters were measured threetimes during the sports season (training period: winter; competitionperiod: spring; resting period: fall): percentage of body fat, hormonalprofile (resting levels of follicle-stimulating hormone, luteinizinghormone, total and free testosterone, and cortisol), and seminograms(quantitative parameters: sperm volume and sperm count; qualitativeparameters: sperm motility and morphology). The following comparisonswere made in the measured parameters:1) within groups (longitudinal design) and 2) between groups ineach of the three periods (cross-sectional design) and over time (mixeddesign). In addition, both the volume and the intensity of training ofeach subject during the season (except for the control group) werequantified. Despite significant differences in training characteristicsand in body fat percent, in general no significant differences(P > 0.05) were found in hormonalprofiles or in semen characteristics between or within groups. A lowersperm motility (46.2 ± 19.5%), however, was observed in thecyclists during the competition period when compared either with theother groups during this same period(P < 0.05) or with themselves duringthe other two periods of study (P < 0.01). In any case, the later phenomenon was attributed to physicalfactors associated with cycling, such as mechanical trauma to thetestis and/or increased gonadal temperature. In conclusion, ourfindings suggest that endurance exercise does not adversely affect the hypothalamic-pituitary-testis axis.