Anaerobic capacity determined by maximal accumulated O2 deficit

We present a method for quantifying the anaerobic capacity based on determination of the maximal accumulated O2 deficit. The accumulated O2 deficit was determined for 11 subjects during 5 exhausting bouts of treadmill running lasting from 15 s to greater than 4 min. The accumulated O2 deficit increased with the duration for exhausting bouts lasting up to 2 min, but a leveling off was found for bouts lasting 2 min or more. Between-subject variation in the maximal accumulated O2 deficit ranged from 52 to 90 ml/kg. During exhausting exercise while subjects inspired air with reduced O2 content (O2 fraction = 13.5%), the maximal O2 uptake was 22% lower, whereas the accumulated O2 deficit remained unchanged. The precision of the method is 3 ml/kg. The method is based on estimation of the O2 demand by extrapolating the linear relationship between treadmill speed and O2 uptake at submaximal intensities. The slopes, which reflect running economy, varied by 16% between subjects, and the relationships had to be determined individually. This can be done either by measuring the O2 uptake at a minimum of 10 different submaximal intensities or by two measurements close to the maximal O2 uptake and by making use of a common Y-intercept of 5 ml.kg-1.min-1. By using these individual relationships the maximal accumulated O2 deficit, which appears to be a direct quantitative expression of the anaerobic capacity, can be calculated after measuring the O2 uptake during one exhausting bout of exercise lasting 2-3 min.     

An alternative method to determine maximal accumulated O2 deficit in runners

An accepted measure of anaerobic capacity is the maximal O2 deficit. But it is not feasible to use O2 deficit if > or =10 submaximal runs are needed to extrapolate the O2 demand of high velocity running (Medb? et al. 1988). Recently, an alternative method to determine O2 deficit was proposed (Hill 1996) using only results of supramaximal cycle ergometer tests. The purpose of this study was to evaluate this alternative method with data from treadmill tests. Twenty-six runners ran at 95%, 100%, 105%, and 110% of their velocity at VO2max. Times to exhaustion, velocity, and accumulated oxygen uptake (VO2) from each individual's four tests were fit to the following equation using iterative nonlinear regression: accumulated VO2 = (O2 demand x velocity x time)-O2 deficit. The mean value s derived for O2 demand and O2 deficit were 0.198+/-0.031 ml x kg(-1) x m(-1) and 42+/-22 ml x kg(-1). SEE for the parameters were 0.007+/-0.007 ml x kg(-1) x m(-1) and 8+/-10 ml x kg(-1), respectively. Mean R2 was 0.998+/-0.003. It was concluded that O2 deficit can be determined from all-out treadmill tests without the need to perform submaximal tests.     

Oxygen deficit is related to the exercise time to exhaustion at maximal aerobic speed in middle distance runners

The purpose of this study was to show the relationship between oxygen deficit and the time to exhaustion (tlim) at maximal aerobic speed (MAS). The minimum speed that elicits VO(2max) was assumed to be the maximal aerobic speed (MAS). Fourteen subelite male runners (mean (SD: age = 27 +/- 5 yrs: VO(2max) = 68.9 +/- 4.6 ml kg (-1). min ( -1); MAS = 21.5 +/- 1 km h (-1) ) participated in the study. Each subject performed an incremental test to determine and MAS. The subjects ran to exhaustion at velocities corresponding to 100 and 120 % MAS. Oxygen deficit was measured during the period exercise to exhaustion at 120% of MAS and was calculated from the difference between O(2) demand and the accumulated O 2 uptake. The tlim values at 100% MAS were correlated with the values of tlim at 120% MAS (r = 0.52). The results reveal that the oxygen deficit was related to the time to exhaustion at MAS and indicate that the greater the oxygen deficit, the greater the time to exhaustion at MAS. It was also noted that the adjustment of oxygen consumption is related to the oxygen deficit. In other words, the subjects who have an important anaerobic capacity are the most efficient during an exercise time to exhaustion at MAS. The time limit values can be expressed by a linear regression making intervene MAS and anaerobic capacity. This conclusion could be of great interest in the training of middle distance runners.     

High-speed running performance is largely unaffected by hypoxic reductions in aerobic power.

We tested the importance of aerobic metabolism to human running speed directly by altering inspired oxygen concentrations and comparing the maximal speeds attained at different rates of oxygen uptake. Under both normoxic (20.93% O2) and hypoxic (13.00% O2) conditions, four fit adult men completed 15 all-out sprints lasting from 15 to 180 s as well as progressive, discontinuous treadmill tests to determine maximal oxygen uptake and the metabolic cost of steady-state running. Maximal aerobic power was lower by 30% (1.00 +/- 0.15 vs. 0.77 +/- 0.12 ml O2. kg-1. s-1) and sprinting rates of oxygen uptake by 12-25% under hypoxic vs. normoxic conditions while the metabolic cost of submaximal running was the same. Despite reductions in the aerobic energy available for sprinting under hypoxic conditions, our subjects were able to run just as fast for sprints of up to 60 s and nearly as fast for sprints of up to 120 s. This was possible because rates of anaerobic energy release, estimated from oxygen deficits, increased by as much as 18%, and thus compensated for the reductions in aerobic power. We conclude that maximal metabolic power outputs during sprinting are not limited by rates of anaerobic metabolism and that human speed is largely independent of aerobic power during all-out runs of 60 s or less.     

Anaerobic energy provision does not limit Wingate exercise performance in endurance-trained cyclists.

The aim of this study was to evaluate the effects of severe acute hypoxia on exercise performance and metabolism during 30-s Wingate tests. Five endurance- (E) and five sprint- (S) trained track cyclists from the Spanish National Team performed 30-s Wingate tests in normoxia and hypoxia (inspired O(2) fraction = 0.10). Oxygen deficit was estimated from submaximal cycling economy tests by use of a nonlinear model. E cyclists showed higher maximal O(2) uptake than S (72 +/- 1 and 62 +/- 2 ml x kg(-1) x min(-1), P < 0.05). S cyclists achieved higher peak and mean power output, and 33% larger oxygen deficit than E (P < 0.05). During the Wingate test in normoxia, S relied more on anaerobic energy sources than E (P < 0.05); however, S showed a larger fatigue index in both conditions (P < 0.05). Compared with normoxia, hypoxia lowered O(2) uptake by 16% in E and S (P < 0.05). Peak power output, fatigue index, and exercise femoral vein blood lactate concentration were not altered by hypoxia in any group. Endurance cyclists, unlike S, maintained their mean power output in hypoxia by increasing their anaerobic energy production, as shown by 7% greater oxygen deficit and 11% higher postexercise lactate concentration. In conclusion, performance during 30-s Wingate tests in severe acute hypoxia is maintained or barely reduced owing to the enhancement of the anaerobic energy release. The effect of severe acute hypoxia on supramaximal exercise performance depends on training background.     

Effects of training on biochemical and functional properties of rodent neonatal heart

This study was undertaken to determine biochemical and functional (in vivo) adaptations of the rodent neonatal heart in response to a training program of endurance running. Ten day-old rats were progressively trained on a treadmill (final intensity, 21 m/min, 30% grade, 1 h/day) until 75 days of age. The training program induced 14, 57, and 24% increases in relative heart mass, skeletal muscle citrate synthase activity, and whole-body maximal O2 uptake, respectively (P less than 0.05). Cardiac myosin (ATPase) and Ca2+-regulated myofibril ATPase were both reduced by approximately 15% in trained vs. sedentary animals (P less than 0.05). In the majority of trained hearts examined, the myosin isozyme profile reflected an estimated 14 +/- 3% shift toward the V3 or low ATPase isozyme. Left ventricular functional indices during submaximal exercise, derived from a fluid-filled indwelling cannula, indicated that the trained animals maintained similar left ventricular (LV) systolic pressure, LV + the time derivative of pressure, and systemic arterial mean blood pressure compared with their sedentary counterparts. These functional parameters were maintained even though the trained animals performed with lower submaximal exercise heart rate. These findings suggest that maximal exercise capacity can be enhanced in neonatal rats even though the biochemical potential for ATP degradation in the cardiac contractile system is lowered. We speculate that the trend to maintain the myosin isozyme pattern further in the direction of the V3 isozyme in the trained neonatal rat heart may reflect a means to economize cross-bridge cycling while maintaining normal levels of ventricle performance at a given submaximal work load.     

Downhill treadmill running trains the rat spinotrapezius muscle.

There are currently no models of exercise that recruit and train muscles, such as the rat spinotrapezius, that are suitable for transmission intravital microscopic investigation of the microcirculation. Recent experimental evidence supports the concept that running downhill on a motorized treadmill recruits the spinotrapezius muscle of the rat. Based on these results, we tested the hypothesis that 6 wk of downhill running (-14 degrees grade) for 1 h/day, 5 days/wk, at a speed of up to 35 m/min, would 1) increase whole body peak oxygen uptake (Vo(2 peak)), 2) increase spinotrapezius citrate synthase activity, and 3) reduce the fatigability of the spinotrapezius during electrically induced 1-Hz submaximal tetanic contractions. Trained rats (n = 6) elicited a 24% higher Vo(2 peak) (in ml.min(-1).kg(-1): sedentary 58.5 +/- 2.0, trained 72.7 +/- 2.0; P < 0.001) and a 41% greater spinotrapezius citrate synthase activity (in mumol.min(-1).g(-1): sedentary 14.1 +/- 0.7, trained 19.9 +/- 0.9; P < 0.001) compared with sedentary controls (n = 6). In addition, at the end of 15 min of electrical stimulation, trained rats sustained a greater percentage of the initial tension than their sedentary counterparts (control 34.3 +/- 3.1%, trained 59.0 +/- 7.2%; P < 0.05). These results demonstrate that downhill running is successful in promoting training adaptations in the spinotrapezius muscle, including increased oxidative capacity and resistance to fatigue. Since the spinotrapezius muscle is commonly used in studies using intravital microscopy to examine microcirculatory function at rest and during contractions, our results suggest that downhill running is an effective training paradigm that can be used to investigate the mechanisms for improved microcirculatory function following exercise training in health and disease.     

Effect of prolonged running on physiological responses to subsequent exercise

The purpose of this study was to compare metabolic and cardiopulmonary responses for submaximal and maximal exercise performed several days preceding (pre-test) and 45 min after (post-test) 21 miles of high intensity (70% VO2 max) treadmill running. Seven aerobically trained subjects' oxygen uptake, oxygen pulse, respiratory exchange ratio, heart rate, pulmonary ventilation, ventilatory equivalent of oxygen, and blood lactate concentration were determined for exercise during the pre- and post-test sessions. No differences were found for submaximal oxygen uptake, oxygen pulse, pulmonary ventilation and ventilatory equivalent of oxygen between the pre- and post-test values. Generally, submaximal heart rate responses were higher, and respiratory exchange ratio values were lower during the post-test. Reductions of maximal work time (12%), maximal oxygen uptake (6%) and maximal blood lactate concentration (47%) were found during the post-test. Thermal stress and glycogen depletion are possible mechanisms which may be responsible for these observed differences.     

Enhanced oxygen extraction and reduced flow heterogeneity in exercising muscle in endurance-trained men

The aim of this study was to investigate the effects of endurance training on skeletal muscle hemodynamics and oxygen consumption. Seven healthy endurance-trained and seven untrained subjects were studied. Oxygen uptake, blood flow, and blood volume were measured in the quadriceps femoris muscle group by use of positron emission tomography and [15O]O2, [15O]H2O, and [15O]CO during rest and one-legged submaximal intermittent isometric exercise. The oxygen extraction fraction was higher (0.49 +/- 0.14 vs. 0.29 +/- 0.12; P = 0.017) and blood transit time longer (0.6 +/- 0.1 vs. 0.4 +/- 0.1 min; P = 0.04) in the exercising muscle of the trained compared with the untrained subjects. The flow heterogeneity by means of relative dispersion was lower for the exercising muscle in the trained (50 +/- 9%) compared with the untrained subjects (65 +/- 13%, P = 0.025). In conclusion, oxygen extraction is higher, blood transit time longer, and perfusion more homogeneous in endurance-trained subjects compared with untrained subjects at the same workload. These changes may be associated with improved exercise efficiency in the endurance-trained subjects.     

Cardiorespiratory and lactate responses to a 1-hour submaximal running at the lactate threshold

Cardiorespiratory and blood lactate (La) responses to prolonged submaximal running at an intensity relative to lactate threshold (LT) were examined in 15 recreational runners, aged 19 to 32. In test 1 where treadmill speed was progressively incremented by 10-20m/min until exhaustion, oxygen uptake at the LT (VO2 @ LT: 2.34 +/- 0.331/min or 41.6 +/- 5.7 ml/kg/min) and VO2max (3.58 +/- 0.341/min or 63.6 +/- 5.5 ml/kg/min) were measured. In test 2, the subject was required to run on the treadmill for 1 hour at a fixed velocity (Vt) which corresponded to his Vt @ LT. As expected, mean VO2 ranged during the 1-h submaximal running from 2.31 +/- 0.411/min or 63.0 +/- 7.8% VO2max at min 10-20 to 2.52 +/- 0.351/min or 69.2 +/- 6.2% VO2max at min 50-60, both of which were close to VO2 @ LT (65.2 +/- 4.4% VO2max). The slight decrease in blood La was found from min 20 to min 60, and this was accompanied by a parallel decline in respiratory exchange ratio. Shifts in the energy substrate toward a reliance on fat oxidation may occur during the course of 1-h running at Vt @t LT. The small oxygen debt observed after the 1-h running may confirm the assumption that prolonged running at Vt at LT would be performed in an almost fully aerobic steady state. We conclude that prolonged running at Vt @ LT may possibly maximize health-related benefits in the healthy adult.     

Proposed tests for measuring the running velocity at the oxygen consumption and heart rate thresholds for treadmill exercise

The purposes of this study were to (a) determine if the mathematical model used to estimate the physical working capacity at the oxygen consumption threshold (PWC(VO(2))) and physical working capacity at the heart rate threshold (PWC(HRT)) for cycle ergometry could be applied to treadmill running; (b) propose new fatigue thresholds called the running velocity at the oxygen uptake threshold (RV(VO(2))) and running velocity at the heart rate threshold (RV(HRT)) for treadmill exercise; and (c) statistically compare the velocities at the RV(VO(2)), RV(HRT), and ventilatory threshold (VT). Seven aerobically trained adult volunteers (mean +/- SD: age 24.0 +/- 3.9 years, Vo(2) max 56.7 +/- 7.1 ml.kg(-1).min(-1)) performed a maximal treadmill test to determine Vo(2) peak and VT as well as four 8-minute submaximal workbouts for the determination of RV(VO(2)) and RV(HRT). One-way repeated-measures analysis of variance indicated that there were no significant (p > 0.05) mean differences among the running velocities for the RV(VO(2)), RV(HRT), and VT. The results of this study indicated that the mathematical model used to estimate PWC(VO(2)) and PWC(HRT) for cycle ergometry could be applied to treadmill running. Furthermore, the RV(VO(2)) and RV(HRT) test may provide submaximal techniques for estimating the VT.     

Endurance training of older men: responses to submaximal exercise.

The purpose of this study was to quantify the exercise response of older subjects on a time-to-fatigue (TTF) submaximal performance test before and after a training program. Eight older men (67.4 +/- 4.8 yr) performed two maximal treadmill tests to determine maximum oxygen uptake (VO2max) and ventilation threshold (TVE) and a constant-load submaximal exercise treadmill test that required an oxygen uptake (VO2) between TVE and VO2max. The submaximal test, performed at the same absolute work rate before and after the training program, was performed to volitional fatigue to measure endurance time. The men trained under supervision at an individualized pace representing approximately 70% of VO2max (80% maximum heart rate) for 1 h, four times per week for 9 wk. Significant increases were demonstrated for VO2max (ml.kg-1.min-1; 10.6%); maximal ventilation (VE, l/min; 11.6%), and TVE (l/min; 9.8%). Weight decreased 2.1%. Performance time on the TTF test increased by 180% (7.3 +/- 3.0 to 20.4 +/- 13.5 min). The similar end points for VO2, VE, and heart rate during the TTF and maximal treadmill tests established that the TTF test was stopped because of physiological limitations. The increase in performance time among the subjects was significantly correlated with improvements in VO2max and TVE, with the submaximal work rate representing a VO2 above TVE by 88% of the difference between TVE and VO2max pretraining and 73% of this difference on posttraining values.     

Oxygen uptake during running as related to body mass in circumpubertal boys: a longitudinal study

To investigate the effect of endurance training on physiological characteristics during circumpubertal growth, eight young runners (mean starting age 12 years) were studied every 6 months for 8 years. Four other boys served as untrained controls. Oxygen uptake (VO2) and blood lactate concentrations were measured during submaximal and maximal treadmill running. The data were aligned with each individual's age of peak height velocity. The maximal oxygen uptake (VO2max; ml.kg-1.min-1) decreased with growth in the untrained group but remained almost constant in the training group. The oxygen cost of running at 15 km.h-1 (VO2 15, ml.kg-1.min-1) was persistently lower in the trained group but decreased similarly with age in both groups. The development of VO2max and VO2 15 (l.min-1) was related to each individual's increase in body mass so that power functions were obtained. The mean body mass scaling factor was 0.78 (SEM 0.07) and 1.01 (SEM 0.04) for VO2max and 0.75 (SEM 0.09) and 0.75 (SEM 0.02) for VO2 15 in the untrained and trained groups, respectively. Therefore, expressed as ml.kg-0.75.min-1, VO2 15 was unchanged in both groups and VO2max increased only in the trained group. The running velocity corresponding to 4 mmol.l-1 of blood lactate (nu la4) increased only in the trained group. Blood lactate concentration at exhaustion remained constant in both groups over the years studied. In conclusion, recent and the present findings would suggest that changes in the oxygen cost of running and VO2max (ml.kg-1.min-1) during growth may mainly be due to an overestimation of the body mass dependency of VO2 during running.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in diastolic coronary resistance during submaximal exercise in conditioned dogs

Diastolic coronary resistance (DCR) was studied in 10 conscious dogs in the untrained (UT) and partially trained (PT) condition. The PT regime consisted of treadmill running 5 days/wk for 4-5 wk. Left circumflex coronary flow, aortic pressure, and heart rate were measured, and diastolic coronary resistance (DCR) was calculated. Adrenergic blockade was achieved with propranolol (1 mg/kg, iv) (beta B) and phentolamine (1 mg/kg, iv) (alpha B). During submaximal exercise in the UT condition, DCR fell from a resting value of 3.84 +/- 0.24 Torr . ml-1 . min with increasing work load to 1.57 +/- 0.12 Torr . ml-1 . min at 6.4 km/h (speed)/16% (grade). The decrease in DCR during submaximal exercise was greater in the PT than in the UT condition. DCR following alpha-adrenergic blockade was not significantly changed in the UT and PT conditions (e.g., at 6.4 km/h (speed)/16% (grade), 1.10 +/- 0.141 vs. 1.03 +/- 0.107 Torr . ml-1 . min, whereas following beta-adrenergic blockade, DCR was larger in the UT compared with the PT condition (e.g., at 6.4 km/h (speed)/16% (grade), 2.03 +/- 0.091 vs. 1.73 +/- 0.073 Torr . ml-1 X min). Myocardial oxygen consumption was not significantly different in the PT and UT conditions, indicating no difference in metabolism with partial training. The present study suggests that during submaximal exercise in the PT condition there is a change in the neurogenic control of the coronary vasculature by a reduction in sympathetic neural activity on the coronary resistance vessels.     

Blood lactate production and recovery from anaerobic exercise in trained and untrained boys

Blood lactate production and recovery from anaerobic exercise were investigated in 19 trained (AG) and 6 untrained (CG) prepubescent boys. The exercises comprised 3 maximal test performances; 2 bicycle ergometer tests of different durations (15 s and 60 s), and running on a treadmill for 23.20 +/- 2.61 min to measure maximal oxygen uptake. Blood samples were taken from the fingertip to determine lactate concentrations and from the antecubital vein to determine serum testosterone. Muscle biopsies were obtained from vastus lateralis. Recovery was passive (seated) following the 60 s test but that following the treadmill run was initially active (10 min), and then passive. Peak blood lactate was highest following the 60 s test (AG, 13.1 +/- 2.6 mmol.1-1 and CG, 12.8 +/- 2.3 mmol.1-1). Following the 15 s test and the treadmill run, peak lactate values were 68.7 and 60.6% of the 60 s value respectively. Blood lactate production was greater (p less than 0.001) during the 15 s test (0.470 +/- 0.128 mmol.1-1.s-1) than during the 60 s test (0.184 +/- 0.042 mmol.1-1.s-1). Although blood lactate production was only nonsignificantly greater in AG, the amount of anaerobic work in the short tests was markedly greater (p less than 0.05-0.01) in AG than CG. Muscle fibre area (type II%) and serum testosterone were positively correlated (p less than 0.05) with blood lactate production in both short tests. Blood lactate elimination was greater (p less than 0.001) at the end of the active recovery phase than in the next (passive) phase.(ABSTRACT TRUNCATED AT 250 WORDS)     

Measurement of maximum oxygen consumption in Guinea fowl Numida meleagris indicates that birds and mammals display a similar diversity of aerobic scopes during running

Judgement of exercise performance in birds has been hampered by a paucity of data on maximal aerobic capacity. We measured the maximal rate of oxygen consumption (Vo2,max) in running guinea fowl Numida meleagris, a bird that has been used in several previous studies of avian running. Mean Vo2,max during level treadmill running was 97.5+/-3.7 mL O(2) kg(-1) min(-1) (mean+/-SEM, N=5). Vo2,max was on average 6% higher when the birds ran uphill compared with the value during level running (paired t-test, P=0.041, N=5). The mean basal rate of oxygen consumption (Vo2,bmr) of the same individuals was 7.9+/-0.5 mL O(2) kg(-1) min(-1). Mean factorial aerobic scope based on individually measured values of Vo2,max and Vo2,bmr was 13.2+/-0.6 (mean+/-SEM, N=5). This value was considerably lower than the factorial aerobic scope previously measured during running in Rhea americana, a large flightless ratite. The difference in factorial scope between these two running birds likely reflects the effects of body size as well as size-independent differences in the ability to deliver and use oxygen. These data confirm a previous prediction that birds have a diversity of factorial aerobic scopes similar to that exhibited by mammals.     

The effects of nightly normobaric hypoxia and high intensity training under intermittent normobaric hypoxia on running economy and hemoglobin mass.

We investigated the effects of nightly intermittent exposure to hypoxia and of training during intermittent hypoxia on both erythropoiesis and running economy (RE), which is indicated by the oxygen cost during running at submaximal speeds. Twenty-five college long- and middle- distance runners [maximal oxygen uptake (Vo(2max)) 60.3 +/- 4.7 ml x kg(-1) x min(-1)] were randomly assigned to one of three groups: hypoxic residential group (HypR, 11 h/night at 3,000 m simulated altitude), hypoxic training group (HypT), or control group (Con), for an intervention of 29 nights. All subjects trained in Tokyo (altitude of 60 m) but HypT had additional high-intensity treadmill running for 30 min at 3,000 m simulated altitude on 12 days during the night intervention. Vo(2) was measured at standing rest during four submaximal speeds (12, 14, 16, and 18 km/h) and during a maximal stage to volitional exhaustion on a treadmill. Total hemoglobin mass (THb) was measured by carbon monoxide rebreathing. There were no significant changes in Vo(2max), THb, and the time to exhaustion in all three groups after the intervention. Nevertheless, HypR showed approximately 5% improvement of RE in normoxia (P < 0.01) after the intervention, reflected by reduced Vo(2) at 18 km/h and the decreased regression slope fitted to Vo(2) measured during rest position and the four submaximal speeds (P < 0.05), whereas no significant corresponding changes were found in HypT and Con. We concluded that our dose of intermittent hypoxia (3,000 m for approximately 11 h/night for 29 nights) was insufficient to enhance erythropoiesis or Vo(2max), but improved the RE at race speed of college runners.     

The effect of acute moderate hypoxia on accumulated oxygen deficit during intermittent exercise in nonacclimatized men

The objective of this study was to determine the effect of acute moderate hypoxia and rest duration on performance and on the accumulated oxygen deficit (AOD) in high-intensity intermittent efforts. After preliminary tests, 2 groups of nonacclimatized men (resident at 690 m above sea level) carried out 3 randomized protocols of effort (EXP1, EXP2, and EXP5) on 3 different days. These tests were performed at acute moderate altitude (2,320 m) by the hypoxia group (H) and in normoxia by the normoxia group (N). During EXP1 the subjects ran a maximum of five 400-m sprints (90% intensity) on a treadmill, with a pause between efforts of 1 minute. In EXP2 and EXP5 the same protocol was repeated, increasing the rest period between sprints to 2 and 5 minutes, respectively. Lactate accumulation and exhaled gases were measured during the tests. Accumulated oxygen deficit was calculated for each sprint. The total AOD (SigmaAOD) for each type of protocol was determined to be the sum of the corresponding accumulated deficits. The AODs were influenced by the length of rest period (p < 0.05) but not by H. The increase in recovery time between sprints increased the SigmaAOD (7,843 +/- 4,435 vs. 7,137 +/- 2,117 ml; 11,013 +/- 4,616 vs. 9,931 +/- 2,731 ml; 12,611 +/- 4,594 vs. 12,907 +/- 3,085 ml for H and N in EXP1, EXP2, and EXP5, respectively). The AOD increased in value when the same sprint was compared from EXP1 to EXP5 (p < 0.05). The results obtained show that exposure to acute moderate altitude does not affect the anaerobic pathway contribution in intermittent high-intensity exercises. Performance during this type of repeated effort is not altered during acute exposure to moderate altitude, which should be taken into account when an acclimatizing period is not possible.     

High-speed running performance: a new approach to assessment and prediction.

We hypothesized that all-out running speeds for efforts lasting from a few seconds to several minutes could be accurately predicted from two measurements: the maximum respective speeds supported by the anaerobic and aerobic powers of the runner. To evaluate our hypothesis, we recruited seven competitive runners of different event specialties and tested them during treadmill and overground running on level surfaces. The maximum speed supported by anaerobic power was determined from the fastest speed that subjects could attain for a burst of eight steps (approximately 3 s or less). The maximum speed supported by aerobic power, or the velocity at maximal oxygen uptake, was determined from a progressive, discontinuous treadmill test to failure. All-out running speeds for trials of 3-240 s were measured during 10-13 constant-speed treadmill runs to failure and 4 track runs at specified distances. Measured values of the maximum speeds supported by anaerobic and aerobic power, in conjunction with an exponential constant, allowed us to predict the speeds of all-out treadmill trials to within an average of 2.5% (R2 = 0.94; n = 84) and track trials to within 3.4% (R2 = 0.86; n = 28). An algorithm using this exponent and only two of the all-out treadmill runs to predict the remaining treadmill trials was nearly as accurate (average = 3.7%; R2 = 0.93; n = 77). We conclude that our technique 1) provides accurate predictions of high-speed running performance in trained runners and 2) offers a performance assessment alternative to existing tests of anaerobic power and capacity.     

Role of brain IL-1beta on fatigue after exercise-induced muscle damage

Brain cytokines, induced by various inflammatory challenges, have been linked to sickness behaviors, including fatigue. However, the relationship between brain cytokines and fatigue after exercise is not well understood. Delayed recovery of running performance after muscle-damaging downhill running is associated with increased brain IL-1beta concentration compared with uphill running. However, there has been no systematic evaluation of the direct effect of brain IL-1beta on running performance after exercise-induced muscle damage. This study examined the specific role of brain IL-1beta on running performance (either treadmill or wheel running) after uphill and downhill running by manipulating brain IL-1beta activity via intracerebroventricular injection of either IL-1 receptor antagonist (ra; downhill runners) or IL-1beta (uphill runners). Male C57BL/6 mice were assigned to the following groups: uphill-saline, uphill-IL-1beta, downhill-saline, or downhill-IL-1ra. Mice initially ran on a motor-driven treadmill at 22 m/min and -14% or +14% grade for 150 min. After the run, at 8 h (wheel cage) or 22 h (treadmill), uphill mice received intracerebroventricular injections of IL-1beta (900 pg in 2 microl saline) or saline (2 microl), whereas downhill runners received IL-1ra (1.8 microg in 2 microl saline) or saline (2 microl). Later (2 h), running performance was measured (wheel running activity and treadmill run to fatigue). Injection of IL-1beta significantly decreased wheel running activity in uphill runners (P<0.01), whereas IL-1ra improved wheel running in downhill runners (P<0.05). Similarly, IL-1beta decreased and Il-1ra increased run time to fatigue in the uphill and downhill runners, respectively (P<0.01). These results support the hypothesis that increased brain IL-1beta plays an important role in fatigue after muscle-damaging exercise.