Effect of acute hypoxia on central fatigue during repeated isometric leg contractions.

To determine whether hypoxia has a direct influence on the central command independently of the working muscles, 16 subjects performed intermittent isometric unilateral knee extensions until exhaustion either in normobaric hypoxia (inspired O(2) fraction=0.11, arterial oxygen saturation approximately 84%) or in normoxia while the knee extensor muscles were exposed to circulatory occlusion with a 250 mmHg cuff. Among the subjects, 11 also performed the tests in hypoxia and normoxia without occlusion. Single electrical stimulations were regularly delivered to the femoral nerve to measure the changes in the knee extensor peak twitch force. With the cuff, the average slope of decrease in peak twitch did not depend on the inspired oxygen fraction. Performance was slightly but significantly lower during hypoxia than in normoxia (8.2+/-2.6 vs 9.4+/-3.1 repetitions, P<0.05) with the cuff on. The number of repetitions was much higher during hypoxia with maintaining leg blood flow (15.6+/-4.5 repetitions) than with circulatory occlusion in normoxia. In conclusion, this study showed that a direct effect of hypoxia in reducing the motor drive to the working muscles exists but this effect is moderate.

Accumulated oxygen deficit during ramp exercise.

This study aimed to compare oxygen deficit during exhaustive ramp exercise (OD ramp and OD lag) with maximal oxygen deficit during a high-intensity constant-power test (MAOD). OD ramp was estimated from the difference between oxygen demand and actual oxygen uptake. OD lag was estimated using a simple equation assuming a linear increase in oxygen uptake lagging behind metabolic requirement. After a first test providing estimation of P peak, 12 healthy males did two 15 W.min(-1) and two 30 W.min(-1) ramp tests to evaluate in duplicate OD ramp and OD lag and an exhaustive exercise at 105% of P peak to evaluate MAOD. OD ramp from the 15 W.min(-1) tests (1.50 +/- 1.83 and 2.60 +/- 2.12 l) and from the 30 W.min(-1) tests (2.41 +/- 1.00 and 2.72 +/- 1.23 l) did not differ from MAOD (2.33 +/- 0.50 l). Contrary to OD lag estimated from the 15 W.min(-1) tests (2.27 +/- 0.30 and 2.31 +/- 0.31 l), OD lag from the 30 W.min(-1) tests (2.51 +/- 0.34 and 2.52 +/- 0.36 l) was significantly greater than MAOD (p < 0.05). The conclusion is that the oxygen deficit would accumulate progressively during a ramp test until attaining the maximal oxygen deficit. This measurement would not however give reliable index of an individual subject due to the elevated test-retest variability.

Evidence of decrease in peak heart rate in acute hypoxia: effect of exercise-induced arterial hypoxemia.

This study focuses on the influence of the arterial oxygen saturation level at exhaustion on peak heart rate under acute moderate hypoxia, in endurance-trained subjects. Nineteen competing male cyclists performed exhaustive ramp exercise (cycle ergometer) under normoxia and normobaric hypoxia (15 % O (2)). After the normoxic trial, the subjects were divided into those demonstrating exercise-induced arterial hypoxemia during exercise (> 5 % decrease in SaO (2) between rest and the end of exercise, n = 10) and those who did not (n = 9). O (2) uptake, heart rate and arterial O (2) saturation (ear-oximeter) levels were measured. Under hypoxia, peak heart rate decreased for both groups (p < 0.001) and to a greater extent for hypoxemic subjects (p < 0.01). Arterial O (2) saturation under hypoxia was lower for the hypoxemic than for the non-hypoxemic subjects (p < 0.001) and it was correlated to the fall in peak heart rate between normoxia and hypoxia for all subjects (p < 0.01; r = 0.65). Hypoxemic subjects presented greater decrease in maximal O (2) uptake than non-hypoxemic ones (19.6 vs. 15.6 %; p < 0.05). The results confirm the greater decrement in arterial O (2) saturation under hypoxia in hypoxemic subjects and demonstrates a more pronounced reduction in peak heart rate in those subjects compared with non-hypoxemic ones. These data confirm the possible influence of arterial oxygenation on the decrease in peak heart rate in acute hypoxia.

A high blood lactate induced by heavy exercise does not affect the increase in submaximal VO2 with hyperoxia.

Few studies evidenced an enhancement in oxygen uptake (VO2) during submaximal exercise in hyperoxia. This O2 "overconsumption" seems to increase above the lactate threshold. The aim of this study was to determine whether the hyperoxia-induced enhancement in VO2 may be related to a higher metabolism of lactate. Nine healthy males (aged 23.1 years, mean VO2 max= 53.8 ml min-1 kg-1) were randomized to two series of exercise in either normoxia or hyperoxia corresponding to an inspired O2 fraction (FIO2) of 30%. Each series consisted of 6 min cycling at 50% VO2 max (Moderate1), 5 min cycling at 95%VO2 max (Near Max) and then 6 min at 50% VO2 max (Moderate2). In both series Near Max was performed in normoxia. VO2 was significantly greater under hyperoxia than in normoxia during Moderate1 (2192 +/- 189 vs. 2025 +/- 172 ml min-1) and during Moderate2 (2352 +/- 173 vs. 2180+ /- 193 ml min-1). However, the effect of the high FIO2 was not significantly different on VO2Moderate2 (+172+/-137 ml min-1 with [La] approximately 6 mmol l-1) compared to VO2Moderate1 (+166 +/- 133 ml min-1 with [La] approximately 2.4 mmol l-1). [La] at the onset of Moderate2 was not different between normoxia and hyperoxia (10.1 +/- 2.2 vs. 10.9 +/- 1.6 mmol l-1). The results show that VO2 is significantly increased during moderate exercise in hyperoxia. But this O2 overconsumption was not modified by a high [La] induced by a prior heavy exercise. It could be concluded that lactate accumulation is not directly responsible for the increase in O2 overconsumption with intensity during exercise in hyperoxia.

Effects of moderate hyperoxia on oxygen consumption during submaximal and maximal exercise.

The present study examined the effect of hyperoxia on oxygen uptake (VO(2)) and on maximal oxygen uptake (VO(2max)) during incremental exercise (IE) and constant work rate exercise (CWRE). Ten subjects performed IE on a bicycle ergometer under normoxic and hyperoxic conditions (30% oxygen). They also performed four 12-min bouts of CWRE at 40, 55, 70 and 85% of normoxic VO(2max) (ex1, ex2, ex3 and ex4, respectively) in normoxia and in hyperoxia. VO(2max) was significantly improved by 15.0 (15.2)% under hyperoxia, while performance (maximum workload, W(max)) was improved by only +4.5 (3.0)%. During IE, the slope of the linear regression relating VO(2) to work rate was significantly steeper in hyperoxia than in normoxia [10.80 (0.88) vs 10.06 (0.66) ml x min(-1) x W(-1)]. During CWRE, we found a higher VO(2) at ex1, ex2, ex3 and ex4, and a higher VO(2) slow component at ex4 under hyperoxia. We have shown that breathing hyperoxic gas increases VO(2max), but to an extent that is difficult to explain by an increase in oxygen supply alone. Changes in metabolic response, fibre type recruitment and VO(2) of non-exercising tissue could explain the additional VO(2) for a given submaximal work rate under hyperoxia.

Modelling the transfers of training effects on performance in elite triathletes.

This study investigated the effects of 40-weeks training in swimming, cycling and running on performances in swimming, running and triathlon competitions in four elite triathletes. The training stimulus was calculated using the exercise heart rate. The level of performance was measured in running by a submaximal 30 min run, in swimming by a 5 x 400 m all-out test and subjectively in triathlon competitions. A mathematical model using one to three first order transfer functions linked actual and modelled performances by minimizing the residual sum of squares between them. The relationships between training and performances were significant in running (tau(1) = 20; tau(2) = 10; r = 0.74; p < 0.001) and in swimming (tau(1) = 31; r = 0.37; p = 0.03), supporting the principle of specificity of the training loads. Cross-transfer training effects were identified between cycling and running (tau(1 = )42; r = 0.56; p < 0.001), but not with swimming performances. In addition, the training loads completed in running were shown to have a major effect on performances in triathlon competition (tau(1 = )52; tau(2 = )4; r = 0.52; p < 0.001), indicating that running training is an essential part of triathlon performance. Swimming appears to be a highly specific activity, which does not gain nor provide benefits from/to other activities (i. e. cycling and running). The present study shows that cross-transfer training effects occur between cycling training and running performance in elite triathletes. A similar cross-training effect does not seem to occur for swimming performance.

Relation between heart rate variability and training load in middle-distance runners.

PURPOSE: Monitoring physical performance is of major importance in competitive sports. Indices commonly used, like resting heart rate, VO2max, and hormones, cannot be easily used because of difficulties in routine use, of variations too small to be reliable, or of technical challenges in acquiring the data. METHODS: We chose to assess autonomic nervous system activity using heart rate variability in seven middle-distance runners, aged 24.6 +/- 4.8 yr, during their usual training cycle composed of 3 wk of heavy training periods, followed by a relative resting week. The electrocardiogram was recorded overnight twice a week and temporal and frequency indices of heart rate variability, using Fourier and Wavelet transforms, were calculated. Daily training loads and fatigue sensations were estimated with a questionnaire. Similar recordings were performed in a sedentary control group. RESULTS: The results demonstrated a significant and progressive decrease in parasympathetic indices of up to -41% (P < 0.05) during the 3 wk of heavy training, followed by a significant increase during the relative resting week of up to +46% (P < 0.05). The indices of sympathetic activity followed the opposite trend, first up to +31% and then -24% (P < 0.05), respectively. The percentage increasing mean nocturnal heart rate variation remained below 12% (P < 0.05). There was no significant variation in the control group. CONCLUSION: This study confirmed that heavy training shifted the cardiac autonomic balance toward a predominance of the sympathetic over the parasympathetic drive. When recorded during the night, heart rate variability appeared to be a better tool than resting heart rate to evaluate cumulated physical fatigue, as it magnified the induced changes in autonomic nervous system activity. These results could be of interest for optimizing individual training profiles.

Analysis of end-tidal and arterial PCO2 gradients using a breathing model.

The aim of this paper was to analyse the difference between end-tidal carbon dioxide tension (PETCO2) and arterial carbon dioxide tension (PaCO2) at rest and during exercise using a homogeneous lung model that simulates the cyclic feature of breathing. The model was a catenary two-compartment model that generated five non-linear first-order differential equations and two equations for gas exchange. The implemented mathematical modelling described variations in CO2 and O2 compartmental fractions and alveolar volume. The model also included pulmonary capillary gas exchange. Ventilatory experimental data were obtained from measurements performed on a subject at rest and during four 5-min bouts of exercise on a cycle ergometer at 50, 100, 150 and 200 W, respectively. Analysis of the PETCO2-PaCO2 difference between experimental and sinusoidally adjusted ventilatory flow profiles at rest and during exercise showed that the model produced similar values in PETCO2-PaCO2 for different respiratory flow dynamics (P approximately equal to 0.75). The model simulations allowed us to study the effects of metabolic, circulatory and respiratory parameters on PETCO2-PaCO2 at rest and during exercise. During exercise, metabolic CO2 production, O2 uptake and cardiac output affected significantly the PETCO2-PaCO2 difference from the 150-W workload (P < 0.001). The pattern of breathing had a significant effect on the PETCO2-PaCO2 difference. The mean (SD) PETCO2-PaCO2 differences simulated using experimental profiles were 0.80 (0.95), 1.65 (0.40), 2.40 (0.20), 3.30 (0.30) and 4.90 (0.20) mmHg, at rest and during exercise at 50, 100, 150 and 200 W, respectively. The relationship between PETCO2-PaCO2 and tidal volume was similar to data published by Jones et al. (J Appl Physiol 47: 954-960, 1979).

Wavelet transform to quantify heart rate variability and to assess its instantaneous changes.

Heart rate variability is a recognized parameter for assessing autonomous nervous system activity. Fourier transform, the most commonly used method to analyze variability, does not offer an easy assessment of its dynamics because of limitations inherent in its stationary hypothesis. Conversely, wavelet transform allows analysis of nonstationary signals. We compared the respective yields of Fourier and wavelet transforms in analyzing heart rate variability during dynamic changes in autonomous nervous system balance induced by atropine and propranolol. Fourier and wavelet transforms were applied to sequences of heart rate intervals in six subjects receiving increasing doses of atropine and propranolol. At the lowest doses of atropine administered, heart rate variability increased, followed by a progressive decrease with higher doses. With the first dose of propranolol, there was a significant increase in heart rate variability, which progressively disappeared after the last dose. Wavelet transform gave significantly better quantitative analysis of heart rate variability than did Fourier transform during autonomous nervous system adaptations induced by both agents and provided novel temporally localized information.

A system to simulate gas exchange in humans to control quality of metabolic measurements.

We have developed a gas exchange simulation system (GESS) to assess the quality control in measurements of metabolic gas exchange. The GESS simulates human breathing from rest to maximal exercise. It approximates breath-by-breath waveforms, ventilatory output, gas concentrations, temperature and humidity during inspiration and expiration. A programmable motion control driving two syringes allows the ventilation to be set at any tidal volume (VT), respiratory frequency (f), flow waveform and period of inspiration and expiration. The GESS was tested at various combinations of VT (0.5-2.51) and f(10-60 stroke x min(-1)) and at various fractional concentrations of expired oxygen (0.1294-0.1795); and carbon dioxide (0.0210-0.0690) for a pre-set flow waveform and for expired gases at the same temperature and humidity as room air. Expired gases were collected in a polyethylene bag for measurement of volume and gas concentrations. Accuracy was assessed by calculating the absolute and relative errors on parameters (error=measured-predicted). The overall error in the gas exchange values averaged less than 2% for oxygen uptake and carbon dioxide output, which is within the accuracy of the Douglas bag method.

Effect of cycling position on ventilatory and metabolic variables.

Three positions are generally used by cyclists: upright posture (UP), dropped posture (DP) and aero posture (AP). They determine different angles of trunk flexion which could be associated with physiological changes. The purpose of this study was to analyse the effect of these rider positions on ventilatory and metabolic variables. Nine male competitive cyclists (26.3+/-3yrs, mean+/-SD) exercised on a cycle ergometer. Subjects performed three 10 min exercise bouts at 70% VO2max (maximal oxygen uptake, I x min(-1)) in UP, DP and AP, in a randomized order. Each bout was separated by a 5 min active recovery period (50% of VO2max). Ventilatory and gas exchange responses to exercise were averaged every min. Blood lactate concentration ([La]b, mM), blood pH were analysed at the 5th and the 10th min. The ventilation, respiratory exchange ratio, mean inspiratory flow, [La]b and perceived exertion were significantly higher in DP (88.4+/-11.41 x min(-1), 0.96+/-0.05 ml x s(-1), 2.52+/-0.84 Mm and 13.6+/-1.2) than in UP (84.8+/-12.31 x min(-1), 0.94+/-0.05 ml x s(-1), 2.14+/-0.99Mm and 12.1+/-1.5). VO2, tidal volume, carbon dioxide output, respiratory rate, inspiratory duty cycle, heart rate and pH remained unchanged between all riding positions (averaged values for the three positions: 3.09+/-0.0061 x min(-1), 2.34+/-0.0061 x br(-1), 3.01+/-0.041 x min(-1), 37.4+/-0.8 br x min(-1), 0.47+/-0, 162+/-1 beat x min(-1) and 7.38+/-0.015). These results showed that the greater changes in ventilatory and metabolic variables occurred in DP. AP appears to be the more suitable position when the aerodynamic drag becomes predominant.

Validity of oxygen uptake measurements during exercise under moderate hyperoxia.

PURPOSE: The validity of oxygen uptake in hyperoxia (FIO2 = 30%) measured by an automated system (MedGraphics, CPX/D system) was assessed during the simulation of gas exchanges during exercise with a mechanical system and during submaximal exercise by human subjects. METHODS: The simulation system reproduced a stable and accurate VO2 for 30 min (sim-test). This trial was repeated nine times in normoxia and nine times in hyperoxia. Ten subjects also performed two submaximal exercises (55% of normoxic VO2max) on a cycle ergometer at the same absolute power in normoxia and in hyperoxia (ex-test). RESULTS: There was a significant downward drift of the oxygen fraction measurement in hyperoxia (< or = 0.10% for FIO2 and FEO2) during sim-test, but VO2 measurement remained stable in the two conditions. There was also a downward drift of the oxygen fraction measurement in the two conditions (< or = 0.07% for FIO2) during ex-test. VO2 was significantly higher in hyperoxia (+4.6%), and this result was confirmed using a modified Douglas bag method. CONCLUSIONS: These findings show that the CPX/D system is stable and valid for assessing VO2 in moderate hyperoxia.

Evaluation of estimates of alveolar gas exchange by using a tidally ventilated nonhomogenous lung model.

The purpose of this study was to evaluate algorithms for estimating O2 and CO2 transfer at the pulmonary capillaries by use of a nine-compartment tidally ventilated lung model that incorporated inhomogeneities in ventilation-to-volume and ventilation-to-perfusion ratios. Breath-to-breath O2 and CO2 exchange at the capillary level and at the mouth were simulated by using realistic cyclical breathing patterns to drive the model, derived from 40-min recordings in six resting subjects. The SD of the breath-by-breath gas exchange at the mouth around the value at the pulmonary capillaries was 59.7 +/- 25.5% for O2 and 22.3 +/- 10.4% for CO2. Algorithms including corrections for changes in alveolar volume and for changes in alveolar gas composition improved the estimates of pulmonary exchange, reducing the SD to 20.8 +/- 10.4% for O2 and 15.2 +/- 5.8% for CO2. The remaining imprecision of the estimates arose almost entirely from using end-tidal measurements to estimate the breath-to-breath changes in end-expiratory alveolar gas concentration. The results led us to suggest an alternative method that does not use changes in end-tidal partial pressures as explicit estimates of the changes in alveolar gas concentration. The proposed method yielded significant improvements in estimation for the model data of this study.

Modeling of adaptations to physical training by using a recursive least squares algorithm.

The present study assesses the usefulness of a systems model with time-varying parameters for describing the responses of physical performance to training. Data for two subjects who undertook a 14-wk training on a cycle ergometer were used to test the proposed model, and the results were compared with a model with time-invariant parameters. Two 4-wk periods of intensive training were separated by a 2-wk period of reduced training and followed by a 4-wk period of reduced training. The systems input ascribed to the training doses was made up of interval exercises and computed in arbitrary units. The systems output was evaluated one to five times per week by using the endurance time at a constant workload. The time-invariant parameters were fitted from actual performances by using the least squares method. The time-varying parameters were fitted by using a recursive least squares algorithm. The coefficients of determination r2 were 0.875 and 0.879 for the two subjects using the time-varying model, higher than the values of 0.682 and 0.666, respectively, obtained with the time-invariant model. The variations over time in the model parameters resulting from the expected reduction in the residuals appeared generally to account for changes in responses to training. Such a model would be useful for investigating the underlying mechanisms of adaptation and fatigue.

Oxygen uptake during submaximal incremental and constant work load exercises in hypoxia.

The effect of acute hypoxia on oxygen uptake (VO2) was studied during incremental (IE) and constant work load exercises. Twenty-two healthy subjects performed two incremental exercises on a bicycle ergometer under normoxic (21% O2) and hypoxic (10.4% O2) conditions. Fifteen subjects performed a constant work load exercise at the same absolute power (CAP) (116 +/- 33 W), while seven other subjects performed three constant work load exercises at the same relative power (CRP) (50, 60 and 70% of VO2max) in both conditions. VO2 was defined as extraventilatory when the estimation of respiratory muscles O2 consumption was subtracted from the total VO2. During IE, the slope of the linear regression relating VO2 to work rate was higher in normoxia than in hypoxia (11.6 +/- 1.2 ml.l-1.W-1 vs 10.1 +/- 1.1 ml.l-1.W-1, p < 0.01). During CAP, VO2 was lower in normoxia than in hypoxia (1.88 +/- 0.45).min-1 vs 1.96 +/- 0.42 l.min-1, p < 0.01) whereas extraventilatory VO2 was not significantly different (1.80 +/- 0.441.min-1 vs 1.77 +/- 0.36) l.min-1). During CRP, the slope relating VO2 to power output computed from the three work loads was not statistically different between normoxia and hypoxia (delta VO2/delta w = 11.9 +/- 3.1 ml.min-1.W-1 vs 12.3 +/- 1.2 ml.min-1.W-1). These findings showed that during CRP, the metabolic efficiency (delta VO2/delta W) was the same in normoxia and in hypoxia. During CAP, the respiratory muscles O2 consumption might have accounted for the difference in VO2 consumption between hypoxia and normoxia.

Breath-to-breath relationships between respiratory cycle variables in humans at fixed end-tidal PCO2 and PO2.

This study examined the statistical properties of breath-to-breath variations in the inspiratory and expiratory volumes and times during rest and light exercise. Sixty data sets were analyzed. Initial data and residuals after fitting time-series models were examined for 1) sustained periodicities with use of spectral analysis, 2) temporal changes in signal power with use of evolutionary spectral analysis, and 3) auto- and cross correlations with use of a portmanteau test. The major findings were as follows: 1) no sustained periodic components were detected; 2) temporal changes in signal power were normally present, but these did not affect significantly the results from time-series modeling; 3) for all variables, a simple autoregressive moving average (ARMA) AR1MA1 model generally described the autocorrelation; 4) considerable cross correlation remained between residuals from the AR1MA1 model; 5) relationships between variables could be described by using a multivariate time-series model; 6) residual fluctuations in end-tidal PCO2 had little influence; and 7) responses were broadly similar between rest and exercise, although some quantitative differences were found. The multivariate model provides a description of the structure of the interrelationships between cycle variables in a quantitative and a qualitative form.

Increase in occlusion pressure with ventilation and response to maximal exercise.

Fifteen sedentary or mildly active men (low fit group) and 15 trained male athletes (high fit group) performed an incremental exercise bout on a cycle ergometer until exhaustion. At each submaximal load, minute ventilation (VE) and rate of change of mouth pressure (dP/dt) during a brief airway occlusion were computed. The airway was occluded for 40-200 ms and adjusted according to the level of ventilation. Maximal oxygen uptake (VO2peak) and minute ventilation (VEpeak) were measured during the last increment. dP/dt was related to VE in all subjects as dP/dt = a VECURV. The CURV parameter was 0.99-1.95 with a median of 1.49. The subjects were divided into four groups of seven or eight according to their physical fitness and their CURV value. Low and high CURV subjects had a CURV below and above the median, respectively. VE/VO2peak and VE/VCO2peak were significantly higher in the low CURV than in the high CURV group (P < 0.01 and P < 0.05, respectively). Although factors other than the increase in pulmonary impedance with ventilation may influence CURV, the present results indicate the possible influence of mechanical constraint of breathing on the ventilatory output.

Comparison of muscle near-infrared spectroscopy and femoral blood gases during steady-state exercise in humans.

Near-infrared spectroscopy (NIRS) is a noninvasive way of measuring muscular oxygenation. We evaluated the relationship between NIRS signal [infrared muscle oxygen saturation (IR-SO2mus)] and the femoral venous oxygen saturation (SfvO2) during cycling exercise. Six healthy subjects performed a 30-min steady-state exercise at 80% maximal oxygen uptake in normoxia and hypoxia (inspired O2 fraction = 0.105). IR-So2mus was recorded continuously throughout the tests with the NIRS probe located on the vastus lateralis. During exercise, blood samples were withdrawn every 5 min from radial artery and femoral vein catheters. In normoxia, IR-So2mus initiated a transient nonsignificant decrease at 5 min, then returned to preexercise level, whereas SfvO2 showed a fast decrease, reaching 18% saturation at 10 min without further change. By contrast, in hypoxia, IR-SO2mus and SfvO2 demonstrated a parallel decrease then stabilized at 10 min. We conclude that IR-SO2mus appears to parallel SfvO2 when both the arterial and venous oxygen contents decrease during steady-state exercise in hypoxia, whereas IR-SO2mus does not follow SfvO2 change in normoxia.

Modeled responses to training and taper in competitive swimmers.

This study investigated the effect of training on performance and assessed the response to taper in elite swimmers (N = 18), using a mathematical model that links training with performance and estimates the negative and positive influences of training, NI and PI. Variations in training, performance, NI, and PI were studied during 3-, 4-, and 6-wk tapers. The fit between modeled and actual performance was significant for 17 subjects; r2 ranged from 0.45 to 0.85, P < 0.05. Training was progressively reduced during tapers. Performance improved during the first two tapers: 2.90 +/- 1.50% (P < 0.01) and 3.20 +/- 1.70% (P < 0.01). Performance improvement in the third taper was not significant (1.81 +/- 1.73%). NI was reduced during the first two tapers (P < 0.01 and P < 0.05, respectively), but not during the third. PI did not change significantly during tapers. Thus, the present results show that the model used is a valuable method to describe the effects of training on performance. Performance improvement during taper was attributed to a reduction in NI. PI did not improve with taper, but it was not compromised by the reduced training periods.

Effects of training on performance in competitive swimming.

The relationships between the mean intensity of a training season, training volume and frequency, and the variations in performance were studied in a group of 18 elite swimmers. Additionally, differences between the swimmers who improved their personal record of the previous year during the follow-up training season (GIR, n = 8) and those who did not (GNI, n = 10) were investigated. The improvement in performance during the follow-up season was significantly correlated with the mean intensity of the training season (r = 0.69, p < 0.01), but not with training volume or frequency. The performance improvement during the follow-up season was negatively related to the initial performance level (r = 0.90, p < 0.01). The decline in performance during detraining from the previous year was less for the GIR than for the GNI (6.21 +/- 2.30% vs. 9.79 +/- 2.18%, p < 0.01). The present findings suggest that training intensity is the key factor in performance improvement in a group of elite swimmers. Factors such as previous detraining and initial performance level could jeopardize success in spite of a good adaptation to training.