The velocity at the VO2max is the main factor predicting the variance of the 10-km performance both in men and women, and high-intensity training contributes to this higher VO2max among men.
In order to investigate the effectiveness of different techniques of water immersion recovery on maximal strength, power and the post-exercise inflammatory response in elite athletes, 41 highly trained (Football, Rugby, Volleyball) male subjects (age = 21.5 ± 4.6 years, mass = 73.1 ± 9.7 kg and height = 176.7 ± 9.7 cm) performed 20 min of exhaustive, intermittent exercise followed by a 15 min recovery intervention. The recovery intervention consisted of different water immersion techniques, including: temperate water immersion (36°C; TWI), cold water immersion (10°C; CWI), contrast water temperature (10-42°C; CWT) and a passive recovery (PAS). Performances during a maximal 30-s rowing test (P(30 s)), a maximal vertical counter-movement jump (CMJ) and a maximal isometric voluntary contraction (MVC) of the knee extensor muscles were measured at rest (Pre-exercise), immediately after the exercise (Post-exercise), 1 h after (Post 1 h) and 24 h later (Post 24 h). Leukocyte profile and venous blood markers of muscle damage (creatine kinase (CK) and lactate dehydrogenase (LDH)) were also measured Pre-exercise, Post 1 h and Post 24 h. A significant time effect was observed to indicate a reduction in performance (Pre-exercise vs. Post-exercise) following the exercise bout in all conditions (P < 0.05). Indeed, at 1 h post exercise, a significant improvement in MVC and P(30 s) was respectively observed in the CWI and CWT groups compared to pre-exercise. Further, for the CWI group, this result was associated with a comparative blunting of the rise in total number of leucocytes at 1 h post and of plasma concentration of CK at 24 h post. The results indicate that the practice of cold water immersion and contrast water therapy are more effective immersion modalities to promote a faster acute recovery of maximal anaerobic performances (MVC and 30″ all-out respectively) after an intermittent exhaustive exercise. These results may be explained by the suppression of plasma concentrations of markers of inflammation and damage, suggesting reduced passive leakage from disrupted skeletal muscle, which may result in the increase in force production during ensuing bouts of exercise.
Training effects on time-to-exhaustion, substrate and blood lactate balances at the maximal lactate steady state velocity (MLSSv) were examined. Eleven male, veteran, long-distance runners performed three tests before and after 6 weeks of training at MLSSv: an incremental test to determine maximum O2 uptake (VO(2,max)) and the velocity at the lactate threshold (vLT), a sub-maximal test of two stages of 20 min at 95 and 105% of vLT separated by 40 min rest to determine the MLSSv and the corresponding lactate concentration (MLSSc) and a time-to-exhaustion run at MLSSv for which the substrate balance was calculated. Duration and distance run at MLSSv increased dramatically respectively from 44+/-10 to 63+/-12 min and from 10.4 to 15.7 km respectively (P<0.01). MLSSv increased significantly with training but the relative fraction of VO(2,max) remained the same (85.2+/-4.5 vs. 85.3+/-5.2%, P=0.93). MLSSc was unaffected by training as determined from the percentage of energy yielded by carbohydrates (80%) during the exhaustive run at MLSSv. These findings show that training at MLSS elicits small increases in MLSSv and VO(2,max), but enhances time-to-exhaustion (endurance) at MLSSv substantially (+50%). Training does not change the proportion of carbohydrate oxidized, which is the major substrate used during an exhaustive run at MLSS lasting 1 h.
VO2max was not attained with the same central and peripheral factors in exhaustive exercises, and tlimDelta50 did not elicit the maximal Q. This might be taken into account if the training aim is to enhance the central factors of VO2max using exercise intensities eliciting VO2max but not necessarily Qmax.
This study aimed to investigate the oxygen uptake and metabolic responses during a 400-m run reproducing the pacing strategy used in competition. A portable gas analyser was used to measure the oxygen uptake (VO2) of ten specifically trained runners racing on an outdoor track. The tests included (1) an incremental test to determine maximal VO2 (VO2max) and the velocity associated with VO2(max) (v - VO2max), (2) a maximal 400-m (400T) and 3) a 300-m running test (300T) reproducing the exact pacing pattern of the 400T. Blood lactate, bicarbonate concentrations [HCO3(-)], pH and arterial oxygen saturation were analysed at rest and 1, 4, 7, 10 min after the end of the 400 and 300T. The peak VO2 recorded during the 400T corresponded to 93.9 +/- 3.9% of VO2max and was reached at 24.4 +/- 3.2 s (192 +/- 22 m). A significant decrease in VO2 (P < 0.05) was observed in all subjects during the last 100 m, although the velocity did not decrease below v - VO2max. The VO2 in the last 5 s was correlated with the pH (r = 0.86, P < 0.0005) and [HCO3(-)] (r = 0.70, P < 0.05) measured at the end of 300T. Additionally, the velocity decrease observed in the last 100 m was inversely correlated with [HCO3(-)] and pH at 300T (r = -0.83, P < 0.001, r = -0.69, P < 0.05, respectively). These track running data demonstrate that acidosis at 300 m was related to both the VO2 response and the velocity decrease during the final 100 m of a 400-m run.
The purpose of this study was to examine whether the heart rate (HR) deflection point (HRDP) in the HR-power relationship is concomitant with the maximal stroke volume (SV(max)) value achievement in endurance-trained subjects. Twenty-two international male cyclists (30.3 +/- 7.3 yr, 179.7 +/- 7.2 cm, 71.3 +/- 5.5 kg) undertook a graded cycling exercise (50 W every 3 min) in the upright position. Thoracic impedance was used to measure continuously the HR and stroke volume (SV) values. The HRDP was estimated by the third-order curvilinear regression method. As a result, 72.7% of the subjects (HRDP group, n = 16) presented a break point in their HR-work rate curve at 89.9 +/- 2.8% of their maximal HR value. The SV value increased until 78.0 +/- 9.3% of the power associated with maximal O(2) uptake (Vo(2 max)) in the HRDP group, whereas it increased until 94.4 +/- 8.6% of the power associated with Vo(2 max) in six other subjects (no-HRDP group, P = 0.004). Neither SV(max) (ml/beat or ml.beat(-1).m(-2)) nor Vo(2 max) (ml/min or ml.kg(-1).min(-1)) were different between both groups. However, SV significantly decreased before exhaustion in the HRDP group (153 +/- 44 vs. 144 +/- 40 ml/beat, P = 0.005). In the HRDP group, 62% of the variance in the power associated with the SV(max) could also be predicted by the power output at which HRDP appeared. In conclusion, in well-trained subjects, the power associated with the SV(max)-HRDP relationship supposed that the HR deflection coincided with the optimal cardiac work for which SV(max) was attained.
Middle-distance running performances (800-1,500 m) relies on both aerobic and anaerobic metabolisms [1]. The relative contribution of each metabolic pathway during a middle-distance run has already been reported in elite athletes, but the performance was for males only performing on a treadmill [2]. Weyand et al. [3] have demonstrated that middle-distance performances depended more on aerobic capacity than on anaerobic capacity. Indeed, Weyand et al. [3] have shown that, in sub-elite runners (2 min 01 sϮ5 s and 2 min 32 sϮ6 s over 800 m for males and females), the peak oxygen deficit was a moderately strong predictor of middle-distance performances (38 and 27% of the variance of the performances over 800 and 1,500 m). Therefore, the energetic factors of performance were expressed with different units: the anaerobic one was reported as capacity (the "anaerobic work capacity" in J), and the aerobic one was expressed as a power (the "maximal aerobic power" in W).Wilkie's model (see method section) gives a physiological background of the hyperbolic function between the total power output (Ė r ) and the exercise duration. According to Wilkie's equation of [4], the aerobic and anaerobic factors of performance can be calculated with the same dimension because it allows the aerobic power (Ė r max aero ) to be distinguished from the Japanese Journal of Physiology, 54, 125-135, 2004 Key words: anaerobic, maximal oxygen uptake, gender, adolescence. Abstract:The aim of this study was to determine the energetic factors of middle-distance running performance in junior elite runners according to gender and by using measurements from on-track performances. Fifteen elite runners (8 males and 7 females) were investigated by means of an incremental test and an all-out run over 600 m performed with a 2-d interval.We calculated (1) the aerobic maximal power (Ė r max aero , in W kg Ė r max aero explained most of the variance in the performance (the personal best performed 8 weeks later) between genders: 65 and 79% over 800 m (T 800 ) and 1,500 m (T 1,500 ). For females, Ė r max aero explained most of the variance of T 1,500 (r 2 ϭ0.66), and Ė r max anaero improved this prediction (r 2 ϭ0.84). No energetic factor predicted the performance on 800 m run in males. In elite junior athletes, the energetic model with individual data measured over an all-out 600 m performed on a track, provides an explanation for most of the variance in middle-distance running performances between genders. The distinction between aerobic power and anaerobic power allowed an improvement in the prediction of middle-distance running performances. [The Japan-
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