No abstract

A group of 12 healthy non-smoking men [mean age 22.3 (SD 1.1) years], performed an incremental exercise test. The test started at 30 W, followed by increases in power output (P) of 30 W every 3 min, until exhaustion. Blood samples were taken from an antecubital vein for determination of plasma concentration lactate [La-]pl and acid-base balance variables. Below the lactate threshold (LT) defined in this study as the highest P above which a sustained increase in [La-]pl was observed (at least 0.5 mmol x l[-1] within 3 min), the pulmonary oxygen uptake (VO2) measured breath-by-breath, showed a linear relationship with P. However, at P above LT [in this study 135 (SD 30) W] there was an additional accumulating increase in VO2 above that expected from the increase in P alone. The magnitude of this effect was illustrated by the difference in the final P observed at maximal oxygen uptake (VO2max) during the incremental exercise test (Pmax,obs at VO2max) and the expected power output at VO2max(Pmax,exp at VO2max) predicted from the linear VO2-P relationship derived from the data collected below LT. The Pmax,obs at VO2max amounting to 270 (SD 19) W was 65.1 (SD 35) W (19%) lower (P < 0.01) than the Pmax,exp at VO2max. The mean value of VO2max reached at Pmax,obs amounted to 3555 (SD 226) ml x min(-1) which was 572 (SD 269) ml x min(-1) higher (P < 0.01) than the VO2 expected at this P, calculated from the linear relationship between VO2 and P derived from the data collected below LT. This fall in locomotory efficiency expressed by the additional increase in VO2, amounting to 572 (SD 269) ml O2 x min(-1), was accompanied by a significant increase in [La-]pl amounting to 7.04 (SD 2.2) mmol x l(-1), a significant increase in blood hydrogen ion concentration ([H+]b) to 7.4 (SD 3) nmol x l(-1) and a significant fall in blood bicarbonate concentration to 5.78 (SD 1.7) mmol x l(-1), in relation to the values measured at the P of the LT. We also correlated the individual values of the additional VO2 with the increases (delta) in variables [La-]pl and delta[H+]b. The delta values for [La-]pl and delta[H+]b were expressed as the differences between values reached at the Pmax,obs at VO2max and the values at LT. No significant correlations between the additional VO2 and delta[La-]pl on [H+]b were found. In conclusion, when performing an incremental exercise test, exceeding P corresponding to LT was accompanied by a significant additional increase in VO2 above that expected from the linear relationship between VO2 and P occurring at lower P. However, the magnitude of the additional increase in VO2 did not correlate with the magnitude of the increases in [La-]pl and [H+]b reached in the final stages of the incremental test.

New Findings r What is the central question of this study?A few weeks of endurance training accelerate the oxygen uptake (V O 2 ) on-kinetics in humans. The main aim of the present study was to determine whether the acceleration ofV O 2 onkinetics obtained by a short period of moderate-intensity training can be explained by an intensification of mitochondrial biogenesis. r What is the main finding and its importance?We demonstrated that 5 weeks of moderate-intensity training accelerates theV O 2 on-kinetics during moderate-intensity cycling in the absence of enhanced mitochondrial biogenesis or capillarization in the trained muscles. We postulate that in the early stages of training an intensification of 'parallel activation' of oxidative phosphorylation could account for the shortening of theV O 2 on-transient.The effects of 5 weeks of moderate-intensity endurance training on pulmonary oxygen uptake kinetics (V O 2 on-kinetics) were studied in 15 healthy men (mean ± SD: age 22.7 ± 1.8 years, body weight 76.4 ± 8.9 kg and maximalV O 2 46.0 ± 3.7 ml kg −1 min −1 ). Training caused a significant acceleration (P = 0.003) ofV O 2 on-kinetics during moderate-intensity cycling (time constant of the 'primary' component 30.0 ± 6.6 versus 22.8 ± 5.6 s before and after training, respectively) and a significant decrease (P = 0.04) in the amplitude of the primary component (837 ± 351 versus 801 ± 330 ml min −1 ). No changes in myosin heavy chain distribution, muscle fibre capillarization, level of peroxisome proliferator-activated receptor γ coactivator 1α and other markers of mitochondrial biogenesis (mitochondrial DNA copy number, cytochrome c and cytochrome oxidase subunit I contents) in the vastus lateralis were found after training. A significant downregulation in the content of the sarcoplasmic reticulum ATPase 2 (SERCA2; P = 0.03) and a tendency towards a decrease in SERCA1 (P = 0.055) was found after training. The decrease in SERCA1 was positively correlated (P = 0.05) with the training-induced decrease in the gain of theV O 2 on-kinetics ( V O 2 at steady state/ power output). In the early stage of training, the acceleration inV O 2 on-kinetics during moderate-intensity cycling can occur without enhanced mitochondrial biogenesis or changes in muscle myosin heavy chain distribution and

Training-induced alleviation of parkinsonian rigidity and muscle tone decrease may be associated with neuroplastic changes caused by a training-induced increase in the level of brain-derived neurotrophic factor.

The aim of this study was to investigate the effect of short-term, moderate intensity and low volume endurance training on gonadal hormone profile in untrained men. Fifteen young, healthy men performed an endurance training of 5-week duration on a cycle ergometer. Before and after the exercise program all participants completed a maximal incremental test. Concentration of testosterone (T), sex hormone-binding globulin (SHBG) and cortisol (C) as well as blood morphology were determined in venous blood samples at rest both before and after the training. The training program resulted in 3.7% improvement of maximal oxygen uptake (VO(2max)) and 8.2% improvement of power output reached at VO(2max) (PO (max)). This was accompanied by significant increase in T (from 18.84+/-5.73 nmol.l(-1) to 22.03+/-6.61 nmol.l(-1), p = 0.0004) and calculated fT concentration (from 374+/-116 pmol.l(-1) to 470+/-153 pmol.l(-1), p = 0.00005). Moreover, the training caused a significant decrease in SHBG concentration (from 34.45+/-11.26 nmol.l(-1) to 31.95+/-10.40 nmol.l(-1), p = 0.01), whereas no significant changes were found in the cortisol concentration (334+/-138 nmol.l(-1) vs. 367+/-135 nmol.l(-1) for pre- and post-training measures, respectively, p = 0.50) and T/C and fT/C ratios. We have concluded that short-term, moderate intensity and low volume endurance training can significantly increase testosterone concentration in previously untrained men.