Oxidative stress may be caused by an increased rate of ATP resynthesis during physical exercise. The aim of this study was to compare changes in the prooxidant-antioxidant state of blood plasma between men and women after maximal-intensity exercise, and to assess the relationship between these changes and the value of the maximal oxygen uptake (VO2max) as well as between these changes and the value of post-exercise disruptions in acid-base balance. Study participants comprised 10 women (20.7±0.5 years) and 10 men (22.3±0.5 years) who were physically active but did no t engage in competitive sports training. VO2max was determined via treadmill incremental test (VO2max relative to body mass: 44.48±1.21 ml/kg/min and 59.16±1.55 ml/kg/min for women and men, respectively). The level of acid-base balance indicators (ABB), lactate concentration (La-), the level of total oxidative status (TOS), the level of total antioxidative capacity (TAC), an d uric acid (UA) concentration were measured before and after the test. An oxidative stress indicator (OSI) was also calculated. Men showed a significant post-exercise increase in the level of TOS and OSI, while women showed a significant post-exercise increase in the level of TAC. Post-exercise changes in UA concentration were insignificant. Post-exercise changes in TOC in men depended on the absolute values of VO2max , on VO2max/LBM, and on post-exercise changes in La- concentration., M. Wiecek, M. Maciejczyk, J. Szymura, Z. Szygula., and Obsahuje bibliografii
The aim of this study was to evaluate the influence of exercise with the intensity progressively increasing from rest until maximal oxygen uptake (VCbmax) on 2,3-DPG levels in red blood cells (RBC) in relation to the changes in the acid-base balance and plasma lactate concentration. Six healthy young men (age 22.5 ±1.5 years, V02max 3.48 ±0.20 1/min) participated in this study. The subjects performed an incremental exercise test on a cycloergometer until exhaustion. Blood samples were tested for acid-base balance indices (pH, HCO3-, BE), plasma lactate and RBC 2,3-DPG concentration. Gas exchange variables were measured continuously breath-bybreath. In this paper we present data concerning 2,3-DPG, plasma lactate, pH, HCO3" and BE measured at rest, at the power output corresponding to the lactate threshold (PO LT), at the power output at maximal oxygen uptake (PO VCbmax), as well as 5, 15 and 30 min after finishing the incremental test. Increase of power output above the lactate threshold to the PO V02max was accompanied by a significant (p<0.01) increase of plasma lactate from 2.58±0.78 mmol/1 to 10.22±3.04 mmol/1. This was also accompanied by a significant drop (p<0.01) in blood pH value from 7.352 ± 0.025 at the PO LT to 7.294 ±0.041 at the PO V02max- No significant changes of the RBC
2,3-DPG level were observed at any of the analysed stages of the exercise. The RBC 2,3-DPG level expressed in relation to the changes of haematocrit showed only minor changes during the exercise period and after 15 min of recovery vs. resting value (3.21 ±1.19). However, after 30 min of recovery, RBC 2,3-DPG decreased to the value of 2.32±1.19 /rmol/ml. We conclude that, during an incremental test, no increase in RBC 2,3-DPG concentration is required to reach the maximal oxygen uptake level. Moreover, a rapid decrease in blood pH, developing during a single bout of exercise, is not a stimulus powerful enough to cause significant changes in the RBC 2,3-DPG level during short-term exercise.
In this experiment we studied the effect of different pedalling rates during cycling at a constant power output (PO) 132±31 W (mean±S.D.), corresponding to 50 % V02 max, on the oxygen uptake and the magnitude of the slow component of V02 kinetics in humans. The PO corresponded to 50 % of V02 max, established during incremental cycling at a pedalling rate of 70 rev.min-1. Six healthy men aged 22.2 ±2.0 years with V02 max 3.89 ±0.92 l.min-1, performed on separate days constant PO cycling exercise lasting 6 min at pedalling rates 40, 60, 80, 100 and 120 rev.min-1, in random order. Antecubital blood samples for plasma lactate [La]pi and blood acid-base balance variables were taken at 1 min intervals. Oxygen uptake was determined breath-by-breath. The total net oxygen consumed throughout the 6 min cycling period at pedalling rates of 40, 60, 80, 100 and 120 rev.min-1 amounted to 7.727± 1.197, 7.705± 1.548, 8.679± 1.262, 9.945± 1.435 and 13.720± 1.862 1, respectively for each pedalling rate. The VO2 during the 6 min of cycling only rose slowly by increasing the pedalling rate in the range of 40-100 rev.min-1. This increase, was 0.142 1 per 20 rev.min-1 on the average. Plasma lactate concentration during the sixth minute of cycling changed little within this range of pedalling rates: the values were 1.83 ±0.70, 1.80 ± 0.48, 2.33 ±0.88 and 2.52 ±0.33 mmoLl-1. The values of [La]pi reached in the 6th minute of cycling were not significantly different from the pre-exercise levels. Blood pH was also not affected by the increase of pedalling rate in the range of 40-100 rev.min-1. However, an increase of pedalling rate from 100 to 120 rev.min-1 caused a sudden increase in the VO2 amounting to 0.747 1 per 20 rev.min-1, accompanied by a significant increase in [La]pj from 1.21 ±0.26 mmol.l-1 in pre-exercise conditions to 5.92±2.46 mmol.l-1 reached in the 6th minute of cycling (P<0.01). This was also accompanied by a significant drop of blood pH, from 7.355 ±0.039 in the pre-exercise period to 7.296 ± 0.060 in the 6th minute of cycling (P<0.01). The mechanical efficiency calculated on the basis of the net VO2 reached between the 4th and the 6th minute of cycling amounted to 26.6 ±2.7, 26.4±2.0, 23.4±3.4, 20.3 ±2.6 and 14.7±2.2 %, respectively for pedalling rates of 40, 60, 80,100 and 120 rev.min-1. No significant increase in the VO2 from the 3rd to the 6th min (representing the magnitude of the slow component of V02 kinetics) was observed at any of the pedalling rates (-0.022±0.056, -0.009±0.029, 0.012±0.073, 0.030±0.081 and 0.122±0.176 l.min-1 for pedalling rates of 40, 60, 80, 100 and 120 rev.min-1, respectively). Thus a significant increase in [La]pi and a decrease in blood pH do not play a major role in the mechanism(s) responsible for the slow component of VO2 kinetics in
humans.