Mechanisms underlying extremely fast muscle V˙O2 on-kinetics in humans.

The time constant of the primary phase of pulmonary V˙O2 on-kinetics (τp ), which reflects muscle V˙O2 kinetics during moderate-intensity exercise, is about 30 s in young healthy untrained individuals, while it can be as low as 8 s in endurance-trained athletes. We aimed to determine the intramuscular factors that enable very low values of t0.63 to be achieved (analogous to τp , t0.63 is the time to reach 63% of the V˙O2 amplitude). A computer model of oxidative phosphorylation (OXPHOS) in skeletal muscle was used. Muscle t0.63 was near-linearly proportional to the difference in phosphocreatine (PCr) concentration between rest and work (ΔPCr). Of the two main factors that determine t0.63 , a huge increase in either OXPHOS activity (six- to eightfold) or each-step activation (ESA) of OXPHOS intensity (>3-fold) was needed to reduce muscle t0.63 from the reference value of 29 s (selected to represent young untrained subjects) to below 10 s (observed in athletes) when altered separately. On the other hand, the effect of a simultaneous increase of both OXPHOS activity and ESA intensity required only a twofold elevation of each to decrease t0.63 below 10 s. Of note, the dependence of t0.63 on OXPHOS activity and ESA intensity is hyperbolic, meaning that in trained individuals a large increase in OXPHOS activity and ESA intensity are required to elicit a small reduction in τp . In summary, we postulate that the synergistic action of elevated OXPHOS activity and ESA intensity is responsible for extremely low τp (t0.63 ) observed in highly endurance-trained athletes

Marathon race performance increases the amount of particulate matter deposited in the respiratory system of runners: an incentive for “clean air marathon runs”

Background In the last decades, marathon running has become a popular form of physical activity among people around the world. It should be noticed that the main marathon races are performed in large cities, where air quality varies considerably. It is well established that breathing polluted air results in a number of harmful effects to the human body. However, there have been no studies to show the impact of marathon run performance on the amount of the deposition of varied fractions of airborne particulate matter (PM) in the respiratory tract of runners. This is why the present study sought to determine the impact of marathon run performance in the air of varying quality on the deposition of the PM1, PM2.5, PM10 in the respiratory tract in humans. Methods The PM1, PM2.5 and PM10 deposition was determined in an “average runner” (with marathon performance time 4 h: 30 min) and in an “elite marathon runner” (with marathon performance time 2 h: 00 min) at rest, and during a marathon race, based on own measurements of the PM content in the air and the size-resolved DF(d) profile concept. Results We have shown that breathing air containing 50 µg m−3 PM10 (a borderline value according to the 2006 WHO standard - still valid) at minute ventilation (VE) equal to 8 L min−1 when at rest, resulted in PM10deposition rate of approximately 9 µg h−1, but a marathon run of an average marathon runner with the VE = 62 L min−1 increased the deposition rate up to 45 µg h−1. In the elite runner, marathon run with the VE= 115 L min−1 increased PM10 deposition rate to 83 µg h−1. Interestingly, breathing the air containing 50 µg m−3of PM10 at the VE = 115 L min−1by the elite marathon runner during the race resulted in the same PM10deposition rate as the breathing highly polluted air containing as much as 466 µg m−3 of PM10 when at rest. Furthermore, the total PM10 deposition in the respiratory tract during a marathon race in average runners is about 22% greater (203 / 166 = 1.22) than in elite runners. According to our calculations, the concentration of PM10in the air during a marathon race that would allow one not to exceed the PM10 deposition rate of 9 µg h−1should be lower than 10 µg m−3 in the case of an average runner, and it should be lower than 5.5 µg m−3 in the case of an elite runner. Conclusions We conclude that a marathon run drastically increases the rate of deposition of the airborne PM in the respiratory tract of the runners, as a consequence of the huge VE generated during the race. A decrease of the PM content in the air attenuates this rate. Based on our calculations, we postulate that the PM10 content in the air during a “clean air marathon run”, involving elite marathon runners, should be below 5.5 µg m−3

Mechanisms of attenuation of pulmonary V'O_{2} slow component in humans after prolonged endurance training

In this study we have examined the effect of prolonged endurance training program on the pulmonary oxygen uptake (V'O2 ) kinetics during heavy-intensity cycling-exercise and its impact on maximal cycling and running performance. Twelve healthy, physically active men (mean\ub1SD: age 22.33\ub11.44 years, V'O2peak 3198\ub1458 mL \ub7 min-1 ) performed an endurance training composed mainly of moderate-intensity cycling, lasting 20 weeks. Training resulted in a decrease (by 3c5%, P = 0.027) in V'O2 during prior low-intensity exercise (20 W) and in shortening of \u3c4 p of the V'O2 on-kinetics (30.1\ub15.9 s vs. 25.4\ub11.5 s, P = 0.007) during subsequent heavy-intensity cycling. This was accompanied by a decrease of the slow component of V'O2 on-kinetics by 49% (P = 0.001) and a decrease in the end-exercise V'O2 by 3c5% (P = 0.005). An increase (P = 0.02) in the vascular endothelial growth factor receptor 2 mRNA level and a tendency (P = 0.06) to higher capillary-to-fiber ratio in the vastus lateralis muscle were found after training (n = 11). No significant effect of training on the V'O2peak was found (P = 0.12). However, the power output reached at the lactate threshold increased by 19% (P = 0.01). The power output obtained at the V'O2peak increased by 14% (P = 0.003) and the time of 1,500-m performance decreased by 5% (P = 0.001). Computer modeling of the skeletal muscle bioenergetic system suggests that the training-induced decrease in the slow component of V'O2 on-kinetics found in the present study is mainly caused by two factors: an intensification of the each-step activation (ESA) of oxidative phosphorylation (OXPHOS) complexes after training and decrease in the "additional" ATP usage rising gradually during heavy-intensity exercise

Factors determining the oxygen consumption rate (\dot{V}o_{2}) on-kinetics in skeletal muscles

Using a computer model of oxidative phosphorylation developed previously [Korzeniewski and Mazat (1996) Biochem. J. 319, 143-148; Korzeniewski and Zoladz (2001) Biophys. Chem. 92, 17-34], we analyse the effect of several factors on the oxygen-uptake kinetics, especially on the oxygen consumption rate (VO2) and half-transition time t(1/2), at the onset of exercise in skeletal muscles. Computer simulations demonstrate that an increase in the total creatine pool [PCr+/-Cr] (where Cr stands for creatine and PCr for phosphocreatine) and in glycolytic ATP supply lengthen the half-transition time, whereas increase in mitochondrial content, in parallel activation of ATP supply and ATP usage, in oxygen concentration, in proton leak, in resting energy demand, in resting cytosolic pH and in initial alkalization decrease this parameter. Theoretical studies show that a decrease in the activity of creatine kinase (CK) [displacement of this enzyme from equilibrium during on-transient (rest-to-work transition)] accelerates the first stage of the VO2 on-transient, but slows down the second stage of this transient. It is also demonstrated that a prior exercise terminated a few minutes before the principal exercise shortens the transition time. Finally, it is shown that at a given ATP demand, and under conditions where CK works near the thermodynamic equilibrium, the half-transition time of VO2 kinetics is determined by the amount of PCr that has to be transformed into Cr during rest-to-work transition; therefore any factor that diminishes the difference in [PCr] between rest and work at a given energy demand will accelerate the VO2 on-kinetics. Our conclusions agree with the general idea formulated originally by Easterby [(1981) Biochem. J. 199, 155-161] that changes in metabolite concentrations determine the transition times between different steady states in metabolic systems