Breakdown of high-energy phosphate compounds and lactate accumulation during short supramaximal exercise

Abstract

Muscle ATP, creatine phosphate and lactate, and blood pH and lactate were measured in 7 male sprinters before and after running 40, 60, 80 and 100 m at maximal speed. The sprinters were divided into two groups, group 1 being sprinters who achieved a higher maximal speed (10.07 +/- 0.13 m X s-1) than group 2 (9.75 +/- 0.10 m X s-1), and who also maintained the speed for a longer time. The breakdown of high-energy phosphate stores was significantly greater for group 1 than for group 2 for all distances other than 100 m; the breakdown of creatine phosphate for group 1 was almost the same for 40 m as for 100 m. Muscle and blood lactate began to accumulate during the 40 m exercise. The accumulation of blood lactate was linear (0.55 +/- 0.02 mmol X s-1 X l-1) for all distances, and there were no differences between the groups. With 100 m sprints the end-levels of blood and muscle lactate were not high enough and the change in blood pH was not great enough for one to accept that lactate accumulation is responsible for the decrease in running speed over this distance. We concluded that in short-term maximal exercise, performance depends on the capacity for using high-energy phosphates at the beginning of the exercise, and the decrease in running speed begins when the high-energy phosphate stores are depleted and most of the energy must then be produced by glycolysis.

Mathematical modelling and analysis of elite athletes’ sprint data to study the rate and regulation of ATP during a maximal exercise of short duration

“…306 All the athletes speed started to reduce at around 5 to 7 seconds during this sprint race and also in 307 the previous studies (Hirvonen et al, 1987). Figure 5 shows this reduce in speed synchronised 308 with the highest rate of decay of the PCr utilisation energy curve.…”

“…Nevertheless, Bogdanis' observations find that there was no correlation between 317 the percentage of PCr and MPO during the last 20-s of the sprint (Bogdanis et al, 1996). In 318 addition, the observations ofBogdanis that an independent study by Hirvonen et al (1987) 319 established, in a series of maximal cycling sprints (40 -100m), that skeletal PCr stores were 320 severely drained after 5 to 7-s. Interestingly, the elite sprinters used more of their available PCr …”

Human muscle metabolism during intermittent maximal exercise

“…In human studies, the decline in maximal power output is noted within the first few seconds of maximal dynamic exercise (Wooton, 1984;Cheetham et al, 1986), possibly suggesting that the tremendously high rates of AlP resynthesis required to sustain such a high power output, could only be maintained for a few seconds. Indeed, under such conditions most of the PCr store is utilised, though not depleted, and a small decrease in ATP concentration is also observed (Boobis et al, 1982;Hirvonen, Rehunen, Rusko and Harkonen, 1987). However, during intermittent maximal isokinetic cycling, the ensuing maximal power output was reported to be substantially less in successive bouts than in the initial exercise period (30s) although resynthesis of PCr was almost complete in the recovery period (4mm), (McCartney et al, 1986).…”

Comparação da potência anaeróbia entre as posições táticas em jogadores de futebol: estudo retrospectivo

“…Isto pode ter sido mais evidente em atletas que apresentaram maiores valores de Pmáx como os LA. Hirvonen et al, 28 observaram em grupo de velocistas de elite, que os atletas com maiores velocidades depletavam seus estoques de PCr em uma maior taxa que os corredores com menores velocidade do mesmo grupo, o que sugere que além da maior participação de PCr há uma menor taxa de ressíntese nos sprints subsequentes.…”