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This article has a correction

Please see: Br J Sports Med 2009;43:310

Br J Sports Med 2008;42:889-893 doi:10.1136/bjsm.2007.043786
  • Original article

High-intensity ultraendurance promotes early release of muscle injury markers

  1. A Bessa1,
  2. M Nissenbaum1,
  3. A Monteiro1,
  4. P G Gandra4,
  5. L S Nunes4,
  6. A Bassini-Cameron1,3,
  7. J P S Werneck-de-Castro1,5,6,
  8. D Vaz de Macedo4,
  9. L-C Cameron1,2,3
  1. 1
    Laboratory of Protein Biochemistry – Federal University of State of Rio de Janeiro, Rio de Janeiro, Brazil
  2. 2
    Graduate Programme in Human Movement Science – University Castelo Branco, Rio de Janeiro, Brazil
  3. 3
    Institute of Genetics and Biochemistry – Federal University of Uberlândia, Uberlândia, Brazil
  4. 4
    Laboratory of Exercise Biochemistry – State University of Campinas, Campinas, Brazil
  5. 5
    Department of Bioscience of Physical Activity – EEFD – Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
  6. 6
    Laboratory of Cellular and Molecular Biology – IBCCF – Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
  1. Professor LC Cameron, Universidade Federal do Estado do Rio de Janeiro Laboratório de Bioquímica de Proteínas, Av. Pasteur, 296 Urca Rio de Janeiro CEP 22290–240, Brazil; cameron{at}unirio.br
  • Accepted 12 December 2007
  • Published Online First 18 January 2008

Abstract

Objective: To evaluate the impact of high-intensity ultraendurance (HIU) cycling, using it as a possible way to understand muscle injury kinetics and blood immune cells’ release during high-intensity prolonged exercise

Design: Male amateur triathletes enrolled during a cycling race of the International Bike Championship 800 km cycling relay (~23 h). Each athlete alternately cycled 20–25 minutes until exhaustion and performed a total of approximately 200 km.

Results: Creatine kinase levels in blood reached a 300% rise in a sigmoidal pattern, while lactate dehydrogenase levels increased by 30–40% following a hyperbolic pattern. Aspartate aminotransferase and alanine aminotransferase levels increased by up to 250% and 140%, respectively. Liver injury markers such as alkaline phosphatase and γ-glutamyltransferase remained stable. Platelets increased by 20–30% from pre-exercise, and there was no change in haematocrit during the race. White blood cells rose by nearly 200%. Leucocytes rose 210% during the race, with a major component coming from neutrophils, which increased more than 300%. Triacylglycerol levels were decreased at the finish and total cholesterol levels remained unchanged. Urate increased (by up to 35%) during the first half of the race, and urea levels increased with a different pattern, increasing by 45% in the second half.

Conclusions: This study showed the blood appearance kinetics of muscle injury markers and some metabolites. It is suggested that the increase in these enzymes came primarily from muscle damage, rather than liver damage, and that white blood cells are selectively mobilised independently of haemoconcentration. The early appearance of muscle injury markers in this kind of exercise was also shown.

Footnotes

  • Competing interests: None.

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