Hoppel 2015 Abstract MiP2015

From Bioblast
Effects of ultramarathon performance on mitochondrial respiration in human platelets.


Hoppel F, Calabria E, Pesta D, Burtscher M, Gnaiger E (2015)

Event: MiP2015

Acute strenuous exercise is linked to severe inflammatory responses [1,2], alterations of mitochondrial function of human skeletal muscle and increased oxidative stress [3]. Due to the invasive nature of muscle biopsies, minimally-invasive alternatives to study mitochondrial function in tissues such as blood cells are gaining significance. Mitochondrial function in human platelets and lymphocytes has been characterized in various disease states. Importantly, respiratory capacity of human PBMCs was linked to physical fitness [4], supporting the concept that mitochondrial function in human blood cells can be used as a systemic mitochondrial marker. In this study we investigated the influence of completion of an ultramarathon on mitochondrial respiration in human platelets.

After informed consent, 10 male recreational athletes (mean age: 39.9 yrs; BMI 24.9 kg2/m) who participated in a competition over 67 km and approximately 4,500 m ascent, were included in the study. Baseline (PRE) measurements were performed on the day before the competition and follow-up sampling was performed within 15 min after finishing the race (POST) by sampling whole blood. To address potential effects of recovery, a third time point was selected 24 h after finishing (REC). Evaluation of mitochondrial respiration was conducted in freshly purified human platelets by the use of six Oroboros Oxygraph-2k operating in parallel. ROUTINE respiration (R), Complex I-linked LEAK and OXPHOS capacity (CI), and CI&II-linked OXPHOS and ET capacity were determined in a single SUIT protocol. Additionally, neutrophils, monocytes and lymphocytes (inflammatory response), creatine kinase (CK; muscular damage) and plasma markers of oxidative damage and repair were quantified at baseline and after the race.

Absolute concentrations of all leukocyte subgroups and serum creatine kinase were changed significantly after the race. No significant changes were found in respiratory substrate control ratios CI/CI&II and CII/CI&II, neither when comparing PRE and POST, nor between POST and recovery. However, the ROUTINE coupling control ratio, R/E (ROUTINE respiration of intact cells, R, divided by uncoupler-stimulated electron transfer-pathway capacity, E) was increased significantly (+25,4% PRE vs. POST; +9,5% PRE vs. REC; p<0.05), indicating the influence of massive physical strain and time of recovery on human platelet metabolism. We found a significant (p<0,05) relationship between BMI and CI/CI&II ratio, whereas age and training time per week were without significant effects on platelet metabolism.

โ€ข O2k-Network Lab: AT Innsbruck Oroboros, AT Innsbruck Burtscher M, IT Verona Calabria E, DE Cologne Pesta D


1-OROBOROS INSTRUMENTS, Innsbruck; 2-Dept Sport Science, Univ Innsbruck, Austria; 3-Dept Neurological Movement Sc, Univ Verona, Italy; 4-D Swarovski Research Lab, Dept Visceral, Transplant, Thoracic Surgery, Med Univ Innsbruck, Austria. - [email protected]

Abstract continued

Alterations in leukocyte content are indicating inflammatory responses to ultramarathon performance. Interestingly, our results demonstrate no significant alterations of the CI/CI&II and CII/CI&II ratios (but compare ref.[2]), indicating no significant changes in the control of flux through these respiratory complexes. However, a significant change of the R/E ratio indicates changes in platelet metabolism. Blood cells emerge as indicators of systemic mitochondrial function [4], including responses to strenuous exercise. The approach can be considered as non-invasive, enabling multiple measurements in time series and extending such studies to a larger number and variety of persons with an interest in obtaining information on their mitochondrial fitness.

References and acknowledgements

  1. de Gonzalo-Calvo D, Dรกvalos A, Montero A, Garcรญa-Gonzรกlez A, Tyshkovska I, Gonzรกlez-Medina A, Soares S, Martรญnez-Camblor P, Casas-Agustench P, Rabadรกn M, Dรญaz-Martรญnez AE, รšbeda N, Iglesias-Gutiรฉrrez E (2015) Circulating inflammatory miRNA signature in response to different doses of aerobic exercise. J Appl Physiol 2:124-34.
  2. de Lucas DR, Caputo F, Mendes de Souza K, Sigwalt AR, Ghisoni K, Lock Silveira PC, Remor AP, da Luz Scheffer D, Antonacci Guglielmo LG, Latini A (2014) Increased platelet oxidative metabolism, blood oxidative stress and neopterin levels after ultraendurance exercise. J Sports Sci 32:22-30.
  3. Tonkonogi M, Walsh B, Svensson M, Sahlin K (2000) Mitochondrial function and antioxidative defence in human muscle: effects of endurance training and oxidative stress. J Physiol 528:379-88.
  4. Tyrrell DJ, Bharadwaj MS, Van Horn CG, Marsh AP, Nicklas BJ, Molina A (2015) Blood-cell bioenergetics are associated with physical function and inflammation in overweight/obese older adults. Exp Gerontol, doi: 10.1016/j.exger.2015.07.015.

Supported by K-Regio project MitoFit and Oroboros.

Labels: MiParea: Respiration, Exercise physiology;nutrition;life style 

Stress:Oxidative stress;RONS  Organism: Human  Tissue;cell: Blood cells, Platelet  Preparation: Permeabilized cells 

Coupling state: ROUTINE, OXPHOS, ET  Pathway: N, S, NS  HRR: Oxygraph-2k  Event: E1, Poster  MiP2015 

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