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Late cardiovascular drift observable during ultra endurance exercise.
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Björn Ekbloms forskningsgrupp.ORCID-id: 0000-0002-0642-4838
Institutionen för Medicin, Enheten för kardiologi, Karolinska Universitetssjukhuset.
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Björn Ekbloms forskningsgrupp.ORCID-id: 0000-0002-1343-8656
Institutionen för Medicin, Enheten för kardiologi, Karolinska Universitetssjukhuset.
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2011 (Engelska)Ingår i: Medicine & Science in Sports & Exercise, ISSN 0195-9131, E-ISSN 1530-0315, Vol. 43, nr 7, s. 1162-1168Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Introduction: The present study investigates the adaptation of the central circulation to ultraenduranceexercise, including the relative contributions of changes in stroke volume (SV) andarterio-venous oxygen difference (a-v O2 diff) to the increased oxygen pulse (VO2/HR).Methods: We evaluated subjects undergoing 12h of mixed exercise at controlled intensity(n=8) and a 53h Adventure race (n=20). Heart rate (HR), oxygen uptake (VO2), and cardiacoutput determined using non-invasive gas rebreathing (CORB) were measured during cyclingat fixed work rate after 0, 4, 8, 12 hours, and 0, 20, and 53 hours of continuous exercise in the12 and 53 h protocol, respectively.Results and Conclusion: The central circulation changed in several steps in response to ultraenduranceexercise. Compared to initial levels, VO2 was increased at every time-point measured.The increase was attributed to peripheral adaptations, confirmed by a close correlation betweenchange in VO2 and change in a-v O2 diff. The first step of the circulatory response was typical ofnormal (early) cardiovascular drift, with increased HR and concomitantly decreased SV andVO2/HR, occurring over the first 4-6 h. The second step, which continued until approximately 12h, included reversed HR-drift, with normalization of SV and VO2/HR. When exercise continueduntil 50 h late cardiovascular drift was noted, characterized by increased VO2/HR, (indicatingmore efficient energy distribution), decreased peripheral resistance, increased stroke volume, anddecreased work of the heart. Since cardiac output was maintained at all time points we interpretthe changes as physiologically appropriate adaptations to ultra-endurance exercise.

Ort, förlag, år, upplaga, sidor
2011. Vol. 43, nr 7, s. 1162-1168
Nyckelord [en]
Cardiac output, oxygen uptake, heart rate, stroke volume, oxygen pulse, adventure race
Nationell ämneskategori
Fysiologi
Forskningsämne
Medicin/Teknik
Identifikatorer
URN: urn:nbn:se:gih:diva-1507DOI: 10.1249/MSS.0b013e318208f773OAI: oai:DiVA.org:gih-1507DiVA, id: diva2:371921
Projekt
Physiology of Adventure RacingTillgänglig från: 2010-11-23 Skapad: 2010-11-23 Senast uppdaterad: 2018-01-12Bibliografiskt granskad
Ingår i avhandling
1. Physiology of Adventure Racing: with emphasis on circulatory response and cardiac fatigue
Öppna denna publikation i ny flik eller fönster >>Physiology of Adventure Racing: with emphasis on circulatory response and cardiac fatigue
2011 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

The overall aims of this thesis were to elucidate the circulatory responses to ultra-endurance exercise (Adventure Racing), and furthermore, to contribute to the clarification of the so called “exercise-induced cardiac fatigue” in relation to said exercise. An Adventure race (AR) varies in duration from six hours to over six days, in which the participants have to navigate through a number of check-points over a pre-set course, using a combination of three or more endurance/outdoor sports, e.g., cycling, running, and kayaking. This thesis is based on the results from four different protocols; 12- and 24-h (n = 8 and 9, respectively) in a controlled setting with fixed exercise intensity, and 53-h and 5-7-day (n = 15 in each) in field setting under race conditions. The subjects in all protocols were experienced adventure racing athletes, competitive at elite level. Study I and II address the circulatory responses and cardiovascular drift, using methods for monitoring heart rate (HR), oxygen uptake (VO2), cardiac output (non-invasive re-breathing) and blood pressure, during ergometer cycling at fixed steady state work rate at periods before, during and after the ultra-endurance exercise. In Study III and IV we examined the possible presence of exercise-induced cardiac fatigue after a 5-7-day AR, from two different perspectives. In Study III analyses were performed with biochemical methods to determine circulating levels of cardiac specific biomarkers (i.e., creatine kinase isoenzyme MB (CK-MB), troponin I, B-type natriuretic peptide (BNP) and N-terminal prohormonal B-type natriuretic peptide (NT-proBNP)). We also made an attempt to relate increases in biomarkers to rated relative performance. In Study IV we used tissue velocity imaging (TVI) (VIVID I, GE VingMed Ultrasound, Norway) to determine whether the high workload (extreme duration) would induce signs of functional cardiac fatigue similar to those that occur in skeletal muscle, i.e., decreased peak systolic velocities. Using conventional echocardiography we also evaluated whether the hearts of experienced ultra-endurance athletes are larger than the normal upper limit. The central circulation changed in several steps in response to ultra-endurance exercise. Compared to initial levels, VO2 was increased at every time-point measured. The increase was attributed to peripheral adaptations, confirmed by a close correlation between change in VO2 and change in arteriovenous oxygen difference. The first step of the circulatory response was typical of normal (early) cardiovascular drift, with increased HR and concomitantly decreased stroke volume (SV) and oxygen pulse (VO2/HR), occurring over the first 4-6 h. The second step, which continued until approximately 12h, included reversed HR-drift, with normalisation of SV and VO2/HR. When exercise continued for 50 h a late cardiovascular drift was noted, characterised by increased VO2/HR, (indicating more efficient energy distribution), decreased peripheral resistance, increased SV, and decreased work of the heart. Since cardiac output was maintained at all-time points we interpret the changes as physiologically appropriate adaptations. Our findings in Study III point towards a distinction between the clinical/pathological and the physiological/exercise-induced release of cardiac biomarkers. The results imply that troponin and CKMB lack relevance in the (healthy) exercise setting, but that BNP, or NT-proBNP adjusted for exercise duration, might be a relevant indicator for impairment of exercise performance. High levels of NTproBNP, up to 2500 ng · l -1 , can be present after ultra-endurance exercise in healthy athletes without any subjective signs or clinical symptoms of heart failure. However, these high levels of NT-proBNP seemed to be associated with decreased relative exercise performance, and might be an indicator of the cardiac fatigue that has previously been described after endurance exercise. Study IV revealed that the sizes of the hearts (left ventricle) of all of our ultra-endurance athletes were within normal limits. The measurements of peak systolic velocities showed (for group average) no signs of cardiac fatigue even after 6 days of continuous exercise. This discrepancy between ours and other studies, involving e.g., marathon or triathlon, might reflect the fact that this type of exercise is performed at relatively low average intensity, suggesting that the intensity, rather than the duration, of exercise is the primary determinant of cardiac fatigue.

Ort, förlag, år, upplaga, sidor
Stockholm: Karolinska Institutet, 2011. s. 112
Nyckelord
cardiovascular drift, cardiac fatigue, adventure race, cardiac biomarkers, cardoac function, exercise echocardiography
Nationell ämneskategori
Fysiologi Kardiologi Idrottsvetenskap
Forskningsämne
Medicin/Teknik
Identifikatorer
urn:nbn:se:gih:diva-1754 (URN)978-91-7457-262-9 (ISBN)
Disputation
2011-03-25, Aulan GIH, Lidingövägen 1, Stockholm, 09:00 (Engelska)
Opponent
Handledare
Projekt
Physiology of Adventure Racing
Tillgänglig från: 2011-03-04 Skapad: 2011-03-03 Senast uppdaterad: 2018-01-12Bibliografiskt granskad

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Mattsson, C. MikaelLarsen, FilipEkblom, Björn

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