TY - BOOK
T1 - Effects of Exercise Training on Haematology and Maximal Cardiac Output
AU - Bonne, Thomas Christian
N1 - CURIS 2015 NEXS 160
PY - 2015
Y1 - 2015
N2 - Qmax may increase within a few weeks of exercise and the underlying mechanisms leading to this are likely to be multi-factorial. Plasma volume is generally thought to rapidly increase in response to exercise training driving an increase in Qmax and hence VO2max. Structural and functional changes to the heart ultra structure possibly also play a role for improving Qmax. Other mechanisms that can improve exercise capacity include hypoxia. It is universally accepted that hypoxia is a main stimulant of erythropoiesis and altitude training is considered a possibility to increase red blood cell volume and hence exercise performance in elite athletes. However, the efficacy of altitude training for sea level performance is still debated and the literature is divergent on this matter. Even if the haematological changes following altitude training may be inadequate to substantially improve performance they can be a challenge in an anti-doping context. In study I nine individuals performed six weeks of endurance exercise. Intravascular volumes, Qmax and VO2max were measured before and after the training intervention. Any increases in BV were then restored by phlebotomy. After the training period, PV, RCV, and BV increased (all P < 0.05) by 147 ± 168 ml (5 ± 5%), 235 ± 64 ml (10 ± 3%), and 382 ± 204 ml (7 ± 4%), respectively. The endurance training intervention resulted in an increased Qmax from 18.9 ± 2.1 l · min-1 to 20.4 ± 2.3 l · min-1 (9 ± 6%, %TE 5.5%) (P < 0.05).
Concomitantly, VO2max increased 10 ± 7% (P < 0.05). After normalization of BV by phlebotomy Qmax returned to pre-training values (18.1 ± 2.5 l.min-1 ; 12 ± 5% reversal P < 0.05) and VO2max decreased by 8 ± 7% after phlebotomy (P < 0.05). Resting measurements of the myocardium by echocardiography was
performed with the subject in a left lateral decubitus position. Left ventricular morphology, diastolic and systolic function was measured before and after training. Measurements revealed no structural adaptations or differences after the training intervention. Left ventricular wall thickness, mass, enddiastolic
and systolic diameter as well as shortening fraction, stroke volume (SV), heart rate and Q was unchanged. This is the first study to add simultaneous measurements of cardiac morphology, BV and Qmax following a six week endurance training period and experimentally reverse the effects by phlebotomy.
In study II the effects of a classical altitude training camp on Hbmass and VO2max were studied in 10 Olympic swimmers. Ten swimmers of comparable characteristics were chosen for a sea level control group. Both the altitude and sea level group completed a similar training intervention at either altitude or sea level. Hbmass significantly increased after altitude training by 6.2 ± 3.9% (P < 0.05) in the altitude group whereas no changes were apparent in the sea level group. Swimming VO2max was similar before and after training camps in both groups (LHTH: n = 7, SL: n = 6). Maximal 200 m speed reached in an incremental swimming step-test (P = 0.051) and time to complete 3000 m tended (P = 0.09) to increase in LHTH but not after sea level training.
In study III haematological parameters were determined weekly three times before and four times after classical altitude and sea level training and ABP thresholds for [Hb], %ret, OFF-score and the abnormal blood profile score (ABPS) were generated using the official ABP software. After altitude training, six swimmers exceeded the 99% ABP thresholds: Two swimmers exceeded the OFF-score thresholds at day 7; One swimmer exceeded the OFF-score threshold at day 28; One swimmer exceeded the threshold for %ret at day 14; One swimmer surpassed the ABPS threshold at day 7 and one swimmer exceeded the ABPS threshold 28 days after altitude training. No values exceeded the individual thresholds in the control group.
In conclusion, this thesis demonstrated that BV is a main determinant of the exercise induced increase in Qmax whereas structural changes to the heart may require years of training to exert an effect. Classical altitude training has the potential to further increase Hbmass and BV through an elevation in RCV and a
strong tendency towards improvements in performance was demonstrated. Moreover, these haematological changes affect the parameters in Athlete Biological Passport that could cause individual reference values to be exceeded up to a month following altitude training.
AB - Qmax may increase within a few weeks of exercise and the underlying mechanisms leading to this are likely to be multi-factorial. Plasma volume is generally thought to rapidly increase in response to exercise training driving an increase in Qmax and hence VO2max. Structural and functional changes to the heart ultra structure possibly also play a role for improving Qmax. Other mechanisms that can improve exercise capacity include hypoxia. It is universally accepted that hypoxia is a main stimulant of erythropoiesis and altitude training is considered a possibility to increase red blood cell volume and hence exercise performance in elite athletes. However, the efficacy of altitude training for sea level performance is still debated and the literature is divergent on this matter. Even if the haematological changes following altitude training may be inadequate to substantially improve performance they can be a challenge in an anti-doping context. In study I nine individuals performed six weeks of endurance exercise. Intravascular volumes, Qmax and VO2max were measured before and after the training intervention. Any increases in BV were then restored by phlebotomy. After the training period, PV, RCV, and BV increased (all P < 0.05) by 147 ± 168 ml (5 ± 5%), 235 ± 64 ml (10 ± 3%), and 382 ± 204 ml (7 ± 4%), respectively. The endurance training intervention resulted in an increased Qmax from 18.9 ± 2.1 l · min-1 to 20.4 ± 2.3 l · min-1 (9 ± 6%, %TE 5.5%) (P < 0.05).
Concomitantly, VO2max increased 10 ± 7% (P < 0.05). After normalization of BV by phlebotomy Qmax returned to pre-training values (18.1 ± 2.5 l.min-1 ; 12 ± 5% reversal P < 0.05) and VO2max decreased by 8 ± 7% after phlebotomy (P < 0.05). Resting measurements of the myocardium by echocardiography was
performed with the subject in a left lateral decubitus position. Left ventricular morphology, diastolic and systolic function was measured before and after training. Measurements revealed no structural adaptations or differences after the training intervention. Left ventricular wall thickness, mass, enddiastolic
and systolic diameter as well as shortening fraction, stroke volume (SV), heart rate and Q was unchanged. This is the first study to add simultaneous measurements of cardiac morphology, BV and Qmax following a six week endurance training period and experimentally reverse the effects by phlebotomy.
In study II the effects of a classical altitude training camp on Hbmass and VO2max were studied in 10 Olympic swimmers. Ten swimmers of comparable characteristics were chosen for a sea level control group. Both the altitude and sea level group completed a similar training intervention at either altitude or sea level. Hbmass significantly increased after altitude training by 6.2 ± 3.9% (P < 0.05) in the altitude group whereas no changes were apparent in the sea level group. Swimming VO2max was similar before and after training camps in both groups (LHTH: n = 7, SL: n = 6). Maximal 200 m speed reached in an incremental swimming step-test (P = 0.051) and time to complete 3000 m tended (P = 0.09) to increase in LHTH but not after sea level training.
In study III haematological parameters were determined weekly three times before and four times after classical altitude and sea level training and ABP thresholds for [Hb], %ret, OFF-score and the abnormal blood profile score (ABPS) were generated using the official ABP software. After altitude training, six swimmers exceeded the 99% ABP thresholds: Two swimmers exceeded the OFF-score thresholds at day 7; One swimmer exceeded the OFF-score threshold at day 28; One swimmer exceeded the threshold for %ret at day 14; One swimmer surpassed the ABPS threshold at day 7 and one swimmer exceeded the ABPS threshold 28 days after altitude training. No values exceeded the individual thresholds in the control group.
In conclusion, this thesis demonstrated that BV is a main determinant of the exercise induced increase in Qmax whereas structural changes to the heart may require years of training to exert an effect. Classical altitude training has the potential to further increase Hbmass and BV through an elevation in RCV and a
strong tendency towards improvements in performance was demonstrated. Moreover, these haematological changes affect the parameters in Athlete Biological Passport that could cause individual reference values to be exceeded up to a month following altitude training.
UR - https://rex.kb.dk/primo-explore/fulldisplay?docid=KGL01009129834&context=L&vid=NUI&search_scope=KGL&tab=default_tab&lang=da_DK
M3 - Ph.D. thesis
SN - 978-87-7611-835-8
BT - Effects of Exercise Training on Haematology and Maximal Cardiac Output
PB - Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen
CY - Copenhagen
ER -