Limiting factors of performance at moderate altitude : consequences for training.
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1 Limiting factors of performance at moderate altitude : consequences for training. Granada Feb 28 Jean-Paul Richalet Laboratoire Réponses cellulaires et fonctionnelles à l hypoxie, Hôpital Avicenne, Bobigny Université Paris 3 - FRANCE
2 BIOLOGICAL DEFINITION OF ALTITUDE 8848 m life impossible? Extreme altitude permanent life impossible 55 m 3 m 2 m High altitude effects at rest training zone Moderate altitude effects on aerobic exercice m Low altitude no effect
3 V 2 max (% NM) training zone Summit of Mt Everest P B (mmhg) Maximal aerobic power (VO 2 max) decreases with altitude Consequence: Training load must be lower when training at high altitude Question? What are the limiting factors of performance? Altitude (km)
4 . VO 2max (ml/min/kg) Female subjects ALTITUDE (m) TW trained UW untrained Male subjects ALTITUDE (m) trained untrained hypoxia vs normoxia trained vs untrained Trained subjects show a greater decrease in VO 2 max with acute hypoxia Woorons et al. 25; Mollard et al., 26; Mollard et al., 27
5 Central control O 2 CO 2 Pulmonary ventilation : CONVECTION O 2 CO 2 Alveolo-capillary transfer of oxygen : DIFFUSION Right heart Left heart Transport of oxygen by the blood : CONVECTION cell O 2 CO 2 oxygen consumption Diffusion of oxygen to the tissues : DIFFUSION Aerobic production of energy
6 Decrease in arterial O 2 saturation at rest and exercise with increasing altitude 9 Rest Maximal exercise SaO 2 (%) Altitude (m)
7 SaO 2 (%) # # SaO 2 at maximal exercise # MALES # untrained trained Altitude (m) # # SaO 2 (%) # # FEMALES Altitude (m) # untrained trained # hypoxia vs normoxia # trained vs untrained Trained subjects show a greater desaturation at exercise in acute hypoxia Woorons et al. 25; Mollard et al., 26
8 Chemoreceptors and acclimatization: Ventilation increases at rest and at each level of exercise
9 Carotid chemoreceptors : hypoxic sensors Blood vessel O 2 O 2 O 2 Glomus cell 2. Oxygen detection 2. Na and Ca action potential (Ca influx) 3. Rise in cytosolic Ca 4. Transmitter release 5. Increase of firing in afferent fibers 3 Nerve ending 2 Ca 2+ influx 4 5 From Lopez-Barneo et al., NIPS, 993 to CNS
10 Max. cardiac output (L/min) Male subjects Female subjects 3 24 Trained 26 Trained Untrained TS US 2 8 Untrained TW UW ALTITUDE (m) ALTITUDE (m) Maximal cardiac output does not change in acute hypoxia Woorons et al. 25; Mollard et al., 26; Mollard et al., 27
11 Adaptation of heart rate in acute and chronic hypoxia 2 Heart rate (beat/min) rest, acute hypoxia max, acute hypoxia maximal, chronic hypoxia rest, chronic hypoxia Altitude (km) Favret and Richalet, 27
12 Hypoxia norepinephrine adenosine acetylcholine Myocyte cell membrane -AR Gs A Adenylate cyclase - Gi M2 + AMPc ITl IF ICa cytosol From: Lerman and Belardinelli, Circulation, 99 ; Richalet et al. 99; Favret and Richalet, 27 IK Ach, Ado
13 QaO 2max (l.min - ) Male subjects trained untrained TS US 4,5 4 3,5 3 2,5 2 Female subjects untrained trained TW SW O 2 transport and extraction of trained and untrained subjects converge at 45m Da-vO 2max (ml.l - ) untrained trained TS US untrained trained TW UW ALTITUDE (m)
14 6 5. _ Q(CaO 2 -CvO 2 ) _ Untrained subjects DO 2 x PvO 2 VO 2 (l.min - ) VO2 max sea level m 25m 45m _ PvO 2 (mmhg)
15 6 5 _ DO 2 x PvO 2. VO2 max Trained subjects VO 2 (l.min - ) _ Q(CaO 2 -CvO 2 ) sea level m 25m 45m _ PvO limit _ 6 8 PvO 2 (mmhg)
16 Subjects 5 endurance trained athletes (59.6 ± 2.8 ml/min/kg) and 6 physically active men (46.2 ± 2.8 ml/min/kg). Protocol Each subject performed five VO 2 peak tests on a cyclo-ergometer at 4 different simulated altitudes: m, m, 25m and 4m Measurements Usual ventilatory and cardio-vascular parameters Cardiac output using thransthoracic bioimpedance Muscle tissue HbO 2 and HHb using Near InfraRed Spectroscopy (NIRS; InSpectra Tissue Spectrometer Model 325, Hutchinson Technology, MN, USA).
17 m m 25m 45m Trained Untrained NIRS Vastus lateralis Trained Untrained HbO 2 HbTot HHb time
18 Training in hypoxia in the endurance-trained athlete Effects on performance Individual response factors Potential risks for health International Olympic Committee Ministère des Sports, France Groupe français de recherche sur l entraînement en hypoxie COMITE INTERNATIONAL OLYMPIQUE
19 4 Scientific teams participated in the study ARPE, Laboratoire «Réponses cellulaires et fonctionnelles à l hypoxie», EA 2363, UFR de Médecine, Université Paris 3, Bobigny Centre National de Ski Nordique, Prémanon Ecole Nationale de Ski et d'alpinisme, Chamonix Service de Physiologie Appliquée, Explorations Fonctionnelles Respiratoires, Hôpital de Strasbourg, Strasbourg Laboratoire de Biologie des Activités Physiques et Sportives, Faculté de Médecine, Clermont-Ferrand EA 3759 Laboratoire «Approche Bio-Psycho-Sociale du Dopage», Faculté des Sciences du Sport, Montpellier Service Central de Physiologie Clinique, CHU de Montpellier Groupe Rhône-Alpes d analyse du système nerveux autonome, St Etienne, Lyon, Grenoble Institut d Anatomie, Université de Berne, Suisse. UFR STAPS, Université de Reims, Reims Laboratoire National de Dépistage du Dopage, Chatenay-Malabry Laboratoire de Biochimie, Hôpital Henri Mondor, Créteil Laboratoire de Neurophysiologie Aérospatiale, IMASSA, Bretigny s/ Orge Université Blaise Pascal, Clermont-Ferrand Laboratoire de Biochimie, H.I.A. Bégin, Paris
20 Main objectives Evaluate the physiological changes induced by various modalities of training in hypoxia and their impact on performance. Hypothesis: these methods improve performance at sea-level Evaluate the individual response to training Hypothesis: there are biological, physiological or psychological markers of the variability of individual response to training in hypoxia Evaluate the potential risks for health Hypothesis: these methods are safe at short, medium and long term, provided a medical control of training procedures
21 «Live/sleep high - train low» Effects of intermittent exposure to hypoxia coupled to training at low altitude on performance in elite endurance athletes (nordic ski, swimming, track and field, using hypoxic rooms) Centre National de Ski Nordique Prémanon, Jura, France
22 VO 2 max (treadmill) time limit at TFM, TDF hypoxic test Blood sampling, PV Nordic ski VO 2 max 25m 3m 35m Hypoxia Control Tests Blood sampling VO 2 max (treadmill) time limit at TFM, TDF hypoxic test Blood sampling, PV VO 2 max 2m recovery 2m 4d 8 nights (3 x 6 nights) 2d 3d
23 VO 2 max (ergocycle) VO 2 max (swim) 2m swin free style Blood sampl., PV TFM, TDF hypoxic test Swimming VO 2 max (swim) 2m swin free style Blood sampl., PV TFM, TDF hypoxic test Hypoxia Control Tests Blood sampl., TDF VO 2 max (ergocycle) VO 2 max (swim) 2m swin free style Blood sampl., PV TFM, TDF 25m 3m 2m 2m recovery 2m 3d 3 nights 2d 2d 3d
24 Track and field Hypoxia Control Tests Blood sampl. TDF VO 2 max (treadmill) field test min at 9% MAS. Blood sampl., PV TFM, TDF hypoxic test VO 2 max (treadmill) field test min at 9% MAS Blood sampl., PV TFM, TDF hypoxic test 25m 3m 2m 2m Recovery 2m 3d 8 nights 3d 3d 2d
25 Red cell mass Red cell mass (l) PRE % N.S. PRE 5.5 Control Group Hypoxic Group
26 . Performance (VO 2 max) VO 2 max (ml/min/kg) % +4.% N.S. +5.8% P = % N.S. Control (n=6) Hypoxic (n=6) P<.5 vs PRE 55 PRE - -5
27 Variations of performance vs hemoglobin VO 2 max (%) ( PRE). Control group Hypoxic group R =.84 P = nhb (%) ( PRE)
28 Field test: min at 9.5 km/h ( 9% of maximal aerobic speed) Mean heart rate (min - ) PRE - -5 Control (n=6) Hypoxic (n=6) P<.5 vs PRE
29 Hypoxic exercise- induced desaturation ( SaO 2 e) SaO 2 e (%) PRE 5 Control PRE 5 Hypoxia PRE P<.5 vs PRE PRE PRE P<.5 vs PRE PRE Control Hypoxia Control Hypoxia Lesser desaturation at exercise ( SaO 2 e) at the end of the training session = sign of ventilatory acclimatization at exercice in hypoxia.
30 Nocturnal oxygen saturation (SaO2) m p<,5 3m p<, ) % ( O2 a S m 25m nuit 3m 3m 35m Sleep in hypoxic chambers induces episodes of desaturation, without apparent consequences on athlete s health
31 Right ventricule diameter in diastole (RVdia) RV Dia (mm) PRE 5 PRE PRE PRE PRE PRE Control Hypoxia Control Hypoxia Control Hypoxia No right ventricular dilatation, classical marker of RV overload due to pulmonary hypertension
32 systolic Pulmonary artery pressure (PAPs) PAPs (mmhg) PRE 5 Control PRE 5 Hypoxia PRE Control PRE Hypoxia PAPs does not vary significantly: no pulmonary hypertension
33 Tolerance and acclimatization «Live high train low» (3/2) does not induce symptoms of Acute Mounatin Sickness. may induce sleep perturbations and fatigue (if 35m and training load not reduced) may induce sleep apneas in some subjects, without apparent clinical consequences during the day.
34 Tolerance and acclimatization «Live high train low» (3/2) is not dangerous for the health of the athlete induces a ventilatory acclimatization (lower desaturation at exercise in hypoxia) that fades away 5 days after the training session
35 Recommendations for «live/sleep high - train low» Altitude: 25-3 Duration: 3 weeks Daily hypoxic exposure: 2-4 hours Reduce training load during the first 3 days Control nocturnal O 2 saturation Control training post hypoxic exposure
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