Why to go to altitude? Oxygen as an ergogenic aid in elite sports Olympic Committee, 7.9.2010, Helsinki Juha Peltonen, PhD Senior exercise physiologist Unit for Sports and Exercise Medicine Institute of Clinical Medicine University of Helsinki Does hypoxia offer such a specific stimulus to enhance exercise capacity that can not be achieved by training at sea level? What happens in acute and chronic hypoxia? How high and how long? When, how often? Natural vs. artificial hypoxia? Supplemental O 2 while at altitude? Do all benefit? Is it possible to screw up? Clinic for Sports and Exercise Medicine Foundation for Sports and Exercise Medicine (Helsingin urheilulääkäriasema) Juha Peltonen Exercise performance at altitude Peronnet et al. J Appl Physiol 70: 399-404, 1991. Muza SR et al. High Alt Med Biol 11: 87-92, 2010 1. If competition will be held at altitude train at altitude 2. If competition will be held at sea level consider LHTH & LHTL Some issues on high altitude physiology Daniels J & Oldridge N. Med Sci Sports, 2, 107-112, 1970 West JB. Respiratory physiology the essentials, 1990. 1
9.9.2010 VO2 in normoxia, hypoxia and hyperoxia Peltonen JE et al. Aviat Space Environ Med 72: 904-911, 2001 Peltonen JE et al. Respir Physiol Neurobiol 169: 24-35, 2009 Peltonen JE et al. Med Sci Sports Exerc 27: 573-579, 1995. Physiological factors affecting VO2 during exercise VO2max decline in hypoxia is associated with Altitude Sea level VO2max (Lawler et al. 1988). Exercise-induced arterial desaturation (EIAH) at sea level (Chapman et al. 1999). Modified from Rowell LB. Human Circulation Regulation during Physical Stress, 1986 5. Central nervous system 6. Peripheral nervous system 2. Central circulation Cardiac output (heart rate, stroke volume) Arterial blood pressure Hemoglobin concentration Red cell mass 1. Respiration O2 diffusion Ventilation Alveolar VA/Q Hb - O2 affinity 3. Peripheral circulation Flow to inactive tissues Muscle blood flow Muscle capillarization O2 diffusion Muscle vascular conductance O2 ekstraction Hb - O2 affinity.. 4. Muscle metabolism Enzyme activity and oxidative potential Energy stores Myoglobin Mitochondria (size and number) Muscle mass and fiber type Substrate delivery Chapman et al. Med Sci Sports Exerc 30, 658-663, 1999 / FIO2 0.187 ~ 1000 m. Acclimatization to hypoxia 2
Ventilation and pulmonary blood flow Cardiovascular responses In acute hypoxia, maximal ventilation is similar or greater than at sea level (Lawler et al. 1988, Chapman et al. 1999). In chronic hypoxia, V Emax increases due to increased ventilatory chemosensitivity (Schoene et al. 1990). Pulmonary vasoconstriction and an increase in pulmonary blood pressure (Alleman et al. 2004). Diffusion capacity unchanged (Sutton et al. 1992) or improved (Calbet et al. 2003). CymermanAet al. J Appl Physiol, 66, 2446-2453, 1989 In acute hypoxia, maximal heart rate, stroke volume and cardiac output are similar (Stenberg et al. 1966) or lower (Lundby et al. 2001, Peltonen et al. 2001) than at sea level. In chronic hypoxia, maximal heart rate, stroke volume and cardiac output are reduced (Sutton et al. 1992, Wagner 2000). Blood flow distribution is altered in chronic hypoxia (Calbet et al. 2003). Wagner PD. Respir Physiol, 120, 1-11, 2000 Why cardiac pumping capacity is reduced in chronic hypoxia? Decrease in max heart rate may be due to Reduced number of cardiac β-reseptors (Richalet et al. 1992) and/or their impaired activity (Lundby et al. 2001). Increased parasympathetic activity (Boushel et al. 2001). Decrease in stroke volume may be due to Decreased blood volume (Robach et al. 2000). Impaired muscle pump (Calbet et al. 2003). Reduced feedforward (Noakes et al. 2001, Calbet et al. 2003). Cardiac contractility is preserved (Reeves et al. 1987). Maximal cardiac output is reduced in chronic hypoxia Muscle blood flow and oxidative capacity Chronic hypoxia without physical activity impairs growth of muscle cells and reduces gene expression of angiogenetic growth factors (Mathieu-Costello 2001). Animal studies: Muscle oxidative capacity may improve in hypoxia (Mathieu-Costello 2001). Human studies: Support for this is weak (Green et al. 1989, Green & Sutton 2001). Acclimatization only has minor effects on metabolic enzyme activity (Green & Sutton 2001). No real benefit on muscle capillarisation (Green & Sutton 2001). Capillary/muscle ratio is increased because of reduced muscle mass. Efficiency may be improved in submaximal work (Green et al. 2000). Central nervous system Motor and cognitive function are impaired in hypoxia (Denison et al. 1966, Ernsting et al. 1978, Kennedy et al. 1989, Hornbein 2001). EMG-activity decreases in hypoxia (Kayser et al. 1994, Peltonen et al. 1997, Amann et al. 2006, 2009). High hypoxic ventilatory chemosensitivity improves arterial O 2 - saturation, but concomitant hypocapnia causes cerebral vasoconstriction (Poulin et al. 1998, Spicuzza et al. 2005, Peltonen et al 2009). Brain is more vulnearble to deoxygenation than muscle in hypoxia, but an absolute level of brain deoxygenation leading to cessation of work has not been found (Peltonen et al. 2009). Energy metabolism in the brain is maintained despite deoxygenation, but the function of neurotransmitters is impaired (Gibson et al. 1981). Anaerobic energy production ATP and PCr homeostasis are maintained at rest and during exercise in hypoxia (Roach & Kayser 2001). Lactic energy production: In acute hypoxia, increased blood lactate concentration at a given submaximal work rate (Peltonen et al. 1999), but no difference in maximal [lactate] (Peltonen et al. 1995). In chronic hypoxia, a reduction in maximal [lactate] (Roach & Kayser 2001): lactate paradox. Few signs of normalization of lactate production as acclimatizations proceeds (van Hall et al. 2001). Blood buffer capacity is reduced at altitude (Grassi et al. 1996), but some studies suggest an improvent in muscle buffer capacity (Mizuno et al. 1990, Gore et al. 2001). 3
9.9.2010 Effects of hypoxia PaO2 & SaO2 Acute hypoxia Ventilation Sympathetic activity Hemoconcentration Heart rate at submax. work Stroke volume Chronic hypoxia Ventilation Red cell production Cardiac output Sympathetic and Natural altitude Simulated altitude At 1800 3000 m VO2max 15-25% Gradual improvement of VO2max Sea level values will not be achieved at altitude parasympathetic activity Efficiency? (cost of VE, CHO use, P/O ratio ) Muscle buffer capacity? (MCT1, MCT4, CA ) Increase in blood O2-carrying capacity is one of the key targets in using hypoxic exposure but this can NOT be followed by measuring EPO Millet GP et al. Sports Med 40: 1-25, 2010 Rusko HK, Tikkanen HO, Peltonen JE. J Sports Sci 22: 928-945, 2004. Total Hb-mass, blood volume and cardiac output vs. VO2max VO2 = SV x HR x C (a-v) O2 thb-mass = RCM Schmidt W & Prommer N. Exerc Sport Sci Rev 38: 68-75, 2010. Blood O2 carrying capacity Schmidt W & Prommer N. Exerc Sports Sci Rev 38: 68-75, 2010 4
[Hb] and Hct are NOT reliable indicators of an increase in RCM measurement of RCM / Hbmass is required. Schmidt W & Prommer N. Exerc Sport Sci Rev 38: 68-75, 2010. Saunders PU et al. High Alt Med Biol 10: 135-148, 2009 8 17 25 33 42 days Saunders PU et al. High Alt Med Biol 10: 135-148, 2009 Schmidt W & Prommer N. Exerc Sport Sci Rev 38: 68-75, 2010. Aims of altitude training TYPE / PURPOSE Planning altitude training TYPE AIM DURATION A Improve general fitness especially aerobic capacity B C To prepare for high intensity training following altitude Improve competitive performance 10 14 days 14-21 days 17 21 days JPNOTE: It is possible to extend duration up to 28-30 days ( ~ 4 wks) to further enhance hematological effects of hypoxic exposure. C B A Week number 5
An example of planning altitude training for winter sports Am example of planning altitude training for summer sports Month PROS AND CONS Millet GP et al. Sports Med 40: 1-25, 2010 Hypoxic exposure may have positive effect negative effect no effect at all Millet GP et al. Sports Med 40: 1-25, 2010 LHTL: 21 d 3000 m ~ 14 h/d CONCLUSIONS: LHTH & LHTL Optimal altitude for living: 2200 2500 m for hematological effect, ie. RCM 1800 1900 m is too low to induce RCM up to 3100 m for non-hematological effects ATHLETE S EXPERIENCE IN HYPOXIA! Optimal duration of hypoxic exposure is dependent on goal 3 4 wks for hematological effects 14 h / day 14 18 d for ventilatory chemosensitivity, efficiency and muscle buffer capacity Recovery between high altitude camps Take care of iron stores, recovery, hydration, CHO Consider extra O 2 or descent ~ 2 /wk during LHTH Clark SA et al. Eur J Appl Physiol 106: 399-406, 2009. 6
How to proceed? Before, during and after hypoxic exposure: Blood analysis (pre and post hypoxic exposure) Blood count (PVK), S-Ferrit, fs-tfr, S-hs-CRP RCM, blood volume Training diary Heart rate monitor data (exercise, rest, sleep) Arterial saturation (exercise, rest, sleep) Weight, mood, amount and quality of sleep Coaches with interest, please contact ari.nummela@kihu.fi ; juha.peltonen@helsinki.fi kari.niemi-nikkola@noc.fi 7