Al#tude and the Athlete
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1 Al#tude and the Athlete Carrie A. Jaworski, MD, FAAFP, FACSM Director, Division of Primary Care Sports Medicine & Fellowship University of Chicago/NorthShore University HealthSystem
2 Objec#ves Understand the effects of al#tude on physiology Discuss al#tude illness spectrum Review use of al#tude in training
3
4 Al#tude defined 0 to 1000 m = Sea level 1000 to 2000 m = Low al#tude 2000 to 3000 m = Moderate al#tude 3000 to 5000 m = High al#tude 5000 to 8900 m = Extreme al#tude
5 Environment at high al#tude (>1500 m or 4920 [) Dry air = risk of dehydra#on Decrease in air density and air resistance Increase in amount of UV light ~4% per 300 min = risk of sunburn Temperature decreases ~6.5 C/1000 m
6 Differences in Atmospheric Condi#ons at Sea Level up Through an Al#tude of 9000 m (29,520 [)
7 Expected Physiologic Effects of Al#tude Barometric pressure is reduced with parallel decrease in inspired par3al pressure of O2 resul3ng in Hypobaric Hypoxia = LOWER arterial pressure of oxygen and arterial oxygen satura3on Other effects Hyperven#la#on Dyspnea on exer#on Nighdme awakenings Increased urina#on Periodic breathing Periods of hyperpnea followed by apnea of 3-10 seconds
8 FACT The reduc1on in PO 2 at al1tude affects the par1al pressure gradient between the blood and the 1ssues and thus oxygen transport. This explains the decrease in endurance sport performance at al1tude.
9 Respiratory Responses to Al#tude Pulmonary ven#la#on increases Pulmonary diffusion does not change Oxygen transport is slightly impaired Oxygen uptake is impaired As the PO 2 decreases, VO 2max decreases at a progressively greater rate
10 FACT Al1tude does not affect VO 2max un1l above 1,500 m. Above. this level, the decrease in VO 2max is approximately 1% for every 100 m.
11 Changes in Maximal Oxygen Uptake With Decrements in Barometric Pressure and Par#al Pressure of Oxygen Data from E.R. Buskirk et al., 1967, "Maximal performance at altitude and on return from altitude in conditioned runners," Journal of Applied Physiology 23:
12 Cardiovascular Responses to Al#tude Ini#al decrease in plasma volume (more red blood cells per unit) Ini#al increase in HR, SV, and Q during submaximal work to compensate for less O 2 Decrease in HR, SV, and Q max during maximal workout, which limits oxygen delivery and uptake
13 The S- shaped Oxygen- Binding Curve for Hemoglobin at Sea Level
14 Hemoglobin (Hb) Concentra#ons of Men Living at Various Al#tudes
15 Metabolic Responses to Al#tude Increase in anaerobic metabolism Increase in lac#c acid produc#on Lower peak blood lactate concentra#on at maximal work rates in acclima#zed people compared to at sea level = Lactate Paradox Newer research demonstrates that this is transient and con#nued exposure to hypoxia results in reversal back to elevated lactate levels
16
17 Effects on Exercise Al#tude induced hypoxia reduces amount of oxygen available to do physical work VO2 max reduced 1% for every 100 m above 1500m For endurance trained athletes, this effect is even greater Reduc#ons seen as early as at 500 m Due to diffusion limita#on in lung and skeletal muscle exacerbated by high pulmonary and systemic blood flow of endurance athletes Ven#la#on, lactate and heart rate greater with same submaximal workload = sensa#on of dyspnea and fa#gue
18 Effects on type of exercise Endurance events: Performance impaired due to reduced VO2 Mixed events: Depends on interplay of oxida#ve and glycoly#c pathways Sprint and Field events: Not dependent on oxygen transport and less air resistance at al#tude so performance improves
19 Acclima#za#on A complex process involving mul#ple physiologic adapta#ons in an effort to maximize oxygen u#liza#on by the body when exposed to the effects of high al#tude. Adapta#ons to improve SUBMAXIMAL work performance at al#tude
20 Begins immediately on ascent Increase in alveolar ven#la#on Reduced venous O2 content Hyperven#la#on = respiratory alkalosis = renal excre#on of bicarbonate (first week) Sympathe#c system ac#va#on (immediate) Increases HR and cardiac output so #ssue oxygen delivery stays near sea- level Increased O2 carrying capacity Plasma volume reduc#on (early) Increased red cell mass (later) Increased peripheral uptake of O2 by muscle RBC 2,3- DPG; days Capillary density; years Acclima#za#on
21 Compe##on at Al#tude Acclima#za#on improves performance Need adequate #me (2-3 weeks) If not possible, compete upon arrival Increase VO 2max at sea level to be able to compete at a lower rela#ve intensity.
22 Al#tude and Performance Ideally wait 2-3 weeks to acclimate for best performance in endurance events At least 5-6 days for ven#latory acclima#za#on Avoid meds as side effects may affect outcome Consider O2 on sidelines to decrease ven#latory demands Skill players need 1-2 days to adjust to differences in air resistance
23 Al#tude Training for Sea- Level Compe##on Not proven that al#tude training improves sea- level performance. Difficult to study since intensity and volume are reduced at al#tude. Live at high al#tude and train as close to sea- level as possible (Live High- Train Low) will improve performance at sea- level. Performance is best immediately upon return Effects last up to 3 weeks
24 Recrea#onal Athletes Recrea#onal ac#vi#es also affected by hypoxia of al#tude Sea- level training is effec#ve at increasing ability to perform at al#tude
25 Training Strategies to Op#mize Al#tude Performance Live High Train High (LHTH) classic method May cause decreased performance Live High - Train Low (LHTL) Natural (descend for training) Ar#ficial live- high Long- con#nuous low- O2 Brief- con#nuous low- O2 Brief- Intermiuent low O2 Live Low Train High in low- O2 Effec#ve for pre- acclima#za#on NOT performance Applica#on of Al#tude/Hypoxic Training by Elite Athletes, Med Sci Sports Exer 2007
26 Live High, Train Low Seems to be best approach Effects last about 3 weeks in both elite and sub- elite athletes Op#mal al#tude appears to be m. Minimum of 3-4 wks for op#mal responses
27 Key Points Performance at Al#tude At al#tude, endurance ac#vity is affected the most due to reliance on oxygen transport and the aerobic energy system. Endurance athletes can prepare for compe##ons at al#tude by performing high- intensity endurance. training at any eleva#on to increase their VO 2max. Anaerobic sprint ac#vi#es are the least affected by al#tude. The thinner air at al#tude provides less aerodynamic resistance and less gravita#onal pull, thus poten#ally improving jumping and throwing events.
28 High- Al#tude Illness Clinical spectrum of signs and symptoms that result from rapid ascent to high al#tude Hypobaric hypoxia is the basis for a spectrum of condi#ons where overlap in presenta#ons can exist Acute Mountain Sickness (AMS) High Al#tude Pulmonary Edema (HAPE) High Al#tude Cerebral Edema (HACE)
29 Incidence 12-25% of unacclima#zed individuals experience symptoms of AMS beginning at 8,000 [ (2440 m) Being fit is not protec#ve Incidence and severity increases at higher al#tudes
30 Epidemiology Summit County, CO: 22% had illness at al#tudes of 7000 to 9000 [; 42% over 10,000 [. Risk Factors: Rate of ascent Al#tude reached Sleeping al#tude Individual physiology History of al#tude illness Residence below 900m
31 HAI Protec#ve Factors Residence at eleva#on >900 m (2950 [) Slow gain in eleva#on <500 m (1640 [) per day in sleeping eleva#on Gene#c factors Physical fitness NOT protec#ve
32 Rest, halt ascent Descend Moderate AMS: >500 m (1640 [) HACE/HAPE: > 1000 m (3280 [) Oxygen if available (keep Pox >90%) Keep warm (esp. for HAPE) Trea#ng HAI: General Principles
33 Acute Mountain Sickness (AMS) Hypoxia causes neurohumoral and hemodynamic responses that result in overperfusion of microvascular beds, elevated capillary pressure, capillary leakage, and consequent edema. Seen at > 2000 m Sx = HA with at least one of the following: nausea, dizziness/lightheadedness, vomi#ng, anorexia, fa#gue/weakness, sleep issues HA alone = High Al#tude Headache
34 AMS Usually mild and self- limited Treatment = Avoid further ascent, rest/acclimate, descend if no response to treatment, analgesics or portable hyperbaric bag Medica#ons = Acetazolamide 250mg BID un#l symptoms resolve Motrin 400 or 600 mg once Preven#on slow ascent/acclimate, hydrate, avoid ETOH, limit training intensity/volume Use of drugs to prevent AMS not recommended for moderate al#tude (<3000 m) unless clear history of recurrent AMS
35 Acetazolamide Carbonic anhydrase inhibitor Reduces absorp#on of bicarb and sodium Results in bicarbonate diuresis and metabolic acidosis Causes compensatory hyperven#la#on Usual dose: mg BID Recommended for people going from sea- level to >8,000 feet with no #me for acclima#za#on, or a history of al#tude illness
36 High Al#tude Pulmonary Edema (HAPE) Occurs 1-4 days a[er arrival at al#tude > 2400m Most common cause of death among HAI 50% mortality rate if not treated quickly 10% of cases fatal Defined by two pulmonary symptoms Cough, dyspnea at rest, exercise intolerance, chest #ghtness/conges#on and two pulmonary signs Crackles, wheezing, cyanosis, tachypnea, tachycardia
37 Treatment of HAPE Immediate descent >1000 m Oxygen to keep SaO 2 >90%. If descent/o 2 not immediately available Portable hyperbaric therapy Nifedipine 30 mg extended release BID (avoid if concomitant HACE) and Salmeterol 125 mcg inhaled Should resolve within hours of descent
38 Recovery from HAPE Variable; liule evidence in literature May take 2 weeks to recover strength Resume some ac#vity when SaO 2 > 90% without supplemental O 2 Remaining at some al#tude fosters acclima#za#on via pulmonary arteriolar remodeling
39 High Al#tude Cerebral Edema (HACE) Takes 2-3 days to develop Rarely occurs below 12,000 feet Increased intracranial pressure Sx: Same as AMS plus altered LOC and Ataxia May result in focal neuro deficits and coma
40 High Al#tude Cerebral Edema (HACE) Pathophysiology: Altered cerebral vascular permeability leads to brain swelling MRI: cerebral edema, lesions of corpus callosum
41 Treatment of HACE Immediate descent > 1000 m and hospitalize Oxygen to maintain SaO 2 >90% Dexamethasone 8 mg PO/IM/IV ini#ally followed by 4 mg QID Consider adding acetazolamide Portable hyperbaric therapy if descent impossible
42 Recovery from HACE Highly variable 1-3 days for symptoms to resolve Days to 12 weeks for neuropsychological func#on to normalize 3-4 weeks for papilledema to resolve Days to 5 weeks for MRI to normalize
43 Preven#on of High Al#tude Illness Acclima#za#on Spend 2 to 3 nights at 8,000 to 10,000 feet before climbing higher Avoid sleeping 2,000 [ (600m) higher than the previous night once higher than 8,000 [ (2,440 m) Spend an extra night for acclima#za#on for every 2,000 to 3,000 ( m) auained.
44 Preven#on of High Al#tude Illness High carbohydrate diet possibly lowers risk of AMS; adequate hydra#on status. Avoid sleeping pills and alcohol. Pharmacologic: Acetazolamide: 5mg/kg/day in 2 to 3 doses for one day prior and first two days at al#tude Dexamathasone: 4mg twice a day for one day prior, than con#nue 3 to 4 days a[er ascent to avoid rebound Ginkgo Biloba: mg BID
45 Return to Al#tude Ac#vity a[er recovery from Moderate AMS & HACE Full recovery prior to ac#vity Strict adherence to acclima#za#on and slow ascent protocols Ascend no more than 500 m/day Rest day every 3-4 days Consider acetazolamide (or dex) Counsel on recogni#on and rapid treatment of HAI
46 Return to Al#tude Ac#vity a[er recovery from HAPE Complete rest un#l fully recovered Strict adherence to acclima#za#on and slow ascent protocols Ascend < m/day Rest day every 3-4 days Consider prophylaxis: Dexamethasone, tadalafil, acetazolamide, nifedipine/salmeterol (especially if ascent will be > 500 m/day)
47 HAI in Children Risk of HAI in kids same as adults Preven#on and treatment largely SAME Strict acclima#za#on/ascent adherence If meds needed: Acetazolamide: 2.5 mg/kd/d divided Dexamethasone: 0.15 mg/kg/dose q6
48 Take home points Acclima#za#on and slow ascent are essen1al in preven#ng High Al#tude Illness Acclima#ze properly Spend 2-3 nights at m before ascent Slow ascent Ascend < 500 m/day of sleeping al#tude Rest day every 3-4 days Prophylac#c meds advised if unable to comply or significant past problems
49 References Hackeu PH et al: High Al#tude Illness. New England Journal of Medicine 345: , The Lake Louise Consensus on the Definition and Quantification of altitude Illness. In: Sutton JR, Houston CS, Coates G, editors. Hypoxia and mountain medicine. Burlington (VT): Queen City Press; Posi#on statement- - al#tude training for improving team- sport players' performance: current knowledge and unresolved issuesbr. J. Sports. Med. 2013;47:Suppl_1 i8- i16 Improving team- sport player's physical performance with al#tude training: from beliefs to scien#fic evidencebr. J. Sports. Med. 2013;47:Suppl_1 i2- i3 Luks AM, McIntosh SE, Grissom CK, Auerbach PS, Rodway GW, Schoene RB, et al. Wilderness Medical Society consensus guidelines for the preven#on and treatment of acute al#tude illness. Wilderness Environ Med Jun;21(2): Luks AM, Swenson ER. Medica#on and dosage considera#ons in the prophylaxis and treatment of high- al#tude illness. Chest Mar;133(3): Maggiorini M, Brunner- La Rocca HP, Peth S, Fischler M, Bohm T, Bernheim A, et al. Both tadalafil and dexamethasone may reduce the incidence of high- al#tude pulmonary edema: a randomized trial. Ann Intern Med Oct 3;145(7): Pollard AJ, Niermeyer S, Barry P, Bartsch P, Berghold F, Bishop RA, et al. Children at high al#tude: an interna#onal consensus statement by an ad hoc commiuee of the Interna#onal Society for Mountain Medicine, March 12, High Alt Med Biol Fall;2(3):
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