layton

I may be there and give clinics on sleeping under bridges, hurling your feces, water color drawing, pan flute playing, focusing the rage, wheelchair racing, helicopter signals, and how to pick up chicks.

i like eat a muffin while practicing safe sects.

NOLSe, don't get overly excited about the north face as a rock route. it's not as inspiring up close. if you want to do it, go over triumph pass...not down from the NE ridge notch.

i live in a giant bucket

his expression says NO, but his festive shirt says YES!

The trip got off to a shaky start...tequilla, more tequilla, and debauchary at Necronomicon's Banned Camp with his lovely bride and Jordop. Jordon, being from Canada, couldn't handle the strong Mexican drink and spend the night and next morning puking more times than i could count on my fingers. Jordan waited till 10:30, when he could finally hold down water to get in the General, and hit the road. Luckily it was one BILLION degrees outsite at the cuttroat lake trailhead, and we quickly packed before the sun's rays melted holes in our cams and slings. Thus began our 30 mile loop of the further reaches of chossington pass in exploratory hope of opening up new lines for the good of humanity. The NE face of golden horn was our objective. (1st photo mine, 2nd Scurlock) click for photo As every electrolite was sweated out of every pore on our bodies, we staggered through some amazing country with fretful bouts of uber alpine hyper stumble-wallowing in the soft snow. A posthole wonderland. Finally after much ballyhoo and dry heavin' we could see our destination, the notch between tower and hardy. Clouds rolled in, but only lasted a little bit. The sun continued to rage. After a friggen long ass walk, we arrived below tower mountain. There's a big ass cave if you look closely. John Scurlock shows a cave also on the N face. Maybe they connect?? Would that be the coolest thing ever! I'll be checking this out for sure. The next day after hitting the snooze for an hour and a half, Jordan and I continued to lose brain cells and electrolites from our bodies, and continued the endless slog to the col overlooking the NE face of Golden Horn. It was pretty brutal. Luckily when we FINALLY got to scope out the route, it was a towering tottering pile of crap. Well, it wasn't that bad. The upper 400 feet looked pretty good, but upon close inspection of the lower half with binocs, it is vertically and horizontally banded with sand and choss. It would be a real prize in chossmungery. After hiking all that way, i was pretty game to try anything no matter how shitty, but looking at it closely, i didn't care how friggin far we hiked. The photos couldn't show the up close chossness, they actually looked kinda sorta do-able. Oh well. We got real good views of tower and Mt Hardy as consolidation prizes. Instead of going back the way we came, we opted to hike out Swamp Creek and hitchike back to the car. It was a lovely little "romp" through the woods and we later decided that hiking in the river would be a lot more fun than meandering though the "lushness" of swamp creek. Then the gods got angry and unleashed the fury, so we got some fun hail and lightning and rain to round out the day. I tried for a long time to get a ride while Jordan hid in the bushed, so I told him it was his turn. I barely hid behind a tree, before Jordan flagged down a ride. I tried not to take it personally. The ride was surreal with an empty VW fan and a dad and freaky kids from everett. We hiked the last mile back to the car, and I drove all the way home to portland by myself. It was really too bad, cuz we both had orange packs and it's not often that a color co-ordinated 1st ascent occurs. I lay awake last night visualize what the climb would've been like. Here is what i think it would have been like, had we actaully attempted it. 1st part of the route: 2nd part of climb: and the final part: I'm sure Jordan will add something or call my b.s.

Nick, here's the best i could find as of early 2000. i'm sure there's more current info, but you can use this for some good background. it's a really really boring read however... Effects of Altitude on Aerobic Capacity By Michael Layton Athletes and scientists have been studying and putting into practice the effects of altitude on aerobic capacity for years. Athletes have been using altitude as a training tool for years despite conflicting scientific evidence (Gore et al., 1998). Athletes use altitude training to boost aerobic capacity (V02max), perform in endurance events, and boost recovery time at sea level (Dick, 1992; Chapman, & Stray-Gunderson, 1998). Hypoxic exercise (altitude training) may increase the training stimulus that increases the effects of endurance training (Levine, & Stray-Gunderson, 1992). There is less oxygen in the air at altitude (Hellemans, 1998), and VO2max is susceptible to changes in oxygen levels (Saltin, 1996). To understand how altitude affects V02max, one must recognize how the body utilizes oxygen in respect to VO2 max, what physiological changes occur when exercising at altitude, how different models of altitude training effect VO2max, what variables besides altitude effect VO2max, and finally, what recommendations should be made to use altitude to effect VO2max. Oxygen supply and use are closely linked: training improves the ability to utilize oxygen delivery (Wagner, 1998). Changes in VO2max to exercising are a measure of the cardiovascular system’s adaptation to hypoxia and endurance performance (Chapman, Stray-Gunderson, &Levine, 1998; Favier et al, 1995). VO2max depends on oxygen supply and peripheral oxygen diffusion (Robergs, Quintana, Parker, & Frankel, 1998; Wagener, 1998), and depends on oxygen supply to muscle mitochondria and mitochondrial metabolic capacity (Wagner, 1998). VO2max is determined by mitochondrial metabolic capacity in untrained subjects, and oxygen supply to muscle mitochondria in trained subjects (Wagner, 1998). The oxygen transport chain starts with ventilation and diffusion of the lungs to circulation and blood flow diffusion to the muscle cells, and finally the processing of oxygen by mitochondria (Wagner, 1998). During maximum work, V02 max measures individual work capacity because it reflects working muscles’ oxygen consumption, and the transport and delivery of oxygen to tissues via the cardiovascular system (Frisancho, 1983). Oxygen consumption reaches a maximum even with greater exertion, although until that point, the rate of oxygen consumption increases linearly with the amount of work. Many positive and negative physiological changes occur at altitude. Hypoxia creates metabolic and musculocardiorespiratory adaptations that affect oxygen transport and utilization (Bailey & Davies, 1997). Negative changes include a V02max decrease with exposure to altitude (Chapman, Stray-Gunderson, & Levine, 1998; Dill, & Adams, 1971; Klausen, Robinson, Micahel, & Myre, 1966; Mizuno et al., 1990; Squires, 1971; Squires, & Buskirk, 1982; Tucker, 1984). The decrease in VO2max at high-altitude ranges from 30%-45% (Cerretelli, 1983). The more altitude, the more decrease in VO2max (Dill & Adams, 1971; Robergs et al., 1998). For each 1000m at altitude, V02max decreases 8% (Favier et al., 1995). The percent decrease in VO2max is greater than the percent decrease in endurance performance that also decreases at altitude (Squires & Buskirk, 1982). Maximum heart rate (HRmax) decreases at altitude (Dick, 1992; Dill & Adams, 1971; Drinkwater, Kramar, Bedi, & Folinsbee, 1982; Klausen et al., 1966; Levine, & Stray-Gunderson, 1997; Saltin, 1996), and resting heart rate increases (Dick, 1992). The HRmax decrease during hypoxia directly affects lung performance (Saltin, 1996), and limits maximum oxygen transport (Drinkwater et al., 1982). A decrease in HRmax at altitude directly affects VO2max because maximum aerobic power decreases despite an increase in hemoglobin concentration (Saltin, 1996). This is because hemoglobin volume increases while plasma volume decreases, which in turn lowers stroke volume while exercising at altitude (Saltin, 1996). The improved oxygen delivery capacity and trend for normalization of stroke volume is offset by the lower HRmax.(Saltin, 1996). HRmax is lowered because hypoxia alters the balance within the sympathetic system (Saltin, 1996). So the net gain of oxygen delivery to tissues versus the work of heart favors limiting cardiac output (Saltin, 1996). In addition to decreased Hrmax, the acclimatization pathway and training response pathway decrease total performance at altitude (Chapman, Stray-Gunderson, & Levin, 1998; Chapman, 1998). Arterial O2 saturation (Sa02) decreases (Wofel et al., 1991), and oxygen uptake is lowered (Levine & Stray-Gunderson, 1992). Plasma volume decreases, and may take months to normalize (Bailey & Davies, 1997), and recovery time also increases at altitude (Dick, 1992). Hypoxia increases demand for iron and may create deficiencies (Bailey & Davies, 1997). There is no increase in red blood cells (RBC) with an iron deficiency (Stray-Gunderson, Hochstein, deLemos, & Levin, 1992). There are decreases of blood flow to skeletal muscles, absolute training intensity, plasma volume, haemopoeisis, and muscle mass (Baliley & Davies, 1997). There are increases in glucogen depletion, chances of acquiring acute mountain sickness, high-altitude pulmonary edema, and high-altitude cerebral edema, and increases in ventilation, dehydration, onset of jet lag, and sunburn potential (Bailey & Davies, 1997). Finally, altitude can suppress the immune system, and increase the amount of free radicals from oxidative stray in the body that destroy membrane integrity, and decrease energy (Bailey & Davies, 1997). There are some positive physiological changes due to altitude exposure, or hypoxia. There is an increase in RBC volume (Chapman, 1998; Levine & Stray-Gunderson, 1992; Levine & Stray-Gunderson, 1997; Stray-Gunderson, Hochstrein, & Levine, 1993). An increase of erythropoeitin (EPO) at altitude is responsible for the increase in RBC volume, and in turn is the primary reason for the increase in V02max after return to sea level (Chapman, 1998; Chapman, Stray-Gunderson, & Levine, 1998; Levine & Stray-Gunderson, 1997). This increase in oxygen carrying capacity allows for a decrease in cardiac output (since more oxygen is in the blood, less needs to be pumped), which increases peripheral diffusion and O2 extraction, and also improves aerobic power 1% for every 100m above 1,500m (Levine & Stray-Gunderson, 1997). Fatty acid metabolism, hemoglobin volume, capillaries (after years), oxidative enzyme activity, and mitochondrial volume also increase (Bailey & Davies, 1997). Finally, blood lactate levels decrease at altitude (Dill & Adams, 1971; Klausen et al., 1966; Levine & Stray-Gunderson, 1997). With this knowledge in mind, several different models of altitude training have been studied and used by scientists and athletes respectively. Altitude training improves performance at altitude, but there is conflicting scientific evidence that altitude training effects performance at sea level (Bailey & Davies, 1997). The debate seems to be between whether athletes should train at altitude, or live at altitude and train near sea level. The case for training at high altitude state that exercising at altitude produces a greater training effect than training at sea level alone (Dill & Adams, 1971; Roskamm et al., 1969). VO2max and hemoglobin volume increase at sea level after altitude training (Dill, 1971; Drinkwater et al, 1982; Horvath, Bedi, Wagner, & Agnew, 1988; Klausen et al, 1966; Rodriguez et al., 1999). In fact, mild altitude is enough to increase RBC volume (Stray-Gunderson et al., 1993), and base training at altitude may increase mitochondrial enzyme activities and maximize peripheral oxygen utilization (Levine & Stray-Gunderson, 1992). However, some studies show VO2max does not change with this train high model (Gore, et al., 1998; Levine & Stray-Gunderson, 1997; Miznuo et al., 1990; Squires & Buskirk, 1982; Tucker et al., 1984). The benefits of the live high-train low model suggest that the high-low model increases performance more than an equivalent sea-level program (Chapman, Stray-Gunderson, & Levin, 1998; Levine & Stray-Gunderson, 1997). VO2max increases in direct proportion to RBC volume in the study of this model, while a sea-level control did not (Levine & Stray-Gunderson, 1997). Performance increases from 1-4% are gained from the high-low model, which is the same percentage difference in race times of athletes who made the finals at the Atlanta Olympics (Chapman, 1998). Training low may also prevent plasma volume loss, and allows for interval training while maintaining VO2max (Chapman, 1998; Chapman, Stray-Gunderson, & Levin, 1998; Levine & Stray-Gunderson, 1992). Some reasons why there seems to be conflicting evidence may be due to the variables that affect physiological changes at altitude. A wide variability of individual response to altitude training divides athletes into responders (those who show benefits of altitude training), and non-responders (those who did not benefit from altitude training). The VO2max at sea-level pre-altitude is the same in responders and non-responders (Chapman, 1998), but VO2max decreases at elevations as low as 601m in 50% of elite athletes (Bailey & Davies, 1997; Chapman, 1998; Chapman, Stray-Gunderson, & Levin, 1998). Non-responders show a decrease in EPO and RBC volume because EPO doesn’t pass threshold (the amount of EPO needed) to produce more RBC (Chapman, 1998). Stem cell sensitivity in bone marrow to EPO levels and its breakdown rate could be one difference between responders and non-responders (Chapman, Stray-Gunderson, & Levine, 1998). Another reason for the difference between responders and non-responders may be a result of genetically inherited traits (Chapman, Stray-Gunderson, & Levine, 1998). The main reason for the difference is manifested through the acclimatization pathway which depends on a hematological adaptation to hypoxia, and a training response pathway which depends on maintenance of interval training velocity and oxygen flux at altitude comparable to sea-level values (Chapman, Stray-Gunderson, & Levine, 1998). Responders have a larger EPO concentration than non-responders, although the hemoglobin increase is the same in both (Chapman Stray-Gunderson, & Levine, 1998). Responders’ hemoglobin increases because the RBC volume increased while the plasma volume decreased, and the non-responders hemoglobin increased because plasma volume decreased and RBC volume did not increase in a study performed on elite athletes (Chapman, Stray-Gunderson, & Levine, 1998). One factor that influences VO2max response to altitude training is the subjects’ fitness level prior to training. VO2max improves most with subjects with the lowest initial values (Gore et al., 1998). VO2max may decrease with altitude training in subjects with high values (Gore et al., 1998; Mizuno et. al, 1990). Elite athletes (athletes who have superior aerobic endurance, and/or power) are more susceptible to VO2max decrease at altitude (Chapman, Stray-Gunderson, & Levine, 1998). Elite athletes may not be able to increase VO2max at altitude because they are near, or at their physiological limits (Gore et. al., 1998) Over-training may decrease VO2max (Gore et al., 1998). There are many other variables that might affect the outcome of all the different studies. For instance, VO2max levels at altitude have been shown to be equal among the genders (Drinkwater et al., 1998; Horvath et al., 1988; Levine & Stray-Gunderson, 1997), and it has been shown to be lower in females (Robergs et al., 1998). This conflicting data may be due to one or more of the variable discussed. Many other variables must be considered while studying altitude’s affect on V02max. Iron levels can also affect results of studies because low iron stores produces a negative hematological response (Chapman, 1998; Chapman, Stray-Gunderson, & Levine, 1998). Disease and testosterone levels have been shown to have a depressive effect on the release of EPO (Chapman, 1998; Gore et al., 1998), and individual differences in peripheral diffusion at altitude may explain why V02max levels differ among studies (Robergs et al., 1998). An increase in anaerobic capacity due to heavy training at altitude could be one of the factors in the increased performance after altitude training (Gore et al., 1998). Testing errors could also be a part of the conflicting study results. From 1956-1997 only 30% of studies used sea-level control groups which makes it difficult to determine if the benefits come from training at altitude or simply the increased training (Bailey & Davies, 1997; Saltin, 1996). By studying natives of high-altitude areas, scientists hope to discover whether the physiological changes are inherited, acquired developmentally, or developed through altitude training. Scientists found that a decrease in VO2max at altitude is not affected by race (Cerretelli, 1993), and that the VO2max of high-altitude native equals those of sea-level natives (Frisancho, 1983; Garrido et al., 1997; Favier et al., 1995). High-altitude natives have the same muscle capillary and mitchondrial volume density as sea level native (Garrido et al., 1997). Changes from development at altitude, or genetics include larger lung volume (Frisancho, 1983; Lindstedt, 1998), greater utilization of glucose, ventilator efficiency, higher anaerobic threshold (Garrido et al., 1997), thicker muscles of the pulmonary artery (Frisancho, 1983), and an increased pulmonary diffusion capacity and adaptations in structural and metabolic organization of skeletal muscles which causes a more efficient cellular respiration system. Therefore, high-altitude natives may have evolved genetically or developmentally by maximizing metabolism (Favier et al., 1995), and oxygen uptake instead of increasing VO2max directly (Garrido et al., 1997). Additionally, there exists a possibility of a gene that gives high-altitude natives higher Sa02 at birth (Garrido et al, 1997). By not taking some of these variables into account could have altered the results of certain studies that reported conflicting results (Dill & Adams, 1971; Gore et al., 1997; Mizuno et al., 1990; Robergs et al., 1998; Roskmm et al., 1969; Saltin, 1996). After understanding how altitude affects VO2max, certain recommendations can be made for athletes deciding to train at altitude. Untrained individuals are unlikely to benefit from altitude training while elite athletes will benefit the most (elite athletes are already near their physiological limit and altitude training could give them an extra benefit, while untrained individuals will benefit from regular sea level training) (Levine & Stray-Gunderson, 1992). For increased performance at altitude, athletes should acclimatize and/or train at altitude (Levine & Stray-Gunderson, 1992). High volume/intensity sessions should not be done at high altitude (Chapman, 1998; Dick, 1992). Athletes need to acclimatize to 2-5 days prior to training (Hellemans, 1998). For increased performance at sea level, the live high-train low model is suggested (Levine & Stray-Gunderson, 1992). Athletes with high hematological adaptation should live at altitude, and those with poor adaptation should live near sea level (Chapman, 1998; Chapman, Stray-Gunderson, & Levine, 1998). Athletes with an ability to train at altitude should train at altitude, while those with a low ability should train near sea level (Chapman, 1998; Chapman, Stray-Gunderson, & Levine, 1998). Any altitude is appropriate for easy aerobic training (Chapman, 1998). The recommendations suggesting the altitude at which athletes should live and train differs from source to source. One source shows athletes need to sleep as high as possible without exceeding 15,000’ (Kutt, 1999), while other state much lower altitudes (Chapman, 1998; Levine & Stray-Gunderson, 1992). The amount of hypoxic stimulus may be necessary to release EPO (Chapman, Stray-Gunderson, & Levine, 1998). The elevation of 3000m or less seems to be the idea training altitude (Bailey & Davies, 1997; Chapman, 1998; Dick, 1992; Levine & Stray-Gunderson, 1992) The longer an athlete stays at altitude, the greater potential for an increase in VO2max (Bailey & Davies, 1997; Frisancho, 1983; Mizuno et al., 1990; Saltin, 1996); however, three weeks is sufficient to gain an increase in performance (Bailey & Davies, 1997; Dick, 1992; Hellemans, 1998). Finally, an athlete will need to decide when to begin training at sea level. Individual differences may determine which days peak performance occurs upon return to sea level (Gore et al., 1998). Days 1 and 2 show an increase in performance (Hellemans, 1998), days +/- 3-10 show a normal or worse performance (Bailey & Davies, 1997; Dick, 1992; Hellemans, 1998), and days +/- 11-24 show another increase in performance (Bailey & Davies, 1997; Dick, 1992; Hellemans, 1998). With these facts in mind athletes and coaches can program a training plan using the effects altitude has on VO2max. Stating that hypoxia brings on a series of physiological adaptations that affect everyone differently can summarize the effects of altitude on V02 max. These changes are even more apparent when elite athletes use altitude as a training tool to possibly increase their performance. Studies done on these athletes report significantly different results (especially when the studies compare those results while using different training models). By looking at some variables that may have affected these studies, one can possibly determine similarities that exist between the conflicting results. It is imprudent to only look at the positive results of studies done on only one or more training models. It could be dangerous to implement a training program only based on studies whose results coincide with the results an athlete wishes to achieve. It is possible that each different model may correlate with the physiology of each different athlete. Scientists should continue to study each model of altitude training to determine their proper use while keeping athletes and trainers updated on the pros and cons of all aspects of each different model. References Bailey, D., & Davies, B. (1997). Physiological implications of altitude training for endurance performance at sea level: A review. British Journal of Sports Medicine, 31, 183-190. Cerretelli, R. (1983). Energy metabolism during exercise at altitude. In E. C. Chamberlayne & P.G. Condliffe (Eds.), Adjustment to high altitude (NIH Publication No. 83-2496, pp. 61-64). Washington, DC: U.S. Department of Health and Human Services. Chapman, P. (1998). Optimum utilization of altitude training: The high-low model. Retrieved October 11, 2000 from the World Wide Web: http://www.sportscience.org.nz/ publications/report/report3.html Chapman, R. F., Stray-Gunderson, J., & Levine, B. D. (1998). Individual variation in response to altitude training. Journal of Applied Physiology, 85, 1448-1456. Dick, F. W. (1992). Training at altitude in practice. International Journal of Sports Medicine, 13, S203-S205. Dill, D. B., & Adams, W. C. (1971). Maximal oxygen uptake at sea level and at 3,090-m altitude in high school champion runners. Journal of Applied Physiology, 30, 854-859. Drinkwater, B. L., Kramar, P. O., Bedi, J. F., & Folinsbee, L. J. (1982). Women at altitude: Cardiovascular responses to hypoxia. Aviation Space and Environmental Medicine, 53, 472-477. Favier, R., Spielvogel, H., Desplanches, D., Ferretti, G., Kayser, B., & Hoppeler, H. (1995). Maximal exercise performance in chronic hypoxia and acute normoxia in high-altitude natives. Journal of Applied Physiology, 78, 1868-1874. Frisancho, R. A. (1983). Developmental components of adaptation to high altitude. In E. C. Chamberlayne & P.G. Condliffe (Eds.), Adjustment to high altitude (NIH Publication No. 83-2496, pp. 27-36). Washington, DC: U.S. Department of Health and Human Services. Garrido, E., Rodas, G., Javierre, C., Segura, R., Estruch, A., & Ventura, J. L. (1997) Cardiorespiratory response to exercise in elite Sherpa climbers transferred to sea level. Medicine and Science in Sports and Exercise, 29, 937-942. Gore, C., Craig, N., Hahn, A., Rice, A., Bourdon, P., Lawrence, S., Walsh, C., Stanef, T., Barnes, P., Parisotto, R., Martin, D., & Payne, D. (1998). Altitude training at 2690m does not increase total haemoglobic mass or sea level V02max in world champion track cyclists. Journal of Science and Medicine in Sport, 13, 156-170. Hellemans, J. (1998). Optimum utilization of altitude training - the high-low model. Retrieved October 11, 2000 from the World Wide Web: http://www.sportscience.org.nz/ publications/report/report10.html Horvath, S. M., Bedi, J. F., Wagner, J. A., & Agrew, J. (1988). Maximal aerobic capacity at several ambient concentrations of CO at several altitudes. Journal of Applied Physiology, 65, 2696-2708. Klausen, K., Robinson, S., Micahel, E. D., & Myhre, L. G. (1966). Effect of high-altitude on maximal working capacity. Journal of Applied Physiology, 21, 1191-1194. Kutt, L. (1999). Altitude training for the new millennium. Retrieved October 11, 2000 from the World Wide Web: http://www.altitudetraining.com/pr4.htm Levine, B. D., & Stray-Gunderson, J. (1992). A practical approach to altitude training: Where to live and train for optimal performance enhancement. International Journal of Sports Medicine, 13, S209-S212. Levine, B. D., & Stray-Gunderson, J. (1997). Living high-training low: Effect of moderate altitude acclimatization with low-altitude training on performance. Journal of Applied Physiology, 83, 102-112. Lindstedt, S. (1998). Exercise hypoxia and limitations to exercise in athletes. Retrieved October 11, 2000 from the World Wide Web: http://www.sportscience.org.na/ publications/report/report4.html Mizuno, M., Juel, L., Bro-Rasmussen, T., Mygind, E., Schibye, B., Rasmussen, B., & Saltin, B. (1990). Limb skeletal muscle adaptation in athletes after training at altitude. Journal of Applied Physiology, 68, 496-502. Robergs, R. A., Quintana, R., Parker, D. L., & Frankel, L. L. (1998). Multiple variables explain variability in decrement in VO2max during acute hypobaric hypoxia. Medicine and Science in Sports and Exercise, 30, 869-879. Roskamm, H., Landry, F., Sanek, L., Schlager, M., Weidemann, H., & Reindell, H. (1969). Effects of a standardized ergometer training program at three different altitudes. Journal of Applied Physiology, 27, 840-847. Rodriguez, F. A., Cacas, H., Casa, M., Pages, T., Rama, R., Ricart, A., Ventura, J., Ibanez, J., & Viscor, G. (1999). Intermittent hypobaric hypoxia stimulates erythropoiesis and improves aerobic capacity. Medicine and Science in Sports and Exercise, 31, 264-268. Saltin, B. (1996). Exercise and the environment: Focus on altitude. Research Quarterly for Exercise and Sport, 67, S1-S10. Squires, R. W. (1979). Effects of acute exposure to moderate simulated altitude on the aerobic capacity of men (Doctoral dissertation, Pennsylvania State University, 1979). Microfilm Publications, International Institute for Sport and Human Performance, University of Oregon, Eugene, Oregon. Squires, R., & Buskirk, E. R. (1982). Aerobic capacity during acute exposure to simulated altitude, 914 to 2286 meters. Medicine and Science in Sports and Exercise, 14, 36-40. Stray-Gunderson, J., Alexander, L., Hochstein, A., deLemos, D., & Levine, B. D. (1992). Failure of red cell volume to increase to altitude exposure in iron deficient runners. Medicine and Science in Sports and Exercise, 24, S90. Stray-Gunderson, J., Hochstein, A., & Levine, B. D. (1993). Effect of 4 weeks altitude exposure and training on red cell mass in trained runners. Medicine and Science in Sports and Exercise, 25, S171. Tucker, A., Stager, J., & Cordain, L. (1984). Arterial 02 saturation and maximum 02 consumption in moderate-altitude runners exposed to sea level and 3,050m. Journal of the American Medical Association, 252, 2876-2871. Wagner, P. (1998). Determinants of maximal oxygen utilization. Retrieved October 11, 2000 from the World Wide Web:http://www.sportscience.org.nz/publications/report/ report6.html Wofel, E. E., Groves, B. M., Brooks, G. A., Butterfield, G. E., Mazzeo, R. S., Moore, L. G., Sutton, J. R., Bender, P. R., Dahms, T. E., McCullough, R. E., McCullough, R. G., Huang, S., Sun, S., Grover, R. F., Hultgren, H. N., & Reeves, J. T. (1991). Oxygen transport during steady-state submaximal exercise in chronic hypoxia. Journal of Applied Physiology, 70, 1129-1136..

i forgot that's what i called her. from her photo! ha ha!

whoops

What a gorgeous mountain Goode is. i wanna be there RIGHT NOW! Have all the various ribs (esp the last one on the right before the hanging glacier) been climbed?

Totally!!!!!!! I call it uber alpine hyper-stumble-wallowing

rappel grappel is the descent for the beckey route. climb the beckey route and then do it...or if you wanna be all about that route, it's just before the col b/t the two spires. the burgundy paisano is totaly realistic for a day trip, just start a little earlier, which even if you weren't going for it is a much better idea than sloggin up Burgundy col in the heat of the day (ugggggh!) it should take 2-4 hours to get to the base

your dog may have had a latex allergy, Jordop

ME and Hopalong the Dog. I love my doggie!

In my opinion, always opt for the least invasive thing possible...bodies don't react well to invasive surgery. Leveling the tibial plateau sounds pretty damn harsh, don't you think it would cause osteoarthritis later on? Also, what do they do with the meniscus that's attached to the tibia. do they remove it, shave down the tibia, and reattach the meniscus? all that vs. something that is routinely done? sounds like they're using dogs as guiny pigs on a new surgery for humans. and "CCL" what colateral is that? do you mean LCL or MCL? if so those aren't that deep so the surgery wouldn't be that complicated. what were the potential drawbacks for the "CCL??" surgery, you didn't list any.

snow lakes is WAY WAY WAY more mellow, although Assgard is pretty scenic. if ya can swing it, snow lakes in, assgard out. the TH aren't very far apart, so hitchin' a ride should be EZ.

so is the new star wars any good?

would you be able to archive this site if you switched...i.e. would all the spray be gone forever?

you all fucking suck and if i ever see any of you i'll pull your balls off, shove them up your ass, so that the next time you take a shit, you'll shit on your balls.

if you do choose the go up above the off-route bolted anchor, you'll score some nice RP's althogh you'd be pretty fucked if ya did

after re-reading what i typed, i still can't see how you guys think i concidered your adventure boring or crowded. i just never figured i'd bother going up there for just a few pitches. shheeeesh.

don't get sucker up to the bolt anchors up left after the 4th pitch (past the 10/5.9 roof)...trend right.

That's pretty cool! Nice goin, looks like y'all had some fun. 5.11 A0...that;s skills. glad you didn't get stabbed, you must have some flippin sweet reflexes. i'm curious about the 8 pitches. how tall is the route? i always thought that the Mole was like 3 pitches. maybe i need to take it off the do'nt bother list! gracias

If you were going slow i'd pass you RuMR, but you're probably faster than me so it wouldn't happen.