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Potential Physiological Benefits of Altitude Training

This is an excellent excerpt reprinted from Burke’s book with permission with permission from Human Kinetics, High-Tech Cycling-2nd Edition.

“Human physiology is affected in different ways at high altitude. In general, the various systems of the human body—pulmonary, cardiovascular, endocrine, skeletal muscles—respond and adjust in an effort to provide enough oxygen to survive in the hypoxic environment of high altitude. Some of these life-supporting physiological responses may also enhance athletic performance, particularly in endurance sports.

The scientific rationale for using altitude training for the enhancement of aerobic performance is based on the body’s response to changes in the partial pressure of inspired oxygen (PIO2) and the partial pressure of oxygen in the arterial blood (PaO2). PIO2 at sea level is equal to 149 mmHg. At Mexico City (2300 m, 7544 ft), PIO2 drops to approximately 123 mmHg. At the summit of Mt. Everest (8852 m, 29,035 ft), PIO2 is approximately 50 mmHg or only about 30% of sea level PIO2.

High-Tech Cycling book coverBecause of the altitude-induced decrease in PIO2, there is a decrease in PaO2, which leads to a drop in renal PaO2 and renal tissue oxygenation (Ou et al. 1998; Richalet et al. 1994). It is hypothesized that this reduction in renal tissue oxygenation stimulates the synthesis and release of erythropoietin (EPO) (Porter and Goldberg 1994; Richalet et al. 1994), the principal hormone that regulates erythrocyte (RBC) and hemoglobin production. In turn, an increase in serum EPO concentration stimulates the synthesis of new RBCs in the red bone marrow by promoting the cellular growth of immature erythrocytes, specifically the colony-forming unit-erythroid (CFU-E). Erythropoietin receptors are present on the surface of CFU-E. Binding of EPO to CFU-E receptors initiates the production of cellular transcription factors, synthesis of membrane and cytoskeletal proteins, synthesis of heme and hemoglobin, and the terminal differentiation of cells (Bell 1996). The RBC maturation process takes five to seven days from the initial altitude-induced increase in serum EPO (Bell 1996; Flaharty et al. 1990).

These hematological changes may significantly improve an athlete’s V·O2max by enhancing the blood’s ability to deliver oxygen to exercising muscles. It has been shown that improvements in RBC mass, hemoglobin concentration, and V·O2max enhance aerobic performance (Berglund and Ekblom 1991; Birkeland et al. 2000; Ekblom and Berglund 1991). Essentially, many athletes and coaches view altitude training as a natural or legal method of blood doping.

Research by Chapman, Stray-Gundersen, and Levine (1998) suggests that some athletes experience a better hematological response at altitude than others do. Female and male collegiate runners who completed either LHTL or traditional “live high, train high” altitude training were classified as responders or nonresponders based on their performance in a postaltitude 5-km run. On average, responders demonstrated a significant 4% improvement (37 s) in the postaltitude 5-km run versus their prealtitude performance; nonresponders were approximately 1% slower (14 s). Hematological data showed that responders had a significantly larger increase in serum EPO (52%) compared with nonresponders, who demonstrated a 34% increase in serum EPO. Similarly, postaltitude RBC mass for responders was 8% higher (p < 0.05), but nonresponders’ RBC mass was only 1% higher (not statistically significant) compared with prealtitude values. A breakdown of responders indicated that 82% came from the LHTL group, and 18% came from the “live high, train high” group. The authors concluded that each athlete may need to follow an altitude training program that places the athlete at an individualized, optimal altitude for living and another altitude for training, thereby producing the best possible hematological response.

Skeletal Muscle
As described, the primary reason endurance athletes train at altitude is to increase RBC mass and hemoglobin concentration. In addition, they may gain secondary physiological benefits as a result of altitude exposure. For example, altitude training has been shown to increase skeletal muscle capillarity (Desplanches et al. 1993; Mizuno et al. 1990). In theory, this physiological adaptation enhances the exercising muscles’ ability to extract oxygen from the blood.

Other favorable skeletal muscle microstructure changes that occur as a result of training at altitude include increased concentrations of myoglobin (Terrados et al. 1990), increased mitochondrial oxidative enzyme activity (Terrados et al. 1990), and a greater number of mitochondria (Desplanches et al. 1993), all of which serve to enhance the rate of oxygen utilization and aerobic energy production.

Nevertheless, scientific data in support of altitude-induced skeletal muscle adaptations are minimal, particularly among well-trained athletes. Only Mizuno and colleagues (1990) examined elite athletes; Desplanches and colleagues (1993) and Terrados and colleagues (1990) examined the effect of altitude training on the skeletal muscle characteristics of untrained individuals. Additional studies conducted on elite athletes failed to demonstrate significant changes in skeletal muscle microstructure caused by altitude training (Saltin et al. 1995; Terrados et al. 1988). Furthermore, Desplanches and colleagues (1993) conducted their study at impractical simulated elevations (4100 to 5700 m, 13,450 to 18,700 ft), an altitude too high for athletes to train at. Thus, based on the current scientific literature, it is unclear whether altitude training, as practiced by most elite athletes at moderate elevations of 1800 to 3050 m (6000 to 10,000 ft) improves oxygen extraction and utilization via favorable changes in skeletal muscle capillarity, myoglobin, mitochondrial oxidative enzyme activity, and mitochondrial density. Additional research is warranted.

Another important physiological adaptation that may occur as a result of exposure to moderate altitude is an improvement in the capacity of the skeletal muscle and blood to buffer the concentration of hydrogen ions (H+). High concentrations of H+ are known to contribute to skeletal muscle fatigue by impairing actin-myosin crossbridge cycling, reducing the sensitivity of troponin for calcium (Ca2+) and inhibiting the enzyme phosphofructokinase (PFK) (McComas 1996). Thus, an enhanced H+ buffering capacity may have a beneficial effect on aerobic and anaerobic performance.

In support of this, Mizuno and colleagues (1990) reported a significant 6% increase in the buffering capacity of the gastrocnemius muscle of elite male cross-country skiers who lived at 2100 m (6890 ft) and trained at 2700 m (8860 ft) for 14 days. Significant improvements in maximal O2 deficit (29%) and treadmill run time to exhaustion (17%) were observed after the athletes returned to sea level. In addition, a positive correlation (r = 0.91, p < 0.05) was demonstrated between the relative increase in buffering capacity of the gastrocnemius muscle and treadmill run time to exhaustion.

Gore and colleagues (2001) reported that skeletal muscle buffer capacity increased 18% (p < 0.05) in male triathletes, cyclists, and cross-country skiers following 23 days of living at 3000 m (9840 ft) and training at 600 m (1970 ft). Furthermore, they found that mechanical efficiency significantly improved during a 4 3 4-min submaximal cycling test following the 23-day LHTL period.

The precise mechanisms responsible for enhanced skeletal muscle buffering capacity following high altitude training are unclear but may be related to changes in creatine phosphate and/or muscle protein concentrations (Mizuno et al. 1990). Improvements in blood buffering capacity may be due to increases in bicarbonate (Nummela and Rusko 2000) or hemoglobin concentration.

The Lactate Curve

What is the lactate curve? Why do I need to know the lactate curve? How does it fit into my triathlon training? When should it fit in my triathlon training? How does it affect my triathlon racing? What does the lactate curve mean to endurance athletes?

Peter Jannsen answers many of these questions in his book, “Lactate Threshold Training.” An excerpt follows that will likely wet your appetite to learn more about how it can help your racing.

lactate threshold training“The lactate content of the blood is a parameter of great importance. This content is measured in millimoles of lactate per liter of blood. Healthy persons at rest have values roughly between 1 and 2 millimoles per liter, and strenuous exercise increases this value. Even slight increases in lactate content (6 to 8 millimoles per liter) may impair an athlete’s coordination. Regularly high lactate values impair aerobic endurance capacity.

For this reason, athletes should be prudent with the number of intensive workloads they undergo in a certain period of time. The workload intensities needed for various workouts can be determined by means of the lactate curve. Graph 89 shows the relationship between lactate content of the blood and the intensity of exercise. Intensity is expressed as running pace in meters per second.

To obtain a lactate curve, the athlete should run the same distance a number of times, each time at a higher pace. After every run, determine the lactate concentration in the blood. Every distance should be run at an even pace, and the running pace should be increased in small steps. The length of the run should be such that the athlete needs at least 5 minutes to cover the distance. When well-trained athletes run slowly, they have low lactate values; their energy supplies are fully aerobic. When the pace is increased, the curve begins to rise; the working muscles do produce lactate, but the quantities are so small that, for the most part, they can be neutralized by the body. It is a widespread belief that this is the case between 2 and 4 millimoles per liter. Therefore, this area is called the aerobic-anaerobic transition zone.

Each athlete can maintain a certain running pace for a long period of time without lactate accumulation in the body. If the pace is increased to a certain point, ongoing acidosis will occur, depending on the degree and duration of the increase, and at a certain moment this acidosis will force the athlete to stop. The lactate content that is measured at this borderline pace is also called the anaerobic threshold. The anaerobic threshold value is around a lactate content of 4 millimoles per liter. Exercise surpassing the anaerobic threshold will inevitably increase lactate content within the body.

Thus, exercise up to this level of the aerobic threshold is fully aerobic. Lactate content at the aerobic threshold is about 2 millimoles per liter. Exercise within the aerobic-anaerobic transition zone is more intensive, and energy supply is both aerobic and anaerobic. Production and neutralization of lactate are balanced. This zone is between 2 and 4 millimoles per liter.

The anaerobic threshold occurs when exercise at a high intensity results in an accumulation of lactate in the blood. Therefore, this type of exercise can be maintained for a limited period of time. But at an intensity just below the anaerobic threshold, this lactate content can be kept at a steady-state level, and this type of exercise may be maintained for a longer period of time, about 1 to 1.5 hours.

Lactate content at the anaerobic threshold is for many athletes about 4 millimoles per liter, but there are wide individual variations among athletes. Anaerobic threshold can be as low as 2 to 3 millimoles per liter or as high as 6 to 8 millimoles per liter. By drawing a lactate curve for every athlete, the anaerobic threshold can be found and subsequently used to set training intensities. The best way to find the anaerobic threshold is to determine maximal lactate steady state (MLSS), which is discussed elsewhere in the book.

Endurance capacity can best be trained by endurance workouts around the level of the anaerobic threshold, that is, workouts with lactate values of 2 to 6 millimoles per liter. These values may be determined according to the athlete’s test results. Very well-trained people mostly train their endurance capacity at somewhat lower values, between 2 and 3 millimoles per liter. Less well-trained persons often cannot help but peak to higher levels. They then surpass their anaerobic threshold and make their workouts less effective. Though they often feel satisfied with a strenuous workout, this type of workout does more damage than good.

The threshold pace is the speed that corresponds with the anaerobic threshold. Above the anaerobic threshold this speed can be maintained for a short period of time, but below the threshold it can be maintained 1 to 1.5 hours. The threshold pace, the running or cycling speed at the heart rate deflection point (HRdefl), is also called the V4 pace, as discussed in chapter 3. However, the term V4 is somewhat misleading, because many athletes have an anaerobic threshold over or under 4 millimoles per liters. For example, an athlete with an anaerobic threshold of 6 millimoles per liter could be said to have a threshold pace of V6.

Sport-specific performance capacity could be defined as the speed that is reached at a lactate content of 4 millimoles per liter, or V4. V4 is an important indicator of the athlete’s capacities. Any improvement of V4 pace will also improve performance capacity. Regular V4 tests indicate the athlete’s condition, so athletes can be monitored in their development and can be mutually compared. But remember that V4 is not the threshold pace for everybody, because many athletes have an anaerobic threshold under or over 4 millimoles per liter. Therefore, it might be better to test MLSS than V4.

Recovery workouts should not be intensive, and lactate content should remain less than 2 millimoles per liter. Intensive interval workouts give high lactate values, far surpassing 4 millimoles per liter. The effect of training will be that the lactate curve shifts to the right, as shown in graph 90.

Therefore, training intensities should be readjusted from time to time, and a new test procedure with blood sampling will be necessary. Not every athlete has access to blood testing, but other methods can supply the same or at least the most important information. All these other methods of finding the anaerobic threshold are discussed elsewhere in this book.”