Exercise is a potent stimulus with a profound ability to alter our bodies over time. For example, intense endurance exercise leads to meaningful adaptations in the various systems that contribute to oxygen transport and utilization. Thus, for every incremental improvement in VO2max we should expect to see increases in hemoglobin mass, improved peripheral circulation, increased left ventricular volumes, or increased muscle mitochondrial density. Given how adaptable all of these systems are, we would expect to see similar exercise-induced adaptations in the airways, pulmonary vasculature, and lungs as well. After all, conventional wisdom states that the rate-limiting factor for maximal oxygen transport and utilization (ie, VO2max) centers around the cardiovascular response to exercise. Additionally, it's traditionally been said that the respiratory system is overbuilt for the demands posed by maximal effort exercise. As a result, the respiratory system cannot be the rate-limiting factor for VO2max.
However, more recent research has revealed several situations in which the respiratory system is underbuilt and incurs high biological costs during maximal effort exercise. As a result, even trained endurance athletes with very high VO2max values may not have enhanced lung volumes and pulmonary diffusion capabilities compared with the average sedentary adult.
The absence of training effects on an athlete's lung structure is shocking when you consider the capacity of the cardiovascular and muscular systems to adapt to exercise. In addition to not showing significant adaptations to exercise, several respiratory system components can be negatively impacted by intense exercise training. For example, elite endurance athletes have a high prevalence of airway narrowing during or immediately following high-intensity exercise. Additionally, high-intensity exercise can lead to disruptions in airway remodeling, hypersensitive airways, and airway injury. This occurs because the ventilatory demands of exercise require flow rates above ten times resting values.
I've even observed arterial desaturation as low as 5–12% below resting values during maximal effort exercise in elite Crossfit competitors. In these athletes, arterial desaturation almost always occurs at intensities above the lactate balance point and reaches the lowest value at maximal intensity. Additionally, oxygen transport to the respiratory muscles does not meet the metabolic requirements of ventilation, which we can observe with muscle oximetry. As a result, there is significant deoxygenation of the trunk’s accessory respiratory muscles during maximal effort exercise.
In the image above we have an intercostal muscle oxygen saturation (SmO2) trend and a peripheral oxygen saturation (SpO2) trend for an advanced Crossfit athlete performing a step test. Note the change in both SmO2 and SpO2 as both reach a nadir at the highest workout intensities. This is indicative of both a pulmonary diffusion limitation and a lack of fatigue resistance of the inspiratory and expiratory musculature.
It’s also worth noting that this phenomenon may be more exaggerated in female elite endurance athletes versus male elite endurance athletes. However, it is also quite common in males as well. High resolution computed tomography has shown that airway cross-sectional areas are comparable between the sexes throughout the maturation process, however, post-pubescent females show a 20–30% reduction in the diameter of the trachea and main stem bronchi. A smaller lung size in adult females accounts for much of these differences in airway size. Still, even when a limited number of comparisons were made at equivalent lung volumes, the adult female had narrowed trachea and bronchi compared to males of an equal body mass. Even when adjusted for age, height, and hemoglobin concentration, resting diffusion capacity and lung volumes are also lower in women versus men. According to Dr. Jermone Dempsey, “we can interpret these data to mean that adult women of all ages and over a wide range of fitness levels have hormonally determined trachea, bronchi, and lung sizes that are underbuilt for the flow rates demanded by heavy intensity exercise. Because the consequences of airway dysanapsis are likely to exist in the majority of women and be manifested even in moderately heavy exercise, we would predict that adult women across the fitness range would experience a greater suscepti- bility to respiratory limitations to exercise than do men."
Knowing that respiratory limitation are so prevalent among elite endurance athletes, we need better tools of diagnosing these limitations and monitoring load on the respiritory system during workouts. Once way we can do that is by monitoring respiratory muscle oxygen kinetics with NIRS-based muscle oximeters.
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