Pulmonary system limitations to endurance exercise performance in humans

Abstract

Accumulating evidence over the past 25 years depicts the healthy pulmonary system as a limiting factor of whole-body endurance exercise performance. This brief overview emphasizes three respiratory system-related mechanisms which impair O(2) transport to the locomotor musculature [arterial O(2) content (C(aO(2))) × leg blood flow (Q(L))], i.e. the key determinant of an individual's aerobic capacity and ability to resist fatigue. First, the respiratory system often fails to prevent arterial desaturation substantially below resting values and thus compromises C(aO(2)). Especially susceptible to this threat to convective O(2) transport are well-trained endurance athletes characterized by high metabolic and ventilatory demands and, probably due to anatomical and morphological gender differences, active women. Second, fatiguing respiratory muscle work (W(resp)) associated with strenuous exercise elicits sympathetically mediated vasoconstriction in limb-muscle vasculature, which compromises Q(L). This impact on limb O(2) transport is independent of fitness level and affects all individuals, but only during sustained, high-intensity endurance exercise performed above ∼85% maximal oxygen uptake. Third, excessive fluctuations in intrathoracic pressures accompanying W(resp) can limit cardiac output and therefore Q(L). Exposure to altitude exacerbates the respiratory system limitations observed at sea level, further reducing C(aO(2)) and substantially increasing exercise-induced W(resp). Taken together, the intact pulmonary system of healthy endurance athletes impairs locomotor muscle O(2) transport during strenuous exercise by failing to ensure optimal arterial oxygenation and compromising Q(L). This respiratory system-related impact exacerbates the exercise-induced development of fatigue and compromises endurance performance.

Figure 1

Relationship between respiratory muscle work and leg blood flow. Fatigue related metabolite accumulation in respiratory muscles activate group III/IV phrenic afferents which reflexly cause increased sympathetic efferent discharge and limb vasoconstriction. This sequence facilitates locomotor muscle fatigue and limits endurance exercise performance. Adapted from (Dempsey et al., 2002).

Figure 2

Effect of exercise-induced arterial desaturation on 5 km cycling time trial performance. During the iso-oxic trial, S_aO₂ was maintained at resting levels (~98%) via progressive increases in inspiratory O₂ content (F_IO₂). Time to completion and mean power output (331 ± 13 W vs 314 ± 13 W) were significantly improved during the iso-oxic time trial. Adapted from (Amann et al., 2006).

Figure 3

Effects of a 60% reduction in inspiratory muscle work (‘Insp. Unload’) on the pre- to post-exercise change in the force-frequency curve of the quadriceps muscle. The y-axis represents the change for the second of the paired quadricep twitch amplitude (Q_tw,T2). The work rate and exercise time was identical during control exercise and inspiratory unloadin (≥90% VO₂max; 292 W, 13 min). Adapted from (Romer et al., 2006b).