The Effects of Caffeine on Ventilation and Pulmonary Function During Exercise - Caffeine: Chemistry, Analysis, Function and Effects - page 338

A simple search of the literature finds no less than two dozen review articles
that have as a primary topic the effects of caffeine on exercise tolerance and
muscular performance (for quality examples, see Graham 2001 and Spriet
2000). With the simple fact that caffeine is the most consumed drug in the
world by humans, it could be easily argued that this large number of reviews is
warranted. When the typical review delves into possible mechanisms for
caffeine to affect exercise performance, three are commonly mentioned: 1)
changes in substrate utilization resulting in glycogen sparing, 2) alterations in
catecholamine release, and 3) central nervous system effects. However, a rarely
discussed consequence of caffeine ingestion is the resulting effect on exercise
ventilation and pulmonary function (Chapman and Mickleborough 2009). In
fact, of the most commonly cited review articles and topic chapters in the
literature on the subject of caffeine ingestion and exercise, only one (Magkos
and Kavouras 2004) briefly mentions the general effects of caffeine on
respiration. Within this chapter, the primary purpose is to highlight the effects
of caffeine on exercise ventilation and pulmonary function, and to suggest
possible effects on exercise performance.

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18.2 Effects of Caffeine on Ventilatory Drive

18.2.1 Central and Peripheral Chemosensitivity Changes With
Caffeine
Caffeine has been historically cited for its stimulating effects on respiration in
both animals and humans (Le Messurier 1936). Clinically, xanthine compounds
have been used as safe and effective ventilatory stimulants for the treatment of
conditions such as chronic obstructive pulmonary disease and neonatal apnea.
Mechanistically, caffeine appears to affect both the central and peripheral
chemoreceptors that control ventilation. Looking first at the effects on
peripheral chemosensitivity, in moderate doses, caffeine has been demonstrated
to significantly raise the resting hypoxic and hypercapnic ventilatory responses
in humans (D'Urzo 1990). The hypoxic ventilatory response relates changes in
arterial oxyhemoglobin saturation (SaO 2 ) with changes in minute ventilation
during progressive isocapnic hypoxia, thus isolating ventilatory drive with
falling inspired PO 2 primarily to the peripheral chemoreceptors located in the
carotid bodies and aortic arch. In one study of 7 mostly caffeine habituated,
untrained adult males, D'Urzo et al (1990) found that 650 mg of orally ingested
caffeine resulted in a 135% increase in the slope of the resting hypoxic ventilatory
response (Figure 18.1). In other words, the change in resting ventilation per
percent change in SaO 2 with hypoxic exposure was nearly doubled with caffeine
ingestion. Similarly, the resting hypercapnic ventilatory response (which relates
changes in minute ventilation to changes in end tidal PCO 2 with progressive
hyperoxic hypercapnia) increased by 31%. Taken together, these data suggest a
strong effect of high dose caffeine augmenting the sensitivity of the peripheral
chemoreceptors in normal untrained adults.