The Effects of Caffeine on Ventilation and Pulmonary Function During Exercise - Caffeine: Chemistry, Analysis, Function and Effects - page 342

caffeine absorption times and habituation status was widely varied in studies
where no increase in exercise ventilation was found.

18.3 Potential Ergogenic Effects of Increased Exercise
Ventilation
What are potential positive ergogenic effects on exercise performance from a
significant increase in exercise ventilation with caffeine ingestion? An increase
in VE could result in a rise in alveolar oxygen partial pressure, improving SaO 2
and ultimately oxygen delivery to the working musculature. In theory, this
could be of benefit in unique situations, such as exercise at altitude, or to
unique individuals, such as athletes who experience pulmonary gas exchange
limitations at sea level. Within the highly endurance trained population, it has
been estimated that approximately 50% of athletes experience exercise induced
arterial hypoxemia (EIH) during heavy exercise (Powers et al 1988). This
phenomenon is hallmarked by a significant reduction in arterial PO 2 and SaO 2
during exercise at sea level, with SaO 2 ,92% often used as a criterion measure
below which VO 2 max is impaired. Although originally thought to occur only
in male athletes with VO 2 max values above 65 mL kg 21 min 21 , EIH appears to
be even more prevalent in female endurance athletes (in part due to smaller
lung volumes, compared to men of the same stature) (Richards et al 2004) as
well as older, masters athletes.
The primary mechanism behind the reduced SaO 2 with EIH is believed to be
a reduced red blood cell transit time in the pulmonary capillary, secondary to
an enlarged stroke volume and fixed pulmonary capillary blood volume in
the athlete (Dempsey et al 1984). However, a blunted or ''inadequate''
hyperventilatory response during exercise in the athlete, resulting in a lower
alveolar oxygen partial pressure in the lung, also appears to play a role in the
formation of EIH (Harms and Stager 1985). To determine if caffeine could be
useful in eliminating the hypoxemia of EIH via increasing minute ventilation, 8
caffeine na¨ve EIH males (VO 2 max 5 69.2 ¡ 4.0 mL kg 21 min 21 ; SaO 2 at
VO 2 max 5 88.0 ¡ 1.7%) were given caffeine (8 mg kg 21 body weight) or
placebo and exercised progressively to VO 2 max (Chapman and Stager 2008).
During submaximal exercise (75%-90% of VO 2 max), caffeine caused a
significant increase in SaO 2 in runners with EIH, secondary to increases in
minute ventilation and end tidal PO 2 (Figure 18.2). However, at the final
minute of exercise corresponding to VO 2 max, SaO 2 was unchanged in EIH
runners, despite a significant increase in VE. In a follow up experiment, during
exercise in simulated altitude (using a hypoxic inspirate), caffeine did not
improve SaO 2 during maximal exercise in highly trained male distance runners
(despite an increase in VE at VO 2 max), but did improve SaO 2 at submaximal
workloads (Chapman et al 1998). One possible explanation for the lack of
improvement of SaO 2 at VO 2 max with caffeine is that as exercise intensity
approached VO 2 max, only about 40% of the increase in VE with caffeine went
towards increasing alveolar ventilation, with the remainder going to dead

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