The cerebral metabolic ratio is not affected by oxygen availability during maximal exercise in humans

Abstract

Intense exercise decreases the cerebral metabolic ratio of O(2) to carbohydrates (glucose + (1/2) lactate) and the cerebral lactate uptake depends on its arterial concentration, but whether these variables are influenced by O(2) availability is not known. In six males, maximal ergometer rowing increased the arterial lactate to 21.4 +/- 0.8 mm (mean +/- s.e.m.) and arterial-jugular venous (a-v) difference from -0.03 +/- 0.01 mm at rest to 2.52 +/- 0.03 mm (P < 0.05). Arterial glucose was raised to 8.5 +/- 0.5 mm and its a-v difference increased from 1.03 +/- 0.01 to 1.86 +/- 0.02 mm (P < 0.05) in the immediate recovery. During exercise, the cerebral metabolic ratio decreased from 5.67 +/- 0.52 at rest to 1.70 +/- 0.23 (P < 0.05) and remained low in the early recovery. Arterial haemoglobin O(2) saturation was 92.5 +/- 0.2% during exercise with room air, and it reached 87.6 +/- 1.0% and 98.9 +/- 0.2% during exercise with an inspired O(2) fraction of 0.17 and 0.30, respectively. Whilst the increase in a-v lactate difference was attenuated by manipulation of cerebral O(2) availability, the cerebral metabolic ratio was not affected significantly. During maximal rowing, the cerebral metabolic ratio reaches the lowest value with no effect by a moderate change in the arterial O(2) content. These findings suggest that intense whole body exercise is associated with marked imbalance in the cerebral metabolic substrate preferences independent of oxygen availability.

Figures

Figure 1. The arterial–internal jugular venous differences (upper) and the metabolic uptake ratio (lower) in response to maximal ergometer rowing in hypoxia (left), normoxia (middle) and hyperoxia (right)

•, lactate; ○, glucose; pre-ex, after warm-up; post-ex, immediately after exercise; *different from rest, #different from hypoxia, +different from normoxia, P < 0.05. Data are mean ± s.e.m., n = 6.