Ide, Kojiro, Allan Horn, and Niels H. Secher. Cerebral metabolic response to submaximal exercise. J. Appl. Physiol. 87(5): 1604-1608.-We studied cerebral oxygenation and metabolism during submaximal cycling in 12 subjects. At two work rates, middle cerebral artery blood velocity increased from 62 Ϯ 3 to 63 Ϯ 3 and 70 Ϯ 5 cm/s as did cerebral oxygenation determined by near-infrared spectroscopy. Oxyhemoglobin increased by 10 Ϯ 3 and 25 Ϯ 3 µmol/l (P Ͻ 0.01), and there was no significant change in brain norepinephrine spillover. The arterial-to-internal-jugularvenous (a-v) difference for O 2 decreased at low-intensity exercise (from 3.1 Ϯ 0.1 to 2.9 Ϯ 0.1 mmol/l; P Ͻ 0.05) and recovered at moderate exercise (to 3.3 Ϯ 0.1 mmol/l). The profile for glucose was similar: its a-v difference tended to decrease at low-intensity exercise (from 0.55 Ϯ 0.05 to 0.50 Ϯ 0.02 mmol/l) and increased during moderate exercise (to 0.64 Ϯ 0.04 mmol/l; P Ͻ 0.05). Thus the molar ratio (a-v difference, O 2 to glucose) did not change significantly. However, when the a-v difference for lactate (0.02 Ϯ 0.03 to 0.18 Ϯ 0.04 mmol/l) was taken into account, the O 2 -to-carbohydrate ratio decreased (from 6.1 Ϯ 0.4 to 4.7 Ϯ 0.3; P Ͻ 0.05). The enhanced cerebral oxygenation suggests that, during exercise, cerebral blood flow increases in excess of the O 2 demand. Yet it seems that during exercise not all carbohydrate taken up by the brain is oxidized, as brain lactate metabolism appears to lower the balance of O 2 -to-carbohydrate uptake. blood pressure; epinephrine; glucose; heart rate; lactate; near-infrared spectroscopy; norepinephrine; norepinephrine spillover CONTROVERSY EXISTS as to whether the metabolic activity of the brain as a whole increases during physical exercise. For example, there appears to be no change in brain O 2 uptake (V O 2 ) during cycling (18, 31), whereas, during vigorous exercise on the treadmill, there is reported to be an increase in brain V O 2 (28). Although the cerebral metabolic rate for O 2 has been taken as the variable most closely coupled to metabolic activity of the brain (18), V O 2 may not be the most sensitive index for an evaluation of the metabolic activity of the brain. In response to neural activation, regional V O 2 increases much less than the increase in cerebral blood flow (7). Also, cerebral oxygenation determined by near-infrared spectroscopy (NIRS) exceeds the increase in O 2 demand in response to motor stimulation (22). Moreover, the increase in regional uptake of glucose surpasses that of O 2 (8), and similar observations have been made for the global value (15). Thus the molar cerebral V O 2 -to-glucose uptake ratio becomes reduced (15, 16).During exercise, blood lactate increases progressively with work rate, and lactate may be of importance for brain metabolism (14). Yet, when there is no increase in blood lactate, as during mental activation, no net brain uptake of lactate has been demonstrated (17). Rather, the increase in lactate uptake by the brain becomes apparent during hyperlactemia ...

The metabolic activity of the brain has not been evaluated during physical exercise. In six volunteers substrate uptake by the brain was determined during graded exercise and recovery from maximal exercise by measuring the arterial‐internal jugular venous concentration differences(a–v differences). The a–v difference for lactate increased from 0.02 ± 0.08 mmol l−1 at rest to 0.39 ± 0.13 mmol l−1 during exercise and remained positive during 30 min of recovery (P < 0.05). The a–v difference for glucose (0.55 ± 0.06 mmol l−1 at rest) did not change significantly during exercise, but during the initial 5 min of recovery it increased to 0.83 ± 0.10 mmol l−1 (P < 0.05). The O2 a–v difference at rest of 3.11 ± 0.30 mmol l−1 remained stable during exercise, then increased during the initial 5 min of recovery (3.77 ± 0.52 mmol l−1) and remained high during the subsequent 30 min recovery period (3.62 ± 0.64 mmol l−1; P < 0.05). Thus the O2/glucose uptake ratio did not change during exercise (pre‐exercise 5.95 ± 0.68; post‐exercise 6.02 ± 1.39) but decreased to 4.93 ± 0.99 during the initial 5 min of recovery (P < 0.05). When lactate uptake was included, the resting O2/carbohydrate uptake ratio of 5.84 ± 0.73 was reduced to 4.42 ± 0.25 during exercise and decreased further during the recovery phase (to 3.79 ± 0.30; P < 0.05). In contrast, in the resting and immobilised rat, lactate infusion to a level similar to that obtained during maximal exercise in humans did not affect the a–v difference for lactate. The large carbohydrate uptake by the brain during recovery from maximal exercise suggests that brain glycogen metabolism is important in the transition from rest to exercise, since this would explain the significant post‐exercise decrease in the O2/carbohydrate uptake ratio.

In a double-blind placebo-controlled cross-over study the effects of epidural morphine (4 mg) on somatosensory functions were investigated in 10 healthy volunteers. Detection, pain detection and pain tolerance thresholds to thermal, mechanical and electrical stimuli as well as magnitude rating of short-lasting stimuli of the same modalities were monitored before and for 10 h after epidural administration of 4 mg of morphine or saline. Epidural morphine induced a naloxone-reversible (0.1 mg/kg, i.v.) increase in pain detection threshold to heat and mechanical stimuli and in pain tolerance threshold to heat, mechanical and electrical stimuli. Morphine induced a more pronounced increase in the pain tolerance than in the pain detection threshold. Magnitude rating of short-lasting radiant heat (argon laser) stimuli were reduced by epidural morphine in comparison to placebo while there was no significant difference between the effects of morphine and placebo on magnitude rating of short-lasting mechanical and electrical stimuli. The warm detection threshold was increased (naloxone reversible) by morphine. Segmental distribution of pruritus was reported by 7 subjects following epidural morphine which was replaced by a short-lasting burning sensation following naloxone administration. Naloxone (0.1 mg/kg) preceeded by placebo did not change somatosensory functions. These results indicate that the somatosensory effect of epidural morphine is dependent on the types of afferent fibres activated as well as on the duration and intensity of the stimulus.