Niels H. Secher

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

Intense exercise decreases the cerebral metabolic ratio of O2 to carbohydrates (glucose +½ lactate) and the cerebral lactate uptake depends on its arterial concentration, but whether these variables are influenced by O2 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 O2 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 O2 fraction of 0.17 and 0.30, respectively. Whilst the increase in a–v lactate difference was attenuated by manipulation of cerebral O2 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 O2 content. These findings suggest that intense whole body exercise is associated with marked imbalance in the cerebral metabolic substrate preferences independent of oxygen availability.

Modelflow underestimates cardiac output in heat stressed individuals

An estimation of cardiac output can be obtained from arterial pressure waveforms using the Modelflow method. However, whether the assumptions associated with Modelflow calculations are accurate during whole body heating is unknown. This project tested the hypothesis that cardiac output obtained via Modelflow accurately tracks thermodilution-derived cardiac outputs during whole body heat stress. Acute changes of cardiac output were accomplished via lower-body negative pressure (LBNP) during normothermic and heat-stressed conditions. In nine healthy normotensive subjects, arterial pressure was measured via brachial artery cannulation and the volume-clamp method of the Finometer. Cardiac output was estimated from both pressure waveforms using the Modeflow method. In normothermic conditions, cardiac outputs estimated via Modelflow (arterial cannulation: 6.1 ± 1.0 l/min; Finometer 6.3 ± 1.3 l/min) were similar with cardiac outputs measured by thermodilution (6.4 ± 0.8 l/min). The subsequent reduction in cardiac output during LBNP was also similar among these methods. Whole body heat stress elevated internal temperature from 36.6 ± 0.3 to 37.8 ± 0.4°C and increased cardiac output from 6.4 ± 0.8 to 10.9 ± 2.0 l/min when evaluated with thermodilution (P < 0.001). However, the increase in cardiac output estimated from the Modelflow method for both arterial cannulation (2.3 ± 1.1 l/min) and Finometer (1.5 ± 1.2 l/min) was attenuated compared with thermodilution (4.5 ± 1.4 l/min, both P < 0.01). Finally, the reduction in cardiac output during LBNP while heat stressed was significantly attenuated for both Modelflow methods (cannulation: -1.8 ± 1.2 l/min, Finometer: -1.5 ± 0.9 l/min) compared with thermodilution (-3.8 ± 1.19 l/min). These results demonstrate that the Modelflow method, regardless of Finometer or direct arterial waveforms, underestimates cardiac output during heat stress and during subsequent reductions in cardiac output via LBNP.

The carotid baroreflex is reset following prolonged exercise in humans

Aim:  Alterations in the carotid baroreflex (CBR) control of arterial pressure may explain the reduction in arterial pressure and left ventricular (LV) function after prolonged exercise. We examined the CBR control of heart rate (HR) and mean arterial pressure (MAP), in addition to changes in LV function, pre‐ to post‐exercise.