Reduced muscle activation during exercise related to brain oxygenation and metabolism in humans

Abstract

Maximal exercise may be limited by central fatigue defined as an inability of the central nervous system to fully recruit the involved muscles. This study evaluated whether a reduction in the cerebral oxygen-to-carbohydrate index (OCI) and in the cerebral mitochondrial oxygen tension relate to the ability to generate a maximal voluntary contraction and to the transcranial magnetic stimulated force generation. To determine the role of a reduced OCI and in central fatigue, 16 males performed low intensity, maximal intensity and hypoxic cycling exercise. Exercise fatigue was evaluated by ratings of perceived exertion (RPE), arm maximal voluntary force (MVC), and voluntary activation of elbow flexor muscles assessed with transcranial magnetic stimulation. Low intensity exercise did not produce any indication of central fatigue or marked cerebral metabolic deviations. Exercise in hypoxia (0.10) reduced cerebral oxygen delivery 25% and decreased 11+/-4 mmHg (P<0.001) together with OCI (6.2+/-0.7 to 4.8+/-0.5, P<0.001). RPE increased while MVC and voluntary activation were reduced (P<0.05). During maximal exercise declined 8+/-4 mmHg (P<0.05) and OCI to 3.8+/-0.5 (P<0.001). RPE was 18.5, and MVC and voluntary activation were reduced (P<0.05). We observed no signs of muscular fatigue in the elbow flexors and all control MVCs were similar to resting values. Exhaustive exercise provoked cerebral deoxygenation, metabolic changes and indices of fatigue similar to those observed during exercise in hypoxia indicating that reduced cerebral oxygenation may play a role in the development of central fatigue and may be an exercise capacity limiting factor.

Figures

Figure 1

Voluntary activation during cycling A, the subject was sitting on the cycling ergometer (not shown) with his right arm flexed 90 deg and fully supinated and the wrist secured in the strain gauge dynamometer. Surface EMG electrodes were placed at the belly and the tendon at the biceps brachii muscle (BB), the triceps brachii muscle (TB) and the brachioradialis muscle (BR). For motorpoint stimulation surface electrodes were placed at BB and a circular coil was positioned over the vertex for TMS stimulation. B, relation between the amplitude of the superimposed twitch evoked by TMS between 60 and 100% of MVC was extrapolated and the y-intercept was used as the estimated biceps resting twitch evoked by TMS. Data from one subject. C, motor point and force tracing (bold line) from TMS stimulation during a MVC. D and E, arm EMG and force tracing from one subject while cycling and while performing a MVC. F, motorpoint stimulation evoked twitch at rest did not change due to the whole-body exercise, which indicates that peripheral fatigue was not present in the biceps muscle at any time of the cycling protocol.

Figure 2

Relation between measurements of fatigue (y-axis) and cerebral metabolism and oxygenation (x-axis) Data are individual and mean (open symbols) for 16 subjects (filled circles) and the four colours illustrates exercise in normoxia at 124 (black), 226 (green) and 279 W (red) and in hypoxia at 124 W (blue). The regression lines are computed according to the mean values. OCI, cerebral oxygen/carbohydrate index; Δ, changes in cerebral mitochondrial oxygen tension; RPE, ratings of perceived exertion; MVC, maximal voluntary contraction.