Prefrontal cortex oxygenation during incremental exercise in chronic fatigue
syndrome
syndrome
J. Patrick Neary(1,*), Andy D.W. Roberts(2), Nina Leavins(2), Michael F.
Harrison(1), James C. Croll(2) and James R. Sexsmith(2)
Harrison(1), James C. Croll(2) and James R. Sexsmith(2)
Summary
This study examined the effects of maximal incremental exercise on cerebral
oxygenation in chronic fatigue syndrome (CFS) subjects. Furthermore, we
tested the hypothesis that CFS subjects have a reduced oxygen delivery to the
brain during exercise. Six female CFS and eight control (CON) subjects
(similar in height, weight, body mass index and physical activity level)
performed an incremental cycle ergometer test to exhaustion, while changes in
cerebral oxy-haemoglobin (HbO_2), deoxy-haemoglobin (HHb), total blood volume
(tHb=HbO_2+HHb) and O_2 saturation [tissue oxygenation index (TOI), %)]
was monitored in the left prefrontal lobe using a near-infrared
spectrophotometer. Heart rate (HR) and rating of perceived exertion (RPE)
were recorded at each workload throughout the test. Predicted VO_2_peak in CFS
(1331 p/m 377 ml) subjects was significantly (P=<0.05) lower than the CON
group (1990 p/m 332 ml), and CFS subjects achieved volitional exhaustion
significantly faster (CFS: 351 p/m 224 s; CON: 715 p/m 176 s) at a lower
power output (CFS: 100 p/m 39 W; CON: 163 p/m 34 W). CFS subjects also
exhibited a significantly lower maximum HR (CFS: 154 p/m 13 bpm; CON: 186 p/m
11 bpm) and consistently reported a higher RPE at the same absolute workload
when compared with CON subjects. Prefrontal cortex HbO_2, HHb and tHb were
significantly lower at maximal exercise in CFS versus CON, as was TOI during
exercise and recovery. The CFS subjects exhibited significant exercise
intolerance and reduced prefrontal oxygenation and tHb response when compared
with CON subjects. These data suggest that the altered cerebral oxygenation
and blood volume may contribute to the reduced exercise load in CFS, and
supports the contention that CFS, in part, is mediated centrally.
This study examined the effects of maximal incremental exercise on cerebral
oxygenation in chronic fatigue syndrome (CFS) subjects. Furthermore, we
tested the hypothesis that CFS subjects have a reduced oxygen delivery to the
brain during exercise. Six female CFS and eight control (CON) subjects
(similar in height, weight, body mass index and physical activity level)
performed an incremental cycle ergometer test to exhaustion, while changes in
cerebral oxy-haemoglobin (HbO_2), deoxy-haemoglobin (HHb), total blood volume
(tHb=HbO_2+HHb) and O_2 saturation [tissue oxygenation index (TOI), %)]
was monitored in the left prefrontal lobe using a near-infrared
spectrophotometer. Heart rate (HR) and rating of perceived exertion (RPE)
were recorded at each workload throughout the test. Predicted VO_2_peak in CFS
(1331 p/m 377 ml) subjects was significantly (P=<0.05) lower than the CON
group (1990 p/m 332 ml), and CFS subjects achieved volitional exhaustion
significantly faster (CFS: 351 p/m 224 s; CON: 715 p/m 176 s) at a lower
power output (CFS: 100 p/m 39 W; CON: 163 p/m 34 W). CFS subjects also
exhibited a significantly lower maximum HR (CFS: 154 p/m 13 bpm; CON: 186 p/m
11 bpm) and consistently reported a higher RPE at the same absolute workload
when compared with CON subjects. Prefrontal cortex HbO_2, HHb and tHb were
significantly lower at maximal exercise in CFS versus CON, as was TOI during
exercise and recovery. The CFS subjects exhibited significant exercise
intolerance and reduced prefrontal oxygenation and tHb response when compared
with CON subjects. These data suggest that the altered cerebral oxygenation
and blood volume may contribute to the reduced exercise load in CFS, and
supports the contention that CFS, in part, is mediated centrally.
