To explore brain involvement in chronic fatigue syndrome (CFS), the statistical parametric mapping of brain MR images has been extended to voxel-based regressions against clinical scores. Using SPM5 we performed voxel-based morphometry (VBM) and analysed T1- and T2-weighted spin-echo MR signal levels in 25 CFS subjects and 25 normal controls (NC). Clinical scores included CFS fatigue duration, a score based on the 10 most common CFS symptoms, the Bell score, the hospital anxiety and depression scale (HADS) anxiety and depression, and hemodynamic parameters from 24-h blood pressure monitoring. We also performed group × hemodynamic score interaction regressions to detect locations where MR regressions were opposite for CFS and NC, thereby indicating abnormality in the CFS group. In the midbrain, white matter volume was observed to decrease with increasing fatigue duration. For T1-weighted MR and white matter volume, group × hemodynamic score interactions were detected in the brainstem [strongest in midbrain grey matter (GM)], deep prefrontal white matter (WM), the caudal basal pons and hypothalamus. A strong correlation in CFS between brainstem GM volume and pulse pressure suggested impaired cerebrovascular autoregulation. It can be argued that at least some of these changes could arise from astrocyte dysfunction. These results are consistent with an insult to the midbrain at fatigue onset that affects multiple feedback control loops to suppress cerebral motor and cognitive activity and disrupt local CNS homeostasis, including resetting of some elements of the autonomic nervous system (ANS). © 2011 The Authors. NMR in Biomedicine published by John Wiley & Sons, Ltd.

This study utilized a hypobaric chamber to compare the effects of mild hypobaria (MH; 50 mmHg, approximately 580 m altitude) on blood O2 status and maximal O2 consumption (VO2max) in 9 untrained and 11 trained (T) cyclists with VO2max values of 51 +/- 3 and 77 +/- 1 ml.kg-1.min-1, respectively. In both groups, arterial O2 saturation (SaO2) decreased significantly during maximal exercise, and this effect was enhanced with MH. Both these responses were significantly greater in the T cyclists in whom the final SaO2 during MH was 86.5 +/- 0.9%. When the group data were combined, approximately 65% of the variance in SaO2 could be attributed to a widened alveolar-arterial Po2 difference. The arterial PO2 during maximal exercise at sea level in the T group was on the steeper portion of the hemoglobin-O2-loading curve (T, 68.3 +/- 1.3 Torr; untrained, 89.0 +/- 2.9 Torr) such that a similar decrease in arterial PO2 in the two groups in response to MH resulted in a significantly greater fall in both SaO2 and calculated O2 content in the T group. As a consequence, the VO2max fell significantly only in the T group (mean change, -6.8 +/- 1.5%; range, + 1.2 to - 12.3%), with approximately 70% of this decrease being due to a fall in O2 content. This is the lowest altitude reported to decrease VO2max, suggesting that T athletes are more susceptible to a fall in inspired PO2.

A modified 2-min CO-rebreathing procedure using capillary or venous blood sampled 8 and 10 min after starting CO-rebreathing allows complete circulatory mixing and provides an accurate and reliable estimate of Hbmass.

The causes of exercise-induced hypoxemia (EIH) remain unclear. We studied the mechanisms of EIH in highly trained cyclists. Five subjects had no significant change from resting arterial PO(2) (Pa(O(2)); 92.1 +/- 2.6 Torr) during maximal exercise (C), and seven subjects (E) had a >10-Torr reduction in Pa(O(2)) (81.7 +/- 4.5 Torr). Later, they were studied at rest and during various exercise intensities by using the multiple inert gas elimination technique in normoxia and hypoxia (13.2% O(2)). During normoxia at 90% peak O(2) consumption, Pa(O(2)) was lower in E compared with C (87 +/- 4 vs. 97 +/- 6 Torr, P < 0.001) and alveolar-to-arterial O(2) tension difference (A-aDO(2)) was greater (33 +/- 4 vs. 23 +/- 1 Torr, P < 0. 001). Diffusion limitation accounted for 23 (E) and 13 Torr (C) of the A-aDO(2) (P < 0.01). There were no significant differences between groups in arterial PCO(2) (Pa(CO(2))) or ventilation-perfusion (VA/Q) inequality as measured by the log SD of the perfusion distribution (logSD(Q)). Stepwise multiple linear regression revealed that lung O(2) diffusing capacity (DL(O(2))), logSD(Q), and Pa(CO(2)) each accounted for approximately 30% of the variance in Pa(O(2)) (r = 0.95, P < 0.001). These data suggest that EIH has a multifactorial etiology related to DL(O(2)), VA/Q inequality, and ventilation.

This study examined the effect of mild hypobaria (MH) on the peak oxygen consumption (VO2peak) and performance of ten trained male athletes [x (SEM); VO2peak = 72.4 (2.2) ml x kg(-1) x min(-1)] and ten trained female athletes [VO2peak = 60.8 (2.1) ml x kg(-1) x min(-1)]. Subjects performed 5-min maximal work tests on a cycle ergometer within a hypobaric chamber at both normobaria (N, 99.33 kPa) and at MH (92.66 kPa), using a counter-balanced design. MH was equivalent to 580 m altitude. VO2peak at MH decreased significantly compared with N in both men [-5.9 (0.9)%] and women [-3.7 (1.0)%]. Performance (total kJ) at MH was also reduced significantly in men [-3.6 (0.8)%] and women [-3.8 (1.2)%]. Arterial oxyhaemoglobin saturation (SaO2) at VO2peak was significantly lower at MH compared with N in both men [90.1 (0.6)% versus 92.0 (0.6)%] and women [89.7 (3.1)% versus 92.1 (3.0)%]. While SaO2 at VO2peak was not different between men and women, it was concluded that relative, rather than absolute. VO2peak may be a more appropriate predictor of exercise-induced hypoxaemia. For men and women, it was calculated that 67-76% of the decrease in VO2peak could be accounted for by a decrease in O2 delivery, which indicates that reduced O2 tension at mild altitude (580 m) leads to impairment of exercise performance in a maximal work bout lasting approximately 5 min.