When compared with healthy sedentary women, female patients with CFS show a significantly decreased exercise capacity. This could affect their physical abilities to a moderate or severe extent. Reaching the age-predicted target heart rate seemed to be a limiting factor of the patients with CFS in achieving maximal effort, which could be due to autonomic disturbances. Arch Intern Med. 2000;160:3270-3277.

The MOSPA-Q provides a relatively valid and reliable estimate of physical activity.

Purpose. Monocytes (Mon1-2-3) play a substantial role in low-grade inflammation associated with high cardiovascular morbidity and mortality of patients with chronic kidney disease (CKD) and chronic heart failure (CHF). The effect of an acute exercise bout on monocyte subsets in the setting of systemic inflammation is currently unknown. This study aims (1) to evaluate baseline distribution of monocyte subsets in CHF and CKD versus healthy subjects (HS) and (2) to evaluate the effect of an acute exercise bout. Exercise-induced IL-6 and MCP-1 release are related to the Mon1-2-3 response. Methods. Twenty CHF patients, 20 CKD patients, and 15 HS were included. Before and after a maximal cardiopulmonary exercise test, monocyte subsets were quantified by flow cytometry: CD14++CD16−CCR2+ (Mon1), CD14++CD16+CCR2+ (Mon2), and CD14+CD16++CCR2− (Mon3). Serum levels of IL-6 and MCP-1 were determined by ELISA. Results. Baseline distribution of Mon1-2-3 was comparable between the 3 groups. Following acute exercise, %Mon2 and %Mon3 increased significantly at the expense of a decrease in %Mon1 in HS and in CKD. This response was significantly attenuated in CHF (P < 0.05). In HS only, MCP-1 levels increased following exercise; IL-6 levels were unchanged. Circulatory power was a strong and independent predictor of the changes in Mon1 (β = −0.461, P < 0.001) and Mon3 (β = 0.449, P < 0.001); and baseline LVEF of the change in Mon2 (β = 0.441, P < 0.001). Conclusion. The response of monocytes to acute exercise is characterized by an increase in proangiogenic and proinflammatory Mon2 and Mon3 at the expense of phagocytic Mon1. This exercise-induced monocyte subset response is mainly driven by hemodynamic changes and not by preexistent low-grade inflammation.

In this study we examined the effect of a dopamine (DA) precursor (L-DOPA) or a serotonin (5-HT) antagonist (Ritanserin) on time to exhaustion. The study had a double-blind, randomised, placebo controlled and cross-over design. Seven moderately trained men performed three tests to exhaustion at 65% Wattmax. Each test was separated by two weeks to allow washout of the drugs (dose: 4 mg/kg Sinemet, and 0.3 mg/kg Ritanserin). Blood lactate, hematocrit, glucose, ammonia, free fatty acids (FFA), growth hormone (GH) and catecholamines were determined before and after exercise. Time to exhaustion did not differ between the three trials. Most of the parameters measured in this study responded as predicted during cycling to exhaustion in man. DA agonism significantly increased heart rate, lactate, and plasma DA values at rest, while other parameters such as FFA, lactate, plasma noradrenaline (NA) and adrenaline (A), and plasma GH showed the highest absolute levels at exhaustion. Ritanserin did not influence basal glucose and heart rate at rest, but this group showed a much lower increase in plasma catecholamine levels. We conclude that under the present conditions, neither a metabolic precursor of DA nor a specific centrally acting 5-HT2A/2C antagonist, when given in two single doses 24 h and immediately before the experiments, influences the time to exhaustion on a bicycle trial at 65% Wattmax.