Breathlessness is the most common symptom limiting exercise in patients with chronic obstructive pulmonary disease (COPD). Exercise training can improve both exercise tolerance and health status in these patients, intensity being of key importance. Nevertheless, in these patients extreme breathlessness and/or peripheral muscle fatigue may prevent patients from higher levels of intensity. In this review article the literature concerning the different ways to optimise exercise tolerance in patients with COPD, with the objective of enhancing the tolerance to higher exercise training intensity, is summarised.Continuous positive airway pressure and different modalities of noninvasive positive pressure ventilation (NPPV) may reduce breathlessness and increase exercise tolerance in these patients. Respiratory muscle unloading and reduction in intrinsic positive end-expiratory pressure have been considered among mechanisms underlying these effects. Nevertheless, the role of NPPV in pulmonary rehabilitation, if any, is still controversial. The addition of nocturnal domiciliary NPPV during a daily exercise programme in patients with severe COPD resulted in an improvement in exercise tolerance and quality of life.In patients with severe COPD application of electrical stimulation combined with active limb mobilisation significantly improved muscle strength, and interval training has been shown capable of inducing physiological training effects.Oxygen supplementation in patients who do not desaturate during exercise seems to be the most promising treatment, since it allows for higher exercise intensities and, therefore, superior training efficacy.In conclusion, further studies are needed to define the appropriate patients in order to generalise such interventions. The modalities discussed should be used as adjuncts to a well designed comprehensive respiratory rehabilitation programme.

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The kinematics characteristics of an upper arm extension of large amplitude (90°) performed in the horizontal plane and the simultaneous activity of the shoulder muscles were recorded in 12 parkinsonian patients and in six normal control subjects. The movement, triggered by an acoustic “go” signal, was preceded by an isometric adduction. Within the whole population of individuals (n = 18) a strong, positive correlation was observed between the root mean square value of agonist EMG activity, evaluated during the acceleration phase of the movement, and both peak velocity and acceleration. In six patients tremor bursts at the frequency of 8–14 Hz (action tremor) were observed during the movement phase in the anterior, middle, and posterior deltoid: all these patients showed low root mean square values and were bradykinetic with respect to the control subjects. The remaining six patients did not show this action tremor during the movement phase. All but one had an agonist activation of normal duration and amplitude, showed high root mean square values, and performed well in the range of control subjects. We conclude that the inability to suppress the activity of pathological oscillator(s) responsible for the action tremor plays a fundamental role in the bradykinesia associated with Parkinson's disease. Mov. Disord. 16:47–57, 2001. © 2001 Movement Disorder Society.

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