Exercise tolerance, the ability to sustain an exercise task, is a key determinant of performance, morbidity, mortality and quality of life. However, the fatigue mechanisms that underpin exercise tolerance remain poorly understood.
The aim of this thesis was to determine: 1) the origins of fatigue causing the limit of tolerance (LoT) during whole-body dynamic exercise in which V̇O2max is attained, and 2) how this is altered by the task demands and in the presence of chronic heart failure (CHF). To assess this, maximum voluntary isokinetic cycling power was measured before, during and instantaneously at LoT of exercise, and compared to the task demands. To provide additional insight these power data were supplemented by gas exchange and electromyography measures.
First, a series of ramp-incremental exercise tests were performed, using different ramp-incrementation rates to change power demand at LoT. Next, the power-tolerable duration relationship was used to investigate the effect of altering the power demand during constant-power exercise. In both studies, reducing power demands, and as a consequence slowing the rate of energy utilisation and metabolite build-up, caused a significant reserve in maximal voluntary power at LoT to become increasingly evident.
A reduced exercise tolerance is a cardinal symptom of CHF, the consequence of fatigue and/or dyspnoeic sensations during exercise. At the LoT in CHF, the magnitude of difference between the maximal voluntary isokinetic power and task demands was different between individuals, suggesting this measurement may distinguish between individuals for which either the exercising muscles, or mechanisms proximal to this, are ultimately limiting exercise.
These data demonstrate that the origins of task failure at V̇O2max can be altered, depending on the exercise task and health status. In future it is hoped these data can inform development of targeted strategies, aimed at increasing exercise tolerance, and as a consequence enhancing quality of life.
