Bassett and Howley

Category: Exercise, Hypertension, Stroke

Last Updated: 26 Jan 2021

Pages: 1 Views: 161

It nas been proposed initially by ( ) that the individuals with more training experience have additional cardiac output, and such individuals are able to operate with even less oxygen saturation. It is also argued that, in elite athletes, decreased transportation time of the RBCs in the pulmonary vessels causes oxygen desaturation in the arteries due to increased cardiac output.

Moreover, increase in flow rate occurs due to increase in volume of blood flow in the vessels or capillaries having constant diameter (Pelliccia et al. , 2002). If flow rate is so fast, then ed blood cells will surpass oxygen hurriedly to the haemoglobin, which will result in less saturation of haemoglobin resulting in reduced oxygen in exercising muscle, causing muscle fatigue (Warpeha, 2003). This theory indicates that maximum oxygen consumption is, to an extent, limited by pulmonary factors during exercise. While other authors indicate that factors such as arterial oxygenation are impossible to affect V02 max (Vogiatzis et al. , 2008). Moreover, Christensen (1931) argued that decline in sub maximal heart rate, without affecting cardiac output, can occur during aerobic exercise.

He concluded that maintaining cardiac output is possible by increasing stroke volume when heart rate is decreased, as cardiac output is the result of heart rate into stroke volume. However, this relationship varies when exercise reaches maximum level. It was evaluated that training time and levels did not affect maximum heart rate, and only an augmented stroke volume caused improvement in performance when exercise reached its maximum levels. Hence, stroke volume was able to maintain appropriate cardiac output, as average heart rate remained the same for both trained and untrained individuals at maximal exercise Christensen, 1931; Saltin and Calbert, 2006).

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