These advanced postural adjustments, which almost did not occur in hypobaric chamber, may have led to increased muscle pumping and increased venous return inflight with respect to the hypobaric chamber.
We hypothesized that standing and pacing between shifts would assist in the maintenance of Q by augmenting venous return and SV by way of peripheral muscle pump action and through a sustained increase in HR.
Ogoh et al. [ 122] increased central blood volume (cardiopulmonary baroreceptor load) by increasing pedal frequency to enhance the muscle pump at the same amount of central command.
Furthermore, there is an increase in cardiac preload, due to muscle pump activation and sympathetic-induced venoconstriction, which together contribute to the SV increment commonly observed during dynamic exercise.
Based on the muscle pump theory, vascular arteries and veins within skeletal muscles are compressed upon muscle contraction, therefore increasing the arteriovenous pressure gradient and promoting capillary filtration [ 22– 22].
Active ankle exercise increases blood velocity in the popliteal [ 11] and femoral veins [ 9, 10] because it can elicit the function of the skeletal muscle pump.
In order to maintain/increase the mobility, the patients are encouraged to maintain normal function and information about the muscle pump is provided.
Muscle contractions increase sympathetic activity but the concomitant enhancement of central blood volume and central venous pressure by the muscle pump elicits a "paradoxical" reduction in sympathetic activity (Ray et al. 1993; Van Lieshout et al. 2001; Secher 2009).
This overall trend may reflect a pathophysiologic phenomenon of increased oxygen extraction during more powerful detrusor muscle contraction which can be explained in the light of the "muscle pump" phenomenon.
It appears that, compared with the respiratory pump, the skeletal muscle pump plays the most important role since the muscle rhythmic contractions occurring during dynamic exercise create intramuscular oscillations which facilitate blood flow to the heart and enhance cardiac preload, thus increasing SV by recruiting the Frank-Starling mechanism [ 13, 21– 26].
