Alam & Smirk discovered that influence from an arm and thereby, presumably, from skeletal muscles affects cardiovascular control during exercise. Physical exercise is associated with reduced muscle oxygenation and they found that post-exercise muscle ischemia maintains the exercise blood pressure rather than heart rate. In patients with Brown-Séquard’s syndrome Alam & Smirk further established that this blood pressure raising effect of muscle ishemia is by a neural mechanism. That observation is confirmed with sensory blockade and in patients with spinal cord lesions. With mild epidural anaesthesia (1% lidocaine), there is no effect on blood pressure or heart rate during cycling exercise, but the blood pressure response becomes attenuated with the use of 0.25% bupivacaine. Furthermore, during paralyzing epidural anaesthesia with 0.5% bupivacaine or 2% lidocaine, electrically evoked exercise is without a pressor response as is the case when similar exercise is carried out in patients with spinal cord injury. In these patients, the increase in heart rate during exercise is eliminated when thigh cuffs hinder that blood from the working muscles reaches the central circulation. Experiments can also be arranged to demonstrate an effect of “central command” (the central nervous system) and cardiac preload for cardiovascular regulation during exercise. Yet, it remains that the elevated blood pressure during exercise with a large muscle mass is dominated by the muscle pressor reflex.