Orthostatic tolerance (OT) refers to a person’s ability to maintain normal blood pressure and consciousness when subjected to gravitational stress. It varies widely between healthy individuals. Gravity imposes a pressure gradient along the body resulting, when upright, in the loss of effective blood volume through distension of dependent veins and transudation through capillaries. This reduces venous return and cardiac output but, due to reflexes, blood pressure does not normally fall. However, if the stress is sufficient, for example by increasing gravity using a centrifuge or applying suction to the lower body, fainting occurs in all subjects. My research, undertaken over several years, has been concerned with ways of assessing orthostatic tolerance, factors which influence it, and methods to increase it. Orthostatic tolerance is usually assessed by determining whether a subject faints when upright for varying periods. However, this is insensitive and unreliable and we have developed a method which combines head-up tilting with graded lower body suction and measures orthostatic tolerance as the time required to induce presyncope. Using this we showed that an important determinant of OT is plasma volume (El-Sayed & Hainsworth, 1995). Interestingly, we have recently shown that Andean high altitude dwellers, who have very large packed cell volumes, also have an exceptionally high OT (Claydon et al. 2004). Blood pressure is regulated mainly through the control of vascular resistance and subjects with good OT show greater increases in vascular resistance. This is partly due to increased sensitivity of the baroreceptor reflex during the orthostatic stress (Cooper & Hainsworth, 2001). The factor that is critical for normal consciousness is actually cerebral blood flow, and autoregulation of this is more effective in subjects with good OT. During orthostatic stress people usually hyperventilate to some extent and the resulting hypocapnia dilates peripheral vessels and constricts those in the brain. Both effects reduce cerebral flow. Norcliffe et al. (2008) showed that both these responses were greater in fainting subjects and this is likely to contribute to their attacks. Strategies for increasing OT are based on manipulating the above factors, particularly plasma volume. Salt loading had been shown to expand plasma volume in dogs and we conducted a double-blind placebo controlled study of the effects of salt supplement in patients with poor OT and fainting attacks (El-Sayed & Hainsworth, 1996). This showed improvement in those taking salt and that all those in whom plasma volume increased OT also increased. The effects of salt, however, are complex as it also results in increased baroreceptor sensitivity and improved autoregulation of cerebral flow (Claydon & Hainsworth, 2004). Interestingly, drinking just water also improves OT although the mechanism is uncertain (Claydon et al. 2006). Of particular relevance to this symposium is the effect of exercise training. Training is known to increase blood volume and so should be of benefit to fainting patients. Mtinangi & Hainsworth (1999) put untrained subjects on a training schedule (5BX/XBX, Royal Canadian Air Force) to reach a “target” level of activity. Fitness increased in all subjects, as assessed by the heart rate-oxygen uptake relationship, and all showed increases in plasma and blood volumes. However, OT increased only in those with a relatively low initial OT and this may be related to earlier observations of fainting in some very highly trained subjects. The same study was then carried out on 14 patients with fainting attacks (Mtinangi & Hainsworth, 1998). Twelve of these trained successfully and all 12 had increases in plasma volume and OT, and were symptomatically improved. Since then we have advocated exercise training as an option for managing such patients. Although increasing plasma volume is usually effecting in increasing OT, another approach is to reduce the actual stress. Venous pooling and capillary fluid loss are minimised by leg movement and the “muscle pump”. We have identified asymptomatic subjects who, despite never normally fainting, have poor orthostatic test results. They apparently compensate by increased postural sway movements during normal standing. Many patients, on the other hand, who have similar poor test results, have smaller postural movements, possibly explaining why they faint and the volunteers don’t (Claydon & Hainsworth, 2006). In conclusion, OT is influenced by several factors including plasma or blood volume, reflex responses and cerebral autoregulation, and any interventions that change these are likely to change OT. However, the stress may be minimised by avoiding standing still and encouraging exaggerated postural movements.