Introduction: The cardiovascular adaptations to high altitude (HA) exposure and its relationship to acute mountain sickness (AMS) are incompletely understood. Aims: This thesis addresses four main hypotheses 1. HA adversely affects biventricular cardiac function leading to an increase in estimated filling pressures which is influenced by the mode of hypoxia. 2. HA exposure leads to myocardial injury that is linked to the development of AMS. 3. HA exposure is associated with a reduction in arterial compliance and an increase in central blood pressure (BP). 4. HA exposure reduces heart rate (HR) variability (HRV) that is linked to AMS an increased risk of cardiac arrhythmias. Methods: This consisted of eight independent studies conducted at terrestrial and 'simulated' HA (hypobaric hypoxia [HH] and normobaric hypoxia [NH] Cardiac function and arterial compliance were examined using portable transthoracic echocardiography and pulse contour analysis respectively. Myocardial injury was measured in venous blood by cardiac troponin T (cTnT) quantification. Cardiac inter-beat interval data for HRV analysis was acquired using single lead ECGs and novel finger and patch sensor technologies. Cardiac rhythm was investigated using a novel implantable cardiac monitor. Results: HA exposure was associated with a non-pathological increase in cTnT, and mild diastolic changes without adversely affecting systolic function or ventricular filling pressures. Resting cardiovascular responses were similar with HH, NH and HA, though notable differences emerged with exercise. Resting central BP, HR and BP-augmentation increased at terrestrial HA. HRV fell (eg reduced time-domain measures, increased LF/HF ratios and less chaos) at HA and was consistently different between men and women. Significant HA (>3500m) was associated with the development of tachyarrhythmia (atrial fibrillation and supraventricular tachycardia) and asymptomatic nocturnal bradycardias and pauses (>3.0 seconds). There were no independent predictors of AMS and its severity. Conclusion: HA-related hypoxia induces early sympathetic activation leading to an increase in resting HR and central BP and may be proarrhythmic. Parasympathetic activation with acclimatisation can trigger nocturnal pauses at higher altitudes. HA exposure does not adversely affect cardiac function.