Background-Although no data exist on the effect of altitude exposure on coronary flow reserve (CFR), patients with coronary artery disease (CAD) are advised not to exceed moderate altitudes of Ϸ2500 m above sea level. We studied the influence of altitude on myocardial blood flow (MBF) in controls and CAD patients. Methods and Results-In 10 healthy controls and 8 patients with CAD, MBF was measured by positron emission tomography and 15 O-labeled water at rest, during adenosine stress, and after supine bicycle exercise. This protocol was repeated during inhalation of a hypoxic gas mixture corresponding to an altitude of 4500 m (controls) and 2500 m (CAD). Workload was targeted to comparable heart rate-blood pressure products at normoxia and hypoxia. Resting MBF increased significantly in controls at 4500 m (ϩ24%, PϽ0.01) and in CAD patients at 2500 m (ϩ24%, PϽ0.05). Altitude had no influence on adenosine-induced hyperemia and CFR. Exercise-induced hyperemia increased significantly in controls (ϩ38%, PϽ0.01) at 4500 m (despite a reduction in workload, Ϫ28%, PϽ0.0001) but not in CAD patients at 2500 m (moderate decrease in workload, Ϫ11%, PϽ0.05). Exercise-induced reserve was preserved in controls (ϩ10%, PϭNS) but decreased in CAD patients (Ϫ18%, PϽ0.005). Conclusions-At 2500 m altitude, there is a significant decrease in exercise-induced reserve in CAD patients, indicating that compensatory mechanisms might be exhausted even at moderate altitudes, whereas healthy controls have preserved reserve up to 4500 m. Thus, patients with CAD and impaired CFR should be cautious when performing physical exercise even at moderate altitude.
To evaluate the complex time course of changes in respiratory sinus arrhythmia (RSA) during the menstrual cycle, daily beat-to-beat morning recordings of heart rate (HR) were carried out in 26 healthy female subjects (age 20-29 years) during two menstrual cycles. For determination of fast, vagally mediated variations of HR we used a robust time-domain measure of RSA (logRSA). We found pronounced changes in HR during the menstrual cycle with a minimum in the early follicular phase and a maximum in the late luteal phase. There were large differences between individuals in the fluctuations of logRSA during the menstrual cycle that were related to average HR: subjects with a low HR exhibited higher values of logRSA in the luteal compared to the follicular phase, whereas the trend was reversed in subjects with a high HR. The difference of extreme points of logRSA fluctuations (early follicular and mid luteal phase) was correlated to average HR (r=-0.64, P < 0.001). We conclude that different patterns of RSA fluctuations occur depending on the level of average HR.
The present study demonstrates that the effect of exercise intensity on the occurrence of coordination between breathing and cycling rhythms differs between men and women.
To investigate interactions between neural (movement) and chemical (hypoxia) respiratory drives during exercise, we analyzed coordination between breathing and cycling rhythms in normoxia (N) and hypoxia (H, 14.5% O(2)). Twenty women [28 (1) years old] cycled for 6 min at three workloads (55%, 75%, and 95% peak oxygen consumption, VO(2peak); WL1, WL2, and WL3) in N and H. Leg movements, respiratory parameters, peripheral oxygen saturation, and heart rate were continuously recorded. The degree of coordination (%COORD) was quantified as the percentage of breaths starting during the same phase of leg movement. Ventilatory response to isocapnic hypoxia (VRH) was assessed at rest during an exposure to an end-tidal PO(2) of 50 mmHg. There were no differences in %COORD between N and H at any of the three workloads, but %COORD increased significantly from WL1 to WL3 in H. There was no correlation between VRH and %COORD. In conclusion, chemical and neural respiratory drives did not competitively interact: coordination between breathing and cycling rhythms was not reduced during H and did not depend on individual VRH.
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