Trends in the workload of the two high altitude aid posts in the Nepal Himalayas.

BACKGROUND: Acute mountain sickness (AMS), High altitude pulmonary edema (HAPE) and High Altitude Cerebral Edema (HACE) are well known problems in the high altitude region of the Nepal Himalayas. To assess the proportion of AMS, HAPE, and HACE from 1983 to 1995 in the Himalaya Rescue Association (HRA) aid posts' patients at the Everest (Pheriche 4,243 m) and Annapurna (Manang 3,499 m) regions, the two most popular trekking areas in the Himalayas. A retrospective study was conducted at the HRA medical aid posts in Manang (3,499 m) and Pheriche (4,243 m) in the Himalayas, where 4,655 trekkers (tourists, mostly Caucasians) and 4,792 Nepalis (mostly porters and villagers) were seen at the two high-altitude clinics from 1983 to 1995, for a variety of medical problems, including AMS. METHODS: The number of trekking permits issued for entering the two most popular regions in the Himalayas was calculated and referenced to the proportion of trekkers with medical conditions. Well established guidelines like the Lake Louise Diagnostic Criteria were used in the assessment of AMS, HAPE and HACE. Linear regression analyses were performed on data collected from the two aid posts to determine the effect of time on each variable. For comparison between the aid posts, angular transformation (arcsine) and analysis of variance (ANOVA) were performed on all proportional (incidence) data. RESULTS: Approximately 20% of all visitors (Nepali plus trekkers) who visited the higher Pheriche aid post were diagnosed with AMS compared to around 6% at the lower Manang aid post. There was a linear increase over time in the number of trekkers entering the Everest (r=0.904, p<.001) and the Annapurna (r=0.887, p<.001) regions. The proportion of trekker patients with any medical condition visiting the two HRA aid posts at Manang and Pheriche, expressed as a function of the total number of trekkers entering the Everest and Annapurna regions, was not significantly different between Pheriche (average 4%) and Manang (average 1%). However, the proportion of AMS, HAPE and HACE in patients (Nepali plus trekkers) to the aid posts was greater in those visiting the higher Pheriche aid post compared to the lower Manang aid post (f=56.74, n=13; p<. 001). Importantly, only the proportion of AMS (r=0.568; p<.05) and not HAPE or HACE increased over time in Pheriche, alongside an unchanged proportion of trekker patients, amongst all Pheriche aid post patients. There was no increase of AMS, HAPE or HACE in Manang. CONCLUSIONS: HAPE and HACE are the life-threatening forms of AMS and although there is a linear increase of trekkers entering the Himalayas in Nepal, the findings revealed that HAPE and HACE have not increased over time. One possible explanation may be that awareness drives by organizations like the Himalayan Rescue Association may be effective in preventing the severe forms of AMS.

Association between aerobic capacity and carotid-cardiac baroreflex responsiveness in women.

The purpose of this study was to determine whether the positive correlation between carotid-cardiac baroreflex responsiveness and aerobic capacity (VO(2)max) that has been reported in men also occurs in women. Carotid-cardiac baroreflex responsiveness was tested in 40 healthy, normotensive women (age 18-35) using the variable neck pressure technique. Participants were subdivided into endurance-trained (ET; n = 11) and untrained (UT; n = 9) groups. No significant between-group difference was found in the range or gain of the carotid-cardiac baroreflex response despite a lower resting HR in the ET group. When participants were subdivided into high (HI; n = 13) and low (LO; n = 17) responders based on reflex RRI responses to CTP changes, no significant between-group differences were found in resting HR or VO(2)max levels. It was concluded that aerobic capacity (VO(2)max) is not a good predictor of cardiac-carotid baroreflex responsiveness in healthy women.

Hemodynamic strategies in blood pressure regulation during orthostatic challenge in women.

Several studies indicate that carotid baroreflex responsiveness is a good predictor of orthostatic tolerance. Two groups of healthy women with high (HI) and low (LO) carotid baroreflex responsiveness were studied (a) to determine any differences in the level of orthostatic tolerance of the two groups, and (b) to study the hemodynamic strategies used by HI and LO responders to regulate arterial pressure during the orthostatic challenge of lower body negative pressure (LBNP). Orthostatic tolerance was similar between the two groups, whereas the hemodynamic strategies recruited to maintain blood pressure at -40 mmHg LBNP differed: HI responders exhibited greater LBNP-induced decreases in stroke volume and cardiac output, as well as a greater increase in peripheral resistance compared to LO responders (p < .05). In addition, a significant increase in plasma renin activity during LBNP was found in the HI responders only. No significant between-group differences were found in arterial and cardiopulmonary control of vascular resistance or arterial baroreflex control of heart rate during LBNP.

Maximal muscle activation is not limited by pulmonary ventilation in chronic hypoxia.

This study was conducted to test the hypothesis that inhibitory reflexes from respiratory centres in the brain or respiratory muscles limit the central motor drive to limb muscles during exhaustive exercise in chronic hypoxia. Experiments were performed on five members of an expedition to the Himalayas, following 56-81 days at altitudes of 5200-7500 m. During the last minute of exhaustive maximal two-legged cycling with and without 4% CO2 inhalation performed on different days, repeated maximal voluntary handgrip contractions (MVC) over 60 s (5 s contraction, 5 s rest; x 6) were performed at rest and exhaustive exercise MVC or rate of decay of MVC was unaffected by simultaneous engagement of a major fraction of the muscle mass (leg muscles) and a very high pulmonary ventilation. With 4% CO2, peak pulmonary ventilation during the exhaustive exercise increased further by 41 L min-1 (140-181 L min-1; P < 0.05) without affecting the handgrip strength. These findings suggest that during exhaustive exercise of large muscle groups in chronic hypoxia, both maximal voluntary contraction force and dynamic muscle contractile force are not limited by extreme activation of respiratory centres or muscles.

Effects of mental state on heart rate and blood pressure variability in men and women.

The effect of different mental states on autonomic modulation of the cardiovascular system was assessed in healthy, normotensive men (n = 18) and women (n = 12). Heart rate variability (HRV), systolic blood pressure variability (BPV) and arterial baroreflex function were assessed during 4 tests at rest ((10 min + 5 min recovery) x 4): (1) Control (spontaneous breathing, (SB) (2) Mental distraction (SB + word puzzle) (3) Conscious control of breathing (paced at SB rate) and (4) Mental stress (SB + computer quiz). There were no significant gender differences in the responses to the interventions in terms of arterial (spontaneous) baroreflex (SPBX) control of HR, and indices of time and frequency domains of HRV and BPV, with the exception of the sympathetic indicator of HRV (low frequency power/total power; P < 0.01) which was lower in women during control and mental stress tests. Conscious control of breathing at SB did not alter HRV, BPV or SPBX in either men or women. Mental distraction and mental stress led to decreases in indices of time and frequency domains of HRV and BPV in all subjects, as well as increases in HR during distraction and in systolic BP during stress. These findings suggest that in studies of cardiovascular control: (1) Paced breathing at SB can be used for individuals with irregular breathing patterns (2) The extent of mental stress achieved is intervention-specific and for the most part, independent of gender and (3) Resting assessment of HRV, BPV and SPBX can be made by having subjects sit quietly without interventions in a controlled laboratory setting.

Cardiovascular response to exercise in humans following acclimatization to extreme altitude.

The purpose of this study was to assess the effects of acclimatization to extreme altitude on the cardiovascular system, using vagal and adrenergic blockade and acute restoration of normoxia during exercise to maximum with one and two legs. Fourteen climbers on an expedition to the Himalayas were studied at a lower base camp (5250 m) following 56-81 days at altitudes between 5250 and 8700 m. After acclimatization, peak heart rate (HRpeak), oxygen uptake (VO2peak) and noradrenaline (NA) were similar during maximal one- and two-legged cycling, whereas peak plasma lactate was higher during the one-legged protocol. HRpeak (range 113-168 beats min-1) was lowest when subjects returned from the higher camps. The degree of partial restoration of HRpeak to more normal values within seconds of 60% O2 inhalation (range 5-35 beats min-1 HRpeak increase) was greatest in subjects with low HRpeak. HR responses to beta-1 blockade increased as a function of HRpeak and the HR responses to atropine were the least in subjects with high HRpeak. These findings suggest that (a) the reduction in HRpeak is linked to the duration and severity of the hypoxaemia, (b) the degree of restoration of HRpeak with acute normoxia is dependent on the level of attenuation or down-regulation of cardiac sympathetic activation (SNA), (c) cardiac vagal drive is masked to a lesser extent in chronic hypoxia because of attenuated SNA and lower HRpeak values, and (d) the lower blood lactate levels at altitude is a function of muscle mass involvement rather than adrenergic activation, as normal peak values were reached during exercise with a small muscle mass.

Cardiovascular response to orthostatic stress: effects of exercise training modality.

The effects of exercise training posture on cardiovascular and baroreflex responses to orthostatic challenge were assessed in highly trained cyclists (CT, n = 8) and swimmers (ST, n = 8), and in untrained men (UT, n = 8). CT demonstrated the lowest orthostatic tolerance to lower body negative pressure (LBNP, 0 to -50 mmHg), with only 3 subjects completing the full LBNP procedures; 5 UT and all ST completed the testing. During LBNP, stroke volume (SV) decreases were similar in CT and ST, but greater than in UT. Mean pulse pressure and systemic vascular resistance (SVR) were reduced in CT relative to ST and UT at the highest levels of LBNP; the slope of the delta SVR/delta Zo and delta SVR/delta SV relationships in CT, used to assess peripheral vascular baroreflex function, were attenuated relative to the other groups. There were no between-group differences in the heart rate response to LBNP. The greater incidence of orthostatic intolerance observed in upright-versus supine-trained athletes during passive LBNP was linked to attenuated baroreflex control of peripheral vascular resistance.

Carotid-cardiac baroreflex and training status: significance of initial responsiveness.

The aim of this study was to demonstrate that within a population of healthy men (n = 15) of varying levels of aerobic fitness (VO2max = 36-74 mL.kg-1.min-1), (i) there are high and low responders with respect to carotid-cardiac baroreflex responsiveness, despite similar baseline heart rates (HRs) both at rest and during dynamic exercise, and (ii) there is a weak association between this responsiveness and training status (VO2max) because of a large overlap in the responses between trained (endurance, ET) and untrained (UT) individuals. Baroreflex function curves were derived during supine rest for each subject by applying varying pressures around the neck in a beat-to-beat ramp (for 12 beats) of +40 to -60 mmHg (1 mmHg = 133.3 Pa). Subjects were divided into low (n = 8) and high (n = 7) responders on the basis of the magnitude of the maximal dynamic R-R interval (RRI) range of the baroreflex curve. Both bradycardic (percent slowing) and tachycardic (percent acceleration) components of the baroreflex curve, and peak sinus node responses (HR, RRI) to continuous neck suction (-60 mmHg) at rest and during exercise (cycling, 45% VO2max) were greater in high compared with low responders (p < 0.05), as assessed using both HR and RRI scales.(ABSTRACT TRUNCATED AT 250 WORDS)

Baroreflex function and cardiac structure with moderate endurance training in normotensive men.

Changes in arterial and cardiopulmonary baroreflex function and cardiac structure were followed throughout 10 wk of moderate endurance training [60 min of cycling, 3 days/wk, 60% maximal O2 uptake (VO2max)] in sedentary normotensive men (22-34 yr old). Subjects were randomly assigned to an exercise training group (ET; n = 9) or to a control group (UT; n = 4). Decreases in resting heart rate (8.9 +/- 2.6%, P < 0.01) and mean arterial pressure (7.0 +/- 2.3%, P < 0.05) and an increase in VO2max occurred after 10 wk in ET. An increase in the gain or slope of the spontaneous baroreflex response at rest was found after 10 wk in ET (50.1 +/- 6.3%, P < 0.01) but not in UT. An upward shift in the resting carotid-cardiac baroreflex response curve also occurred after 10 wk in ET, although the maximum range and gain of the response and the vagally mediated peak reflex sinus node responses were unchanged. Cardiopulmonary baroreflex function (reflex changes in forearm vascular conductance) and measured indexes of left ventricular structure were not altered in either ET or UT, although peak transmitral inflow velocity increased in ET (P < 0.05). These findings demonstrate that moderate exercise training results in an enhancement in the ability to reflexly adjust heart rate with spontaneous changes in arterial pressure within the operating range. This occurs independently of any changes in carotid-cardiac baroreflex function over the full response range in cardiopulmonary baroreflex function or in cardiac structure.

Norepinephrine spillover from skeletal muscle during exercise in humans: role of muscle mass.

The purpose of this study was to determine the effect of increasing muscle mass involvement in dynamic exercise on both sympathetic nervous activation and local hemodynamic variables of individual active and inactive skeletal muscle groups. Six male subjects performed 15-min bouts of one-legged knee extension either alone or in combination with the knee extensors of the other leg and/or with the arms. The range of work intensities varied between 24 and 71% (mean) of subjects' maximal aerobic capacity (% VO2max). Leg blood flow, measured in the femoral vein by thermodilution, was determined in both legs. Arterial and venous plasma concentrations of norepinephrine (NE) and epinephrine were analyzed, and the calculated NE spillover was used as an index of sympathetic nervous activity to the limb. NE spillover increased gradually both in the resting, and to a larger extent in the exercising legs, with a steeper rise occurring approximately 70% VO2max. These increases were not associated with any significant changes in leg blood flow or leg vascular conductance at the exercise intensities examined. These results suggest that, as the total active muscle mass increases, the rise in sympathetic nervous activity to skeletal muscle, either resting or working at a constant load, is not associated with any significant neurogenic vasoconstriction and reduction in flow or conductance through the muscle vascular bed, during whole body exercise demanding up to 71% VO2max.

Muscle blood flow is not reduced in humans during moderate exercise and heat stress.

The effect of heat stress on circulation in an exercising leg was determined using one-legged knee extension and two-legged bicycle exercise, both seated and upright. Subjects exercised for three successive 25-min periods wearing a water-perfused suit: control [CT, mean skin temperature (Tsk) = 35 degrees C], hot (H, Tsk = 38 degrees C), and cold (C, Tsk = 31 degrees C). During the heating period, esophageal temperature increased to a maximum of 37.91, 39.35, and 39.05 degrees C in the three types of exercise, respectively. There were no significant changes in pulmonary O2 uptake (VO2) throughout the entire exercise period with either one or two legs. Leg blood flow (LBF), measured in the femoral vein of one leg by thermodilution, remained unchanged between CT, H, and C periods. Venous plasma lactate concentration gradually declined over time, and no trend for an increased lactate release during the heating period was found. Similarly, femoral arteriovenous O2 difference and leg VO2 remained unchanged between the three exercise periods. Although cardiac output (acetylene rebreathing) was not significantly higher during H, there was a tendency for an increase of 1 and 2 l/min in one- and two-legged exercise, respectively, which could account for part of the increase in total skin blood flow during heating (gauged by changes in forearm blood flow). Because LBF was not reduced during exercise and heat stress in these experiments, the additional increase in skin blood flow must have been met by redistribution of blood away from vascular beds other than active skeletal muscle.

Peripheral blood flow during rewarming from mild hypothermia in humans.

During the initial stages of rewarming from hypothermia, there is a continued cooling of the core, or after-drop in temperature, that has been attributed to the return of cold blood due to peripheral vasodilatation, thus causing a further decrease of deep body temperature. To examine this possibility more carefully, subjects were immersed in cold water (17 degrees C), and then rewarmed from a mildly hypothermic state in a warm bath (40 degrees C). Measurements of hand blood flow were made by calorimetry and of forearm, calf, and foot blood flows by straingauge venous occlusion plethysmography at rest (Ta = 22 degrees C) and during rewarming. There was a small increase in skin blood flow during the falling phase of core temperature upon rewarming in the warm bath, but none in foot blood flow upon rewarming at room air, suggesting that skin blood flow seems to contribute to the after-drop, but only minimally. Limb blood flow changes during this phase suggest that a small muscle blood flow could also have contributed to the after-drop. It was concluded that the after-drop of core temperature during rewarming from mild hypothermia does not result from a large vasodilatation in the superficial parts of the periphery, as postulated. The possible contribution of mechanisms of heat conduction, heat convection, and cessation of shivering thermogenesis were discussed.