Physiology of accidental hypothermia in the mountains : a forgotten story

Pour maintenir l'équilibre thermique, il est aussi nécessaire de de faciliter la déperdition calorique, en particulier pendant les périodes d'effort soutenu, que de maintenir la production de chaleur et conserver l'isolement. Au moyen d'ajustements vestimentaires, les régions anatomiques les plus concernées par les échanges de chaleurs devraient être ventilées un maximum pendant l'activité et isolées au cours de l'inactivité

Estimating human energy expenditure: a review of techniques with particular reference to doubly labelled water

Estimating human energy expenditure: a review of techniques with particular reference to doubly labelled water. Ainslie P, Reilly T, Westerterp K. Department of Physiology and Biophysics, University of Calgary, Faculty of Medicine, Heritage Medical Research Building Room 209, 3330 Hospital Drive NW, Calgary, Alberta T2N 4N1, Canada. [email protected] This review includes an historical overview of the techniques for measuring energy expenditure (EE). Following this overview, the "gold standard" method of measuring EE, the doubly labelled water (DLW) method, is emphasised. Other methods, such as direct calorimetry, indirect calorimetry systems, heart rate and EE relationships, questionnaires and activity recall, motion sensors, combined heart rate and motion sensors for the estimation of EE are then highlighted in relation to their validation against the DLW method. The major advantages and disadvantages for each method are then considered. The preferred method to determine EE is likely to depend principally on factors such as the number of study participants to be monitored, the time period of measurements and the finances available. Small study participant numbers over a short period may be measured accurately by means of indirect calorimetric methods (stationary and portable systems). For periods over 3-4 days, EE should ideally be measured using the DLW method. However, the use of motion sensors is very promising in the measurement of EE, and has a number of advantages over the DLW method. Furthermore, if used correctly, both heart rate and questionnaire methods may provide valuable estimates of EE. Additional studies are needed to examine the possibility of improving the accuracy of measurement by combining two or more techniques. Such information, if confirmed by scientific rigour, may lead to an improvement in the estimation of EE and population-based physical activity levels. The accurate measurement of physical activity and EE is critical from both a research and health prospective. A consideration of the relevant techniques used for the estimation of EE may also help improve the quality of these frequently reported measurement

Dynamic Cerebral Autoregulation Is Impaired In Acute Mountain Sickness; Focus On Redox Regulation of Systemic Nitric Oxide Bioavailability

PURPOSE: The present study examined whether a decrease in systemic nitric oxide (NO) bioavailability subsequent to increased oxidative stress in hypoxia would impair cerebral autoregulation (CA), elevate intracranial pressure (ICP) and increase susceptibility to acute mountain sickness (AMS). METHODS: Arterial blood pressure (ABP-photoplethysmography) and middle cerebral artery velocity (MCAv-transcranial Doppler) were measured in 18 males at rest in normoxia and following 6h passive exposure to normobaric hypoxia (12%O2). A dynamic rate of CA was determined by the rate of regulation (RoR) and transfer function (TF) analysis (0.07-0.20Hz) during a transient period of hypotension (leg-cuff technique). Venous samples (not corrected for volume shifts) were assayed for total nitric oxide (NOx) via ozone-based chemiluminescence and the ascorbate radical (A·-) by electron paramagnetic resonance spectroscopy. Clinical AMS (moderate to severe) was diagnozed as a Lake Louise score of <=5 points and Environmental Symptoms Questionnaire cerebral symptoms score <=0.7 points. RESULTS: Nine subjects were diagnozed with AMS (AMS+) and were characterized by a greater increase in plasma A·- during hypoxia (AMS+: +461 ± 215 arbitrary units (AU)[square root]Gauss (G) vs. AMS-: +30 ± 237 AU[square root]G, P 0.05). The AMS+ subgroup experienced a greater reduction in RoR and increase in TF gain (P< 0.05 vs. AMS-) which was consistently related to the increase in symptom scores (r= -0.66 to -0.70, P< 0.05). This translated into a greater increase in eICP (AMS: +8.5 ± 9.1 vs. AMS-: -6.5 ± 9.5 mmHg, P < 0.05). CONCLUSION: These findings identify oxidative stress, impaired CA and intracranial hypertension as potential risk factors for AMS whereas systemic NO metabolism appears unimportant

Mechanisms of orthostatic intolerance following very prolonged exercise

Nine men completed a 24-h exercise trial, with physiological testing sessions before (T1, ∼0630), during (T2, ∼1640; T3, ∼0045; T4, ∼0630), and 48-h afterwards (T5, ∼0650). Participants cycled and ran/trekked continuously between test sessions. A 24-h sedentary control trial was undertaken in crossover order. Within testing sessions, participants lay supine and then stood for 6 min, while heart rate variability (spectral analysis of ECG), middle cerebral artery perfusion velocity (MCAv), mean arterial pressure (MAP; Finometer), and end-tidal Pco2 (PetCO2) were measured, and venous blood was sampled for cardiac troponin I. During the exercise trial: 1) two, six, and four participants were orthostatically intolerant at T2, T3, and T4, respectively; 2) changes in heart rate variability were only observed at T2; 3) supine MAP (baseline = 81 ± 6 mmHg) was lower (P < 0.05) by 14% at T3 and 8% at T4, whereas standing MAP (75 ± 7 mmHg) was lower by 16% at T2, 37% at T3, and 15% at T4; 4) PetCO2 was reduced (P < 0.05) at all times while supine (−3–4 Torr) and standing (−4–5 Torr) during exercise trial; 5) standing MCAv was reduced (P < 0.05) by 23% at T3 and 30% at T4 during the exercise trial; 6) changes in MCAv with standing always correlated (P < 0.01) with changes in PetCO2 (r = 0.78–0.93), but only with changes in MAP at T1, T2, and T3 (P < 0.05; r = 0.62–0.84); and 7) only two individuals showed minor elevations in cardiac troponin I. Recovery was complete within 48 h. During prolonged exercise, postural-induced hypotension and hypocapnia exacerbate cerebral hypoperfusion and facilitate syncope