[Ocular phototoxicity and altitude among mountain guides]. / Phototoxicité oculaire et altitude chez des guides de haute montagne.

PURPOSE: This study aimed to evaluate ocular phototoxicity in mountaineer guides who experience overexposure to ultraviolet related to the altitude at which they work, as well as light reflection on snow. MATERIALS AND METHODS: Ninety-six guides and 90 controls living in plains, over 50 years old, underwent complete examinations. They responded to a questionnaire assessing altitude exposure and protective eyewear. We compared the two groups and performed a logistic regression within the guide group so as to identify risk and protective factors. RESULTS: Guides develop more ocular surface diseases. They exhibit more anterior cortical cataract (P<0.01) and cataract surgery (P=0.01). Only 61.5% of guides had a normal ocular fundus versus 81.1% in control group (P<0.01). They exhibit more drusen (27.2% vs. 15.6%, P<0.01). Among the guide group, exposure at an altitude above 3000 m is risk factor for anterior cortical cataract (OR=1.16, P<0.01). Wearing ski masks (OR=0.50, P=0.04) or photochromic lenses (OR=0.53, P=0.03) reduces this risk. Exposure to snow increases the risk of maculopathy (OR=1.9, P<0.01). Wearing a hat reduces this risk (OR=0.40, P=0.02) and the risk of cataract formation (OR=0.46, P=0.04). CONCLUSIONS: Guides develop more ocular surface diseases, anterior cortical lens opacities and drusen. These results underscore the potential deleterious role of ultraviolet radiation and the importance of light reflection on snow. The best ocular protection includes sunglasses and a hat with a visor or brim.

Operation Everest III: role of plasma volume expansion on VO(2)(max) during prolonged high-altitude exposure.

We hypothesize that plasma volume decrease (DeltaPV) induced by high-altitude (HA) exposure and intense exercise is involved in the limitation of maximal O(2) uptake (VO(2)(max)) at HA. Eight male subjects were decompressed for 31 days in a hypobaric chamber to the barometric equivalent of Mt. Everest (8,848 m). Maximal exercise was performed with and without plasma volume expansion (PVX, 219-292 ml) during exercise, at sea level (SL), at HA (370 mmHg, equivalent to 6, 000 m after 10-12 days) and after return to SL (RSL, 1-3 days). Plasma volume (PV) was determined at rest at SL, HA, and RSL by Evans blue dilution. PV was decreased by 26% (P < 0.01) at HA and was 10% higher at RSL than at SL. Exercise-induced DeltaPV was reduced both by PVX and HA (P < 0.05). Compared with SL, VO(2)(max) was decreased by 58 and 11% at HA and RSL, respectively. VO(2)(max) was enhanced by PVX at HA (+9%, P < 0.05) but not at SL or RSL. The more PV was decreased at HA, the more VO(2)(max) was improved by PVX (P < 0.05). At exhaustion, plasma renin and aldosterone were not modified at HA compared with SL but were higher at RSL, whereas plasma atrial natriuretic factor was lower at HA. The present results suggest that PV contributes to the limitation of VO(2)(max) during acclimatization to HA. RSL-induced PVX, which may be due to increased activity of the renin-aldosterone system, could also influence the recovery of VO(2)(max).

Operation Everest III (COMEX '97). Effects of prolonged and progressive hypoxia on humans during a simulated ascent to 8,848 M in a hypobaric chamber.

Exposure to high altitude induces physiological or pathological modifications that are not always clearly attributable to a specific environmental factor: hypoxia, cold, stress, inadequate food. The principal goal of hypobaric chamber studies is to determine the specific effect of hypoxia. Eight male volunteers ("altinauts"), aged 23 to 37 were selected. They were first preacclimatized in the Observatoire Vallot (4,350 m) before entering the chamber. The chamber was progressively decompressed down to 253 mmHg barometric pressure, with a recovery period of 3 days at 5,000 m in the middle of the decompression period. They spent a total of 31 days in the chamber. Eighteen protocols were organized by 14 European teams, exploring the limiting factors of physical and psychological performance, and the pathophysiology of acute mountain sickness (AMS). All subjects reached 8,000 m and 7 of them reached the simulated altitude of 8,848 m. Three altinauts complained of transient neurological symptoms which resolved rapidly with reoxygenation. Body weight decreased by 5.4 kg through a negative caloric balance. Only four days after the return to sea-level, subjects had recovered 3.4 kg, i.e. 63% of the total loss. At 8,848 m (n = 5), PaO2 was 30.6 +/- 1.4 mmHg, PCO2 11.9 +/- 1.4 mmHg, pH 7.58 +/- 0.02 (arterialized capillary blood). Hemoglobin concentration increased from 14.8 +/- 1.4 to 18.4 +/- 1.5 g/dl at 8,000 m and recovered within 4 days at sea-level. AMS score increased rapidly at 6,000 m and was maximal at 7,000 m, especially for sleep. AMS was related to alteration in color vision and elevation of body temperature. VO2MAX decreased by 59% at 7,000 m. The purpose of this paper is to give a general description of the study and the time course of the main clinical and physiological parameters. The altinauts reached the "summit" (for some of them three consecutive times) in better physiological conditions than it would have been possible in the mountains, probably because acclimatization and other environmental factors such as cold and nutrition were controlled.

Recovery processes after repeated supramaximal exercise at the altitude of 4,350 m.

We tested the hypothesis that prolonged exposure to high altitude would impair the restoration of muscle power during repeated sprints. Seven subjects performed two 20-s Wingate tests (WT1 and WT2) separated by 5 min of recovery, at sea level (N) and after 5-6 days at 4,350 m (H). Mean power output (MPO) and O2 deficit were measured during WT. O2 uptake (VO2) and ventilation (VE) were measured continuously. Blood velocity in the femoral artery (FBV) was recorded by Doppler ultrasound during recovery. Arterialized blood pH and concentrations of bicarbonate ([HCO3-]), venous plasma lactate ([La-]), norepinephrine ([NE]), and epinephrine ([Epi]) were measured before and after WT1 and WT2. MPO decreased between WT1 and WT2 by 6.9% in N (P < 0.05) and by 10.7% in H (P < 0.01). H did not further decrease MPO. O2 deficit decreased between WT1 and WT2 in H only (P < 0.01). Peak VO2 after WT was reduced by 30-40% in H (P < 0.01), but excess postexercise O2 consumption was not significantly lowered in H. During recovery in H compared with N, VE, exercise-induced acidosis, and [NE] were higher, [Epi] tented to be higher, [La-] was not altered, and [HCO3-] and FBV were lower. The similar [La-] accumulation was associated with a higher exercise-induced acidosis and a larger increase in [NE] in H. We concluded from this study that prolonged exposure to high altitude did not significantly impair the restoration of muscle power during repeated sprints, despite a limitation of aerobic processes during early recovery.

[Epilepsy, cerebral calcifications and celiac disease]. / Epilepsie, calcifications cérébrales et maladie coeliaque.

Epilepsy, frequently with complex partial seizures, is observed in 5.5 p. 100 of all cases of celiac sprue. Bilateral parieto-occipital calcifications in the cortical or subcortical areas are found in about one-half of these patients. This triple association is apparently not fortuitous. Prognosis of epilepsy would depend on how early the gluten-free diet was started. The diagnosis of celiac sprue should be entertained in patients with brain calcifications and epilepsy. Search for anti-endomysium antibodies could provide useful information although villosity atrophy in the proximal portion of the small bowel and its regression with gluten-free diet remain the essential elements for the diagnosis of celiac sprue.

[Cardiovascular effects of a calcium channel blocker in hypoxia caused by altitude]. / Effets cardiovasculaires d'un bloqueur calcique en hypoxie d'altitude.

OBJECTIVE: High altitude pulmonary oedema can be successfully treated and prevented by calcium channel blockers. Moreover, calcium entering in the cells could explain the congestive phenomena of acute mountain sickness (AMS). These findings led us to study the action of a calcium channel blocker, isradipine, in the prevention of non-complicated AMS. METHODS: In a double blind randomized study, 20 healthy volunteers received 5 mg of isradipine (n = 6) or placebo (n = 6) for 8 days. After 5 days of treatment in normoxia, the subjects were rapidly transported to an altitude of 4350 m. The efficiency of the treatment was then estimated by the AMS symptom score, haemodynamic parameters and renal function. RESULTS: The administration of isradipine did not significantly modify AMS symptom score nor most of other parameters measured in high altitude hypoxia. Heart rate was an average of 15 b/min lower in the isradipine group, probably because of a direct action of isradipine on the sinus node. Otherwise, the effects of hypoxia were similar in both groups and were in accordance with the literature. There was no clear explanation for the increase in cardiac output and stroke volume when the subjects moved from supine to standing position. Renal blood flow, measured by Doppler or para-aminohippuric acid clearance was not modified by hypoxia. Cerebral blood flow was elevated, due to the direct vasodilator effect of hypoxia. However this increase did not seem to be the main mechanism responsible for the congestive phenomena. On the other hand, the increase in capillary permeability (demonstrated by the increased transcapillary escape rate of albumin, and albuminuria) appeared to play a major role in the pathogenesis of AMS and high altitude cerebral oedema. Isradipine had no protective effect on these phenomena and its use should be restricted to the treatment of high altitude pulmonary oedema.

Pressurization and acute mountain sickness.

Numerous cases of acute mountain sickness (AMS) during trekking were reported to have been successfully treated with portable pressure chambers. The effect of early pressurization during acute altitude exposure in the Alps had not been previously studied. In order to test the hypothesis that an early pressurization of unacclimatized subjects for 3 h could prevent or delay the appearance of symptoms of AMS, 51 previously healthy subjects climbed from 1,030 to 4,360 m within 12 h. Upon arrival at 4,360 m, AMS scores (Lake Louise Consensus Questionnaire '91), oxygen saturation (SaO2), and heart rate (HR) were determined at rest. The subjects were then randomly divided in two groups; one group was pressurized to 200 mBar for 3 h while the other rested. AMS score, HR, and SaO2 were similar in both groups before treatment. AMS score had decreased (from 2.44 +/- 0.41 (S.E.) to 0.89 +/- 0.26, p < 0.05) and SaO2 had increased (from 75.22 +/- 1.32% to 79.07 +/- 1.27%, p < 0.05) in the treatment group 15 min after leaving the pressure chamber whereas the control group had unchanged AMS score (2.50 +/- 0.40 vs. 2.40 +/- 0.40, N.S.) and SaO2 (77.83 +/- 1.41 vs. 76.67 +/- 1.24, N.S.). The next morning, however, AMS score, HR, and SaO2 were similar for both groups. It is concluded that during acute ascent in the Alps, an early 3-h pressurization of unacclimatized subjects does slightly delay the onset of AMS but does not prevent the illness nor does it attenuate its severity upon appearance.

Energy expenditure climbing Mt. Everest.

Weight loss is a well-known phenomenon at high altitude. It is not clear whether the negative energy balance is due to anorexia only or an increased energy expenditure as well. The objective of this study was to gain insight into this matter by measuring simultaneously energy intake, energy expenditure, and body composition during an expedition to Mt. Everest. Subjects were two women and three men between 31 and 42 yr of age. Two subjects were observed during preparation at high altitude, including a 4-day stay in the Alps (4,260 m), and subsequently during four daytime stays in a hypobaric chamber (5,600-7,000 m). Observations at high altitude on Mt. Everest covered a 7- to 10-day interval just before the summit was reached in three subjects and included the summit (8,872 m) in a fourth. Energy intake (EI) was measured with a dietary record, average daily metabolic rate (ADMR) with doubly labeled water, and resting metabolic rate (RMR) with respiratory gas analysis. Body composition was measured before and after the interval from body mass, skinfold thickness, and total body water. Subjects were in negative energy balance (-5.7 +/- 1.9 MJ/day) in both situations, during the preparation in the Alps and on Mt. Everest. The loss of fat mass over the observation intervals was 1.4 +/- 0.7 kg, on average two-thirds of the weight loss (2.2 +/- 1.5 kg), and was significantly correlated with the energy deficit (r = 0.84, P < 0.05). EI on Mt. Everest was 9-13% lower than during the preparation in the Alps.(ABSTRACT TRUNCATED AT 250 WORDS)

Myoelectrical and metabolic changes in muscle fatigue.

In isometric contraction-induced fatigue force loss has been related to mostly myoelectrical or intramuscular events. However, some factors potentially involved may interfere at more than one site in these events and it has proven difficult to distinguish between those influences. The study of the relationships between force generating capacity, the metabolic state of a muscle and its myoelectrical properties may therefore help broaden our understanding of the fatigue process. In order to investigate these relationships, we have evaluated changes in force-generating capacity, NMR-determined metabolic variables, and myoelectrical activity, as measured from surface EMG, simultaneously in brachial biceps muscle of healthy subjects, during different types of fatiguing isometric exercise and during recovery. Factors studied include intramuscular pH, inorganic phosphate and its diprotonated form concentrations, root-mean square and mean power frequency of the EMG power spectrum, and neuromuscular efficiency index. Results show that different mechanisms are likely to contribute to force loss in fatiguing muscle and during different phases of recovery from fatigue. Indeed, relationships between variables from the three groups differed according to exercise protocol as well as in fatiguing and recovering muscle.

Use of a hypobaric chamber for pre-acclimatization before climbing Mount Everest.

Climbing Mount Everest needs an acclimatization period of 3 to 4 weeks between 3000 and 6000 m. In order to reduce this period of time spent in dangerous conditions, an experience of pre-acclimatization was performed with 5 elite alpinists (4 male, 1 female), aged 30 +/- 4 yrs (mean +/- SD), before their attempt to climb Mount Everest. Subjects first remained one week on Mont-Blanc (between 4350 and 4807 m), then spent a total of 38 hours in a hypobaric chamber (in 4 consecutive days) from 5000 to 8500 m standard altitude. Then, they flew to Kathmandu and reached 7800 m five days only after leaving the base camp. The pre-acclimatization period showed a 12% increase in hemoglobin concentration, and no change in ventilatory response to hypoxia. Arterial oxygen saturation at submaximal exercise in hypoxia (FIO2 = 0.115) increased from 75 +/- 4 to 82 +/- 3%, probably because of an efficient ventilatory acclimatization. On Mount Everest, the speed of ascent was very high (5600 m of altitude gain in 6 days), knowing that in conventional expeditions, 12 to 32 days are generally necessary to reach, safe, the same altitude. In conclusion, pre-acclimatization seems to have triggered efficient mechanisms which allowed climbers to save 1 to 3 weeks of time in mountain conditions.

Detection of high-risk subjects for high altitude diseases.

The variability in sensitivity to acute mountain sickness among individuals is a phenomenon well known to physicians and high altitude alpinists. The measurement of cardiac and respiratory responses to hypoxia (FIO2 = 0.115) at rest and during exercise (50% VO2max) allows the detection of those subjects who are more liable to suffer from high altitude diseases. In a retrospective study performed on 288 subjects evaluated with a hypoxic test during a Mountain medicine consultation, we found that the most clinically susceptible subjects had at least one abnormal response to the hypoxic tests, especially during exercise. The observation of one or several abnormal values in cardiac or respiratory responses to hypoxia leads us to advise a modification in the alpine or trekking objective, an increase in the acclimatization time and/or prevention by acetazolamide.

Acute hypoxia decreases cardiac response to catecholamines in exercising humans.

Cardiac chronotropic response to adrenergic activity at rest and exercise has been studied in 8 sea-level natives on the first two days of exposure to high altitude hypoxia (3823 m, 473 mmHg). Maximal O2 uptake (VO2max) was determined at low altitude (day 0:D0) and high altitude (day 2:D2). Submaximal exercise tests were performed at low altitude (day 1:D1) and high altitude (days 3 and 4: D3, D4). Plasma venous norepinephrine (NE) and epinephrine (E) concentrations were determined at rest and at the end of submaximal exercise. From D0 to D2, maximal heart rate decreased by 7% (p less than 0.01), and VO2max decreased by 17% (p less than 0.01). During submaximal exercise, plasma NE did not vary significantly (D1: 1.36 +/- 0.57, D3: 1.48 +/- 0.51, D4: 1.31 +/- 0.54 ng.ml-1). In contrast, relative work load decreased at high altitude (% VO2max at D1, D3 and D4 were respectively: 90.2 +/- 6.1, 83.3 +/- 9.8, 76.9 +/- 8.2). Linear relationships were found, both at low and high altitudes, between NE and VO2, NE and % VO2max, and between the increases in NE and heart rate during exercise. Covariance analysis indicates that these relations shifted to the left at high altitude:for the same NE or increase in NE, VO2 or increase in heart rate was lower at high altitude. Variations in E were similar but not significant. We conclude that hypoxia induced a decrease in cardiac chronotropic response to adrenergic activation during submaximal exercise.