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Prolonged, exhaustive exercise frequently leads to an increased incidence of upper respiratory tract illness (URTI) which is linked to transient immunodepression. We investigated potential biochemical markers of stress and fatigue, and URTI symptoms as a surrogate of immunodepression, in US Marines undergoing intensive winter training at altitude. Selected plasma amino acids and leptin (p[Lep]) were measured as possible markers of fatigue and immunodepression, together with nonesterified fatty acids (p[NEFA]) and total antioxidant capacity (p[TAC]). Changes were observed in plasma free tryptophan (p[FT]), p[Gln], p[Lep], p[NEFA], p[TAC] but not branched chain amino acids (p[BCAA]). p[FT] decreased markedly. Resting p[Gln] decreased overall after one month at altitude. p[Gln] routinely decreases 1-2 hrs after prolonged exercise. Importantly, we observed early morning decreases in p[Gln], suggesting a cumulative effect of prolonged activity, stress, and fatigue. Concomitantly, individuals with highest illness scores had the greatest p[Gln] decrease: low p[Gln] may therefore be associated with a diminished stress tolerance.

Four compounds derived from 2-aminothiazole and 2-amino-2-thiazoline were prepared by coupling the respective bases with the acid chlorides of either 3- or 4-(N,N-dimethylamino)benzoic acid. Products were identified using infrared spectroscopy, 1H NMR spectroscopy and electrospray mass spectroscopy and in two cases by single-crystal X-ray diffraction. Of the four, N-(thiazol-2-yl)-3-(N,N-dimethylamino)-benzamide (1), N-(thiazolin-2-yl)-4-(N,N-dimethylamino)benzamide (2), N-(thiazolin-2-yl)-3-(N,N-dimethylamino) benzamide (3) and N-(thiazolin-2-yl)-4-(N,N-dimethylamino)benzamide (4), the hydrochloride salts of compounds 3 and 4 showed anti-inflammatory activity across a concentration range of 10−2−5 × 10−4 M while 3 (at a concentration of 10−5 M) was found to have no adverse effect on myocardial function. The X-ray crystal structure of 2 and the 1:1 adduct structure of 3 with 3-(N,N-dimethylamino)benzoic acid are reported.

Oxygen delivery (DO 2 ) calculated from cardiac output, haematocrit (Hct) and arterial oxygen saturation (SaO 2 ), has been obtained on six subjects at sea level (London) and after slow ascent to 5000 meters (Chamlang base camp) at rest and during mild exercise (25 watts and 50 watts). Haematocrit was increased in all six subjects at 5000 m and expressed as haemoglobin (Hb) rose from a mean (+/- standard error; SEM) of 13.8 +/-0.1 g (100 ml) -1 to 15.8 +/-0.3 g (100 ml) -1 (t = 6.3, p = 0.0014). SaO 2 was almost constant with exercise at sea level (rest 98.5%, 25 w 98.3% and 50 w 98.3%) but declined more steeply with exercise at 5000 m (rest 88.8 +/-0.6%, 25 w 85.4 +/-0.4% and 50 w 84.4 +/-0.5%). Arterial oxygen content (CaO 2 ) was very similar for 25 watts exercise at altitude (5000 m, 18.1 ml per decilitre - dl) as at sea level (London, CaO 2 18.2 ml dl -1 ). At rest CaO 2 was higher at altitude (18.8 +/-0.2 ml dl -1 ) than at sea level (18.3 +/-0.4 ml dl -1 ) and at 50 w CaO 2 was lower at altitude (17.9 +/-0.4 ml dl -1 ) than at sea level (18.2 +/-0.2 ml dl -1 ). Hence, similar cardiac output values at rest (sea level, 5.0 +/-0.4 litres min -1 l min -1 ; altitude, 5.6 +/-0.3 l min -1 ) and at 25 w exercise (sea level, 8.2 +/-0.7 l min -1 ; altitude, 8.3 +/-0.9 l min -1 ) resulted in similar values for DO 2 at rest (sea level, 0.9 +/-0.1 I min -1 ; altitude, 1.0 +/-0.1 I min -1 ) and 25 w exercise (sea level, 1.5 +/-0.1 l min -1 ; altitude, 1.5 +/-0.2 l min -1 ). For 50 w exercise cardiac output and oxygen delivery were greater at altitude in one subject but were significantly reduced for the remaining five (cardiac output mean difference 3.0 +/-0.9 1 l min -1 , p = 0.015; DO 2 mean difference, 0.56 +/-0.2 1 1 min -1 , p = 0.028). Acclimatization was therefore adequate to sustain a normal value for oxygen delivery for rest and 25 watts exercise (via compensatory erythropoiesis) but insufficient for 50―watt exercise in five of the six subjects.