Running a marathon from -45°C to +55°C in a climate chamber: a case study.

BACKGROUND: We describe a runner who completed a self-paced marathon (42.195 km) in a climate chamber with a temperature difference of 100°C, starting at an ambient temperature (Tambient) of -45°C and finishing at an Tambient of +55°C. METHODS: Tambient was set at -45°C at the start, and was steadily increased at a rate of 1°C at 4.5-minute intervals to +55°C. Before the start, after every 10.5 km, and at the end of the marathon, body mass, urine, and sweat production were measured and samples of venous blood and urine were collected. The runner's temperature was recorded every 10 seconds at four sites, ie, the rectum for body core temperature (Tcore), and at the forehead, right wrist, and right ankle for surface temperatures (Tskin). RESULTS: The subject took 6.5 hours to complete the marathon, during which Tcore varied by 0.9°C (start 37.5°C, peak 38.4°C). The largest difference (∆) of Tskin was recorded at the ankle (∆16°C). The calculated amount of sweat produced increased by 888% from baseline. In the blood samples, myoglobin (+250%) showed the highest change. Of the pituitary hormones, somatotropic hormone (+391%) and prolactin (+221%) increased the most. Regarding fluid regulation hormones, renin (+1145%) and aldosterone (+313%) showed the greatest increase. CONCLUSION: These results show that running a marathon in a climate chamber with a total ∆Tambient of 100°C is possible, and that the Tambient to Tcore relationship is maintained. These results may offer insight into regulatory mechanisms to avoid hypothermia and hyperthermia. The same study is to be performed using more subjects with the same characteristics to validate the present findings.

Time-dependent changes of the susceptibility of cardiac contractile function to hypoxia-reoxygenation after myocardial infarction in rats.

In this study we analyzed the susceptibility of contractile function of the myocardium to hypoxia-reoxygenation after infarction. For this purpose, the contractility of isolated papillary muscles from rats was studied at high oxygen tension (pO2 80 kPa) and during hypoxia (pO2 3 kPa) with subsequent reoxygenation at variable intervals between 15 h and 9 weeks after permanent ligation of the left coronary artery. Hypoxic exposure reduced the contractile performance of the preparations to a similar extent in both groups. Notably, the contractility and, in particular, the relaxation rates recovered more completely from hypoxia in the hypertrophied myocardium of rats with coronary artery ligation than in sham-operated (SO) animals. The recovery of contractile function was improved maximally between 6 and 9 weeks after myocardial infarction (MI). The lower sensitivity of the (post)ischemic myocardium to hypoxia-reoxygenation correlated with enhanced left ventricular glutathione peroxidase (GSH-Px) activity (15 h to 9 weeks post-MI) and 2-3-fold increased expression levels (15 h to 6 weeks post-MI) of the 72 kDa heat shock protein (HSP72) in the papillary muscles. These findings suggest that the greater antioxidant potential and, possibly, stimulation of HSPs contribute to the sustained tolerance of the myocardium to hypoxia-reoxygenation injury after infarction.

Decreased susceptibility of cardiac function to hypoxia-reoxygenation in renin-angiotensinogen transgenic rats.

We tested the hypothesis that the renin-angiotensin system (RAS) protects the contractile function of the myocardium against the damaging effect of hypoxia-reoxygenation. For this purpose, the contractility of isolated papillary muscles from wild-type (WT) rats and from rats expressing human renin and angiotensinogen as transgenes (TGR) was compared. After 15 min of hypoxia, peak force (PF) was decreased to 24 +/- 5% of the normoxic values in TGR (n = 10) and to 18 +/- 1% in WT rats (n = 12). PF and relaxation rates recovered completely in TGR but not in WT rats during 45 min of reoxygenation. Improved contractility of the papillary muscles from TGR during hypoxia-reoxygenation correlated with increased glutathione peroxidase activities and creatine kinase (CK)-MB and CK-BB isoenzyme levels. On the other hand, inhibition of the RAS with ramipril (1 mg/kg body wt for 3 wk) in WT animals resulted in deterioration of the contractile function of the papillary muscles during reoxygenation compared with untreated rats. These findings suggest that activation of the RAS protects contractile function of the cardiac muscle against hypoxia-reoxygenation, possibly through changes in CK isoenzymes and enhanced antioxidant capacity.