Control of erythropoiesis after high altitude acclimatization.

Erythropoiesis was studied in 11 subjects submitted to a 4-h hypoxia (HH) in a hypobaric chamber (4,500 m, barometric pressure 58.9 kPa) both before and after a 3-week sojourn in the Andes. On return to sea level, increased red blood cells (+3.27%), packed cell volume (+4.76%), haemoglobin (+6.55%) ( P<0.05), and increased arterial partial pressure of oxygen (+8.56%), arterial oxygen saturation (+7.40%) and arterial oxygen blood content ( C(a)O(2)) (+12.93%) at the end of HH ( P<0.05) attested high altitude acclimatization. Reticulocytes increased during HH after the sojourn only (+36.8% vs +17.9%, P<0.01) indicating a probable higher reticulocyte release and/or production despite decreased serum erythropoietin (EPO) concentrations (-46%, P<0.01). Hormones (thyroid, catecholamines and cortisol), iron status (serum iron, ferritin, transferrin and haptoglobin) and renal function (creatinine, renal, osmolar and free-water clearances) did not significantly vary (except for lower thyroid stimulating hormone at sea level, P<0.01). Levels of 2,3-diphosphoglycerate (2,3-DPG) increased throughout HH on return (+14.7%, P<0.05) and an inverse linear relationship was found between 2,3-DPG and EPO at the end of HH after the sojourn only ( r=-0.66, P<0.03). Inverse linear relationships were also found between C(a)O(2) and EPO at the end of HH before ( r=-0.63, P<0.05) and after the sojourn ( r=-0.60, P=0.05) with identical slopes but different ordinates at the origin, suggesting that the sensitivity but not the gain of the EPO response to hypoxia was modified by altitude acclimatization. Higher 2,3-DPG levels could partly explain this decreased sensitivity of the EPO response to hypoxia. In conclusion, we show that altitude acclimatization modifies the control of erythropoiesis not only at sea level, but also during a subsequent hypoxia.

Normo- and hypobaric hypoxia: are there any physiological differences?

Since Bert (1878) and Barcroft (1925), studies on hypoxia are realized by lowering ambient O(2) partial pressure (PO(2)) either by barometric pressure reduction (hypobaric hypoxia HH) or by lowering the O(2) fraction (normobaric hypoxia NH). Today, a question is still debated: "are there any physiological differences between HH and NH for the same ambient PO(2)?" Since published studies are scarce and controversial, we submitted 18 subjects in a random order to a 40-min HH test and to a 40-min NH test at an ambient PO(2) equal to 120 hPa (4500 m). Cardioventilatory variables [breathing frequency (f), tidal volume (V(t)), minute ventilation (V(E)), O(2) and CO(2) end-tidal fractions or pressures (FET(O2) and FET(CO2) or PET(O2) and PET(CO2) respectively), heart rate (HR) and O(2) arterial saturation by pulse oxymetry (SpO(2))] were measured throughout the tests. At the end of the tests, arterial blood samples were taken to measure arterial blood gases [O(2) and CO(2) arterial partial pressures ( Pa(O2) and Pa(CO2)), pH and O(2) arterial saturation (SaO(2))]. Results show that during HH compared to NH, f is greater (P

Thermoregulation in the cold after physical training at different ambient air temperatures.

Since human thermoregulation at rest is altered by cold exposure, it was hypothesized that physical training under cold conditions would alter thermoregulation. Three groups (n = 8) of male subjects (mean age 24.3 +/- 0.9 years) were evaluated: group T (interval training at 21 degrees C), group CT (interval training at 1 degrees C), and group C (no training, equivalent exposure to 1 degrees C). Each group was submitted, before and after 4 weeks of interval training (5 d/week), to a cold air test at rest (SCAT) (dry bulb temperature (Tdb) = 1 degrees C) for a 2-h period for evaluation of the thermoregulatory responses. During SCAT, after the training/acclimation period, group T exhibited a higher rectal temperature (Tre) (P < 0.05) without significant change in mean skin temperature (Tsk) whereas metabolic heat production (M) was higher at the beginning of the SCAT (P < 0.05). For group CT, no thermoregulatory change was observed. Group C showed a lower Tre (P < 0.05) without significant change in either Tsk or in M, suggesting the development of a hypothermic general cold adaptation. This study showed, first, that the cold thermoregulatory responses induced by an interval training differed following the climatic conditions of the training and, second, that this training performed in the cold prevented the development of a general cold adaptation.

Circadian rhythm of rectal temperature during sleep deprivation with modafinil.

BACKGROUND: Sleep deprivation (SD) induces many adverse psychological and physiological effects, particularly on vigilance and the thermoregulatory system. The drug modafinil appears to suppress or diminish the harmful effects on vigilance. However, the effects of modafinil combined with SD on the circadian rhythm of core temperature are not well established. HYPOTHESIS: We studied the circadian rhythm of rectal temperature (CRTre) during 62 h of SD alone or with three dosage levels of modafinil. METHODS: Six men underwent repeated SD experiments lasting 7 d each, including a 24-h control period, 62 h of SD, and a 24-h recovery period. Experiments were repeated four times in mixed order for placebo and three levels of modafinil (50, 150, or 300 mg x 24 h(-1)). The Tre was recorded each minute throughout the experiment and the CRTre was studied by the single cosinor method. RESULTS: Independent of modafinil, SD increased the mesor (p < 0.05) and reduced the amplitude (p < 0.01) of the CRTre without changing the acrophase. During the recovery period, a rebound increase was seen in the amplitude of the CRTre (p < 0.01). The 50 mg x 24 h(-1) dose of modafinil, but not the higher doses, induced a lower mesor (p < 0.01) independent of SD. CONCLUSIONS: The observed changes may reflect a threshold for the central action of modafinil on core temperature. The hyperthermic effect reported in the literature for SD with modafinil may actually result from the sleep deprivation alone.

Effects of modafinil on heat thermoregulatory responses in humans at rest.

The effects of modafinil on heat thermoregulatory responses were studied in 10 male subjects submitted to a sweating test after taking 200 mg of modafinil or placebo. Sweating tests were performed in a hot climatic chamber (45 degrees C, relative humidity <15%, wind speed = 0.8 m x s(-1), duration 1.5 h). Body temperatures (rectal (Tre) and 10 skin temperatures (Tsk)), sweat rate, and metabolic heat production (M) were studied as well as heart rate (HR). Results showed that modafinil induced at the end of the sweating test higher body temperatures increases (0.50 +/- 0.04 versus 0.24 +/- 0.05 degrees C (P < 0.01) for deltaTre and 3.64 +/- 0.16 versus 3.32 +/- 0.16 degrees C (P < 0.05) for deltaTsk (mean skin temperature)) and a decrease in sweating rate throughout the heat exposure (P < 0.05) without change in M, leading to a higher body heat storage (P < 0.05). AHR was also increased, especially at the end of the sweating test (17.95 +/- 1.49 versus 12.52 +/- 1.24 beats/min (P < 0.01)). In conclusion, modafinil induced a slight hyperthermic effect during passive dry heat exposure related to a lower sweat rate, probably by its action on the central nervous system, and this could impair heat tolerance.

Anthropological and thermoregulatory changes induced by a survival sojourn in a tropical climate.

OBJECTIVE: A survival sojourn in a tropical climate exposes subjects to 2 main constraints: food restriction and tropical climatic conditions. We hypothesized that such a sojourn could modify anthropological characteristics and thermoregulatory responses to heat and cold on return. METHODS: Eight European male subjects were submitted to a sweating test (ST) for 90 minutes (dry bulb temperature [Tdb] = 47 degrees C, relative humidity (RH) = 10%, and wind speed = 0.8 m x s(-1)) and to a whole-body cold-air test (Tdb = 1 degrees C, RH = 40%, and wind speed = 0.8 m x s(-1)) for 120 minutes in thermoclimatic chambers both before and after a 4-week survival sojourn in French Guyana. RESULTS: The survival sojourn resulted in a decrease in lean body mass (P < .05) without any significant change in body fat content. Heat thermoregulatory changes studied during the ST were characterized both by a lower mean skin temperature (Tsk) (P < .05) and a higher sweat rate measured after the sojourn than before it (m(sw); P < .05). Cold thermoregulatory changes were characterized by a higher T(sk) value (P < .05) and a decreased onset for continuous shivering without any significant change in internal temperature or metabolic heat production (M). CONCLUSIONS: This study showed that this type of sojourn modifies not only biometrical characteristics of the subjects but also the thermoregulatory responses, inducing an adaptation of the thermoregulatory system to heat and an increase in the sensitivity of the thermoregulatory system to cold. This finding could have practical implications on return after such a sojourn.