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We investigated the effect of hypoxic acclimatization per se, without any concomitant influence of strenuous physical activity on muscle and cerebral oxygenation. Eight healthy male subjects participated in a crossover-designed study. In random order, they conducted a 10-day normoxic (CON) and a 10-day hypoxic (EXP) confinement. Pre and post both CON and EXP confinements, subjects conducted two incremental-load cycling exercises to exhaustion; one under normoxic, and the other under hypoxic (F(I)O(2)  = 0.154) conditions. Oxygen uptake (V˙O(2)), ventilation (V˙(E)), and relative changes in regional hemoglobin oxygenation (Δ([HbO(2)]) in the cerebral cortex and in the serratus anterior (SA) and vastus lateralis (VL) muscles were measured. No changes were observed in the CON confinement. Peak work rate and V˙O(2peak) were similar pre and post in the EXP confinement, whereas V˙(E) increased in the EXP post normoxic and hypoxic trials (P < 0.05). The exercise-induced drop in VL Δ[HbO(2)] was less in the post- than pre-EXP trial by 4.0 ± 0.4 and 4.2 ± 0.6 μM during normoxic and hypoxic exercise, respectively. No major changes were observed in cerebral or SA oxygenation. These results demonstrate that a 10-day hypoxic exposure without any concomitant physical activity had no effect on normoxic or hypoxic V˙O(2peak), despite the enhanced VL oxygenation., (© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Previous findings of a narcosis-induced reduction in heat production during cold water immersion, as reflected in oxygen uptake (VO2), have been attributed to the attenuation of the shivering response. The possibility of reduced oxygen utilization (VO2) by the muscles could not, however, be excluded. Accordingly, the present study tested the hypothesis that mild narcosis, induced by inhalation of a normoxic gas mixture containing 30% nitrous oxide (N2O), would affect VO2. Nine male subjects participated in both maximal and submaximal exercise trials, inspiring either room air (AIR) or a normoxic mixture containing 30% N2O. In the submaximal trials, the subjects exercised at 50% of maximal exercise intensity (Wmax) as determined in the maximal AIR trial. Though the subjects attained the same Wmax in the AIR and N2O trials, maximal VO2 was significantly higher (P < 0.05) during the N2O condition [58.9 (SEM 3.1) ml x kg(-1) x min(-1)] compared to the AIR condition [55.0 (SEM 2.4) ml x kg(-1) x min(-1)]. However, the VO2-relative exercise intensity relationship was similar during both maximal AIR and maximal N2O at submaximal exercise intensities. There were no significant differences in the responses of oesophageal temperature, sweating rate, heart rate and ventilation between AIR and N2O in the maximal and submaximal tests. It was concluded that the previously reported narcosis-induced reductions in VO2 observed during cold water immersion can be attributed solely to a reduction in the shivering response rather than to decreased oxygen utilization by the muscles.

It is generally assumed that exercise and shivering are analogous processes with regard to substrate utilisation and that, as a consequence, exercise can be used as a model for shivering. In the present study, substrate utilisation during exercise and shivering at the same oxygen consumption (VO2) were compared. Following an overnight fast, eight male subjects undertook a 2-h immersion in cold water, designed to evoke three different intensities of shivering. At least 1 week later they undertook a 2-h period of bicycle ergometry during which the exercise intensity was varied to match the VO2 recorded during shivering. During both activities hepatic glucose output (HGO), the rate of glucose utilisation (Rd), blood glucose, plasma insulin, free fatty acid (FFA) and beta-hydroxybutyrate (B-HBA) concentrations were measured. The VO2 measured during the different levels of shivering averaged 0.49 l.min-1 (level 1: low), 0.6 l.min-1 (level 2: low-moderate), and 0.9 l.min-1 (level 3: moderate), and corresponded closely to the levels measured during exercise. HGO and Rd were greater (P < 0.05) during exercise than during shivering at the same VO2 (9.5% and 14.7%, respectively). The average (SD). HGO during level 3 exercise was 3.0 (0.91) mg.kg-1.min-1 compared to 2.76 (1.0) mg.kg-1.min-1 during shivering. The values for Rd were 3.06 (0.98) mg.kg-1.min-1 during level 3 exercise and 2.68 (0.82) mg.kg-1.min-1 during shivering. Blood glucose levels did not differ between conditions averaging 5.4 (0.3) mmol.l-1 over all levels of shivering and 5.2 (0.3) mmol.l-1 during exercise. Plasma FFA and B-HBA were higher (P < 0.01) during shivering than during corresponding exercise (12.3% and 33.3%, respectively). FFA averaged 0.61 (0.2) mmol.l-1 over all levels of shivering and 0.47 (0.16) mmol.l-1 during exercise. The figures for L-HBA were 0.44 (0.13) mmol. l-1 during all levels of shivering and 0.32 (0.1) mmol.l-1 during exercise. Plasma insulin was higher (P < 0.05) during level 2 and 3 shivering compared to corresponding exercise; at these levels the average value for plasma insulin was 95.9 (21.9) pmol.l-1 during shivering and 80.6 (16.1) pmol.l-1 during exercise. On the basis of the present findings it is concluded that, with regard to substrate utilisation, shivering and exercise of up to 2 h duration should not be regarded as analogous processes.

The principal cause of the immediate transient elevation in ventilation (VE, L.min-1) and oxygen uptake (VO2, L.min-1), when a human subject is immersed in cold water is considered to be the stimulation of cutaneous cold receptors. The present study demonstrates that the initial VE and VO2 responses are comprised of a thermogenic and a hydrostatic component. The peak values in VE reached (mean +/- SD) 66.8 +/- 22.3, 53.9 +/- 38.1, 32.2 +/- 15.4, 22.5 +/- 3.6, 19.5 +/- 4.6 L.min-1 during the first minute of immersion in 10 degrees, 15 degrees, 20 degrees, 28 degrees and 40 degrees C water, respectively. Similarly, peaks (mean +/- SD) in VO2 of 1.22 +/- 0.25, 1.01 +/- 0.32, 0.98 +/- 0.39, 0.81 +/- 0.09, and 0.78 +/- 0.26 L.O2.min-1, were reached when subjects were immersed in 10 degrees, 15 degrees, 20 degrees, 28 degrees, and 40 degrees C water. It is concluded that the observed increases in VO2 during the first minute of immersion are partly due to the increased hydrostatic pressure causing a shift of venous blood towards the thoracic region, and a transient increase in the uptake of oxygen into the blood.

The study examined the effects of a 10-day normobaric hypoxic confinement ( FiO2: 0.14), with [hypoxic exercise training ( HT); n = 8)] or without [hypoxic ambulatory ( HA; n = 6)] exercise, on the hand temperature responses during and after local cold stress. Before and after the confinement, subjects immersed their right hand for 30 min in 8 ° C water [cold water immersion ( CWI)], followed by a 15-min spontaneous rewarming ( RW), while breathing either room air ( AIR), or a hypoxic gas mixture ( HYPO). The hand temperature responses were monitored with thermocouples and infrared thermography. The confinement did not influence the hand temperature responses of the HA group during the AIR and HYPO CWI and the HYPO RW phases; but it impaired the AIR RW response (−1.3 ° C; P = 0.05). After the confinement, the hand temperature responses were unaltered in the HT group throughout the AIR trial. However, the average hand temperature was increased during the HYPO CWI (+0.5 ° C; P ≤ 0.05) and RW (+2.4 ° C; P ≤ 0.001) phases. Accordingly, present findings suggest that prolonged exposure to normobaric hypoxia per se does not alter the hand temperature responses to local cooling; yet, it impairs the normoxic RW response. Conversely, the combined stimuli of continuous hypoxia and exercise enhance the finger cold-induced vasodilatation and hand RW responses, specifically, under hypoxic conditions. [ABSTRACT FROM AUTHOR]