An integrative evaluation of oxidative metabolism was carried out in 9 healthy young men (age, 24.1 ± 1.7 yr mean ± SD) before (CTRL) and after a 10-day horizontal bed rest carried out in normoxia (N-BR) or hypoxia (H-BR, FiO2 = 0.147). H-BR was designed to simulate planetary habitats. Pulmonary O2 uptake (V̇o2) and vastus lateralis fractional O2 extraction (changes in deoxygenated hemoglobin+myoglobin concentration, Δ[deoxy(Hb+Mb)] evaluated using near-infrared spectroscopy) were evaluated in normoxia and during an incremental cycle ergometer (CE) and one-leg knee extension (KE) exercise (aimed at reducing cardiovascular constraints to oxidative function). Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in permeabilized vastus lateralis fibers. During CE V̇o2peak and Δ[deoxy(Hb+Mb)]peak were lower (P < 0.05) after both N-BR and H-BR than during CTRL; during KE the variables were lower after N-BR but not after H-BR. During CE the overshoot of Δ[deoxy(Hb+Mb)] during constant work rate exercise was greater in N-BR and H-BR than CTRL, whereas during KE a significant difference vs. CTRL was observed only after N-BR. Maximal mitochondrial respiration determined ex vivo was not affected by either intervention. In N-BR, a significant impairment of oxidative metabolism occurred downstream of central cardiovascular O2 delivery and upstream of mitochondrial function, possibly at the level of the intramuscular matching between O2 supply and utilization and peripheral O2 diffusion. Superposition of hypoxia on bed rest did not aggravate, and partially reversed, the impairment of muscle oxidative function in vivo induced by bed rest. The effects of longer exposures will have to be determined.

To assess the effect of normobaric hypoxia on metabolism, gut hormones, and body composition, 11 normal weight, aerobically trained (O2peak: 60.6 ± 9.5 ml·kg−1·min−1) men (73.0 ± 7.7 kg; 23.7 ± 4.0 years, BMI 22.2 ± 2.4 kg·m−2) were confined to a normobaric (altitude ≃ 940 m) normoxic (NORMOXIA; PIO2 ≃ 133.2 mmHg) or normobaric hypoxic (HYPOXIA; PIO was reduced from 105.6 to 97.7 mmHg over 10 days) environment for 10 days in a randomized cross-over design. The wash-out period between confinements was 3 weeks. During each 10-day period, subjects avoided strenuous physical activity and were under continuous nutritional control. Before, and at the end of each exposure, subjects completed a meal tolerance test (MTT), during which blood glucose, insulin, GLP-1, ghrelin, peptide-YY, adrenaline, noradrenaline, leptin, and gastro-intestinal blood flow and appetite sensations were measured. There was no significant change in body weight in either of the confinements (NORMOXIA: −0.7 ± 0.2 kg; HYPOXIA: −0.9 ± 0.2 kg), but a significant increase in fat mass in NORMOXIA (0.23 ± 0.45 kg), but not in HYPOXIA (0.08 ± 0.08 kg). HYPOXIA confinement increased fasting noradrenaline and decreased energy intake, the latter most likely associated with increased fasting leptin. The majority of all other measured variables/responses were similar in NORMOXIA and HYPOXIA. To conclude, normobaric hypoxic confinement without exercise training results in negative energy balance due to primarily reduced energy intake.

The purpose of the study was to investigate the effect of interval training combined with a thigh cuffs pressure of +90 mmHg on maximal and submaximal cycling performance. Twenty untrained individuals were assigned either to a control (CON) or to an experimental (CUFF) training group. Both groups trained 3 days per week for 6 weeks at the same relative intensity; each training session consisted of 2-min work bout at 90% of VO(2max): 2-min active recovery bout at 50% of VO(2max). An incremental exercise test to exhaustion, a 6-min constant-power test at 80% of VO(2max) (Sub(80)) and a maximal constant-power test to exhaustion (TF(150)) were performed pre- and post-training. Despite the unchanged VO(2max), both groups significantly increased peak power output (CON: ∼12%, CUFF: ∼20%) that was accompanied by higher deoxygenation (ΔStO(2)) measured with near-infrared muscle spectroscopy. These changes were more pronounced in the CUFF group. Moreover, both groups reduced VO(2) during the Sub(80) test without concomitant changes in ΔStO(2). TF(150) was enhanced in both groups. Thus, an interval exercise training protocol under moderate restricted blood flow conditions does not provide any additive effect on maximal and submaximal cycling performance. However, it seems to induce peripheral muscular adaptations, despite the lower absolute training intensity.

The study examined the effects of hypoxia and horizontal bed rest, separately and in combination, on peak oxygen uptake (V̇o2 peak) during upright cycle ergometry. Ten male lowlanders underwent three 21-day confinement periods in a counterbalanced order: 1) normoxic bed rest [NBR; partial pressure of inspired O2 (PiO2 ) = 133.1 ± 0.3 mmHg]; 2) hypoxic bed rest (HBR; PiO2 = 90.0 ± 0.4 mmHg), and 3) hypoxic ambulation (HAMB; PiO2 = 90.0 ± 0.4 mmHg). Before and after each confinement, subjects performed two incremental-load trials to exhaustion, while inspiring either room air (AIR), or a hypoxic gas (HYPO; PiO2 = 90.0 ± 0.4 mmHg). Changes in regional oxygenation of the vastus lateralis muscle and the frontal cerebral cortex were monitored with near-infrared spectroscopy. Cardiac output (CO) was recorded using a bioimpedance method. The AIR V̇o2 peak was decreased by both HBR (∼13.5%; P ≤ 0.001) and NBR (∼8.6%; P ≤ 0.001), with greater drop after HBR (P = 0.01). The HYPO V̇o2 peak was also reduced by HBR (-9.7%; P ≤ 0.001) and NBR (-6.1%; P ≤ 0.001). Peak CO was lower after both bed-rest interventions, and especially after HBR (HBR: ∼13%, NBR: ∼7%; P ≤ 0.05). Exercise-induced alterations in muscle and cerebral oxygenation were blunted in a similar manner after both bed-rest confinements. No changes were observed in HAMB. Hence, the bed-rest-induced decrease in V̇o2 peak was exaggerated by hypoxia, most likely due to a reduction in convective O2 transport, as indicated by the lower peak values of CO.

Cold-induced vasodilatation (CIVD) is a cyclical increase in finger temperature that has been suggested to provide cryoprotective function during cold exposures. Physical fitness has been suggested as a potential factor that could affect CIVD response, possibly via central (increased cardiac output, decreased sympathetic nerve activity) and/or peripheral (increased microcirculation) cardiovascular and neural adaptations to exercise training. Therefore, the purpose of this study was to investigate the effect of endurance exercise training on the CIVD response. Eighteen healthy males trained 1 h d(-1) on a cycle ergometer at 50% of peak power output, 5 days week(-1) for 4-weeks. Pre, Mid, Post, and 10 days after the cessation of training and on separate days, subjects performed an incremental exercise test to exhaustion (.VO(2peak)) and a 30-min hand immersion in 8 degrees C water to examine their CIVD response. The exercise-training regimen significantly increased .VO(2peak) (Pre: 46.0 +/- 5.9, Mid: 52.5 +/- 5.7, Post: 52.1 +/- 6.2, After: 52.6 +/- 7.6 ml kg(-1) min(-1); P < 0.001). There was a significant increase in average finger skin temperature (Pre: 11.9 +/- 2.4, After: 13.5 +/- 2.5 degrees C; P < 0.05), the number of waves (Pre: 1.1 +/- 1.0, After: 1.7 +/- 1.1; P < 0.001) and the thermal sensation (Pre: 1.7 +/- 0.9, After: 2.5 +/- 1.4; P < 0.001), after training. In conclusion, the aforementioned endurance exercise training significantly improved the finger CIVD response during cold-water hand immersion.

Keramidas, Michail E, Roger Kölegård, Igor B. Mekjavic, and Ola Eiken. Acute effects of normobaric hypoxia on hand-temperature responses during and after local cold stress. High Alt Med Biol. 15:183-191, 2014.-The purpose was to investigate acute effects of normobaric hypoxia on hand-temperature responses during and after a cold-water hand immersion test. Fifteen males performed two right-hand immersion tests in 8°C water, during which they were inspiring either room air (Fio 2 : 0.21; AIR), or a hypoxic gas mixture (Fio 2 : 0.14; HYPO). The tests were conducted in a counterbalanced order and separated by a 1-hour interval. Throughout the 30-min cold-water immersion (CWI) and the 15-min spontaneous rewarming (RW) phases, finger-skin temperatures were measured continuously with thermocouple probes; infrared thermography was also employed during the RW phase to map all segments of the hand. During the CWI phase, the average skin temperature (Tavg) of the fingers did not differ between the conditions (AIR: 10.2 -0.5°C, HYPO: 10.0 -0.5°C; p = 0.67). However, Tavg was lower in the HYPO than the AIR RW phase (AIR: 24.5 -3.4°C; HYPO: 22.0 -3.8°C; p = 0.002); a response that was alike in all regions of the immersed hand. Accordingly, present findings suggest that acute exposure to normobaric hypoxia does not aggravate the cold-induced drop in hand temperature of normothermic males. Still, hypoxia markedly impairs the rewarming responses of the hand.

The purpose of the study was to evaluate the recuperative efficacy of pre-exercise napping on physical capacity after military sustained operations (SUSOPS) with partial sleep deprivation. Before and after a 2-day SUSOPS, 61 cadets completed a battery of questionnaires, and performed a 2-min lunges trial and a 3,000-m running time-trial. After the completion of SUSOPS, subjects were randomized to either a control [without pre-exercise nap (CON); n = 32] or a nap [with a 30-min pre-exercise nap (NAP); n = 29] group. SUSOPS enhanced perceived sleepiness and degraded mood in both groups. Following SUSOPS, the repetitions of lunges, in the CON group, were reduced by ~ 2.3%, albeit the difference was not statistically significant (p = 0.62). In the NAP group, however, the repetitions of lunges were increased by ~ 7.1% (p = 0.01). SUSOPS impaired the 3,000-m running performance in the CON group (~ 2.3%; p = 0.02), but not in the NAP group (0.3%; p = 0.71). Present results indicate, therefore, that a relatively brief pre-exercise nap may mitigate physical performance impairments ensued by short-term SUSOPS.

Skeletal muscle oxidative function was evaluated in 11 healthy males (mean ± SD age 27 ± 5 years) prior to (baseline data collection, BDC) and following a 21 day horizontal bed rest (BR), carried out in normoxia ( = 133 mmHg; N-BR) and hypoxia ( = 90 mmHg; H-BR). H-BR was aimed at simulating reduced gravity habitats. The effects of a 21 day hypoxic ambulatory confinement ( = 90 mmHg; H-AMB) were also assessed. Pulmonary O uptake ( ), vastus lateralis fractional O extraction (changes in deoxygenated haemoglobin + myoglobin concentration, Δ[deoxy(Hb + Mb)]; near-infrared spectroscopy) and femoral artery blood flow (ultrasound Doppler) were evaluated during incremental one-leg knee-extension exercise (reduced constraints to cardiovascular O delivery) carried out to voluntary exhaustion in a normoxic environment. Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in permeabilized vastus lateralis fibres. decreased (P< 0.05) after N-BR (0.98 ± 0.13 L min ) and H-BR (0.96 ± 0.17 L min ) vs. BDC (1.05 ± 0.14 L min ). In the presence of a decreased (by ∼6-8%) thigh muscle volume, normalized per unit of muscle mass was not affected by both interventions. Δ[deoxy(Hb + Mb)] decreased (P < 0.05) after N-BR (65 ± 13% of limb ischaemia) and H-BR (62 ± 12%) vs. BDC (73 ± 13%). H-AMB did not alter or Δ[deoxy(Hb + Mb)] . An overshoot of Δ[deoxy(Hb + Mb)] was evident during the first minute of unloaded exercise after N-BR and H-BR. Arterial blood flow to the lower limb during both unloaded and peak knee extension was not affected by any intervention. Maximal ADP-stimulated mitochondrial respiration decreased (P < 0.05) after all interventions vs. control. In 21 day N-BR, a significant impairment of oxidative metabolism occurred downstream of cardiovascular O delivery, affecting both mitochondrial respiration and presumably the intramuscular matching between O supply and utilization. Superposition of H on BR did not worsen the impairment induced by BR alone.