Michail E. Keramidas

Muscle and cerebral oxygenation during exercise performance after short-term respiratory work.

The purpose of the study was to investigate the effect of 30-min voluntary hyperpnoea on cerebral, respiratory and leg muscle balance between O(2) delivery and utilization during a subsequent constant-power test. Eight males performed a V˙O(2max) test, and two exercise tests at 85% of peak power output: (a) a control constant-power test (CPT), and (b) a constant-power test after a respiratory maneuver (CPT(RM)). Oxygenated (Δ[O(2)Hb]), deoxygenated (Δ[HHb]) and total (Δ[tHb]) hemoglobin in cerebral, intercostal and vastus lateralis were monitored with near-infrared spectroscopy. The performance time dropped ∼15% in CPT(RM) (6:55±2:52min) compared to CPT (8:03±2:33min), but the difference was not statistically significant. The vastus lateralis and intercostal Δ[tHb] and Δ[HHb] were lower in CPT(RM) than in CPT (P≤0.05). There were no differences in cerebral oxygenation between the trials. Thus, respiratory work prior to an exercise test influences the oxygenation during exercise in the leg and respiratory muscles, but not in the frontal cortex.

The Effect of Normobaric Hypoxic Confinement on Metabolism, Gut Hormones, and Body Composition

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.

Acute Effects of Normobaric Hypoxia on Hand-Temperature Responses During and After Local Cold Stress

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 (Fio2: 0.21; AIR), or a hypoxic gas mixture (Fio2: 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.

PlanHab: hypoxia exaggerates the bed-rest-induced reduction in peak oxygen uptake during upright cycle ergometry.

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.

Hand temperature responses to local cooling after a 10-day confinement to normobaric hypoxia with and without exercise

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.

Separate and combined effects of a 10-d exposure to hypoxia and inactivity on oxidative function in vivo and mitochondrial respiration ex vivo in humans

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.

Forearm–finger skin temperature gradient as an index of cutaneous perfusion during steady-state exercise

The purpose of this study was to examine whether the forearm–finger skin temperature gradient (Tforearm–finger), an index of vasomotor tone during resting conditions, can also be used during steady‐state exercise. Twelve healthy men performed three cycling trials at an intensity of ~60% of their maximal oxygen uptake for 75 min separated by at least 48 h. During exercise, forearm skin blood flow (BFF) was measured with a laser‐Doppler flowmeter, and finger skin blood flow (PPG) was recorded from the left index fingertip using a pulse plethysmogram. Tforearm–finger of the left arm was calculated from the values derived by two thermistors placed on the radial side of the forearm and on the tip of the middle finger. During exercise, PPG and BFF increased (P<0·001), and Tforearm–finger decreased (P<0·001) from their resting values, indicating a peripheral vasodilatation. There was a significant correlation between Tforearm–finger and both PPG (r = −0·68; P<0·001) and BFF (r = −0·50; P<0·001). It is concluded that Tforearm–finger is a valid qualitative index of cutaneous vasomotor tone during steady‐state exercise.

The Effect of a Sleep High–Train Low Regimen on the Finger Cold-Induced Vasodilation Response

The present study evaluated the effect of a sleep high-train low regimen on the finger cold-induced vasodilation (CIVD) response. Seventeen healthy males were assigned to either a control (CON; n=9) or experimental (EXP; n=8) group. Each group participated in a 28-day aerobic training program of daily 1-h exercise (50% of peak power output). During the training period, the EXP group slept at a simulated altitude of 2800 meters (week 1) to 3400 m (week 4) above sea level. Normoxic (CIVD(NOR); CON and EXP groups) and hypoxic (CIVD(HYPO); F(I)O(2)=0.12; EXP group only) CIVD characteristics were assessed before and after the training period during a 30-min immersion of the hand in 8°C water. After the intervention, the EXP group had increased average finger skin temperature (CIVD(NOR): +0.5°C; CIVD(HYPO): +0.5°C), number of waves (CIVD(NOR): +0.5; CIVD(HYPO): +0.6), and CIVD amplitude (CIVD(NOR): +1.5°C; CIVD(HYPO): +3°C) in both CIVD tests (p<0.05). In contrast, the CON group had an increase in only the CIVD amplitude (+0.5°C; p<0.05). Thus, the enhancement of aerobic performance combined with altitude acclimatization achieved with the sleep high-train low regimen contributed to an improved finger CIVD response during cold-water hand immersion in both normoxic and hypoxic conditions.

PlanHab: Hypoxia counteracts the erythropoietin suppression, but seems to exaggerate the plasma volume reduction induced by 3 weeks of bed rest

The study examined the distinct and synergistic effects of hypoxia and bed rest on the erythropoietin (EPO) concentration and relative changes in plasma volume (PV). Eleven healthy male lowlanders underwent three 21‐day confinement periods, in a counterbalanced order: (1) normoxic bed rest (NBR; PIO2: 133.1 ± 0.3 mmHg); (2) hypoxic bed rest (HBR; PIO2: 90.0 ± 0.4 mmHg, ambient simulated altitude of ~4000 m); and (3) hypoxic ambulation (HAMB; PIO2: 90.0 ± 0.4 mmHg). Blood samples were collected before, during (days 2, 5, 14, and 21) and 2 days after each confinement to determine EPO concentration. Qualitative differences in PV changes were also estimated by changes in hematocrit and hemoglobin concentration along with concomitant changes in plasma renin concentration. NBR caused an initial reduction in EPO by ~39% (P = 0.04). By contrast, HBR enhanced EPO (P = 0.001), but the increase was less than that induced by HAMB (P < 0.01). All three confinements caused a significant reduction in PV (P < 0.05), with a substantially greater drop in HBR than in the other conditions (P < 0.001). Thus, present results suggest that hypoxia prevents the EPO suppression, whereas it seems to exaggerate the PV reduction induced by bed rest.

Peak oxygen uptake and regional oxygenation in response to a 10-day confinement to normobaric hypoxia.

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 (FIO2 = 0.154) conditions. Oxygen uptake ( V ˙ O 2 ), ventilation ( V ˙ E ), and relative changes in regional hemoglobin oxygenation (Δ([HbO2]) 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 2 p ⁢ e a k 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[HbO2] 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 2 p ⁢ e a k , despite the enhanced VL oxygenation.