Energy Intake of Men With Excess Weight During Normobaric Hypoxic Confinement.

Due to the observations of weight loss at high altitude, normobaric hypoxia has been considered as a method of weight loss in obese individuals. With this regard, the aim of the present study was to determine the effect of hypoxia per se on metabolism in men with excess weight. Eight men living with excess weight (125.0 ± 17.7 kg; 30.5 ± 11.1 years, BMI: 37.6 ± 6.2 kg⋅m-2) participated in a randomized cross-over study comprising two 10-day confinements: normobaric (altitude of facility ≃ 940 m) normoxia (NORMOXIA; P I O2 = 133 mmHg), and normobaric hypoxia (HYPOXIA). The P I O2 in the latter was reduced from 105 (simulated altitude of 2,800 m) to 98 mmHg (simulated altitude of 3,400 m over 10 days. Before, and at the end of each confinement, participants completed a meal tolerance test (MTT). Resting energy expenditure (REE), circulating glucose, GLP-1, insulin, catecholamines, ghrelin, peptide-YY (PYY), leptin, gastro-intestinal blood flow, and appetite sensations were measured in fasted and postprandial states. Fasting REE increased after HYPOXIA (+358.0 ± 49.3 kcal⋅day-1, p = 0.03), but not after NORMOXIA (-33.1 ± 17.6 kcal⋅day-1). Postprandial REE was also significantly increased after HYPOXIA (p ≤ 0.05), as was the level of PYY. Furthermore, a tendency for decreased energy intake was concomitant with a significant body weight reduction after HYPOXIA (-0.7 ± 0.2 kg) compared to NORMOXIA (+1.0 ± 0.2 kg). The HYPOXIA trial increased the metabolic requirements, with a tendency toward decreased energy intake concomitant with increased PYY levels supporting the notion of a hypoxia-induced appetite inhibition, that could potentially lead to body weight reduction. The greater postprandial blood-glucose response following hypoxic confinement, suggests the potential development of insulin resistance.

A 10-day confinement to normobaric hypoxia impairs toe, but not finger temperature response during local cold stress.

The study examined the effects of a 10-day normobaric hypoxic confinement on the finger and toe temperature responses to local cooling. Eight male lowlanders underwent a normoxic (NC) and, in a separate occasion, a normobaric hypoxic confinement (HC; FO2: 0.154; simulated altitude ~3400m). Before and after each confinement, subjects immersed for 30min their right hand and, in a different session, their right foot in 8°C water, while breathing either room air (AIR) or a hypoxic gas mixture (HYPO). Throughout the cold-water immersion tests, thermal responses were monitored with thermocouples on fingers and toes. Neither confinement influenced thermal responses in the fingers during the AIR or HYPO test. In the foot, by contrast, HC, but not NC, reduced the average toe temperature by ~1.5°C (p=0.03), both during the AIR and HYPO test. We therefore conclude that a 10-day confinement to normobaric hypoxia per se augments cold-induced vasoconstriction in the toes, but not in the fingers. The mechanism underlying this dissimilarity remains to be established.

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.

Intermittent normobaric hypoxic exposures at rest: effects on performance in normoxia and hypoxia.

INTRODUCTION: It has been speculated that short (-1-h) exposures to intermittent normobaric hypoxia at rest can enhance subsequent exercise performance. Thus, the present study investigated the effect of daily resting intermittent hypoxic exposures (IHE) on peak aerobic capacity and performance under both normoxic and hypoxic conditions. METHODS: Eighteen subjects were equally assigned to either a control (CON) or IHE group and performed a 4-wk moderate intensity cycling exercise training (1 h x d(-1), 5 d x wk(-1)). The IHE group additionally performed IHE (60 min) prior to exercise training. IHE consisted of seven cycles alternating between breathing a hypoxic gas mixture (5 min; F1O2 = 0.12-0.09) and room air (3 min; F1O2 = 0.21). Normoxic and hypoxic peak aerobic capacity (VO2(peak)) and endurance performance were evaluated before (PRE), during (MID), upon completion (POST), and 10 d after (AFTER) the training period. RESULTS: Similar improvements were observed in normoxic VO2(peak) tests in both groups [IHE: delta(POST-PRE) = +10%; CON: delta(POST-PRE) = + 14%], with no changes in the hypoxic condition. Both groups increased performance time in the normoxic constant power test only [IHE: delta(POST-PRE) = +108%; CON: delta(POST-PRE) = +114%], whereas only the IHE group retained this improvement in the AFTER test. Higher levels of minute ventilation were noted in the IHE compared to the CON group at the POST and AFTER tests. CONCLUSION: Based on the results of this study, the IHE does not seem to be beneficial for normoxic and hypoxic performance enhancement.

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.

Normoxic and hypoxic performance following 4 weeks of normobaric hypoxic training.

INTRODUCTION: Although training in hypoxia has been suggested to improve sea level and altitude performance, most studies have only evaluated its effect on maximal aerobic capacity in either normoxia or hypoxia. The present study evaluated the effect of a live low-train high training regimen on both normoxic and hypoxic endurance performance and aerobic capacity. METHODS: There were 18 male subjects who performed 20 training sessions in either a normoxic (F(IO2) = 0.21) or hypoxic (F(IO2) = 0.12) environment. Both the Control (N = 9) and Hypoxic (N = 9) group subjects trained at an intensity that maintained their heart rate at a level corresponding to that elicited at 50% of peak power output attained in normoxia or hypoxia, respectively. Before, during, upon completion, and 10 d after the protocol, subjects' aerobic capacity (VO2 peak) and endurance performance (80% of VO2 peak) were determined under normoxic and hypoxic conditions. RESULTS: Mean +/- SD normoxic VO2 peak increased significantly only in the Control group from 45.7 +/- 6.1 to 53.9 +/- 3.9 (ml x kg(-1) x min(-1)), whereas hypoxic VO2 peak did not improve in either group. The Control group exhibited significant improvements in normoxic, but not hypoxic peak power output (PPO) and time to exhaustion, whereas the Hypoxic group only exhibited improvements in normoxic time to exhaustion. During each testing period, we also assessed pulmonary function, selected hematological variables, and anthropometry. There were no significant changes in these variables in either group after the training protocol. CONCLUSION: The hypoxic training regimen used in the present study had no significant effect on altitude and sea level performance.

Respiratory muscle endurance training: effect on normoxic and hypoxic exercise performance.

The aim of this study was to investigate the effect of respiratory muscle endurance training on endurance exercise performance in normoxic and hypoxic conditions. Eighteen healthy males were stratified for age and aerobic capacity; and randomly assigned either to the respiratory muscle endurance training (RMT = 9) or to the control training group (CON = 9). Both groups trained on a cycle-ergometer 1 h day(-1), 5 days per week for a period of 4 weeks at an intensity corresponding to 50% of peak power output. Additionally, the RMT group performed a 30-min specific endurance training of respiratory muscles (isocapnic hyperpnea) prior to the cycle ergometry. Pre, Mid, Post and 10 days after the end of training period, subjects conducted pulmonary function tests (PFTs), maximal aerobic tests in normoxia (VO(2max)NOR), and in hypoxia (VO(2max)HYPO; F(I)O(2) = 0.12); and constant-load tests at 80% of VO(2max)NOR in normoxia (CLT(NOR)), and in hypoxia (CLTHYPO). Both groups enhanced VO(2max)NOR (CON: +13.5%; RMT: +13.4%), but only the RMT group improved VO(2max)HYPO Post training (CON: -6.5%; RMT: +14.2%). Post training, the CON group increased peak power output, whereas the RMT group had higher values of maximum ventilation. Both groups increased CLT(NOR) duration (CON: +79.9%; RMT: +116.6%), but only the RMT group maintained a significantly higher CLT(NOR) 10 days after training (CON: +56.7%; RMT: +91.3%). CLT(HYPO) remained unchanged in both groups. Therefore, the respiratory muscle endurance training combined with cycle ergometer training enhanced aerobic capacity in hypoxia above the control values, but did not in normoxia. Moreover, no additional effect was obtained during constant-load exercise.