Exercise In Moderate Hypoxia Research Articles

Substrate utilization during exercise and recovery at moderate altitude

Recent studies have shown that exercise training at moderate altitude or in moderate hypoxia improved glycemic parameters. From these data, it has been supposed that endurance exercise in moderate hypoxia affects substrate utilization and that exposure to moderate hypoxia in combination with exercise may be utilized as part of metabolic or diabetes prevention program. However, the influence of exercise at moderate hypoxia on circulating metabolites and hormones in terms of substrate utilization is unclear. The purpose of this study was to elucidate the influence of exercise in moderate hypoxia on substrate utilization. We determined cardiorespiratory, metabolic, and hormonal parameters during exercise and postexercise recovery at a simulated moderate altitude of 2000 m, and then we compared these variables with values obtained at sea level. Seven men participated in this study; subjects reported to the laboratory on 4 occasions. Two maximal exercise tests were performed to estimate peak oxygen uptake at the simulated 2000-m altitude and sea level on different days. Afterward, submaximal exercise tests were carried out at a simulated altitude of 2000 m or sea level, separated by 1 week. Subjects performed submaximal exercise at the same relative exercise intensity (50% peak oxygen uptake) at a simulated altitude of 2000 m and at sea level for 30 minutes. The tests were performed in random order, and subjects were blinded to the respective altitudes. Venous blood samples and expired gases were obtained before, during exercise (15 and 30 minutes), and during postexercise recovery periods (15, 30, 45, and 60 minutes). The respiratory exchange ratio during exercise and recovery at moderate altitude was greater than at sea level. The epinephrine and norepinephrine concentrations during exercise and recovery were higher ( P < .05) at moderate altitude than at sea level. Free fatty acids and glycerol concentrations during recovery were lower ( P < .05) at moderate altitude than at sea level. These results suggest that carbohydrate utilization is increased during exercise and postexercise recovery period in moderate hypoxia as compared with normoxia. It is also suggested that moderate hypoxia influences the changes in circulating metabolites and hormones in terms of substrate metabolism during exercise and the recovery.

Moderate exercise in hypoxia induces a greater arterial desaturation in trained than untrained men

During moderate exercise breathing a low inspired O(2) fraction (F(I)O(2)), arterial O(2) desaturation may depend on the fitness level. Seven trained (TM) and seven untrained men (UTM) cycled in normoxia and in hypoxia (F(I)O(2)=0.187, 0.173, 0.154, 0.13 and 0.117). We compared TM and UTM at submaximal intensities below the ventilatory threshold. Ventilatory variables were monitored and arterial oxygen saturation was measured by pulse oximetry. O(2) saturation was not different between groups at sea level. In hypoxia, O(2) saturation was lower in TM than in UTM at F(I)O(2)=0.154 (87.3 +/- 2.9% vs 90.4 +/- 1.5% at 90 W) and below. Both the ventilatory-equivalent and the end-tidal O(2) pressure were lower in TM at sea level and at every F(I)O(2), with the differences between TM and UTM becoming apparent at lower exercise intensity and increasing in magnitude as the severity of hypoxia increased. O(2) saturation was correlated with the ventilatory parameters at every F(I)O(2) and the correlations were stronger in severe hypoxia. These results demonstrate that a moderate exercise carried out in hypoxia, contrary to normoxic conditions, can lead to a greater arterial desaturation in TM compared with UTM. This phenomenon could be partly attributed to a relative hypoventilation in trained subjects.

Effects Of Acute Moderate Hypoxia On Anaerobic Capacity In Endurance-trained Runners

While there is some controversy whether anaerobic capacity might be improved after altitude training little is known about changes in anaerobic capacity during hypoxic exposure in highly trained athletes. PURPOSE To find out if acute exposure to moderate hypoxia affects anaerobic capacity in endurance-trained athletes. METHODS 18 male middle-/long-distance runners and triathletes (23.9 ± 3.9 yrs, 182 ± 6 cm, 70.8 ± 6.7 kg, VO2max 68.1 ± 4.3 ml · kg-1 · min-1) performed two supra- VO2max treadmill tests with the same speed, one in normoxia and one on a separate day after a 4 h exposure to normobarc hypoxia (FiO2 0.15). Maximal accumulated oxygen de.cit (MAOD) was determined as described by Medbø et al. (1988). Capillary blood samples from the earlobe were drawn at rest and repeatedly during 15 min of recovery for measurement of lactate and ammonia. RESULTS MAOD showed a tendency (p = 0.061) to be increased in hypoxia by 9 % on the average while maximal capillary lactate (12.8 ± 2.0 vs. 13.7 ± 2.1 mmol · L−1, p = 0.036) and maximal capillary ammonia concentration (95 ± 49 vs. 121 ± 42 μmol · L−1, p = 0.008) were significantly decreased. The reduction in time to exhaustion (144 ± 33 vs. 203 ± 55 s, p <0.001) was significantly correlated to the decrement in oxygen uptake during exercise in hypoxia (R = 0.797, p <0.001). CONCLUSION The slight increase in MAOD shows that performance during exhaustive supra-VO2max exercise in moderate hypoxia is not impaired by changes in anaerobic capacity. Supported by the Bundesinstitut für Sportwissenschaft (VF0408/01/01/2000–2001)

Role of catecholamines and β-receptors in ventilatory response during hypoxic exercise

The ventilatory response to moderate exercise in hypoxia is potentiated in goats, decreasing Pa CO 2 more than in normoxic exercise. We investigated the hypothesis that this potentiation results from a ventilatory stimulus provided by increased levels of circulating catecholamines (norepinephrine and/or epinephrine), acting via β-receptors. Plasma norepinephrine [NE] and epinephrine [E] concentrations, arterial blood gases and ventilation were measured in normoxia and hypoxia ( Pa O 2 = 34–38 Torr ) at rest and during moderate exercise (5.6 kph; 5% grade) in seven female goats. Pa CO 2 decreased from rest to exercise in normoxia ( 2.9 ± 0.7 Torr; P < 0.01 ), and decreased significantly more from rest during hypoxic exercise ( 6.4 ± 0.6 Torr; P < 0.01 ). [NE] increased in both normoxic ( 1.1 ± 0.4 ng/ml; P < 0.05 ) and hypoxic exercise ( 2.5 ± 0.5 ng/ml; p < 0.01 ); the [NE] increase in hypoxia was significantly greater ( P < 0.01). [E] increased in normoxic ( 0.3 ± 0.1 ng/ml; P < 0.05 ) but not hypoxic exercise ( 0.6 ± 0.5 ng/ml; P > 0.2 ). Experiments were repeated following administration of the β-adrenergic receptor blocker, propranolol (2 mg/kg, i.v.). After β-blockade, Pa CO 2 decreases from rest to exercise in normoxia ( 3.2 ± 0.7 Torr; P < 0.01 ) and hypoxia ( 8.1 ± 0.7 Torr; P < 0.001 ) were not significantly different from control. The data indicate that β-adrenergic receptor stimulation is not necessary for a greater decrease in Pa CO 2 during hypoxic versus normoxic exercise. The greater rise in [NE] suggests a possible role in ventilatory control during hypoxic exercise, perhaps via α-adrenergic receptors. However, recent evidence suggests that NE is inhibitory in goats, and that NE is unlikely to mediate extra ventilatory stimulation during hypoxic exercise.