Pascal Mollard

The Ergogenic Effect of Recombinant Human Erythropoietin on V̇O2max Depends on the Severity of Arterial Hypoxemia

Treatment with recombinant human erythropoietin (rhEpo) induces a rise in blood oxygen-carrying capacity (CaO2) that unequivocally enhances maximal oxygen uptake (V̇O2max) during exercise in normoxia, but not when exercise is carried out in severe acute hypoxia. This implies that there should be a threshold altitude at which V̇O2max is less dependent on CaO2. To ascertain which are the mechanisms explaining the interactions between hypoxia, CaO2 and V̇O2max we measured systemic and leg O2 transport and utilization during incremental exercise to exhaustion in normoxia and with different degrees of acute hypoxia in eight rhEpo-treated subjects. Following prolonged rhEpo treatment, the gain in systemic V̇O2max observed in normoxia (6–7%) persisted during mild hypoxia (8% at inspired O2 fraction (FIO2) of 0.173) and was even larger during moderate hypoxia (14–17% at FIO2 = 0.153–0.134). When hypoxia was further augmented to FIO2 = 0.115, there was no rhEpo-induced enhancement of systemic V̇O2max or peak leg V̇O2. The mechanism highlighted by our data is that besides its strong influence on CaO2, rhEpo was found to enhance leg V̇O2max in normoxia through a preferential redistribution of cardiac output toward the exercising legs, whereas this advantageous effect disappeared during severe hypoxia, leaving augmented CaO2 alone insufficient for improving peak leg O2 delivery and V̇O2. Finally, that V̇O2max was largely dependent on CaO2 during moderate hypoxia but became abruptly CaO2-independent by slightly increasing the severity of hypoxia could be an indirect evidence of the appearance of central fatigue.

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

During moderate exercise breathing a low inspired O2 fraction (FIO2), arterial O2 desaturation may depend on the fitness level. Seven trained (TM) and seven untrained men (UTM) cycled in normoxia and in hypoxia (FIO2=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. O2 saturation was not different between groups at sea level. In hypoxia, O2 saturation was lower in TM than in UTM at FIO2=0.154 (87.3 ± 2.9% vs 90.4 ± 1.5% at 90 W) and below. Both the ventilatory‐equivalent and the end‐tidal O2 pressure were lower in TM at sea level and at every FIO2, with the differences between TM and UTM becoming apparent at lower exercise intensity and increasing in magnitude as the severity of hypoxia increased. O2 saturation was correlated with the ventilatory parameters at every FIO2 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.

Validity of arterialized earlobe blood gases at rest and exercise in normoxia and hypoxia

The purpose of this study was to compare arterial and arterialized blood gases during normoxic and hypoxic exercise. In the same conditions, earlobe pulse oximetry O(2) saturation (Sp(O2)) was compared to arterial oxygen saturation (Sa(O2)). Ten men performed incremental cycle ergometer tests, in normoxia and hypoxia (FI(O2) = 0.127). Blood samples were drawn simultaneously from the radial artery and pre-warmed earlobe capillary blood of subjects at rest, submaximal and near maximal exercise. R(2) between the two samples were 0.99 for P(O2) and S(O2), 0.86 for P(CO2) and 0.97 between Sp(O2) and Sa(O2). Earlobe P(O2) mean was 4.4+/-3.6 mmHg lower than Pa(O2) in normoxia but in hypoxia only 1.1+/-2.2 mmHg low. The mean difference were low in normoxia between Sa(O2) and Sp(O2) and increased in hypoxia, were acceptable for P(CO2), S(O2), pH in all conditions. In conclusion, except for P(O2) in normoxia, pre-warmed earlobe capillary blood is a good substitute to arterial blood to allow measurement of blood gas values in normoxia and hypoxia at rest and exercise.

Effects of a 4-week training with voluntary hypoventilation carried out at low pulmonary volumes.

This study investigated the effects of training with voluntary hypoventilation (VH) at low pulmonary volumes. Two groups of moderately trained runners, one using hypoventilation (HYPO, n=7) and one control group (CONT, n=8), were constituted. The training consisted in performing 12 sessions of 55 min within 4 weeks. In each session, HYPO ran 24 min at 70% of maximal O(2) consumption ( [V(02max)) with a breath holding at functional residual capacity whereas CONT breathed normally. A V(02max) and a time to exhaustion test (TE) were performed before (PRE) and after (POST) the training period. There was no change in V(O2max), lactate threshold or TE in both groups at POST vs. PRE. At maximal exercise, blood lactate concentration was lower in CONT after the training period and remained unchanged in HYPO. At 90% of maximal heart rate, in HYPO only, both pH (7.36+/-0.04 vs. 7.33+/-0.06; p<0.05) and bicarbonate concentration (20.4+/-2.9 mmolL(-1) vs. 19.4+/-3.5; p<0.05) were higher at POST vs. PRE. The results of this study demonstrate that VH training did not improve endurance performance but could modify the glycolytic metabolism. The reduced exercise-induced blood acidosis in HYPO could be due to an improvement in muscle buffer capacity. This phenomenon may have a significant positive impact on anaerobic performance.

Prolonged expiration down to residual volume leads to severe arterial hypoxemia in athletes during submaximal exercise.

The goal of this study was to assess the effects of a prolonged expiration (PE) carried out down to the residual volume (RV) during a submaximal exercise and consider whether it would be worth including this respiratory technique in a training programme to evaluate its effects on performance. Ten male triathletes performed a 5-min exercise at 70% of maximal oxygen consumption in normal breathing (NB(70)) and in PE (PE(70)) down to RV. Cardiorespiratory parameters were measured continuously and an arterialized blood sampling at the earlobe was performed in the last 15s of exercise. Oxygen consumption, cardiac frequency, end-tidal and arterial carbon dioxide pressure, alveolar-arterial difference for O(2) (PA(O2) - Pa(O2)) and P(50) were significantly higher, and arterial oxygen saturation (87.4+/-3.4% versus 95.0+/-0.9%, p<0.001), alveolar (PA(O2)) or arterial oxygen pressure, pH and ventilatory equivalent were significantly lower in PE(70) than NB(70). There was no difference in blood lactate between exercise modalities. These results demonstrate that during submaximal exercise, a prolonged expiration down to RV can lead to a severe hypoxemia caused by a PA(O2) decrement (r=0.56; p<0.05), a widened PA(O2) - Pa(O2) (r=-0.85; p<0.001) and a right shift of the oxygen dissociation curve (r=-0.73; p<0.001).

Non-invasive evaluation of the capillary recruitment in the human muscle during exercise in hypoxia

This study proposes a non-invasive evaluation of capillary recruitment in human muscle from resting state to maximal exercise while under hypoxic conditions. Our work is based on the analysis of oxygen transport variables measured during incremental exercise in endurance-trained men (n=8) and in their sedentary counterparts (n=8). Maximal exercise tests were performed on a cycloergometer in normoxia and at three simulated normobaric levels of hypoxia (altitude equivalent to 1000, 2500 and 4500 m). We made the assumption that the relationship between the oxygen diffusion coefficient (Kt) and cardiac output (Qc) was: Kt=kQcNc where Nc is the capillary recruitment coefficient during exercise. Our results demonstrate that Nc increases with altitude and that the increase is greater in trained compared with untrained subjects at high altitude (4500 m). Moreover, the venous PO2 threshold beyond which capillary recruitment increases is lower in trained men. Despite their greater increase in capillary recruitment, trained men are not able to compensate for their drastic drop in arterial oxygen content during exercise in acute hypoxia, which results in a greater drop in maximal oxygen consumption than in sedentary men.

'Oxygen uptake efficiency slope' in trained and untrained subjects exposed to hypoxia

We assessed the ability of the oxygen uptake efficiency slope, whether calculated on 100 and 80% of maximal exercise test duration (OUES(100) and OUES(80)), to identify the change in cardiorespiratory capacities in response to hypoxia in subjects with a broad range of V(O2 peak). Four maximal exercise tests were performed in trained (T) and untrained subjects (UT) in normoxia and at 1000, 2500 and 4500 m. The mean reductions in maximal exercise capacities at 4500 m were the same in T subjects for V(O2 peak) (-30%), OUES(80) (-26%) and OUES(100) (-26%) whereas in UT subjects only OUES(100) (-14%), but not OUES(80) (-20%), was lower compared with V(O2 peak) (-21%, p<0.05). OUES(100) and OUES(80) were correlated with V(O2 peak) and the ventilatory anaerobic threshold in both groups. Multiple regression analyses showed that V(O2 peak), OUES(100) and OUES(80) were significantly linked to O(2) arterial-venous difference. The OUES(80) could be considered as an interesting sub-maximal index of cardiorespiratory fitness in normal or hypoxemic subjects unable to reach V(O2 peak).