Aurélien Pichon

Interchangeability between heart rate and photoplethysmography variabilities during sympathetic stimulations

Photoplethysmography variability (PPGV) is currently considered to be a good surrogate to heart rate variability (HRV) measurements using the time between two pulse waves instead of RR intervals. Nevertheless, the interchangeability between HRV and PPGV has never been evaluated in situations with severe alterations in the autonomic nervous system (ANS). We aimed to identify the conditions for a correct utilization of PPGV in evaluating the consequences of sympathetic stimulations. Nine subjects performed three tests: active orthostatic test, slow walk and moderate and exhaustive cycling exercises in the supine position. Pulse waves at the fingertip and RR intervals were recorded at the same time. We used correlations and the Bland and Altman method to compare and evaluate interchangeability between several HRV indices. Bland and Altman analysis highlighted small discrepancies between PPGV and HRV for all HRV indices in the supine position and for LF(ms)(2), HF(ms)(2), LF(peak) and RMSSD in the upright position. During the slow walk, it was impossible to detect properly PPG peaks. We observed large differences between the two methods during the cycling exercise. In conclusion, PPGV can be used instead of HRV without reserve in the supine position but only for some HRV indices in the upright position and not during slow walk and cycling exercise.

Polar Activity Watch 200: a new device to accurately assess energy expenditure

Objectives Energy expenditure (EE) based on movement detection is calculated by a new device, the Activity Watch 200 (AW200). The aim of this study was to validate EE measured by this device against indirect calorimetry (IC) and to assess the reproducibility of AW200 measurements. Design EE was assessed during a 9.7 km hike. 10 men and 10 women in the age range 35–45 years, and 5 men and 6 women in the age range 50–55 years were tested. One in five participants of each age- and sex-matched group was equipped with a portable metabograph (Oxycon Mobil) for IC measurements. Data were collected every 30 min during the hike, and IC was extrapolated for the remaining four other participants of the group. Results During the total hike, there was a high correlation between EE obtained from the AW200 and the IC calculation (r = 0.987, p<0.001). Identical values of EE were calculated by both methods during the first 90 min of the hike. However, EE calculated by the AW200 at 120 min and at the end of the hike was lower (p<0.05). Bland–Altman analysis showed limits of agreements between 105 and 279 kJ after 30 and 120 min, respectively. EE measured by the AW200 was well correlated with IC measurements, and limits of agreement between devices were below 10% of the measured values for hike durations longer than 60 min. Conclusion The AW200 appears to be a very useful and accurate device for measuring EE during exercise in recreational hikers and provides a useful tool for keeping track of personal EE.

Cerebral adaptations to chronic anemia in a model of Erythropoietin deficient mice exposed to hypoxia

Anemia and hypoxia in rats result in an increase in factors potentially involved in cerebral angiogenesis. Therefore, the aim of this study was to assess the effect of chronic anemia and/or chronic hypoxia on cerebral cellular responses and angiogenesis in wild-type and anemic transgenic mice. These studies were done in erythropoietin-deficient mice (Epo-TAg(h)) in normoxia and following acute (one day) and chronic (14 days, barometric pressure = 420 mmHg) hypoxia. In normoxia, Epo-TAg(h) mice showed an increase in transcript and protein levels of hypoxia-inducible factor 1alpha (HIF-1alpha), vascular endothelial growth factor (VEGF), erythropoietin receptors (EpoR), phospho-STAT-5/STAT-5 ratio, and neuronal neuronal nitric oxide synthase (nNOS) along with a higher cerebral capillary density. In wild-type (WT) mice, acute hypoxia increased all of the studied factors, while in chronic hypoxia, HIF-1alpha, EpoR, phospho-STAT-5/STAT-5 ratio, nNOS, and inducible NOS remained elevated, with an increase in capillary density. Surprisingly, in Epo-TAg(h) mice, chronic hypoxia did not further increase any factor except the nitric oxide metabolites, while HIF-1alpha, EpoR, and phospho-STAT-5/STAT-5 ratio were reduced. Normoxic Epo-TAg(h) mice developed cerebral angiogenesis through the HIF-1alpha/VEGF pathway. In acute hypoxia, WT mice up-regulated all of the studied factors, including cerebral NO. Polycythemia and angiogenesis occurred with acclimatization to chronic hypoxia only in WT mice. In Epo-TAg(h), the decrease in HIF-1alpha, VEGF proteins, and phospho-STAT-5 ratio in chronic hypoxia suggest that neuroprotective and angiogenesis pathways are altered.

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.

Cardiac output during exercise: A comparison of four methods

Several techniques assessing cardiac output (Q) during exercise are available. The extent to which the measurements obtained from each respective technique compares to one another, however, is unclear. We quantified Q simultaneously using four methods: the Fick method with blood obtained from the right atrium (QFick‐M), Innocor (inert gas rebreathing; QInn), Physioflow (impedance cardiography; QPhys), and Nexfin (pulse contour analysis; QPulse) in 12 male subjects during incremental cycling exercise to exhaustion in normoxia and hypoxia (FiO2 = 12%). While all four methods reported a progressive increase in Q with exercise intensity, the slopes of the Q/oxygen uptake (VO2) relationship differed by up to 50% between methods in both normoxia [4.9 ± 0.3, 3.9 ± 0.2, 6.0 ± 0.4, 4.8 ± 0.2 L/min per L/min (mean ± SE) for QFick‐M, QInn, QPhys and QPulse, respectively; P = 0.001] and hypoxia (7.2 ± 0.7, 4.9 ± 0.5, 6.4 ± 0.8 and 5.1 ± 0.4 L/min per L/min; P = 0.04). In hypoxia, the increase in the Q/VO2 slope was not detected by Nexfin. In normoxia, Q increases by 5–6 L/min per L/min increase in VO2, which is within the 95% confidence interval of the Q/VO2 slopes determined by the modified Fick method, Physioflow, and Nexfin apparatus while Innocor provided a lower value, potentially reflecting recirculation of the test gas into the pulmonary circulation. Thus, determination of Q during exercise depends significantly on the applied method.

Long-term ventilatory adaptation and ventilatory response to hypoxia in plateau pika (Ochotona curzoniae): role of nNOS and dopamine

We assessed ventilatory patterns and ventilatory responses to hypoxia (HVR) in high-altitude (HA) plateau pikas, repetitively exposed to hypoxic burrows, and control rats. We evaluated the role of neuronal nitric oxide synthase (nNOS) and dopamine by using S-methyl-l-thiocitrulline (SMTC) inhibitor and haloperidol antagonist, respectively. Ventilation (Vi) was measured using a whole body plethysmograph in conscious pikas (n = 9) and low-altitude (LA) rats (n = 7) at different Pi(O(2)) (56, 80, 111, 150, and 186 mmHg) and in HA acclimatized rats (n = 9, 8 days at 4,600 m) at two different Pi(O(2)) (56 and 80 mmHg). The effects of NaCl, SMTC, and haloperidol on ventilatory patterns were assessed in pikas at Pi(O(2)) = 56 and 80 mmHg. We observed a main species effect with larger Vi, tidal volume (VT), inspiratory time/total time (T(i)/T(tot)), and a lower expiratory time in pikas than in LA rats. Pikas had also a larger VT and lower respiratory frequency compared with HA rats in hypoxia. HVR of pikas and rats were not statistically different. In pikas, SMTC induced a significant increase in Vi and VT for a Pi(O(2)) of 56 mmHg, but had no effect for a PiO(2) of 80 mmHg, i.e., the living altitude of pikas. In pikas, haloperidol injection had no effect on any ventilatory parameter. Long-term ventilatory adaptation in pikas is mainly due to an improvement in respiratory pattern (VT and T(i)/T(tot)) with no significant improvement in HVR. The sensitivity to severe acute hypoxia in pikas seems to be regulated by a peripheral nNOS mechanism.

The role of haemoglobin mass on VO 2 max following normobaric 'live high-train low' in endurance-trained athletes

It remains unclear by which mechanism ‘live high–train low’ (LHTL) altitude training increases exercise performance. Haematological and skeletal muscle adaptations have both been proposed. To test the hypotheses that (i) LHTL improves maximal oxygen uptake (VO2max) and (ii) this improvement is related to hypoxia-induced increases in total haemoglobin mass (Hbmass) and not to improved maximal oxidative capacity of skeletal muscle, we determined VO2max before LHTL and after LHTL, before and after the altitude-induced increases in Hbmass (measured by carbon-monoxide rebreathing) had been abolished by isovolumic haemodilution. We obtained skeletal muscle biopsies to quantify mitochondrial oxidative capacity and efficiency. Sixteen endurance-trained athletes were assigned (double-blinded, placebo controlled) to ≥16 h/day over 4 weeks to normoxia (placebo, n=6) or normobaric hypoxia equivalent to 3000 m altitude (LHTL, n=10). Four-week LHTL did not increase VO2max, irrespective of treatment (LHTL: 1.5%; placebo: 2.0%). Hbmass was slightly increased (4.6%) in 5 (of 10) LHTL subjects but this was not accompanied by a concurrent increase in VO2max. In the subjects demonstrating an increase in Hbmass, isovolumic haemodilution elicited a 5.8% decrease in VO2max. Cycling efficiency was altered neither with time nor by LHTL. Neither maximal capacity of oxidative phosphorylation nor mitochondrial efficiency was modified by time or LHTL. The present results suggest that LHTL has no positive effect on VO2max in endurance-trained athletes because (i) muscle maximal oxidative capacity is not improved following LHTL and (ii) erythrocyte volume expansion after LHTL, if any, is too small to alter O2 transport.

Blood viscosity and hemodynamics during exercise

We tested the effects of submaximal exercise on blood viscosity (η(b)), nitric oxide production (NO) and hemodynamics. Relationships between the exercise-induced changes that occurred in these parameters were investigated. Nine subjects performed exercise for 15 min at 105% of the first ventilatory threshold. Mean arterial pressure (MAP) and cardiac output (Qc) were measured, allowing the determination of systemic vascular resistance (SVR). Blood was sampled at rest and at the end of exercise. The η(b) was determined at high shear rate and was used to calculate systemic vascular hindrance (VH). NO production was estimated by measuring plasma concentrations of NO stable end products (NOx). Qc, MAP, η(b) and NOx, increased with exercise, whereas SVR and VH decreased. The changes between rest and exercise were calculated and tested for correlations. We observed: 1) a positive correlation between the increase in η(b) and the increase in NOx; 2) a negative correlation between the increase in NOx and the decrease in VH; 3) a negative correlation between the increase in η(b) and the decrease in SVR. Although the increase in Qc and blood flow during exercise probably promoted NO production due to shear dependent stimulation of the endothelium, the present results also support that the rise in η(b) during exercise may be necessary for NO production and adequate vasodilation.

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.

Swimmers can train in hypoxia at sea level through voluntary hypoventilation.

This study used an innovative technique of pulse oximetry to investigate whether swimmers can train under hypoxic conditions through voluntary hypoventilation (VH). Ten trained subjects performed a front crawl swimming series with normal breathing (NB), VH at high (VHhigh) and low pulmonary volume (VHlow). Arterial oxygen saturation was continuously measured via pulse oximetry (SpO2) with a waterproofed forehead sensor. Gas exchanges were recorded continuously and lactate concentration ([La]) was assessed at the end of each test. In VHlow, SpO2 fell down to 87% at the end of the series whereas it remained above 94% in VHhigh during most part of the series. Ventilation, oxygen uptake and end-tidal O2 pressure were lower in both VHhigh and VHlow than in NB. Compared to NB, [La] significantly increased in VHlow and decreased in VHhigh. This study demonstrated that swimmers can train under hypoxic conditions at sea level and can accentuate the glycolytic stimulus of their training if they perform VH at low but not high pulmonary volume.