Biomedical subjects

Christian Denis

Publications and source records attributed to Christian Denis.

6 recordsLinked to original sources

PubMed2003

Decrease in peak heart rate with acute hypoxia in relation to sea level VO(2max).

The aim of this study was to evaluate the influence of arterial oxygen saturation ( SaO(2)) on maximal heart rate during maximal exercise under conditions of acute hypoxia compared with normoxia. Forty-six males were divided into three groups depending on their sea level maximal oxygen consumption ( VO(2max)): high [GH, VO(2max)=64.2 (3.3) ml x min(-1) x kg(-1)], medium [GM, 50.8 (3.9) ml x min(-1) x kg(-1)] and low [GL, 41.0 (1.9) ml x min(-1) x kg(-1)]. All subjects performed a maximal exercise test in two conditions of inspired oxygen tension ( PIO(2), (149 mmHg and 70 mmHg). Among the GM group, seven subjects performed five supplementary incremental exercise tests at PIO(2) 136, 118, 104, 92, and 80 mmHg. Measurements of VO(2max) and SaO(2) using an ear-oxymeter were carried out at all levels of PIO(2). The decrease in SaO(2 )and peak heart rate (HR(peak)) with PIO(2) became significant from 104 and 92 mmHg. SaO(2) correlated with the decrease in HR(peak). For PIO(2)=70 mmHg, the decrease in VO(2max), SaO(2) and HR(peak) was, respectively, 44%, 62%, and 17.0 bpm for GH, 38%, 68%, and 14.7 bpm for GM, and 34%, 68%, and 11.8 bpm for GL. During maximal exercise in hypoxia, SaO(2) was lower for GH than GM and GL ( p<0.01). Among subjects in GH, five presented exercise-induced hypoxemia (EIH) when exercising in normoxia. The EIH group exhibited a greater decrement in HR(peak) than the non-EIH group at maximal hypoxic exercise (21.2 bpm vs. 15.0 bpm; p<0.05). When subjects are exposed to acute hypoxia, the lower SaO(2), due either to lower PIO(2) or to training status, is associated with lower HR(peak).

Acute Disease↗

PubMed2003

Effects of endurance training on satellite cell frequency in skeletal muscle of old men.

We investigated the effects of endurance training on satellite cells, which are a major component of the regenerative capacity of muscles. Muscle biopsies were obtained from the vastus lateralis of 11 men aged between 70 and 80 years who trained for 14 weeks (work load corresponding to 65-95% of peak oxygen consumption, VO(2) peak). Satellite cells were identified by immunohistochemistry. There was a significant increase in satellite cell number. Additionally, VO(2) peak, citrate synthase activity, and the area of type IIA fibers were significantly increased. Fiber type distribution and the myonuclear number were not significantly affected. The enhancement of satellite cell frequency and fiber area indicate that endurance training is an efficient strategy to improve muscle function in the elderly.

Aged↗

PubMed2003

A methodology to assess the accuracy of a portable metabolic system (VmaxST).

PURPOSE: Validity of a portable metabolic system (VmaxST) was investigated during gas exchanges simulations by a mechanical system (GESS) and during human exercise. METHODS: Three tests were conducted while gas exchanges were measured continuously by VmaxST. Test 1 was composed of six simulations of gas exchanges during steady-state exercise (20 min at V̇E = 80 L.min-1). Test 2 was composed of seven simulations of gas exchanges during incremental exercise (V̇O(2) from 300 to 5600 mL.min-1). In the human trial, 11 subjects performed an incremental running exercise on a treadmill while gas exchanges were measured at the end of each stage with the Douglas bag method (DBM). RESULTS: Test 1 showed that the VmaxST measurements were stable, despite inaccurate measurements of gas concentrations at the start of the test. During test 2, the mean error (difference between measured and predicted value) and the upper and lower limits of agreement were -8.0%, -12.6%, and -3.4% for V̇O(2); -4.6%, -12.0%, and +2.8% for V̇CO(2); and -0.7%, -4.7%, and +3.3% for V̇E. During the human trial, no significant difference was shown between V̇O(2) measured by VmaxST and by DBM at any stage of exercise. The mean difference and the upper and lower limits of agreement between the VmaxST and the DBM measurements were -0.5%, -14.3%, and +13.3% for V̇O(2); -6.3%, -20.9%, and +8.3% for V̇CO(2); and -9.9%, -25.5%, and +5.7% for V̇E. CONCLUSIONS: The use of GESS showed that measurements of V̇O(2) by VmaxST could be biased in a standardized condition. In more realistic condition of use, this bias was lower but the accuracy of measurements was impaired.

Adult↗

PubMed2002

Modeling of end-tidal and arterial PCO2 gradient: comparison with experimental data.

PURPOSE: The aim of this study was to test whether a tidally ventilated homogeneous lung model can correctly describe arterial and end-tidal gas partial pressures and thus the difference in end-tidal and arterial gas partial pressures at rest and during exercise. METHODS: The implemented mathematical modeling described variations during the breathing cycle in CO2 and O2 fractions, alveolar volume, and pulmonary capillary gas exchange. Experimental data were obtained from measurements performed by 17 healthy subjects at rest and during 40, 50, 65, and 75% exercise .VO(2max) on a cycle ergometer. VO2, VCO2, and PET,CO2 were continuously measured using the MedGraphics CPX/D gas exchange system. Arterial gases were measured in brachial artery blood samples drawn simultaneously with gas exchange. Cardiac output was measured using the CO2 rebreathing method corrected by the blood sample data. The model was driven using experimental data for ventilation, VO2, VCO2, and cardiac output. RESULTS: The mean difference and the upper and lower limits of agreement between measured and simulated data were -0.004, +0.84, and -0.84 Torr for Pa,CO2; -0.06, +0.64, and -0.76 Torr for Pa,O2; -1.96, +2.84, and -6.76 Torr for PET,CO2; and +7.20, +25.80, and -11.40 Torr for PET,O2. Actual PET,CO2-Pa,CO2 difference increased significantly with workload (P < 0.0001) from 0.3 +/- 3 Torr at rest to 4.7 +/- 2.5 Torr at 75% .VO(2max). Model-simulated PET,CO2-Pa,CO2 difference also increased significantly with exercise (P < 0.0001) from 0.7 +/- 1.7 Torr at rest to 9.1 +/- 3.4 Torr at 75% .VO(2max). CONCLUSION: The lung model described actual arterial CO2 partial pressures better than variations in end-tidal CO2 partial pressures and thus better than the gradient in end-tidal arterial CO2 partial pressures.

Adult↗

PubMed2002

Assessment of arterial gas pressures and cardiac output using a breathing lung model.

PURPOSE: The aim of this investigation was to evaluate a breathing lung model to estimate arterial gas partial pressures and cardiac output at rest and during exercise. METHODS: A mathematical model was used to describe variations in gas fractions, alveolar volume, and gas exchange in the pulmonary capillaries during the breathing cycle. Experimental data were obtained from 17 healthy subjects at rest and during exercise at 40, 50, 65, and 75% VO(2max) on a cycle ergometer. VO(2), VCO(2), and P(ET,CO2) were monitored continuously with a MedGraphics CPX/D gas exchange system. Arterial gases were measured in brachial artery blood samples drawn simultaneously with gas exchange. Cardiac output was measured using the CO(2) rebreathing method corrected by the arterial blood sample data. The model parameters including cardiac output, end-expiratory alveolar volume, and mixed-venous gas contents were estimated by fitting modelVCO(2) to experimental values over 50 breaths. RESULTS: The fit of model parameters gave arterial gas partial pressures not significantly different from measured data. Measured P(a,C02) and P(a,O2) were significantly correlated with model outputs (R(2) = 0.991 for P(a,CO2) and R(2) = 0.999 for P(a, CO2); P < 0.0001). The cardiac output values estimated using the breathing lung model were significantly correlated with the values obtained with the corrected CO rebreathing method (R(2) = 0.71; P < 0.0001). There was, however, a significant 2.3 L x min(-1) difference between these two methods. CONCLUSION: Results obtained with the proposed method were in good agreement with measured arterial gas partial pressures. Despite a certain degree of bias, the promising results for cardiac output demonstrate the reliability of this method that should be now evaluated using a gold standard method.

Adult↗

PubMed2002

Mitochondrial biogenesis during skeletal muscle regeneration.

Myogenesis requires energy production for the execution of a number of regulatory and biosynthesis events. We hypothesized that mitochondrial biogenesis would be stimulated during skeletal muscle regeneration. Tibialis anterior muscles of male Sprague-Dawley rats were injected with 0.75% bupivacaine and removed at 3, 5, 7, 10, 14, 21, or 35 days after injection (n = 5-7/group). Two main periods emerged from the histochemical analyses of muscle sections and the expression of proliferating cell nuclear antigen, desmin, and creatine phosphokinase: 1) activation/proliferation of satellite cells (days 3-14) and 2) differentiation into muscle fibers (days 5-35). The onset of muscle differentiation was accompanied by a marked stimulation of mitochondrial biogenesis, as indicated by a nearly fivefold increase in citrate synthase activity and state 3 rate of respiration between days 5 and 10. Peroxisome proliferator-activated receptor-gamma coactivator-1 (PGC-1) mRNA level and mitochondrial transcription factor A (mtTFA) protein level peaked on day 10 concurrently with the state 3 rate of respiration. Therefore, transcriptional activation by PGC-1 and mtTFA may be one of the mechanisms regulating mitochondrial biogenesis in regenerating skeletal muscle. Taken together, our results suggest that mitochondrial biogenesis may be an important regulatory event during muscle regeneration.

Animals↗