PubMed Health⌕ Search

Biomedical subjects

Jean Lonsdorfer

Publications and source records attributed to Jean Lonsdorfer.

11 recordsLinked to original sources
PubMed2006

Deciphering the metabolic and mechanical contributions to the exercise-induced circulatory response: insights from eccentric cycling.

Metabolic demand and muscle mechanical tension are closely coupled during exercise, making their respective drives to the circulatory response difficult to establish. This coupling being altered in eccentric cycling, we implemented an experimental design featuring eccentric vs. concentric constant-load cycling bouts to gain insights into the control of the exercise-induced circulatory response in humans. Heart rate (HR), stroke volume (SV), cardiac output (Q), oxygen uptake (V(.-)(O(2))), and electromyographic (EMG) activity of quadriceps muscles were measured in 11 subjects during heavy concentric (heavy CON: 270 +/- 13 W; V(.-)(O(2)) = 3.59 +/- 0.20 l/min), heavy eccentric (heavy ECC: 270 +/- 13 W, V(.-)(O(2)) = 1.17 +/- 0.15 l/min), and light concentric (light CON: 70 +/- 9 W, V(.-)(O(2)) = 1.14 +/- 0.12 l/min) cycle bouts. Using a reductionist approach, the circulatory responses observed between heavy CON vs. light CON (difference in V(.-)(O(2)) and power output) was ascribed either to metabolic demand, as estimated from heavy CON vs. heavy ECC (similar power output, different V(.-)(O(2))), or to muscle mechanical tension, as estimated from heavy ECC vs. light CON (similar V(.-)(O(2)), different power output). 74% of the Q response was determined by the metabolic demand, also accounting for 65% and 84% of HR and SV responses, respectively. Consequently, muscle mechanical tension determined 26%, 35%, and 16% of the Q, HR, and SV responses, respectively. Q was significantly related to V(.-)(O(2)) (r(2) = 0.83) and EMG activity (r(2) = 0.82; both P < 0.001). These results suggest that the exercise-induced circulatory response is mainly under metabolic control and support the idea that the level of muscle activation plays a role in the cardiovascular regulation during cycle exercise in humans.

Adult↗
PubMed2006

Exercise training in normobaric hypoxia in endurance runners. I. Improvement in aerobic performance capacity.

This study investigates whether a 6-wk intermittent hypoxia training (IHT), designed to avoid reductions in training loads and intensities, improves the endurance performance capacity of competitive distance runners. Eighteen athletes were randomly assigned to train in normoxia [Nor group; n = 9; maximal oxygen uptake (VO2 max) = 61.5 +/- 1.1 ml x kg(-1) x min(-1)] or intermittently in hypoxia (Hyp group; n = 9; VO2 max = 64.2 +/- 1.2 ml x kg(-1) x min(-1)). Into their usual normoxic training schedule, athletes included two weekly high-intensity (second ventilatory threshold) and moderate-duration (24-40 min) training sessions, performed either in normoxia [inspired O2 fraction (FiO2) = 20.9%] or in normobaric hypoxia (FiO2) = 14.5%). Before and after training, all athletes realized 1) a normoxic and hypoxic incremental test to determine VO2 max and ventilatory thresholds (first and second ventilatory threshold), and 2) an all-out test at the pretraining minimal velocity eliciting VO2 max to determine their time to exhaustion (T(lim)) and the parameters of O2 uptake (VO2) kinetics. Only the Hyp group significantly improved VO2 max (+5% at both FiO2, P < 0.05), without changes in blood O2-carrying capacity. Moreover, T(lim) lengthened in the Hyp group only (+35%, P < 0.001), without significant modifications of VO2 kinetics. Despite similar training load, the Nor group displayed no such improvements, with unchanged VO2 max (+1%, nonsignificant), T(lim) (+10%, nonsignificant), and VO2 kinetics. In addition, T(lim) improvements in the Hyp group were not correlated with concomitant modifications of other parameters, including VO2 max or VO2 kinetics. The present IHT model, involving specific high-intensity and moderate-duration hypoxic sessions, may potentialize the metabolic stimuli of training in already trained athletes and elicit peripheral muscle adaptations, resulting in increased endurance performance capacity.

Adaptation, Physiological↗
PubMed2005

Ventilation efficiency and pulmonary function after a wheelchair interval-training program in subjects with recent spinal cord injury.

OBJECTIVE: To study the effect of a wheelchair interval-training program on the ventilatory function of subjects with recent spinal cord injury (SCI). DESIGN: Evaluation trial before and after a training program. SETTING: Center of reeducation and university hospital. PARTICIPANTS: Six subjects (5 men, 1 woman) hospitalized after a recent SCI. INTERVENTION: On a wheelchair ergometer, subjects with SCI performed 30 minutes of interval training 3 times a week for 6 weeks. The training program was part of their reeducation program. MAIN OUTCOME MEASURES: Spirometric values at rest and dynamic ventilatory responses were studied before and after this training program with a spirometric test, a maximal exercise test that increased by 5W every 2 minutes, and a submaximal test. RESULTS: Spirometric values at rest did not change after training. At maximal exercise, peak ventilation (Vepeak, 7.5%), peak breathing frequency (f peak) (-13.4%), peak tidal volume (Vtpeak +28.9%), and the ventilatory reserve (12.9%) improved after training. The oxygen cost of Ve decreased significantly (-20%) after training. We observed for the wheelchair tests that, at the same workload after training, Ve and f decreased and Vt increased. CONCLUSIONS: After 6 weeks of our interval-training program in subjects with recent SCI, the increase of Vt and the decrease of oxygen cost of Ve indicated better ventilatory efficiency.

Ergometry↗
PubMed2005

Exercising with a denervated heart after cardiac transplantation.

Heart transplantation (HTR) is now an accepted life-extending procedure for those dying of intractable heart failure (CHF). HTR patients expect a high quality of life which implies a reasonable exercise capacity. Nevertheless HTR present unique exercise challenges with both central and peripheral factors of limitation that result in peak oxygen uptakes of 60-70% of age-matched normal subjects. Among central factors persistent chronotropic incompetence questions the occurrence and role of the graft reinnervation. Among peripheral factors the energetic impairement of the skeletal muscle seem to result more from microvascular abnormalities than from an actual deficit in oxidative capacity, questioning the mechanism of recovery from the CHF peripheral myopathy and the role of immunosuppressive drugs. Endurance and resistance training programs may reverse at least in part most but not all of these abnormalities. Training permits patients to engage in sports and even to participate in competitive events that are rewarding to them but also to the community because it promotes organ donation and confidence in medical achievements. Mechanisms of exercise impairments and improvements resulting from training are discussed in the perspective of current literature. Areas of future research and recommendations for the practice of sports after HTR are suggested.

Exercise↗
PubMed2004

Cardiac output and oxygen release during very high-intensity exercise performed until exhaustion.

Our objectives were firstly, to study the patterns of the cardiac output (Q(.)) and the arteriovenous oxygen difference [(a-nu(-))O(2)] responses to oxygen uptake (V(.)O(2)) during constant workload exercise (CWE) performed above the respiratory compensation point (RCP), and secondly, to establish the relationships between their kinetics and the time to exhaustion. Nine subjects performed two tests: a maximal incremental exercise test (IET) to determine the maximal V(.)O(2) (V(.)O(2)peak), and a CWE test to exhaustion, performed at p Delta50 (intermediate power between RCP and V(.)O(2)peak). During CWE, V(.)O(2) was measured breath-by-breath, Q(.) was measured beat-by-beat with an impedance device, and blood lactate (LA) was sampled each minute. To calculate ( a-nu(-)O(2), the values of V(.)O(2) and Q(.) were synchronised over 10 s intervals. A fitting method was used to describe the V(.)O(2), Q(.) and ( a-nu(-))O(2) kinetics. The ( a-nu(-)O(2) difference followed a rapid monoexponential function, whereas both V(.)O(2) and Q(.) were best fitted by a single exponential plus linear increase: the time constant (tau) V(.)O(2) [57 (20 s)] was similar to tau ( a-nu(-)O(2), whereas tau for Q(.) was significantly higher [89 (34) s, P <0.05] (values expressed as the mean and standard error). LA started to increase after 2 min CWE then increased rapidly, reaching a similar maximal value as that seen during the IET. During CWE, the rapid component of V(.)O(2) uptake was determined by a rapid and maximal ( a-nu(-)O(2) extraction coupled with a two-fold longer Q(.) increase. It is likely that lactic acidosis markedly increased oxygen availability, which when associated with the slow linear increase of Q(.), may account for the V(.)O(2) slow component. Time to exhaustion was larger in individuals with shorter time delay for ( a-nu(-)O(2) and a greater tau for Q(.).

Adult↗
PubMed2004

Intermittent exercise test in chronic obstructive pulmonary disease patients: how do the pulmonary hemodynamics adapt?

PURPOSE: Endurance training is an important component of rehabilitation in patients with chronic obstructive pulmonary disease (COPD). In our study, we investigated the pulmonary hemodynamics' adaptation during a high-intensity intermittent exercise in such patients. METHODS: Eight patients underwent a 30-min exercise, alternating a 4-min work set at their first ventilatory threshold with a 1-min exercise set at 90% of their maximal tolerated power output. Pulmonary arterial pressure was measured by means of a right heart catheter. Cardiac output was calculated using the Fick's principle applied to oxygen. RESULTS: VO(2), cardiac output, and ventilation increased during the first minutes of exercise and remained stable thereafter. Heart rate increased significantly and progressively to its maximal value from rest to the end of the test (P < 0.001). After an initial increase, stroke volume decreased significantly (P < 0.05). Pulmonary arterial pressure increased from rest (mean +/- SEM 23.9 +/- 2.1 mm Hg) to the fifth minute of exercise (41.6 +/- 2.8 mm Hg), and decreased significantly thereafter (35.2 +/- 3.3 mm Hg at the 30th minute) (P < 0.001). Total pulmonary vascular resistance decreased from rest to the end of the test (P < 0.001). CONCLUSION: The high-intensity 1-min bouts of work of our intermittent work exercise are well tolerated without pushing the pulmonary arterial pressure dramatically high in COPD patients.

Adaptation, Physiological↗
PubMed2003

Preserved response of mitochondrial function to short-term endurance training in skeletal muscle of heart transplant recipients.

OBJECTIVES: We sought to determine whether intrinsic mitochondrial function and regulation were altered in heart transplant recipients (HTRs) and to investigate the response of mitochondrial function to six-week endurance training in these patients. BACKGROUND: Despite the normalization of central oxygen transport during exercise, HTRs are still characterized by limited exercise capacity, which is thought to result from skeletal muscle metabolic abnormalities. METHODS: Twenty HTRS agreed to have vastus lateralis biopsies and exercise testing: before and after training for 12 of them and before and after the same control period for eight subjects unwilling to train. Mitochondrial respiration was evaluated on saponin-permeabilized muscle fibers in the absence or presence (maximum respiration rate [V(max)]) of saturating adenosine diphosphate. RESULTS: Mitochondrial function was preserved at the level of sedentary subjects in untrained HTRs, although they showed 28 +/- 5% functional aerobic impairment (FAI). After training, V(max), citrate synthase, cytochrome c oxidase, and mitochondrial creatine kinase (CK) activities were significantly increased by 48%, 40%, 67%, and 53%, respectively (p < 0.05), whereas FAI decreased to 12 +/- 5% (p < 0.01). The control of mitochondrial respiration by creatine and mitochondrial CK was also improved (p < 0.01), suggesting that phosphocreatine synthesis and transfer by the mitochondrial CK become coupled to oxidative phosphorylation, as shown in trained, healthy subjects. CONCLUSIONS: In HTRs, the mitochondrial properties of skeletal muscle were preserved and responded well to training, reaching values of physically active, healthy subjects. This suggests that, in HTRs, immunosuppressive drugs do not alter the intrinsic muscle oxidative capacities and that the patients' physical handicap results from nonmitochondrial mechanisms.

Cell Respiration↗
PubMed2003

Pulmonary hemodynamics during a strenuous intermittent exercise in healthy subjects.

PURPOSE: It has been suggested that an intermittent work exercise test (IWET) is as efficient but better tolerated than continuous exercise for rehabilitation. Although systemic and pulmonary cardiovascular adjustments have been investigated for continuous exercise, it has not been done for IWET with exercise bouts near maximal work rate. METHODS: In seven healthy subjects, the pulmonary hemodynamics have been studied by the aid of heart catheterization during a strenuous 30-min bicycle IWET where a 4-min work set at the first ventilatory threshold (VT1) alternated with a 1-min work set at the second ventilatory threshold (VT2). RESULTS: During the IWET, cardiac output increased then remained stable with decreasing stroke volume and increasing heart rate, which became near maximal at the end of the test. Mean pulmonary arterial pressure increased from rest to the fifth minute of exercise and decreased significantly thereafter (P<0.01). An identical evolution was observed for mean systemic arterial pressure (SAP). CONCLUSION: Pulmonary hemodynamics adapt well in healthy subjects during a strenuous IWET despite the performance of exercise bouts of near maximal intensity.

Adult↗
PubMed2002

Mitochondrial respiratory chain function in skeletal muscle of ALS patients.

Evidence implicating mitochondrial dysfunction in the central nervous system of patients with sporadic amyotrophic lateral sclerosis (SALS) has recently been accumulating. In contrast, data on mitochondrial function in skeletal muscle in SALS are scarce and controversial. We investigated the in situ properties of muscle mitochondria in patients with early-stage SALS and sedentary (SED) controls using the skinned fiber technique to determine whether respiration of muscle tissue is altered in early-stage SALS in comparison with SED. Musculus vastus lateralis biopsies were obtained from 7 SED group members and 14 patients with early-stage SALS (mean disease duration, 9 months). Muscle fibers were permeabilized with saponine and then skinned and placed in an oxygraphic chamber to measure basal (V(0)) and maximal (V(max)) adenosine diphosphate-stimulated respiration rates and to assess mitochondrial regulation by adenosine diphosphate. Muscle oxidative capacity, evaluated with V(max), was identical in patients in the SALS and SED groups (V(0): SALS, 1.1 +/- 0.1; SED, 0.8 +/- 0.1, micromol 0(2). min(-1). gm(-1)dw and V(max): SALS, 3.1 +/- 0.3; SED, 2.5 +/- 0.3, micromol 0(2). min(-1). gm(-1)dw). This study shows an absence of large mitochondrial damage in skeletal muscle of patients with early-stage SALS, suggesting that mitochondrial dysfunction in the earlier stages of SALS is almost certainly not systemic.

Amyotrophic Lateral Sclerosis↗