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Biomedical subjects

F Piquard

Publications and source records attributed to F Piquard.

At least 19 recordsLinked to original sources
PubMed2006

Chronic L-arginine supplementation enhances endurance exercise tolerance in heart failure patients.

The purpose of the study was to determine the potential beneficial effect of six weeks oral L-arginine supplementation (LAS) on endurance exercise, an important determinant of daily-life activity in patients with chronic stable heart failure (CHF). After an initial incremental maximal exercise test, CHF patients performed an identical thirty-minute interval endurance exercise test before and after six weeks with (L-arginine group; ARG) or without LAS (control group; CTL). Hemodynamic, respiratory, and metabolic parameters were determined at rest, during exercise, and during recovery. Mean heart rate decreased throughout exercise and recovery after LAS (- 8.2 +/- 1.4 b x min(-1); p = 0.003 and - 6.7 +/- 1.6 b x min(-1); p < 0.001, respectively), systemic blood pressure and respiratory parameters remaining unchanged. Resting L-argininaemia increased from 102 +/- 11 to 181 +/- 37 micromol x l(-1) (p < 0.004) and exercise-induced peak increase in plasma lactate was blunted after LAS (4.13 +/- 0.75 vs. 3.13 +/- 0.39 mmol x l(-1); p = 0.02). No significant change was observed in the control group. In heart failure patients, six weeks oral LAS enhances endurance exercise tolerance, reducing both heart rate and circulating lactates. This suggests that chronic LAS might be useful as a therapeutic adjuvant in order to improve the patient's physical fitness.

Administration, Oral↗
PubMed2006

Relationship between very high physical activity energy expenditure, heart rate variability and self-estimate of health status in middle-aged individuals.

In middle-aged persons, moderate physical activity energy expenditure (PAEE) has been shown to be associated with increased vagal-related heart rate variability (HRV) indexes and better health status. The purpose of this study was to determine whether a very high PAEE has greater effect on vagal-related HRV indexes and self-estimates of well-being in middle-aged subjects having distinct long-term physical activity profiles. Forty-four subjects were divided into three groups on the basis of the sport score of the Modified Baecke Questionnaire for Older Adults: sedentary (SED, n = 15), moderately-trained (MT, n = 16), and highly-trained subjects (HT, n = 13). PAEE was estimated by triaxial accelerometry during one week. Time and frequency domain HRV indexes were determined during quiet periods in the morning on 5-min R-R interval segments under controlled breathing. Quality of life was evaluated using the SF-36 health survey questionnaire. PAEE was significantly different for each group (374.5 +/- 13.8, 616.8 +/- 22.4, and 1086.6 +/- 43.2 kcal . day (-1) for SED, MT, and HT, respectively, p < 0.001). MT presented significantly higher vagal-related HRV indexes than SED and HT (p < 0.05). None of the HRV indexes was significantly greater in HT than in SED. MT and HT had similar health status scores, which were significantly higher than for SED. These results indicate that in middle-aged subjects, habitual moderate PAEE is associated with greater vagal tone and self-estimates of well-being compared to low PAEE. In contrast, very high PAEE is associated with similar vagal-related indexes as low PAEE, despite better overall health status.

Aging↗
PubMed2005

Acute myocardial ischaemia induces specific alterations of ventricular mitochondrial function in experimental pigs.

AIMS: As cardiac metabolic flexibility is crucial, this study examined whether acute ischaemia can induce specific qualitative alterations of the mitochondrial metabolic pathways as well as energy transfer systems. METHODS: Left descending coronary artery ligation was performed after sternotomy in eight pigs and the heart was excised after 45 min of ischaemia. Maximal O2 uptake (V(max), micromol O2 min(-1) g(-1) dry weight) of saponin-skinned myofibres were measured from ischaemic and non-ischaemic area of ventricular myocardium. RESULTS: V(max) decreased by approximately 20% in ischaemic myocardium with both glutamate-malate (18.1 +/- 1.3 vs. 22.1 +/- 1.7 in control, P < 0.05) and pyruvate substrates (19.3 +/- 1.0 vs. 23.3 +/- 2.0 in control, P < 0.05) whereas no difference was observed with palmitoyl carnitine (15.6 +/- 1.8 vs. 16.6 +/- 0.9 in control). The K(m) of mitochondrial respiration for ADP decreased in ischaemic heart by 24% (679 +/- 79 vs. 899 +/- 84 microm of ADP in control, P < 0.05). Moreover, the mitochondrial creatine kinase efficacy (K(m) without creatine/K(m) with creatine), representative of the coupling of oxidative phosphorylation process with the mitochondrial creatine kinase, was reduced in ischaemic heart (11.6 +/- 2.5 in ischaemic vs. 18.0 +/- 2.2 in control, P < 0.05). CONCLUSIONS: These findings argue for specific mitochondrial impairments at the level of pyruvate oxidation and creatine kinase channelling system after an acute period of in vivo ischaemia, whereas the lipid mitochondrial oxidation pathway seems to be preserved. Such a loss of metabolic flexibility following acute ischaemia could become an early feature of metabolic dysregulation of the heart.

Adenosine Diphosphate↗
PubMed2004

Effects of increased training load on vagal-related indexes of heart rate variability: a novel sleep approach.

There is little doubt that moderate training improves cardiac vagal activity and thus has a cardioprotective effect against lethal arrhythmias. Our purpose was to learn whether a higher training load would further increase this beneficial effect. Cardiac autonomic control was inferred from heart rate variability (HRV) and analyzed in three groups of young subjects (24.5 +/- 3.0 yr) with different training states in a period free of stressful stimuli or overload. HRV was analyzed in 5-min segments during slow-wave sleep (SWS, a parasympathetic state that offers high electrocardiographic stationarity) and compared with data collected during quiet waking periods in the morning. Sleep parameters, fatigue, and stress levels checked by questionnaire were identical for all three groups with no signs of overtraining in the highly trained (HT) participants. During SWS, a significant (P <0.05) increase in absolute and normalized vagal-related HRV indexes was observed in moderately trained (MT) individuals compared with sedentary (Sed) subjects; this increase did not persist in HT athletes. During waking periods, most of the absolute HRV indexes indistinctly increased in MT individuals compared with controls (P < 0.05) but did not increase in HT athletes. Normalized spectral HRV indexes did not change significantly among the three groups. Heart rate was similar for MT and Sed subjects but was significantly (P <0.05) lower in HT athletes under both recording conditions. These results indicate that SWS discriminates the state of sympathovagal balance better than waking periods. A moderate training load is sufficient to increase vagal-related HRV indexes. However, in HT individuals, despite lower heart rate, vagal-related HRV indexes return to Sed values even in the absence of competition, fatigue, or overload.

Adult↗
PubMed2004

Abnormal heart rate variability in a subject with second degree atrioventricular blocks during sleep.

OBJECTIVE: We compare the profiles of heart rate variability (HRV) during sleep stages in 9 healthy controls and one subject with second degree atrioventricular blocks (AVB), investigating the role of sympathovagal balance in such pathology. METHOD: Sleep and cardiac records were taken for one night in 9 male subjects from 21:00 to 07:00 h and for two nights in a male subject with AVB. Time and frequency domain indexes of HRV were calculated over 5 min-periods. RESULTS: In one subject without any daytime heart disease, 253 and 318 AVB of type 2 (Mobitz 2) were observed during the two experimental nights, predominantly during rapid eye movement (REM) sleep and the surrounding sleep stage 2 in the second half of the night. In the 9 control subjects, absolute HRV indexes and low frequency (LF)/(LF+high frequency, HF) (where LF and HF are low frequency and high frequency power) were low during slow wave sleep, and significantly increased during REM sleep and the preceding sleep stage 2. In the subject with AVB, these HRV indexes were abnormally low during all sleep stages, with a predominant increase in parasympathetic activity as inferred from low LF/(LF+HF). During wake, however, LF/(LF+HF) normally increased, and the tachycardia observed with the arousal that terminates SWS was preserved in the subject with AVB. CONCLUSION: These results suggest that in the subject with second degree atrioventricular blocks, sleep processes, particularly during REM sleep, create a specific neurological background that prevents an increase in sympathetic tone and triggers cardiac pauses.

Adult↗
PubMed2003

Mechanisms of renal hyporesponsiveness to ANP in heart failure.

The atrial natriuretic peptide (ANP) plays an important role in chronic heart failure (CHF), delaying the progression of the disease. However, despite high ANP levels, natriuresis falls when CHF progresses from a compensated to a decompensated state, suggesting emergence of renal resistance to ANP. Several mechanisms have been proposed to explain renal hyporesponsiveness, including decreased renal ANP availability, down-regulation of natriuretic peptide receptors and altered ANP intracellular transduction signal. It has been demonstrated that the activity of neutral endopeptidase (NEP) is increased in CHF, and that its inhibition enhances renal cGMP production and renal sodium excretion. In vitro as well as in vivo studies have provided strong evidence of an increased degradation of intracellular cGMP by phosphodiesterase in CHF. In experimental models, ANP-dependent natriuresis is improved by phosphodiesterase inhibitors, which may arise as new therapeutic agents in CHF. Sodium-retaining systems likely contribute to renal hyporesponsiveness to ANP through different mechanisms. Among these systems, the renin-angiotensin-aldosterone system has received particular attention, as angiotensin II and ANP have renal actions at the same sites and inhibition of angiotensin-converting enzyme and angiotensin-receptor blockade improve ANP hyporesponsiveness. Less is known about the interactions between the sympathetic nervous system, endothelin or vasopressin and ANP, which may also blunt ANP-induced natriuresis. To summarize, renal hyporesponsiveness to ANP is probably multifactorial. New treatments designed to restore renal ANP efficiency should limit sodium retention in CHF patients and thus delay the progression to overt heart failure.

Arginine Vasopressin↗
PubMed2002

Time-courses in renin and blood pressure during sleep in humans.

We previously described a strong concordance between nocturnal oscillations in plasma renin activity (PRA) and the rapid eye movement (REM) and non-REM (NREM) sleep cycles, but the mechanisms inducing PRA oscillations remain to be identified. This study was designed to examine whether they are linked to sleep stage-related changes in arterial blood pressure (ABP). Analysis of sleep electroencephalographic (EEG) activity in the delta frequency band, intra-arterial pressure, and PRA measured every 10 min was performed in eight healthy subjects. Simultaneously, the ratio of low frequency power to low frequency power + high frequency power [LF/(LF + HF)] was calculated using spectral analysis of R--R intervals. The cascade of physiological events that led to increased renin release during NREM sleep could be characterized. First, the LF/(LF + HF) ratio significantly (P < 10(-4) decreased, indicating a reduction in sympathetic tone, concomitantly to a significant (P < 10(- 3) decrease in mean arterial pressure (MAP). Delta wave activity increased (P < 10(-4) 10-20 min later and was associated with a lag of 0-10 min with a significant rise in PRA (P < 10(-4) . Rapid eye movement sleep was characterized by a significant increase (P < 10(-4) in the LF/(LF + HF) ratio and a decrease (P < 10(-4) in delta wave activity and PRA, whereas MAP levels were highly variable. Overnight cross-correlation analysis revealed that MAP was inversely correlated with delta wave activity and with PRA (P < 0.01 in all subjects but one). These results suggest that pressure-dependent mechanisms elicit the nocturnal PRA oscillations rather than common central processes controlling both the generation of slow waves and the release of renin from the kidney.

Adult↗
PubMed2002

L-arginine reduces exercise-induced increase in plasma lactate and ammonia.

To investigate the effect of L-arginine supplementation (L-ARG) on physiological and metabolic changes during exercise, we determined in a double-blind study the cardiorespiratory (heart rate, oxygen consumption (VO(2)) and carbon dioxide production (VCO(2)) and the metabolic (lactate and ammonia) responses to maximal exercise after either an intravenous L-ARG hydrochloride salt or placebo load in 8 healthy subjects. Exercise-induced increases in heart rate, VO(2) and VCO(2) were not significantly different after L-ARG or placebo. By contrast, peak plasma ammonia and lactate were significantly decreased after L-ARG load (60.6 +/- 8.2 vs. 73.1 +/- 9.1 micro mol x l(-1), p < 0.01 and 7.1 +/- 0.7 vs. 8.2 +/- 1.1 mmol x l(-1), p < 0.01, for ammonia and lactate, respectively). Plasma L-citrulline increased significantly during exercise only after L-ARG load, despite a concomitant decrease in plasma L-ARG. Furthermore, a significant inverse relationship was observed between changes in lactate and L-citrulline concentrations after L-ARG load (r = -0.84, p = 0.009). These results demonstrate that intravenous L-ARG reduces significantly exercise-induced increase in plasma lactate and ammonia. Taken together, the specific L-citrulline increase and the inverse relationship observed between L-citrulline and plasma lactate after L-ARG might support that L-ARG supplementation enhances the L-arginine-nitric oxide (NO) pathway during exercise.

Adult↗
PubMed2001

Inverse coupling between ultradian oscillations in delta wave activity and heart rate variability during sleep.

OBJECTIVE: We investigate the relationship between changes in heart rate variability and electroencephalographic (EEG) activity during sleep. METHOD: Nine male subjects with regular non-rapid-eye movement-rapid-eye movement (NREM-REM) sleep cycles were included in the study. They underwent EEG and cardiac recordings during one experimental night. Heart rate variability was determined over 5-min periods by the ratio of low frequency to low frequency plus high frequency power [LF/(LF+HF)] calculated using spectral analysis of R-R intervals. EEG spectra were analyzed using a fast Fourier transform algorithm. RESULTS: We found an ultradian 80-120 min rhythm in the LF/(LF+HF) ratio, with high levels during rapid eye movement (REM) sleep and low levels during slow wave sleep (SWS). During sleep stage 2 there was a progressive decrease in the transition from REM sleep to SWS, and an abrupt increase from SWS to REM sleep. These oscillations were significantly coupled in a 'mirror-image' to the overnight oscillations in delta wave activity, which reflect sleep deepening and lightening. Cardiac changes preceded EEG changes by about 5 min. CONCLUSIONS: These findings demonstrate the existence of an inverse coupling between oscillations in delta wave activity and heart rate variability. They indicate a non-uniformity in sleep stage 2 that underlies ultradian sleep regulation.

Activity Cycles↗
PubMed2001

Sleep deprivation blunts the night time increase in aldosterone release in humans.

The aim of this study was to determine the effect of sleep deprivation on the 24-h profile of aldosterone and its consequences on renal function. Aldosterone and its main hormonal regulatory factors, ACTH (evaluated by cortisol measurement) and the renin-angiotensin system [RAS, evaluated by plasma renin activity (PRA) measurement] were determined every 10 min for 24 h in eight healthy subjects in the supine position, once with nocturnal sleep and once during total 24-h sleep deprivation. Plasma Na(+) and K(+) were measured every 10 min in four of these subjects. In an additional group of 13 subjects under enteral nutrition, diuresis, natriuresis and kaliuresis were measured once during the sleep period (23.00--07.00 h) and once during a 23.00--07.00 hours sleep deprivation period. During sleep deprivation, aldosterone displayed lower plasma levels and pulse amplitude in the 23.00--07.00-hour period than during sleep. Similarly, PRA showed reduced levels and lower pulse frequency and amplitude. Plasma cortisol levels were slightly enhanced during sleep deprivation. Overnight profiles of plasma K(+) and Na(+) were not affected. Diuresis and kaliuresis were not influenced by sleep deprivation. In contrast, natriuresis significantly increased during sleep deprivation. This study demonstrates that sleep deprivation modifies the 24-h aldosterone profile by preventing the nocturnal increase in aldosterone release and leads to altered overnight hydromineral balance.

Adrenocorticotropic Hormone↗
PubMed2000

Effect of sleep deprivation on overall 24 h growth-hormone secretion.

After sleep deprivation, the blunting of the normal sleep-related growth-hormone (GH) pulse is compensated during the day. Consequently, the amount of GH secreted during a 24 h period is similar whether or not a person has slept during the night. These results argue against the belief that sleep disorders in children can inhibit growth through a daily GH deficit.

Adult↗
PubMed2000

Lack of acute cyclosporine nephrotoxicity in late heart-transplant recipients.

BACKGROUND: Cyclosporine induces daily renal hypoperfusion in subjects with normal atrial natriuretic peptide (ANP) levels, but its acute effects in heart transplant patients with increased ANP remain to be determined. METHODS: Cyclosporinemia and creatinine clearance were monitored during 7 hours following cyclosporine administration in 6 heart transplant patients. RESULTS CONCLUSIONS: No acute cyclosporine-induced decrease in creatinine clearance was observed after heart transplantation. These data suggest that maintenance cyclosporine dose may be less nephrotoxic than suspected and that increased ANP might protect the renal function late after heart transplantation.

Acute Disease↗
PubMed2000

VO(2) kinetics reveal a central limitation at the onset of subthreshold exercise in heart transplant recipients.

Because the cardiocirculatory response of heart transplant recipients (HTR) to exercise is delayed, we hypothesized that their O(2) uptake (VO(2)) kinetics at the onset of subthreshold exercise are slowed because of an impaired early "cardiodynamic" phase 1, rather than an abnormal subsequent "metabolic" phase 2. Thus we compared the VO(2) kinetics in 10 HTR submitted to six identical 10-min square-wave exercises set at 75% (36 +/- 5 W) of the load at their ventilatory threshold (VT) to those of 10 controls (C) similarly exercising at the same absolute (40 W; C40W group) and relative load (67 +/- 14 W; C67W group). Time-averaged heart rate, breath-by-breath VO(2), and O(2) pulse (O(2)p) data yielded monoexponential time constants of the VO(2) (s) and O(2)p increase. Separating phase 1 and 2 data permitted assessment of the phase 1 duration and phase 2 VO(2) time constant (). The VO(2) time constant was higher in HTR (38.4 +/- 7.5) than in C40W (22.9 +/- 9.6; P < or = 0. 002) or C67W (30.8 +/- 8.2; P < or = 0.05), as was the O(2)p time constant, resulting from a lower phase 1 VO(2) increase (287 +/- 59 vs. 349 +/- 66 ml/min; P < or = 0.05), O(2)p increase (2.8 +/- 0.6 vs. 3.6 +/- 1.0 ml/beat; P < or = 0.0001), and a longer phase 1 duration (36.7 +/- 12.3 vs. 26.8 +/- 6.0 s; P < or = 0.05), whereas the was similar in HTR and C (31.4 +/- 9.6 vs. 29.9 +/- 5.6 s; P = 0.85). Thus the HTR have slower subthreshold VO(2) kinetics due to an abnormal phase 1, suggesting that the heart is unable to increase its output abruptly when exercise begins. We expected a faster in HTR because of their prolonged phase 1 duration. Because this was not the case, their muscular metabolism may also be impaired at the onset of subthreshold exercise.

Adult↗
PubMed2000

Exercise-induced increase in circulating adrenomedullin is related to mean blood pressure in heart transplant recipients.

Adrenomedullin (ADM) is a newly discovered potent vasorelaxing and natriuretic peptide that recently has been shown to be increased after heart transplantation. To investigate the hemodynamic factors modulating its release and the eventual role of ADM in blood pressure regulation after heart transplantation, seven matched heart-transplant recipients (Htx) and seven normal subjects performed a maximal bicycle exercise test while monitoring for heart rate, blood pressure, and circulating ADM. Baseline heart rate and systemic blood pressure were higher in Htx; left ventricular mass index and ADM tended to be higher after heart transplantation and correlated positively in Htx (r = 0.79, P = 0.03). As expected, exercise-induced increase in heart rate was lower in Htx than in controls (60 +/- 11 % vs. 121 +/- 14 %, respectively) and blood pressure increase was similar in both groups. Maximal exercise increased significantly plasma ADM in both groups (from 25.3 +/- 3.1 to 30.7 +/- 3.5 pmol/L, P < 0.05 and from 15.2 +/- 1.4 to 29.1 +/- 4.4 pmol/L, P = 0.02 in Htx and controls, respectively), the hypotensive peptide level remaining elevated until the 30th min of recovery. A significant inverse relationship was observed between peak mean blood pressure and circulating ADM in Htx (r = -0.86, P < 0.02). Besides showing that circulating ADM is increased after heart transplantation, the present study demonstrates a positive relationship between baseline ADM and left ventricular mass index. Furthermore, maximal exercise-induced increase in ADM is inversely related to mean blood pressure in Htx, suggesting that ADM might participate in blood pressure regulation during exercise after heart transplantation.

Adrenomedullin↗