Use of botulinum toxin type A in symptomatic accessory soleus muscle: first five cases.

Symptomatic accessory soleus muscle (ASM) can cause exercise-induced leg pain due to local nerve/vascular compression, muscle spasm, or local compartment syndrome. As intramuscular injections of botulinum toxin type A (BTX-A) can reduce muscle tone and mass, we investigated whether local BTX-A injections relieve the pain associated with symptomatic ASM. We describe five patients presenting peri/retromalleolar exertional pain and a contractile muscle mass in the painful region. Com-pression neuropathy was ruled out by electromyo-graphic analysis of the lower limb muscles. Doppler ultrasonography was normal, excluding a local vascular compression. ASM was confirmed by magnetic resonance imaging. After a treadmill stress test, abnormal intramuscular pressure values in the ASM, confirmed the diagnosis of compartment syndrome only in one patient. All five patients received BTX-A injections in two points of the ASM. The treatment efficacy was evaluated based on the disappearance of exercise-induced pain and the resumption of normal physical and sports activities. After BTX-A injection, exertional pain disappeared and all five patients resumed their normal level of physical and sports performances. Neither side effects nor motor deficits were observed. BTX-A is well tolerated in patients with ASM and could be used as a new conservative therapeutic strategy for the treatment of symptomatic ASM before surgery.

Effect of a short-term intermittent exercise-training programme on the pulse wave velocity and arterial pressure: a prospective study among 71 healthy older subjects.

AIMS OF THE STUDY: Stiffening of large arteries has been associated with increased cardiovascular outcomes among older subjects. Endurance exercises might attenuate artery stiffness, but little is known about the effects of intermittent training programme. We evaluate the effect of a short Intermittent Work Exercise Training Program (IWEP) on arterial stiffness estimated by the measure of the pulse wave velocity (PWV). METHODS AND SUBJECTS: Seventy-one healthy volunteers (mean age: 64.6 years) free of symptomatic cardiac and pulmonary disease performed a 9-week IWEP that consisted of a 30-min cycling twice a week over a 9-week period. Each session involved six 5-min bouts of exercise, each of the latter separated into 4-min cycling at the first ventilatory threshold alternated with 1-min cycling at 90% of the pretraining maximal tolerated power. Before and after the IWEP, the following measurements were made: carotid-radial PWV and carotid-femoral PWV with a tonometer and systolic and diastolic blood pressure. RESULTS: Training resulted in a non-significant decrease of the carotid-radial PWV, a significant decrease of the carotid-femoral PWV from 10.2 to 9.6 m/s (p < 0.001) (that was no longer significant after adjustment for mean arterial pressure) and a significant decrease in both systolic and diastolic blood pressure, respectively, from 129.6 ± 14.9 mmHg to 120.1 ± 14.1 mmHg (p < 0.001) and from 77.2 ± 8.8 mmHg to 71.4 ± 10.1 mmHg (p < 0.001). CONCLUSION: The present results support the idea that a short-term intermittent aerobic exercise programme may be an effective lifestyle intervention for reducing rapidly blood pressure and probably central arterial stiffness among older healthy subjects.

Muscle phosphorylase kinase deficiency: a neutral metabolic variant or a disease?

OBJECTIVE: To examine metabolism during exercise in 2 patients with muscle phosphorylase kinase (PHK) deficiency and to further define the phenotype of this rare glycogen storage disease (GSD). METHODS: Patient 1 (39 years old) had mild exercise-induced forearm pain, and EMG showed a myopathic pattern. Patient 2 (69 years old) had raised levels of creatine kinase (CK) for more than 6 months after statin treatment. Both patients had increased glycogen levels in muscle and PHK activity <11% of normal. Two novel pathogenic nonsense mutations were found in the PHKA1 gene. The metabolic response to anaerobic forearm exercise and aerobic cycle exercise was studied in the patients and 5 healthy subjects. RESULTS: Ischemic exercise showed a normal 5-fold increase in plasma lactate (peak 5.7 and 6.9 mmol/L) but an exaggerated 5-fold increase in ammonia (peak 197 and 171 µmol/L; control peak range 60-113 µmol/L). An incremental exercise test to exhaustion revealed a blunted lactate response (5.4 and 4.8 mmol/L) vs that for control subjects (9.6 mmol/L; range 7.1-14.3 mmol/L). Fat and carbohydrate oxidation rates at 70% of peak oxygen consumption were normal. None of the patients developed a second wind phenomenon or improved their work capacity with an IV glucose infusion. CONCLUSION: Our findings demonstrate that muscle PHK deficiency may present as an almost asymptomatic condition, despite a mild impairment of muscle glycogenolysis, raised CK levels, and glycogen accumulation in muscle. The relative preservation of glycogenolysis is probably explained by an alternative activation of myophosphorylase by AMP and P(i) at high exercise intensities.

Diffusing capacity of the lung for CO and pulmonary blood flow during incremental and intermittent exercise.

The aims of this study were to evaluate the feasibility of successive diffusing capacity of the lung for carbon monoxide (DLCO) measurements during two different exercise tests (upright cycling), and to compare the relationships between DLCO and pulmonary blood flow (Qc). Eight healthy subjects performed an incremental test (1-min step) and a strenuous 30-min intermittent-work exercise test (4 min at low and 2 min at high workload). Intrabreath DLCO and Qc were calculated by assessing the uptake of CO and C2H2 during exhalation. DLCO could be measured reliably up to 73-90% of peak oxygen consumption (VO2) during the incremental test, and up to 85-95% of peak VO2 during the intermittent test. The coefficients of variation of DLCO and Qc measured during two successive constant-load exercise tests were 5-6% and 7-11%, respectively. The highest values of DLCO, Qc and VO2 measured during the incremental and intermittent tests were similar (56 and 51 mL/mmHg/min for DLCO, 18.7 and 18.3 L/min, for Qc and 2.4 and 2.3 L/min for VO2, respectively). The main observed result was that the linear relationships between DLCO and Qc were similar whatever the exercise type. This allows DLCO comparisons, with regards to Qc, during different exercise protocols.

A comparison of four algorithms for the measurement of interrupter respiratory resistance in adults.

The aim of our study was to compare four algorithms for the measurement of respiratory resistance in adults using the interrupter technique. Four methods to estimate alveolar pressure from the mouth pressure during occlusion were assessed in 122 normal adults (57 males, 65 females, aged 18-79 yr, mean 41.2 +/- 15.6): taking the mean oscillation pressure (Rint), performing a linear back extrapolation (RintL) or a linear regression for the whole curve (RintRL), taking the end-occlusion pressure (RintE). Mean values for Rint, RintL and RintRL in males were respectively 0.23 +/- 0.04, 0.22 +/- 0.04 and 0.22 +/- 0.04 kPa s L(-1), not statistically different. In females values were respectively 0.27 +/- 0.05, 0.26 +/- 0.05 and 0.26 +/- 0.05 kPa s L(-1), not statistically different. RintE was higher than the remainder and was the only measure correlating weakly with morphometric variables: RintE = 1.152 - (0.00152 x age (yr)) - (0.00382 x height (cm)), r = 0.31 (p < 0.05) in females; RintE = 0.227 - (0.00122 x age (yr)) + (0.00830 x body mass index (kg m(-2))) with r = 0.34 (p < 0.05) in males. We conclude that it is equivalent to estimate alveolar pressure from or extrapolating it to the beginning of occlusion in healthy adults but when taking the end-occlusion pressure, resistance is higher and depends in part on morphometric parameters.

Effect of acute hypoxia on heart rate variability at rest and during exercise.

The purpose of this study was to investigate sympathovagal balance as inferred from heart rate variability (HRV) responses to acute hypoxia at rest and during exercise. HRV was evaluated in 12 healthy subjects during a standardized hypoxic tolerance test which consists of four periods alternating rest and moderate exercise (50 % V.O (2)max) in normoxic and hypoxic conditions. Ventilatory responses were determined and HRV indexes were calculated for the last 5 min of each period. In well-tolerant subjects, hypoxia at rest induced a decrease of root-mean-square of successive normal R-R interval differences (RMSSD) (p < 0.05) and of absolute high frequency (HF) power (p < 0.001). All absolute HRV indexes were strongly reduced during exercise (p < 0.001) with no further changes under the additional stimulus of hypoxia. A significant increase (p < 0.05) in the HF/(LF+HF) ratio (where LF is low frequency power) was found during exercise in hypoxia compared to exercise in normoxia, associated with similar mean changes in ventilation and tidal volume. These results indicate a vagal control withdrawal under hypoxia at rest. During exercise at 50 % V.O (2)max, HRV indexes cannot adequately represent cardiac autonomic adaptation to acute hypoxia, or possibly to other additional stimuli, due to the dominant effect of exercise and the eventual influence of confounding factors.

Non-invasive cardiac output evaluation during a maximal progressive exercise test, using a new impedance cardiograph device.

One of the greatest challenges in exercise physiology is to develop a valid, reliable, non-invasive and affordable measurement of cardiac output (CO). The purpose of this study was to evaluate the reproducibility and accuracy of a new impedance cardiograph device, the Physio Flow, during a 1-min step incremental exercise test from rest to maximal peak effort. A group of 12 subjects was evaluated to determine the reproducibility of the method as follows: (1) each subject performed two comparable tests while their CO was measured by impedance cardiography using the new device (COImp1, COImp2), and (2) in a subgroup of 7 subjects CO was also determined by the direct Fick method (COFick) during the second test. The mean difference between the values obtained by impedance (i.e. COImp1-COImp2) was -0.009 l.min-1 (95% confidence interval: -4.2 l.min-1, 4.2 l.min-1), and CO ranged from 3.55 l.min-1 to 26.75 l.min-1 (n = 146). When expressed as a percentage, the difference (COImp1-COImp2) did not vary with increasing CO. The correlation coefficient between the values of COImp and COFick obtained during the second exercise test was r = 0.94 (P < 0.01, n = 50). The mean difference expressed as percentage was -2.78% (95% confidence interval: -27.44%, 21.78%). We conclude that COImp provides a clinically acceptable evaluation of CO in healthy subjects during an incremental exercise.

Exercise training with a heart device: a hemodynamic, metabolic, and hormonal study.

PURPOSE: The mechanisms of the training-induced improvements in left ventricular assist (LVAD) patients are unknown. METHODS: We measured the hemodynamic, gas exchange, and metabolic and hormonal effects of 6-wk exercise training in a cardiogenic shock patient who was assisted by an LVAD. RESULTS: After training, the peak power and VO2 increased by 166% and 56%, respectively (80 W and 16.1 mL x min(-1) x kg(-1)), whereas the ventilatory drive decreased. Although the LVAD output increased little with exercise, the systemic cardiac output rose (adequately for the VO2) from 5.91 and 4.90 L x min(-1) at rest to 9.75 and 9.47 L x min(-1) at peak work rate, before and after training, respectively. Thus, the left ventricle ejected again through the aortic valve. Unloading and/or retraining resulted in a left ventricular filling pressure decrease. Although the right ventricular ejection fraction increased with exercise, it decreased again at the maximal load after training. For a given work rate the arterial lactate, the norepinephrine (NE) and epinephrine (E) concentrations fell after training, but the enhanced maximal work rate elicited higher NE and E concentrations (4396 and 1848 pg x mL(-1), respectively). The lack of right ventricular unloading might have kept the atrial natriuretic peptide higher after training, but the blood cyclic GMP and endothelin were lower after training. CONCLUSION: In an LVAD patient, retraining returns the exercise capacity to the class III level by peripheral and left ventricular hemodynamic improvements, but the safety of maximal exercise remains to be proven in terms of right ventricular function and orthosympathetic drive.

A new impedance cardiograph device for the non-invasive evaluation of cardiac output at rest and during exercise: comparison with the "direct" Fick method.

The objectives of this study were to evaluate the reliability and accuracy of a new impedance cardiograph device, the Physio Flow, at rest and during a steady-state dynamic leg exercise (work intensity ranging from 10 to 50 W) performed in the supine position. We compared cardiac output determined simultaneously by two methods, the Physio Flow (QcPF) and the direct Fick (QcFick) methods. Forty patients referred for right cardiac catheterisation, 14 with sleep apnoea syndrome and 26 with chronic obstructive pulmonary disease, took part in this study. The subjects' oxygen consumption values ranged from 0.14 to 1.19 l x min(-1). The mean difference between the two methods (QcFick - QcPF) was 0.04 l x min(-1) at rest and 0.29 l x min(-1) during exercise. The limits of agreement, defined as mean difference +/- 2SD, were -1.34, +1.41 l x min(-1)] at rest and -2.34, +2.92 l x min(-1) during exercise. The difference between the two methods exceeded 20% in only 2.5% of the cases at rest, and 9.3% of the cases during exercise. Thoracic hyperinflation did not alter QcPF. We conclude that the Physio Flow provides a clinically acceptable and non-invasive evaluation of cardiac output under these conditions. This new impedance cardiograph device deserves further study using other populations and situations.

Aldosterone release during the sleep-wake cycle in humans.

The aim of this study was to assess the relative influence on the 24-h aldosterone profile of the adrenocorticotropic system, primarily modulated by a circadian rhythmicity, and the renin-angiotensin system, which is influenced by sleep. Cortisol, plasma renin activity (PRA), and aldosterone were measured for 24 h in healthy subjects under basal conditions, once with nocturnal sleep and once with a night of sleep deprivation followed by 8 h of daytime sleep. The sleep period displayed high mean aldosterone levels, pulse amplitude, and frequency that were reduced during waking periods. During sleep, aldosterone pulses were mainly related to PRA oscillations, whereas they were mainly associated with cortisol pulses during waking periods. Cross-correlation analysis between sleep electroencephalographic activity in the delta band and aldosterone levels yielded significant results, aldosterone following delta waves by approximately 30 min. This study demonstrates that the 24-h aldosterone profile is strongly influenced by sleep processes. A dual influence, by the renin-angiotensin system during sleep and by the adrenocorticotropic system during wakefulness, is exerted on aldosterone pulses throughout the 24-h period.

Oscillations in sympatho-vagal balance oppose variations in delta-wave activity and the associated renin release.

To determine the potential role of the sympathetic nervous system in the generation of the oscillations in PRA over the 24-h period, we used the autocorrelation coefficient of RR interval (rRR), a new tool to evaluate the sympatho-vagal balance continuously. We determined the influence of the sympathetic nervous system both on the nocturnal PRA oscillations associated to increases in delta-wave activity and on the daytime oscillations that occur randomly in awake subjects. PRA and rRR were determined every 10 min during 24 h in nine healthy subjects under continuous bed rest. Electroencephalographic spectral analysis was used to establish the variations in delta-wave activity during sleep, from 2300-0700 h. The overnight profiles in PRA, rRR and delta-wave activity were analyzed using a modified version of the pulse detection program ULTRA. The temporal link among the profiles of rRR, PRA, and delta-wave activity was quantified using cross-correlation analysis. During sleep, large oscillations in PRA were strongly linked to variations in delta-wave activity. They were preceded by opposite oscillations in rRR, decreases in rRR reflecting predominant vagal activity, and increases in rRR reflecting sympathetic dominance. During the waking periods, the levels of rRR were higher, with smaller variations. The daytime PRA oscillations were not associated with any significant changes in rRR, and conversely, significant oscillations in rRR were not followed by any significant changes in PRA. In conclusion, the sympathetic nervous system is not directly involved in the generation of renin oscillations observed under basal conditions. During sleep, the oscillations in sympatho-vagal balance are inversely related to the variations in delta-wave activity and the associated renin release. The processes that give the intermittent signal for concomitant increases in slow wave activity and renin release from the kidney remain to be identified.