[Geriatric patients with chronic kidney insufficiency: which antalgia?]. / Patients gériatriques insuffisants rénaux chroniques: quelle antalgie ?

Pain is a leading cause of office visits. In the geriatric population, it is known that the prevalence of renal failure increases exponentially with age, modifing the elimination of drugs and of their metabolites. What analgesia should be offered to these patients? The holy grail would be a medication without renal elimination, without toxic metabolites and without nephrotoxicity. Based on the literature we try to propose a specific approach to analgesia in older patients with kidney insufficiency, in order to help practitioners to better prescribe for this group of patients.

Hyperoxia does not accelerate quadriceps muscle deoxygenation kinetics at the onset of heavy exercise cycle.

AIM: The aim of this study was to determine whether an increase in O2 availability induces an alteration of the balance between O2 consumption ((V)O2) and O2 delivery ((Q)O2) at the muscle level. For that, we examined the effect of moderate hyperoxia on muscle deoxygenation kinetics at the onset of heavy-intensity cycling exercise. METHODS: Eight young male adults performed step transitions from 35 W to heavy-intensity exercise corresponding to a power output half-way between the first ventilatory threshold and (V)O2max in normoxia and in hyperoxia (FIO2=0.30). Muscle deoxygenation (HHb) and total hemoglobin (Hbtot) were monitored continuously by near-infrared spectroscopy. HHb data were fit with a mono-exponential model from the onset of exercise up to 90 seconds. RESULTS: Hyperoxia neither altered the delay before the increase in HHb (normoxia: 10.7±1.8 s vs. hyperoxia: 9.5±1.9 s; NS) nor the HHb mean response time (normoxia: 20.6±2.8 s vs. hyperoxia: 19.6±2.3 s; NS). Likewise, Hbtot was not different between normoxia and hyperoxia. CONCLUSION: These results indicate that moderate hyperoxia has no effect on muscle deoxygenation kinetics at the onset of heavy exercise. It suggests that muscle (V)O2 increases at the same rate than O2 delivery when O2 availability is enhanced.

Effect of high-intensity interval training and detraining on extra VO2 and on the VO2 slow component.

To examine the effect of 6-week of high-intensity interval training (HIT) and of 6-week of detraining on the VO2/Work Rate (WR) relationship and on the slow component of VO2, nine young male adults performed on cycle ergometer, before, after training and after detraining, an incremental exercise (IE), and a 6-min constant work rate exercise (CWRE) above the first ventilatory threshold (VT1). For each IE, the slope and the intercept of the VO2/WR relationship were calculated with linear regression using data before VT1. The difference between VO2max measured and VO2max expected using the pre-VT1 slope was calculated (extra VO2). The difference between VO2 at 6th min and VO2 at 3rd min during CWRE (DeltaVO2(6'-3')) was also determined. HIT induced significant improvement of most of the aerobic fitness parameters while most of these parameters returned to their pre-training level after detraining. Extra VO2 during IE was reduced after training (130 +/- 100 vs. -29 +/- 175 ml min(-1), P = 0.04) and was not altered after detraining compared to post-training. DeltaVO2(6'-3') during CWRE was unchanged by training and by detraining. We found a significant correlation (r2 = 0.575, P = 0.02) between extra VO2 and DeltaVO2(6'-3') before training. These results show that an alteration of extra VO2 can occur without any change in the VO2 slow component, suggesting a possible dissociation of the two phenomena. Moreover, the fact that extra VO2 did not change after detraining could indicate that this improvement may remain after the loss of other adaptations.

Effect of prior heavy exercise on muscle deoxygenation kinetics at the onset of subsequent heavy exercise.

This study examines the effect of prior heavy exercise on muscle deoxygenation kinetics at the onset of heavy-intensity cycling exercise. Ten young male adults (20 +/- 2 years) performed two repetitions of step transitions (6 min) from 35 W to heavy-intensity exercise preceded by either no warm-up or by a heavy-intensity exercise. VO2 was measured breath-by-breath, and muscle deoxygenation (HHb) and total hemoglobin (Hb(tot)) were monitored continuously by near-infrared spectroscopy. We used a two-exponential model to describe the VO2 kinetics and a mono-exponential model for the HHb kinetic. The parameters of the phase II VO2 kinetics (TD1 VO2, tau1 VO2 and A1 VO2) were unaffected by prior heavy exercise, while some parameters of local muscle deoxygenation kinetics were significantly faster (TD HHb: 7 +/- 2 vs. 5 +/- 2 s; P < 0.001, MRT HHb: 20 +/- 3 vs. 15+/- 4 s; P < 0.05). Blood lactate, heart rate and Hb(tot) values were significantly higher before the second bout of heavy exercise. These results collectively suggest that the prior heavy exercise probably increased muscle O2 availability and improved O2 utilization at the onset of a subsequent bout of heavy exercise.

Respiratory muscle oxygenation kinetics: relationships with breathing pattern during exercise.

This work aimed to investigate accessory respiratory muscle oxygenation (RMO(2)) during exercise, using near-infrared spectroscopy, and to study relationships between RMO(2) kinetics and breathing parameters. Nineteen young males (19.3 +/- 1.5 years) performed a maximal incremental test on a cycle ergometer. Changes in breathing pattern were characterized by accelerated rise in the breathing frequency (f (Racc)), plateau of tidal volume (V (Tplateau)) and inflection point in the V. (E)/V (T) relationship (V. (E)/V (T inflection)). First and second ventilatory thresholds (VT1 and VT2) were also determined. RMO (2) kinetics were monitored by NIRS on the serratus anterior. During exercise, all subjects showed reduced RMO (2) (deoxygenation) with a breakdown (B-RMO(2)) at submaximal workload (86 % .VO(2max)). .VO(2) corresponding to B-RMO (2) and to f (Racc), V (Tplateau), .V(E)/V(T inflection), or VT2 were not different. Relationships were found between the .VO(2) at B-RMO(2) and the .VO(2) at f (Racc) (r = 0.88, p < 0.001), V (Tplateau) (r = 0.84, p < 0.001), V. (E)/V (T inflection) (r = 0.58, p < 0.05) or VT2 (r = 0.79, p < 0.001). The amplitude of RMO(2) at maximal workload was weakly related to .VO(2max) (r = 0.58, p < 0.05). B-RMO (2) seems to be due to the change in breathing pattern and especially to the important rise in breathing frequency at the VT2 exercise level. Moreover, subjects who exhibit higher .VO(2max) also exhibit a higher decrease in respiratory muscle oxygenation during exercise.

Evidence of exercise-induced O2 arterial desaturation in non-elite sportsmen and sportswomen following high-intensity interval-training.

The aim of this study was to investigate the development of exercise-induced hypoxemia (EIH defined as an exercise decrease > 4 % in oxygen arterial saturation, i. e. SaO (2) measured with a portable pulse oximeter) in twelve sportsmen and ten sportswomen (18.5 +/- 0.5 years) who were non-elite and not initially engaged in endurance sport or training. They followed a high-intensity interval-training program to improve V.O (2)max for eight weeks. The training running speeds were set at approximately 140 % V.O (2)max running speed up to 100 % 20-m maximal running speed. Pre- and post-training pulmonary gas exchanges and SaO (2) were measured during an incremental running field-test. After the training period, men and women increased their V.O (2)max (p < 0.001) by 10.0 % and 7.8 %, respectively. Nine subjects (seven men and two women) developed EIH. This phenomenon appeared even in sportsmen with low V.O (2)max from 45 ml x min (-1) x kg (-1) and seemed to be associated with inadequate hyperventilation induced by training: because only this hypoxemic group showed 1) a decrease in maximal ventilatory equivalent in O (2) (V.E/V.O (2), p < 0.01) although maximal ventilation increased (p < 0.01) with training, i. e. in EIH-subjects the ventilatory response increased less than the metabolic demand after the training program; 2) a significant relationship between SaO (2) at maximal workload and the matched V.E/V.O (2) (p < 0.05, r = 0.67) which strengthened a relative hypoventilation implication in EIH. In conclusion, in this field investigation the significant decrease in the minimum SaO (2) inducing the development of EIH after high-intensity interval-training indicates that changes in training conditions could be accompanied in approximately 40 % non-endurance sportive subjects by alterations in the degree of arterial oxyhemoglobin desaturation developing during exercise.

Time spent at VO2max: a methodological issue.

This study was designed to propose a standardised procedure to determine the time spent at VO2max (tVO2max) based on the VO2max of the day (i. e. the VO2max value measured the day of the test). Ten male subjects first performed a graded field test, followed by a continuous running exercise to exhaustion, at the velocity of the Université de Montréal Track Test (V(UMTT)) plus 1 km x h(-1) (V(UMTT)(+1)). The second test consisted of an exhaustive run at 100 % of V(UMTT), followed by a V(UMTT)(+1) test. Different methods were used to compare time spent at VO2max, based on the VO2max of the graded field test, and time spent at VO2max, based on the VO2max of the day, during an exhaustive run at 100 % of V(UMTT). Results have shown that V(UMTT)(+1) tests were of sufficient intensity and duration to identify the VO2max of the day. Time spent at VO2max ranged from 25 +/- 53 s to 139 +/- 76 s according to the method used. However, the tVO2max method based on the sum of each value higher than 95 % of VO2max of the day appeared more robust than methods based on the time to exhaustion minus time to reach VO2 reference value, or the method based on the sum of values higher than VO2max minus 2.1 ml x kg(-1) x min(-1).

Effects of high intensity intermittent training on peak VO(2) in prepubertal children.

This study was designed to examine peak VO(2) responses of prepubescent children following a 7-week aerobic training. Twenty-three boys and thirty girls (9.7 +/- 0.8 years) were divided into a high intensity experimental group (HIEG: 20 girls and 13 boys) and a control group (CG: 10 girls and 10 boys). A graded 20-m shuttle run with measurement of gas exchange values was performed prior to and after the 7-week training program. The test consisted of a 3-min run at 7 km x h(-1) to determine energy cost of running, immediately followed by a 20-meter shuttle run test. HIEG had two 30 min-sessions of short intermittent aerobic training per week at velocities ranging from 100 up to 130 % of the maximal aerobic speed. For HIEG, absolute peak VO(2)(9.1 %) and relative to body mass peak VO(2)(8.2 %) increased significantly (p < 0.001); it was unchanged in the CG. Similarly, maximal shuttle run improved significantly in HIEG (5.1 %, p < 0.001). In contrast, there was no significant change for CG. For both groups energy cost of running remained unchanged. These findings show that prepubescent children could significantly increase their peak VO(2) and maximal shuttle velocity with high intensity short intermittent aerobic exercises.

Relationship between run times to exhaustion at 90, 100, 120, and 140% of vVO2max and velocity expressed relatively to critical velocity and maximal velocity.

The aim of the present study was to explain the inter-individual variability in running time to exhaustion (tlim) when running speed was expressed as a percentage of the velocity, associated with maximal oxygen uptake (vVO2max). Indeed for the same percentage of vVO2max the anaerobic contribution to energy supply is different and could be dependent on the critical velocity (Cv) and also on the maximal running velocity (vmax). Ten subjects ran four tlim at 90, 100, 120, and 140% of vVO2max; mean and standard deviation for tlim were 839 +/- 236 s, 357 +/- 110 s, 122 +/- 27 s, and 65 +/- 17s, respectively. Each velocity was then expressed 1) as a percentage of the difference between vVO2max and Cv (%AeSR); 2) as a percentage of the difference between vmax and Cv (%MSR); 3) as a percentage of the difference between vmax and vVO2max (%AnSR). Highest correlations were found between tlim90 and tlim100 and velocity expressed as %MSR (r = -0.82, p < 0.01 and r = -0.75, p < 0.01), and between tlim120 and tlim140 and velocity expressed as %AnSR (r = -0.83, p < 0.01 and r = -0.94, p < 0.001). These results show that the same intensity relative to aerobic contribution did not represent the same absolute intensity for all and could partly explain variability in tlim. Therefore expressing intensity as a percentage of MSR for sub-maximal and maximal velocities and as a percentage of AnSR for supra-maximal velocities allows individual differences in anaerobic work capacity to be taken into account and running times to exhaustion to be predicted accurately.

Oxygen kinetics and modelling of time to exhaustion whilst running at various velocities at maximal oxygen uptake.

The purpose of this study was to characterise the relationship between running velocity and the time for which a subject can run at maximal oxygen uptake (VO2max), (tlimVO2max). Seven physical education students ran in an incremental test (3-min stages) to determine VO2max and the minimal velocity at which it was elicited (vVO2max). They then performed four all-out running tests on a 200-m indoor track every 2 days in random order. The mean times to exhaustion tlim at 90%, 100%, 120% and 140% vVO2max were 13 min 22 s (SD 4 min 30 s), 5 min 47 s (SD 1 min 50 s), 2 min 11 s (SD 38 s) and 1 min 12 s (SD 18 s), respectively. Five subjects did not reach VO2max in the 90% vVO2max test. All the subjects reached VO2max in the runs at 100% vVO2max. All the subjects, except one, reached VO2max in the runs at 120% vVO2max. Four subjects did not reach VO2max in the 140% vVO2max test. Time to achieve VO2max was always about 50% of the time to exhaustion irrespective of the intensity. The time to exhaustion-velocity relationship was better fitted by a 3- than by a 2-parameter critical power model for running at 90%, 100%, 120%, 140% vVO2max as determined in the previous incremental test. In conclusion, tlimVO2max depended on a balance between the time to attain VO2max and the time to exhaustion tlim. The time to reach VO2max decreased as velocity increased. The tlimVO2max was a bi-phasic function of velocity, with a peak at 100% vVO2max.

Determination of the velocity associated with the longest time to exhaustion at maximal oxygen uptake.

The so-called velocity associated with VO2max, defined as the minimal velocity which elicits VO2max in an incremental exercise protocol (v(VO2max)), is currently used for training to improve VO2max. However, it is well known that it is not the sole velocity which elicits VO2max and it is possible to achieve VO2max at velocities lower and higher than v(VO2max). The goal of this study was to determine the velocity which allows exercise to be maintained the longest time at v(VO2max). Using the relationship between time to exhaustion at VO2max in the all-out runs at 90%, 100%, 120% and 140% of v(VO2max) and distance run at VO2max, the velocity which elicits the longest time to exhaustion at VO2max (CV') was determined. For the six subjects tested (physical education students), this velocity was not significantly different from v(VO2max) (16.96+/-0.92 km x h(-1) vs 17.22+/-1.12 km x h(-1), P = 0.2 for CV' and v(VO2max), respectively) and these two velocities were correlated (r = 0.88, P = 0.05).

Validity of the Université de Montréal Track Test to assess the velocity associated with peak oxygen uptake for adolescents.

BACKGROUND: The purpose of the study was to test the ability to determine the velocity associated with peak oxygen uptake for adolescents by means of a simple field test, the Université de Montréal Track Test (UMTT). METHODS: Fifteen adolescents, 13.4 +/- 1.0 years, performed two maximal field tests where oxygen uptake and heart rate were continuously monitored. The first test (graded field test, first stage 8 km.h-1, increment 1.5 km.h-1, duration 3 min) allowed the subjects to reach a steady-state oxygen uptake. Then, the velocity associated with peak oxygen uptake was calculated from the ratio between peak oxygen uptake above resting level to energy cost of running. The calculated velocity was kept as the criterion velocity. For the second test (UMTT, first stage 8 km.h-1; increment 1 km.h-1; duration 2 min), the velocity measured at the last completed stage was retained. RESULTS: The measured peak oxygen uptake for the graded field test (51.8 +/- 6.5 ml.kg-1.min-1) and for the UMTT (51.0 +/- 7.9 ml.kg-1.min-1) were not significantly different. The calculated velocity (12.9 +/- 1.0 km.h-1) and the measured velocity (12.7 +/- 0.9 km.h-1) were not significantly different and were significantly correlated (r = 0.80, p < 0.001). CONCLUSIONS: It was concluded that, for adolescents, the velocity measured at the last completed stage of the UMTT allows a valid estimation of the velocity associated with peak oxygen uptake.