Maximal aerobic power in patients with chronic low back pain: a comparison with healthy subjects.

The objective of the study was to compare the maximal aerobic capacity of patients with chronic low back pain with healthy asymptomatic controls matched for age, gender and level of physical activity at work and during sports activities. Reported data in the literature with respect to aerobic capacity in patients with chronic low back pain are not conclusive. Nevertheless, based on the assumption that chronic low back pain leads to deconditioning, physical training programs are widely used as a treatment. A total of 70 patients with chronic low back pain and 70 healthy asymptomatic subjects completed questionnaires regarding demographics and performed a graded maximal exercise test until exhaustion on a cycle ergometer. The maximal aerobic power was measured by indirect calorimetry. Heart rate, respiratory exchange ratio and blood lactate levels were also measured. The test was considered maximal when VO2max achievement criteria were obtained. VO2max values were compared among groups. The absolute and normalized for weight values of VO2max measured in patients with chronic low back pain were significantly lower than that of the control group. Independent comparison between men and women showed that absolute values of VO2max are also significantly lower in men and women with chronic low back pain. Women reached absolute and normalized for weight VO2max values significantly lower than those of men, both in chronic low back pain and control group. In conclusion, chronic low back pain patients, especially women, seem to have a reduced aerobic capacity compared to healthy asymptomatic subjects.

Aerobic fitness and limiting factors of maximal performance in chronic low back pain patients.

BACKGROUND: Studies of measurement of maximal aerobic uptake in patients with chronic low back pain have shown inconsistent results and none has focused on clinical endpoints of ergometry tests. OBJECTIVE: To determine the level of cardiorespiratory fitness and to establish factors limiting the maximal effort during the ergometry. METHODS: Patients with chronic low back pain performed a graded maximal exercise test. Clinical endpoints of the test were determined and grouped as "maximal effort" and "symptom-limited effort" endpoints. RESULTS: 101 patients aged 29.8 +/- 7.5 achieved a VO2 max value of 30.0 (+/- 7.27) ml.kg(-1).min(-1). In men and women independently, a linear regression analysis demonstrated that VO2 max was inversely and weakly related to age. When compared to normative categories of VO2 max, men and women were situated in the fair category. Quadriceps/leg fatigue was reported by 47.5% of patients and was the most frequent limiting factor of the tests. "Symptom limited effort" endpoints were reported by 54.4% of the subjects. CONCLUSIONS: Clinical limiting factors of maximal exertion interfere the achievement of maximal oxygen uptake in patients with low back pain during ergometry. Further, there exists an association among the clinical endpoints of the tests and the VO2 value achieved. CLBP patients have a lower level of aerobic fitness than healthy controls.

A new non exercise-based VO2max prediction equation for patients with chronic low back pain.

UNLABELLED: INTRODUCTION The measurement of the maximal oxygen uptake as a parameter of cardiorespiratory fitness is useful in exercise prescription in functional restoration programs but this measurement requires the subject's maximal exertion which is not always possible in patients with chronic low back pain. The purpose of this study was to develop a regression equation to predict maximal oxygen uptake based on non-exercise data in adult patients with chronic low back pain. METHODS: Cross sectional study in which 70 participants completed a maximal graded exercise test in cycle ergometer to assess maximal oxygen uptake. RESULTS: Patients achieved a mean +/- SD value of VO(2)max of 30.8 (+/-7.7) ml kg(-1) min(-1). The regression model included as data of non-exercise the patient's gender, body mass index and the intensity of physical activity during leisure time. Multiple linear regression analysis generated the following formula (R (2) = 38.3, SEE = 6.08 ml kg(-1) min(-1)): VO(2)max (ml kg(-1) min(-1)) = 35.3377 - 0.475411 x BMI + 0.155232 x PALT + 7.97682 x gender; where BMI = body mass index, PALT = physical activity during leisure time, women = 0, men = 1. The Durbin Watson statistic showed no problems with serial autocorrelation (D-W = 1.86). The Kolmogorov-Smirnov normality test demonstrated that the errors are distributed normally. CONCLUSIONS: This study provides a new and relatively precise non-exercise regression model to predict VO(2)max in patients with chronic low back pain.

Physical deconditioning in chronic low back pain.

OBJECTIVE: To establish the level of cardiorespiratory fitness and the rate of decrease in maximal aerobic capacity according to age in patients with chronic low back pain and compare these with normative data. DESIGN: Prospective case series with historical controls. SUBJECTS/PATIENTS: Seventy patients with chronic low back pain. METHODS: A maximal cycle ergometer protocol was used to measure VO2max, heart rate, respiratory exchange ratio and blood lactate levels. RESULTS: Seventy patients achieved absolute and normalized for weight VO2max values of 2.17 (standard deviation (SD) 0.65) l/min and 30.79 (SD 7.77) ml/kg/min, respectively. Absolute VO2max was poorly related to age in both men and women with chronic low back pain (r = -0.22 and r = -0.28, respectively). VO2max normalized for weight was also inversely related to age in both men and women (r = -0.36 and r = -0.42, respectively). The rate of VO2max decline between 20 and 59 years was -3.3 ml/kg/min/decade for the entire population and -1.2 and -5.4 ml/kg/min/decade in men and women, respectively. CONCLUSION: The level of physical fitness of patients with chronic low back pain is comparable to the physical fitness of healthy, but poorly conditioned subjects. Patients with chronic low back pain show a VO2max decline with ageing that is slower than of active subjects.

Cerebral adaptations to chronic anemia in a model of erythropoietin-deficient mice exposed to hypoxia.

Anemia and hypoxia in rats result in an increase in factors potentially involved in cerebral angiogenesis. Therefore, the aim of this study was to assess the effect of chronic anemia and/or chronic hypoxia on cerebral cellular responses and angiogenesis in wild-type and anemic transgenic mice. These studies were done in erythropoietin-deficient mice (Epo-TAg(h)) in normoxia and following acute (one day) and chronic (14 days, barometric pressure = 420 mmHg) hypoxia. In normoxia, Epo-TAg(h) mice showed an increase in transcript and protein levels of hypoxia-inducible factor 1alpha (HIF-1alpha), vascular endothelial growth factor (VEGF), erythropoietin receptors (EpoR), phospho-STAT-5/STAT-5 ratio, and neuronal neuronal nitric oxide synthase (nNOS) along with a higher cerebral capillary density. In wild-type (WT) mice, acute hypoxia increased all of the studied factors, while in chronic hypoxia, HIF-1alpha, EpoR, phospho-STAT-5/STAT-5 ratio, nNOS, and inducible NOS remained elevated, with an increase in capillary density. Surprisingly, in Epo-TAg(h) mice, chronic hypoxia did not further increase any factor except the nitric oxide metabolites, while HIF-1alpha, EpoR, and phospho-STAT-5/STAT-5 ratio were reduced. Normoxic Epo-TAg(h) mice developed cerebral angiogenesis through the HIF-1alpha/VEGF pathway. In acute hypoxia, WT mice up-regulated all of the studied factors, including cerebral NO. Polycythemia and angiogenesis occurred with acclimatization to chronic hypoxia only in WT mice. In Epo-TAg(h), the decrease in HIF-1alpha, VEGF proteins, and phospho-STAT-5 ratio in chronic hypoxia suggest that neuroprotective and angiogenesis pathways are altered.

Effects of a 4-week training with voluntary hypoventilation carried out at low pulmonary volumes.

This study investigated the effects of training with voluntary hypoventilation (VH) at low pulmonary volumes. Two groups of moderately trained runners, one using hypoventilation (HYPO, n=7) and one control group (CONT, n=8), were constituted. The training consisted in performing 12 sessions of 55 min within 4 weeks. In each session, HYPO ran 24 min at 70% of maximal O(2) consumption ( [V(02max)) with a breath holding at functional residual capacity whereas CONT breathed normally. A V(02max) and a time to exhaustion test (TE) were performed before (PRE) and after (POST) the training period. There was no change in V(O2max), lactate threshold or TE in both groups at POST vs. PRE. At maximal exercise, blood lactate concentration was lower in CONT after the training period and remained unchanged in HYPO. At 90% of maximal heart rate, in HYPO only, both pH (7.36+/-0.04 vs. 7.33+/-0.06; p<0.05) and bicarbonate concentration (20.4+/-2.9 mmolL(-1) vs. 19.4+/-3.5; p<0.05) were higher at POST vs. PRE. The results of this study demonstrate that VH training did not improve endurance performance but could modify the glycolytic metabolism. The reduced exercise-induced blood acidosis in HYPO could be due to an improvement in muscle buffer capacity. This phenomenon may have a significant positive impact on anaerobic performance.

Prolonged expiration down to residual volume leads to severe arterial hypoxemia in athletes during submaximal exercise.

The goal of this study was to assess the effects of a prolonged expiration (PE) carried out down to the residual volume (RV) during a submaximal exercise and consider whether it would be worth including this respiratory technique in a training programme to evaluate its effects on performance. Ten male triathletes performed a 5-min exercise at 70% of maximal oxygen consumption in normal breathing (NB(70)) and in PE (PE(70)) down to RV. Cardiorespiratory parameters were measured continuously and an arterialized blood sampling at the earlobe was performed in the last 15s of exercise. Oxygen consumption, cardiac frequency, end-tidal and arterial carbon dioxide pressure, alveolar-arterial difference for O(2) (PA(O2) - Pa(O2)) and P(50) were significantly higher, and arterial oxygen saturation (87.4+/-3.4% versus 95.0+/-0.9%, p<0.001), alveolar (PA(O2)) or arterial oxygen pressure, pH and ventilatory equivalent were significantly lower in PE(70) than NB(70). There was no difference in blood lactate between exercise modalities. These results demonstrate that during submaximal exercise, a prolonged expiration down to RV can lead to a severe hypoxemia caused by a PA(O2) decrement (r=0.56; p<0.05), a widened PA(O2) - Pa(O2) (r=-0.85; p<0.001) and a right shift of the oxygen dissociation curve (r=-0.73; p<0.001).

Living high-training low: effect on erythropoiesis and maximal aerobic performance in elite Nordic skiers.

The "living high-training low" model (Hi-Lo) may improve aerobic performance in athletes, and the main mechanism of this improvement is thought to be augmented erythropoiesis. A positive effect of Hi-Lo has been demonstrated previously by using altitudes of 2,000-3,000 m. Since the rate of erythropoiesis is altitude-dependent, we tested whether a higher altitude (3,500 m) during Hi-Lo increases erythropoiesis and maximal aerobic performance. Nordic skiers trained for 18 days at 1,200 m, while sleeping at 1,200 m in ambient air (control group, n = 5) or in hypoxic rooms (Hi-Lo, n = 6; 3 x 6 days at simulated altitudes of 2,500, 3,000 and finally 3,500 m, 11 h day(-1)). Measurements were done before, during (blood samples only) and 2 weeks after the intervention (POST). Maximal aerobic performance was examined from VO(2max) and time to exhaustion (T(exh)) at vVO(2max) (minimum speed associated with VO(2max)), respectively. Erythropoietin and soluble transferrin receptor responses were higher during Hi-Lo, whereas reticulocytes did not change. In POST (vs. before): hematological parameters were similar to basal levels, as well as red blood cell volume, being 2.68 +/- 0.83 l (vs. 2.64+/-0.54 l) in Hi-Lo and 2.62+/-0.57 l (vs. 2.87 +/- 0.59 l) in controls. At that time, neither VO(2max) nor T(exh) were improved by Hi-Lo, VO(2max) being non-significantly decreased by 2.0% (controls) and 3.7% (Hi-Lo). The present results suggest that increasing the altitude up to 3,500 m during Hi-Lo stimulates erythropoiesis but does not confer any advantage for maximal O2 transport.

Living high-training low: tolerance and acclimatization in elite endurance athletes.

The "living high-training low" (LHTL) model is frequently used to enhance aerobic performance. However, the clinical tolerance and acclimatization process to this intermittent exposure needs to be examined. Forty one athletes from three federations (cross-country skiers, n=11; swimmers, n=18; runners, n=12) separately performed a 13 to 18-day training at the altitude of 1,200 m, by sleeping either at 1,200 m (CON) or in hypoxic rooms (HYP), with an O2 fraction corresponding to 2,500 m (5 nights for swimmers and 6 for skiers and runners), 3,000 m (6 nights for skiers, 8 for swimmers and 12 for runners) and 3,500 m (6 nights for skiers). Measurements performed before, 1 or 15 days after training were ventilatory response (HVRe) and desaturation (deltaSaO2e) during hypoxic exercise, an evaluation of cardiac function by echocardiography, and leukocyte count. Lake Louise AMS score and arterial O2 saturation during sleep were measured daily for HYP. Subjects did not develop symptoms of AMS. Mean nocturnal SaO2 decreased with altitude down to 90% at 3,500 m and increased with acclimatization (except at 3,500 m). Leukocyte count was not affected except at 3,500 m. The heart function was not affected by LHTL. Signs of ventilatory acclimatization were present immediately after training (increased HVRe and decreased deltaSaO2e) and had disappeared 15 days later. In conclusion, LHTL was well tolerated and compatible with aerobic training. Comparison of the three patterns of training suggests that a LHTL session should not exceed 3,000 m, for at least 18 days, with a minimum of 12 h day(-1) of exposure.

Living high-training low: effect on erythropoiesis and aerobic performance in highly-trained swimmers.

The "living high-training low" model (LHTL), i.e., training in normoxia but sleeping/living in hypoxia, is designed to improve the athletes performance. However, LHTL efficacy still remains controversial and also little is known about the duration of its potential benefit. This study tested whether LHTL enhances aerobic performance in athletes, and if any positive effect may last for up to 2 weeks after LHTL intervention. Eighteen swimmers trained for 13 days at 1,200 m while sleeping/living at 1,200 m in ambient air (control, n=9) or in hypoxic rooms (LHTL, n=9, 5 days at simulated altitude of 2,500 m followed by 8 days at simulated altitude of 3,000 m, 16 h day(-1)). Measures were done before 1-2 days (POST-1) and 2 weeks after intervention (POST-15). Aerobic performance was assessed from two swimming trials, exploring .VO(2max) and endurance performance (2,000-m time trial), respectively. Reticulocyte, serum EPO and soluble transferrin receptor responses were not altered by LHTL, whereas reticulocytes decreased in controls. In POST-1 (vs. before): red blood cell volume increased in LHTL only (+8.5%, P=0.03), .VO(2max) tended to increase more in LHTL (+8.1%, P=0.09) than in controls (+2.5%, P=0.21) without any difference between groups (P=0.42) and 2,000-m performance was unchanged with LHTL. In POST-15, both performance and hematological parameters were similar to initial levels. Our results indicate that LHTL may stimulate red cell production, without any concurrent amelioration of aerobic performance. The absence of any prolonged benefit after LHTL suggests that this LHTL model cannot be recommended for long-term purposes.