The Quebec Low Back Pain Study: a protocol for an innovative 2-tier provincial cohort.

INTRODUCTION: The neurobiological mechanisms underlying recovery from or persistence of low back pain (LBP) remain misunderstood, limiting progress toward effective management. We have developed an innovative two-tier design to study the transition from acute to chronic LBP. The objective of the first tier is to create a provincial web-based infrastructure to recruit and monitor the trajectory of individuals with acute LBP. The objective of the second tier is to fuel hypothesis-driven satellite data collection centers with specialized expertise to study the role of biomechanical, epigenetic, genetic, neuroanatomical, ontological, physiological, psychological, and socioeconomic factors in LBP chronicity. METHODS: This article describes the first tier of the protocol: establishment of the Core Dataset and Cohort. Adults with acute LBP will be recruited through networks, media, and health care settings. A web-based interface will be used to collect self-reported variables at baseline and at 3, 6, 12, and 24 months. Acute LBP will be defined according to the Dionne 2008 consensus. Measurements will include the Canadian minimum data set for chronic LBP research, DN4 for neuropathic pain, comorbidities, EQ-5D-5L for quality of life, and linkage with provincial medico-administrative databases. The primary outcome will be the transition to chronic LBP, as defined by Deyo 2014. Secondary outcomes include health care resource utilization, disability, sick leave, mood, and quality of life. PERSPECTIVE: This study brings together diverse research expertise to investigate the transition from acute to chronic LBP, characterize the progression to recovery or chronicity, and identify patterns associated with that progression.

Muscle Oxygen Supply and Use in Type 1 Diabetes, From Ambient Air to the Mitochondrial Respiratory Chain: Is There a Limiting Step?

OBJECTIVE: Long before clinical complications of type 1 diabetes (T1D) develop, oxygen supply and use can be altered during activities of daily life. We examined in patients with uncomplicated T1D all steps of the oxygen pathway, from the lungs to the mitochondria, using an integrative ex vivo (muscle biopsies) and in vivo (during exercise) approach. RESEARCH DESIGN AND METHODS: We compared 16 adults with T1D with 16 strictly matched healthy control subjects. We assessed lung diffusion capacity for carbon monoxide and nitric oxide, exercise-induced changes in arterial O2 content (SaO2, PaO2, hemoglobin), muscle blood volume, and O2 extraction (via near-infrared spectroscopy). We analyzed blood samples for metabolic and hormonal vasoactive moieties and factors that are able to shift the O2-hemoglobin dissociation curve. Mitochondrial oxidative capacities were assessed in permeabilized vastus lateralis muscle fibers. RESULTS: Lung diffusion capacity and arterial O2 transport were normal in patients with T1D. However, those patients displayed blunted exercise-induced increases in muscle blood volume, despite higher serum insulin, and in O2 extraction, despite higher erythrocyte 2,3-diphosphoglycerate. Although complex I- and complex II-supported mitochondrial respirations were unaltered, complex IV capacity (relative to complex I capacity) was impaired in patients with T1D, and this was even more apparent in those with long-standing diabetes and high HbA1c. [Formula: see text]O2max was lower in patients with T1D than in the control subjects. CONCLUSIONS: Early defects in microvascular delivery of blood to skeletal muscle and in complex IV capacity in the mitochondrial respiratory chain may negatively impact aerobic fitness. These findings are clinically relevant considering the main role of skeletal muscle oxidation in whole-body glucose disposal.

Exercise training and high-fat diet elicit endocannabinoid system modifications in the rat hypothalamus and hippocampus

The purpose of the present study was to examine the effect of chronic exercise on the hypothalamus and hippocampus levels of the endocannabinoids (eCBs) anandamide (AEA) and 2-arachidonoylglycerol (2-AG) and of two AEA congeners and on the expression of genes coding for CB1, CB2 receptors (Cnr1 and Cnr2, respectively), and the enzymes responsible for eCB biosynthesis and degradation, in rats fed with a standard or high-fat diet. Male Wistar rats (n = 28) were placed on a 12-week high-fat (HFD) or standard diet period, followed by 12 weeks of exercise training for half of each group. Tissue levels of eCBs and related lipids were measured by liquid chromatography mass spectrometry, and expression of genes coding for CB1 and CB2 receptors and eCB metabolic enzymes was measured by quantitative real-time polymerase chain reaction (qPCR). HFD induced a significant increase in 2-AG (p < 0.01) in hypothalamus. High-fat diet paired with exercise training had no effect on AEA, 2-AG, and AEA congener levels in the hypothalamus and hippocampus. Cnr1 expression levels were significantly increased in the hippocampus in response to HFD, exercise, and the combination of both (p < 0.05). Our results indicate that eCB signaling in the CNS is sensitive to diet and/or exercise

The effects of voluntary exercise and prazosin on capillary rarefaction and metabolism in streptozotocin-induced diabetic male rats.

Type-1 diabetes mellitus (T1D) causes impairments within the skeletal muscle microvasculature. Both regular exercise and prazosin have been shown to improve skeletal muscle capillarization and metabolism in healthy rats through distinct angiogenic mechanisms. The aim of this study was to evaluate the independent and additive effects of voluntary exercise and prazosin treatment on capillary-to-fiber ratio (C:F) in streptozotocin (STZ)-treated diabetic rats. STZ (65 mg/kg) was intraperitoneally administered to male Sprague-Dawley rats (n = 36) to induce diabetes, with healthy, nondiabetic, sedentary rats (n = 10) as controls. The STZ-treated rats were then divided into sedentary (SED) or exercising (EX; 24-h access to running wheels) groups and then further subdivided into prazosin (Praz) or water (H2O) treatment groups: nondiabetic-SED-H2O, STZ-SED-H2O, STZ-EX-H2O, STZ-SED-Praz, and STZ-EX-Praz. After 3 wk, untreated diabetes significantly reduced the C:F in tibialis anterior (TA) and soleus muscles in the STZ-SED-H2O animals (both P < 0.05). Voluntary exercise and prazosin treatment independently resulted in a normalization of C:F within the TA (1.86 ± 0.12 and 2.04 ± 0.03 vs 1.71 ± 0.09, P < 0.05) and the soleus (2.36 ± 0.07 and 2.68 ± 0.14 vs 2.13 ± 0.12, P < 0.05). The combined STZ-EX-Praz group resulted in the highest C:F within the TA (2.26 ± 0.07, P < 0.05). Voluntary exercise volume was negatively correlated with fed blood glucose levels (r2 = -0.7015, P < 0.01) and, when combined with prazosin, caused further enhanced nonfasted glucose (P < 0.01). Exercise and prazosin reduced circulating nonesterified fatty acids more than either stimulus alone (P < 0.05). These results suggest that the distinct stimulation of angiogenesis, with both regular exercise and prazosin treatment, causes a cooperative improvement in the microvascular complications associated with T1D.NEW & NOTEWORTHY It is currently well established that poorly controlled diabetes reduces both skeletal muscle mass and muscle capillarization. These muscle-specific features of diabetes may, in turn, compromise insulin sensitivity and glucose control. Using a model of streptozotocin-induced diabetes, we show the vascular complications linked with disease and how chronic exposure to exercise and prazosin (an α1-adrenergic antagonist) can reduce these complications and improve glycemic control.

Glucagon responses to exercise-induced hypoglycaemia are improved by somatostatin receptor type 2 antagonism in a rat model of diabetes.

AIMS/HYPOTHESIS: Regular exercise is at the cornerstone of care in type 1 diabetes. However, relative hyperinsulinaemia and a blunted glucagon response to exercise promote hypoglycaemia. Recently, a selective antagonist of somatostatin receptor 2, PRL-2903, was shown to improve glucagon counterregulation to hypoglycaemia in resting streptozotocin-induced diabetic rats. The aim of this study was to test the efficacy of PRL-2903 in enhancing glucagon counterregulation during repeated hyperinsulinaemic exercise. METHODS: Diabetic rats performed daily exercise for 1 week and were then exposed to saline (154 mmol/l NaCl) or PRL-2903, 10 mg/kg, before hyperinsulinaemic exercise on two separate occasions spaced 1 day apart. In the following week, animals crossed over to the alternate treatment for a third hyperinsulinaemic exercise protocol. RESULTS: Liver glycogen content was lower in diabetic rats compared with control rats, despite daily insulin therapy (p < 0.05). Glucagon levels failed to increase during exercise with saline but increased three-to-six fold with PRL-2903 (all p < 0.05). Glucose concentrations tended to be higher during exercise and early recovery with PRL-2903 on both days of treatment; this difference did not achieve statistical significance (p > 0.05). CONCLUSIONS/INTERPRETATION: PRL-2903 improves glucagon counterregulation during exercise. However, liver glycogen stores or other factors limit the prevention of exercise-induced hypoglycaemia in rats with streptozotocin-induced diabetes.

Exercise training and high-fat diet elicit endocannabinoid system modifications in the rat hypothalamus and hippocampus.

The purpose of the present study was to examine the effect of chronic exercise on the hypothalamus and hippocampus levels of the endocannabinoids (eCBs) anandamide (AEA) and 2-arachidonoylglycerol (2-AG) and of two AEA congeners and on the expression of genes coding for CB1, CB2 receptors (Cnr1 and Cnr2, respectively), and the enzymes responsible for eCB biosynthesis and degradation, in rats fed with a standard or high-fat diet. Male Wistar rats (n = 28) were placed on a 12-week high-fat (HFD) or standard diet period, followed by 12 weeks of exercise training for half of each group. Tissue levels of eCBs and related lipids were measured by liquid chromatography mass spectrometry, and expression of genes coding for CB1 and CB2 receptors and eCB metabolic enzymes was measured by quantitative real-time polymerase chain reaction (qPCR). HFD induced a significant increase in 2-AG (p < 0.01) in hypothalamus. High-fat diet paired with exercise training had no effect on AEA, 2-AG, and AEA congener levels in the hypothalamus and hippocampus. Cnr1 expression levels were significantly increased in the hippocampus in response to HFD, exercise, and the combination of both (p < 0.05). Our results indicate that eCB signaling in the CNS is sensitive to diet and/or exercise.

Voluntary exercise improves metabolic profile in high-fat fed glucocorticoid-treated rats.

Diabetes is rapidly induced in young male Sprague-Dawley rats following treatment with exogenous corticosterone (CORT) and a high-fat diet (HFD). Regular exercise alleviates insulin insensitivity and improves pancreatic ß-cell function in insulin-resistant/diabetic rodents, but its effect in an animal model of elevated glucocorticoids is unknown. We examined the effect of voluntary exercise (EX) on diabetes development in CORT-HFD-treated male Sprague-Dawley rats (∼6 wk old). Animals were acclimatized to running wheels for 2 wk, then given a HFD, either wax (placebo) or CORT pellets, and split into 4 groups: placebo-sedentary (SED) or -EX and CORT-SED or -EX. After 2 wk of running combined with treatment, CORT-EX animals had reduced visceral adiposity, and increased skeletal muscle type IIb/x fiber area, oxidative capacity, capillary-to-fiber ratio and insulin sensitivity compared with CORT-SED animals (all P < 0.05). Although CORT-EX animals still had fasting hyperglycemia, these values were significantly improved compared with CORT-SED animals (14.3 ± 1.6 vs. 18.8 ± 0.9 mM). In addition, acute in vivo insulin response to an oral glucose challenge was enhanced ∼2-fold in CORT-EX vs. CORT-SED (P < 0.05) which was further demonstrated ex vivo in isolated islets. We conclude that voluntary wheel running in rats improves, but does not fully normalize, the metabolic profile and skeletal muscle composition of animals administered CORT and HFD.

Regional cerebral hemodynamic response to incremental exercise is blunted in poorly controlled patients with uncomplicated type 1 diabetes.

OBJECTIVE: Cerebral vasoreactivity to pharmacologically induced hypercapnia is impaired in poorly controlled patients with type 1 diabetes but otherwise free from microangiopathy. However, whether this response is also compromised during exercise, a daily-life physiological condition challenging regional cerebral hemodynamics, is unknown. We aimed to investigate prefrontal cortex hemodynamics during incremental maximal exercise in patients with uncomplicated type 1 diabetes, taking into account long-term glycemic control as well as exercise- and diabetes-influenced vasoactive stimuli. RESEARCH DESIGN AND METHODS: Two groups of patients (type 1 diabetes with adequate glycemic control [T1D-A], n = 8, HbA1c 6.8 ± 0.7% [51 ± 7.7 mmol/mol]; type 1 diabetes with inadequate glycemic control [T1D-I], n = 10, HbA1c 9.0 ± 0.7% [75 ± 7.7 mmol/mol]) were compared with 18 healthy control subjects (CON-A and CON-I) matched for physical activity and body composition. Throughout exercise, near-infrared spectroscopy allowed investigation of changes in oxyhemoglobin (O2Hb), deoxyhemoglobin (HHb), and total hemoglobin (THb) in the prefrontal cortex. Venous and arterialized capillary blood was sampled during exercise to assess for factors that may alter prefrontal cortex hemodynamics and oxygenation. RESULTS: No differences were observed between T1D-A and CON-A, but VO2max was impaired (P < 0.05) and cerebral blood volume (THb) increase blunted (P < 0.05) in T1D-I compared with CON-I. Nonetheless, O2Hb appeared unaltered in T1D-I probably partly due to blunting of simultaneous neuronal oxygen extraction (i.e., a lower HHb increase; P < 0.05). There were no intergroup differences in arterial oxygen content, Paco2, pH, [K(+)], and free insulin levels. CONCLUSIONS: Maximal exercise highlights subtle disorders of both hemodynamics and neuronal oxygenation in the prefrontal cortex of poorly controlled patients with type 1 diabetes. These findings may warn clinicians of brain endothelial dysfunction occurring even before overt microangiopathy during exercise.

Muscle oxygen supply impairment during exercise in poorly controlled type 1 diabetes.

PURPOSE: Aerobic fitness, as reflected by maximal oxygen (O2) uptake (VO2max), is impaired in poorly controlled patients with type 1 diabetes. The mechanisms underlying this impairment remain to be explored. This study sought to investigate whether type 1 diabetes and high levels of glycated hemoglobin (HbA1c) influence O2 supply including O2 delivery and release to active muscles during maximal exercise. METHODS: Two groups of patients with uncomplicated type 1 diabetes (T1D-A, n = 11, with adequate glycemic control, HbA1c <7.0%; T1D-I, n = 12 with inadequate glycemic control, HbA1c >8%) were compared with healthy controls (CON-A, n = 11; CON-I, n = 12, respectively) matched for physical activity and body composition. Subjects performed exhaustive incremental exercise to determine VO2max. Throughout the exercise, near-infrared spectroscopy allowed investigation of changes in oxyhemoglobin, deoxyhemoglobin, and total hemoglobin in the vastus lateralis. Venous and arterialized capillary blood was sampled during exercise to assess arterial O2 transport and factors able to shift the oxyhemoglobin dissociation curve. RESULTS: Arterial O2 content was comparable between groups. However, changes in total hemoglobin (i.e., muscle blood volume) was significantly lower in T1D-I compared with that in CON-I. T1D-I also had impaired changes in deoxyhemoglobin levels and increase during high-intensity exercise despite normal erythrocyte 2,3-diphosphoglycerate levels. Finally, VO2max was lower in T1D-I compared with that in CON-I. No differences were observed between T1D-A and CON-A. CONCLUSIONS: Poorly controlled patients displayed lower VO2max and blunted muscle deoxyhemoglobin increase. The latter supports the hypotheses of increase in O2 affinity induced by hemoglobin glycation and/or of a disturbed balance between nutritive and nonnutritive muscle blood flow. Furthermore, reduced exercise muscle blood volume in poorly controlled patients may warn clinicians of microvascular dysfunction occurring even before overt microangiopathy.

Mechanical ventilatory constraints during incremental exercise in healthy and cystic fibrosis children.

AIM: To analyze breathing pattern and mechanical ventilatory constraints during incremental exercise in healthy and cystic fibrosis (CF) children. METHODS: Thirteen healthy children and 6 children with cystic fibrosis volunteered to perform an incremental test on a treadmill. Exercise tidal flow/volume loops were plotted every minute within a maximal flow/volume loop (MFVL). Expiratory flow limitation (expFL expressed in %Vt) was evaluated and end-expiratory and end-inspiratory lung volumes (EELV and EILV) were estimated from expiratory reserve volume relative to vital capacity (ERV/FVC) and from inspiratory reserve volume relative to vital capacity (IRV/FVC). RESULTS: During the incremental exercise, expFL was first observed at 40% of maximal aerobic speed in both groups. At maximal exercise, 46% of healthy children and 83% of CF children presented expFL, without significant effect of cystic fibrosis on the severity of expFL. According to the two-way ANOVA results, both groups adopted similar breathing pattern and breathing strategies as no significant effect of CF has been revealed. But, according to one-way ANOVA results, a significant increase of ERV/FVC associated with a significant decrease of IRV/FVC from resting value shave been observed in healthy children at maximal exercise, but not in CF children. DISCUSSION: The hypothesis of this study was based on the assumption that mild cystic fibrosis could induce more frequent and more severe mechanical ventilatory constraints due to pulmonary impairment and breathing pattern disturbances. But, this study did not succeed to highlight an effect of mild cystic fibrosis on the mechanical ventilatory constraints (expFL and dynamic hyperinflation) that occur during an incremental exercise. This absence of effect could be due to the absence of an impact of the disease on spirometric data, breathing pattern regulation during exercise and breathing strategy.

A test to assess aerobic and anaerobic parameters during maximal exercise in young girls.

The Wingate cycle test (WAnT) is a 30-s test commonly used to estimate anaerobic work capacity (AWC). However, the test may be too short to fully deplete anaerobic energy reserves. We hypothesized that a 90-s all-out isokinetic test (ISO_90) would be valid to assess both aerobic and anaerobic capacities in young females. Eight girls (11.9 ± 0.5 y) performed an exhaustive incremental test, a WAnT and an ISO_90. Peak VO2 attained during the ISO_90 was significantly greater than VO2peak. Mean power, end power, fatigue index, total work done and AWC were not significantly different between the WAnT and after 30 s of the 90-s test (i.e., ISO_30). However, 95% limits of agreement showed large variations between the two tests when comparing all anaerobic parameters. It is concluded that an ISO-90 may be a useful test to assess aerobic capacity in young girls. However, since the anaerobic parameters derived from the ISO_30 did not agree with those derived from a traditional WAnT, the validity of using an ISO_90 to assess anaerobic performance and capacity within this population group remains unconfirmed.

Time to exhaustion and time spent at a high percentage of VO2max in severe intensity domain in children and adults.

The aim of the study was to compare time spent at a high percentage of VO2max (>90% of VO2max) (ts90%), time to achieve 90% of VO2max (ta90%), and time to exhaustion (TTE) for exercise in the severe intensity domain in children and adults. Fifteen prepubertal boys (10.3 ± 0.9 years) and 15 men (23.5 ± 3.6 years) performed a maximal graded exercise to determine VO2max, maximal aerobic power (MAP) and power at ventilatory threshold (PVTh). Then, they performed 4 constant load exercises in a random order at PVTh plus 50 and 75% of the difference between MAP and PVTh (PΔ50 and PΔ75) and 100 and 110% of MAP (P100 and P110). VO2max was continuously monitored. The P110 test was used to determine maximal accumulated oxygen deficit (MAOD). No significant difference was found in ta90% between children and adults. ts90% and TTE were not significantly different between children and adults for the exercises at PΔ50 and PΔ75. However, ts90% and TTE during P100 (p < 0.05 and p < 0.01, respectively) and P110 (p < 0.001) exercises were significantly shorter in children. Children had a significantly lower MAOD than adults (34.3 ± 9.4 ml · kg vs. 53.6 ± 11.1 ml · kg). A positive relationship (p < 0.05) was obtained between MAOD and TTE values during the P100 test in children. This study showed that only for intensities at, or higher than MAP, lower ts90% in children was linked to a reduced TTE, compared to adults. Shorter TTE in children can partly be explained by a lower anaerobic capacity (MAOD). These results give precious information about exercise intensity ranges that could be used in children's training sessions. Moreover, they highlight the implication of both aerobic and anaerobic processes in endurance performances in both populations.

Comparison of mechanical ventilatory constraints between continuous and intermittent exercises in healthy prepubescent children.

BACKGROUND: The aim of this study was to evaluate the occurrence and severity of mechanical ventilatory constraints in healthy prepubescent children during continuous and intermittent exercise. METHODS: Twelve prepubescent children (7-11 years old) performed 7 exercises on a treadmill: one graded test for the determination of maximal aerobic speed (MAS), three continuous exercises (CE) at 60, 70, and 80% of MAS and three intermittent exercises (IE), alternating 15 sec of exercise with 15 sec of passive recovery, at 90, 100, and 110% of MAS. During each CE and IE, tidal flow/volume loops were plotted within a maximal flow/volume loop (MFVL) measured at rest before each exercise. Expiratory flow limitation (expFL expressed in %Vt) was defined as the part of exercise tidal volume (Vt) meeting the boundary of MFVL. Breathing strategy was estimated by measuring inspiratory capacity relative to forced vital capacity and tidal volume relative to inspiratory capacity. Other breathing pattern parameters (ventilation VE, Vt, respiratory frequency f) were continuously recorded during exercise. RESULTS: An "intensity" effect was found for VE during CE (P < 0.001) but not during IE (P = 0.08). The increase in VE was predominantly assumed by an increase in f for both exercise modalities. During each exercise, several children heterogeneously experienced expFL ranging between 10 and 90%Vt. For all exercises, Vt was predominantly regulated by an increase in Vt/IC with no change in IC/FVC from rest to exercise. Finally, no significant "modality" effect was found for mechanical ventilatory constraint parameters (expFL, Vt/IC, and IC/FVC). DISCUSSION: We could conclude that neither of the modalities studied induced more mechanical ventilatory constraints than the other, but that exercise intensities specific to each modality might be greater sources of exacerbation for mechanical ventilatory constraints.

Assessment of child-specific aerobic fitness and anaerobic capacity by the use of the power-time relationships constants.

This study first aimed to compare critical power (CP) and anaerobic work capacity (AWC), to laboratory standard evaluation methods such as maximal oxygen uptake (VO(2)max) and maximal accumulated oxygen deficit (MAOD). Secondly, this study compared child and adult CP and AWC values. Subjects performed a maximal graded test to determine VO(2)max and maximal aerobic power (MAP); and four constant load exercises. In children, CP (W * kg(-1)) was related to VO(2)max (ml * kg(-1) * min(-1); r = .68; p = .004). AWC (J * kg(-1) in children was related to MAOD (r = .58; p = .018). Children presented lower AWC (J * kg(-1); p = .001) than adults, but similar CP (%MAP) values. CP (%MAP and W * kg(-1) and AWC (J * kg(-1) were significantly related to laboratory standard evaluation methods but low correlation indicated that they cannot be used interchangeably. CP (%MAP) was similar in children and adults, but AWC (J * kg(-1) was significantly lower in children. These conclusions support existing knowledge related to child-adults characteristics.

Reproducibility of measurement of muscle deoxygenation in children during exercise.

This study was designed to test the reproducibility of muscle oxygenation by NIRS in children during exercise. Twelve healthy non-obese and non-trained children performed one maximal graded test, and four 6-min constant load cycle exercises. Deoxy-hemoglobin (Hb/Mb- H+) data were averaged every 1, 5, 10, 20 and 30s. Hb/Mb- H+ data averaged every 5, 10, 20 and 30s showed good reproducibility. When averaged every second, Hb/Mb-H+ values were reproducible after the first minute of exercise. Based on 1s averaged signal modeling, time period and t values for Hb/Mb-H+ were not reproducible but mean response time values showed an acceptable reproducibility.

Correspondences between continuous and intermittent exercises intensities in healthy prepubescent children.

The aim of this article is to determine correspondences between three levels of continuous and intermittent exercise (CE and IE, respectively) in terms of steady-state oxygen uptake (VO(2SS)) and heart rate (HR) in children. Fourteen healthy children performed seven exercises on a treadmill: one graded test for the determination of maximal aerobic speed (MAS), three CE at 60, 70 and 80% of MAS (CE60, CE70 and CE80) and three IE (alternating 15 s of exercise intercepted with 15 s of passive recovery) at 90, 100 and 110% of MAS (IE90, IE100 and IE110). Mean VO(2SS) and mean HR were determined for both continuous and intermittent exercises. For comparison, three associations were designed: CE60 versus IE90, CE70 versus IE100 and CE80 versus IE110. No VO(2SS) difference was observed for CE60 versus IE90 and CE70 versus IE100 whereas a significant difference (P < 0.01) was found for CE80 versus IE110 (1.36 +/- 0.45 vs. 1.19 +/- 0.38 L min(-1), respectively). Significant linear regressions were found for the three CE versus IE associations for VO(2SS) (0.60 < r (2) < 0.99, P < 0.05). For the three associations, mean HR presented no significant difference. Only one significant relation was found for CE80 versus IE110 association (r(2) = 0.49, P < 0.05). Correspondences between CE and IE intensities are possible in terms of VO(2SS) whatever the level of exercise; even if for high intensities, VO(2SS) was higher during CE. These results demonstrated that it is possible to diversify the exercise modality while conserving exercise individualization.

Influence of recovery intensity on time spent at maximal oxygen uptake during an intermittent session in young, endurance-trained athletes.

In this study, we examined the effects of three recovery intensities on time spent at a high percentage of maximal oxygen uptake (t90[Vdot]O(2max)) during a short intermittent session. Eight endurance-trained male adolescents (16 +/- 1 years) performed four field tests until exhaustion: a graded test to determine maximal oxygen uptake ([Vdot]O(2max); 57.4 +/- 6.1 ml x min(-1) . kg(-1)) and maximal aerobic velocity (17.9 +/- 0.4 km x h(-1)), and three intermittent exercises consisting of repeat 30-s runs at 105% of maximal aerobic velocity alternating with 30 s active recovery at 50% (IE(50)), 67% (IE(67)), and 84% (IE(84)) of maximal aerobic velocity. In absolute values, mean t90[Vdot]O(2max) was not significantly different between IE(50) and IE(67), but both values were significantly longer compared with IE(84). When expressed in relative values (as a percentage of time to exhaustion), mean t90[Vdot]O(2max) was significantly higher during IE(67) than during IE(50). Our results show that both 50% and 67% of maximal aerobic velocity of active recovery induced extensive solicitation of the cardiorespiratory system. Our results suggest that the choice of recovery intensity depends on the exercise objective.