Recovery (Passive vs. Active) during Interval Training ...

Training & Testing 1

IJSM/3025/12.10.2012/Macmillan IJSM/3025/12.10.2012/Macmillan

Recovery (Passive vs. Active) during Interval Training and Plasma Catecholamine Responses

Authors

A. B. Abderrahmane1, J. Prioux2, K. Chamari3, Z. Tabka4, A. Bouslama5, I. Mrizek6, H. Zouhal7

Affiliations

Affiliation addresses are listed at the end of the article

Key words ▶ adrenaline ● ▶ noradrenaline ● ▶ intermittent exercise ● ▶ endurance ●

Abstract

▼

The effect of recovery mode (Active [AR] vs. Passive [PR]) on plasma catecholamine (Adrenaline [A] and Noradrenaline [NA]) responses to maximal exercise (Exemax) was studied during interval training (IT). 24 male subjects (21.1 ± 1.1 years) were randomly assigned to a control group (CG, n = 6), AR training group (ARG, n = 9) or PR group (PRG, n = 9). ARG and PRG participated in an IT program 3 times a week for 7 weeks. Before and after training, maximal oxygen uptake (VO2max) and maximal aerobic velocity (MAV) were measured. Plasma A and NA were determined at rest,

Introduction

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accepted after revision September 27, 2012 Bibliography DOI http://dx.doi.org/ 10.1055/s-0032-1327697 Int J Sports Med 2012; 33: 1–6 © Georg Thieme Verlag KG Stuttgart · New York ISSN 0172-4622 Correspondence Dr. Hassane Zouhal, PhD Laboratoire Mouvement Sport Sante UFR APS Campus la Harpe Av Charles Tillon 35044 Rennes France Tel.: + 33/2/99 14 17 75 Fax: + 33/2/99 14 17 74 [email protected]

Intermittent running exercise (interval training [IT]) is well known as an effective method to improve aerobic fitness [13]. IT allows a high level of oxygen uptake to be elicited [22] and longitudinal studies have demonstrated its effectiveness in improving VO2max [3]. This type of exercise is known to be characterized by several factors such as intensity and duration of exercise and recovery, with or without series (e. g. a number of repetitions interspersed by a relatively long recovery) and the recovery mode, i. e., passive vs. active recovery) [1]. Concerning the latter factor, there is a belief in the training field that active recovery allows for better performance during the next period of high-intensity exercise than does passive recovery. In this context, Dorado et al. [4] have shown that during a highintensity IT performed until exhaustion (around 2 min at 110 % of maximal power output, alternated with 5 min, active/passive recovery); active recovery enhanced work capacity in the second exercise bout by increasing the aerobic energy yield compared with passive recovery. These authors partly explained their findings by accelerated VO2 kinetics.

at the end of Exemax and after 10 and 30 min of recovery. Training induced significant changes only in ARG: an increase of VO2max and MAV along with a significant increase of A and NA at the end of Exemax (2.82 ± 0.15 vs. 1.03 ± 0.15 nmol/l and 7.22 ± 0.36 vs. 6.65 ± 0.57 nmol/l, respectively p < 0.05). The ratio A/NA measured at the end of Exemax also increased significantly after training (0.41 ± 0.11 vs. 0.16 ± 0.08, P > 0.05). The present results show that IT with AR induces a significant increase of A and NA concentrations in response to maximal exercise. The study furthermore shows that IT program with AR may induce more stress than the same program with PR.

Considerable information is available concerning the physiological adaptations responsible for the improvements in endurance performance observed following high-intensity IT in sedentary and recreationally trained individuals [13]. In contrast, relatively little is known concerning the hormonal responses that occur following high-intensity interval training and their implication on the enhancement of performance. Catecholamines (adrenaline (A) and noradrenaline (NA)), known as stress hormones, are responsible for many adaptive processes both at rest and during exercise [11, 29]. In fact these hormones are known to affect the regulation of intermediary metabolism, affecting glucose production, muscle glycogen mobilization and lipolysis, all of which affect exercise metabolism and performance [11, 29]. At rest and in response to exercise, catecholamine concentrations are influenced by several factors such as exercise characteristics, gender, and training status [29]. Indeed, endurance continuous training exercises are known to increase A and NA both at rest and in response to several stimuli [28, 29]. Several studies have reported greater plasma A concentrations in endurance-trained subjects compared to untrained ones [18, 29]. These differences were

■ Proof copy for correction only. All forms of publication, duplication or distribution prohibited under copyright law. ■ Abderrahmane AB et al. Recovery (Passive vs. Active)… Int J Sports Med 2012; 33: 1–6

2 Training & Testing


Table 1 Morphological characteristics and physiological values of the participants determined during the maximal graded test for both trained and control groups ARG, (n = 9), PRG, (n = 9) and CG, (n = 6). ARG (n = 9) age (year) height (cm) weight (kg) %fat mass ( %) MAV (km.h-1) VO2max (l.min-1) VO2max (ml.min-1.kg-1) HR (bpm) RER [La]rest [La]end [La] 10’

PRG (n = 9)

CG (n = 6)

BT

AT

BT

AT

BT

AT

21.1 ± 1.0 179 ± 4 76.8 ± 10.9 $$ 10.6 ± 3.4 16.0 ± 1.7 4.4 ± 0.7 59 ± 9 198 ± 6 1.10 ± 0.03 2.1 ± 0.3 6.5 ± 1.8 5.6 ± 1.4

21.1 ± 1.0 179 ± 4 77.5 ± 10.4 $$ 10.9 ± 3.5 17.3 ± 1.2 * 4.8 ± 0.7 63 ± 10* 197 ± 6 1.10 ± 0.05 2.4 ± 0.7 6.6 ± 1.2 5.6 ± 0.9

21.0 ± 1.0 182 ± 5 73.5 ± 10.8 ££ 11.8 ± 4.1 15.6 ± 1.4 4.2 ± 0.4 59 ± 5 200 ± 5 1.10 ± 0.06 1.7 ± 0.3 6.8 ± 1.4 5.8 ± 1.3

21.0 ± 1.0 181 ± 4 74.2 ± 10.3 ££ 12.5 ± 4.6 16.6 ± 1.5 4.4 ± 0.5 60 ± 6 198 ± 4 1.10 ± 0.04 2.1 ± 0.6 6.3 ± 1.4 6.0 ± 1.7

21.1 ± 1.0 177 ± 4 66.2 ± 6.1 10.7 ± 1.9 16.1 ± 0.4 4.1 ± 0.4 60 ± 2 200 ± 6 1.10 ± 0.10 2.5 ± 0.6 6.7 ± 0.9 4.9 ± 2.8

21.1 ± 1.0 177 ± 4 67.0 ± 6.5 10.9 ± 2.2 15.8 ± 0.6 4.0 ± 0.4 60 ± 4 199 ± 3 1.20 ± 0.10 2.2 ± 0.8 6.2 ± 1.2 3.9 ± 1.9

Data are means ( ± SD) Heart rate (HR), Respiratory exchange ratio (RER), Oxygen consumption (VO2max (l.min-1)), Blood lactate (Lac), Maximal aerobic velocity (MAV), Active recovery group (ARG), Passive recovery group (PRG) and Control group (CG), Before training (BT), After training (AT) *: Significantly different from rest values: *: p < 0.05 $: Significantly different between ARG and CG: $$: p < 0.01 £: Significantly different between PRG and CG: ££ p < 0.01

observed both in response to physical exercises and to other different stimuli such as insulin-induced hypoglycaemia as well as after stimulation with hypoxia, glucagon or caffeine. This phenomenon was called “sports adrenal medulla” [9–11] which corresponds to a higher capacity to secrete A in trained subjects. Nevertheless, concerning the type of training sessions, which preferentially increase the adrenergic responses to exercise, data remain conflicting. In fact, while [9] reported greater A responses in endurance-trained subjects compared to untrained ones in response to 2 min at 110 % of VO2max, [26] they did not find any significant differences between endurance-trained and untrained subjects in response to a Wingate-test. However, these authors reported significant higher plasma A concentration in sprint-trained subjects. Other results from the same lab [8] observed no significant differences between middle and long distance runners concerning catecholamine responses to the Wingate-test. Thus, these authors suggested that endurance-trained subjects involved in the study [9] might have been more intensively trained than those tested in study [19]. Also in line with this, [19] when comparing anaerobic-trained subjects and aerobic-trained subjects, also reported greater A concentration in the anaerobic-trained group in response to a 2-min prolonged sprint. These authors also suggested that the intensity of the training sessions rather than training volume is the most important factor that is able to induce a higher catecholamine response to exercise. In other words, intensity of training may represent the most important factor that is able to increase A responses to exercise. In this context, IT exercise with passive recovery is more intense than the same exercise with active recovery [21]. However, little is known about the effect of endurance interval training exercises on catecholamine responses and especially the effect of the mode of recovery, active vs. passive recovery. Consequently, because of the paucity of data that relate directly to our understanding of the catecholamine responses that occur following high-intensity interval training, this study investigated the effects of recovery mode, i. e., active vs. passive recovery during an IT program on plasma catecholamine responses at rest and in response to maximal exercise after IT exercise train-

ing. IT exercise with active recovery is known to be more stressful than the same exercise (e. g. same volume) with passive recovery [3, 4, 21, 22]. In fact, it has been shown that IT exercise with active recovery induces higher values of heart rate, oxygen uptake and blood lactate concentrations than when the same exercise is executed with passive recovery [3, 4]. Consequently, we hypothesized that plasma catecholamine responses will be higher after the IT program with active than with passive recovery. In this study, the maximal graded test was chosen as it has been reported that the catecholamine responses reach higher values immediately after this type of exercise than in response to submaximal aerobic exercise [16]. To investigate the responsiveness of the adrenal medulla to the sympathetic nervous input, the A/ NA ratio was also compared between the 2 groups [28, 26].

Materials and Methods

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Subjects 24 adult male subjects volunteered to participate in this study. Their morphological characteristics measured before and after ▶ Table 1. The subjects were modertraining are displayed in ● ately trained and never practiced IT before this study. The participants were randomly assigned in counterbalanced order to a control group (CG, n = 6, 21.1 ± 1.0 years old) and to 2 intermittent recovery groups: active recovery group (ARG, n = 9, 21.1 ± 1.0 years old) and passive recovery group (PRG, n = 9, 21.0 ± 1.0 years old). Prior to testing, the participants underwent a medical examination and were fully informed about the experimental procedures. Written informed consent was obtained from all participants in accordance with the international ethical standards [7].

Testing procedure The participants visited the laboratory for a familiarization session with all the material of the experiment. During this session the anthropometric measurements (height, body mass and % body fat mass [ %FM]) were determined. The %FM was estimated




Table 2 The training program for the trained groups: active recovery group (ARG) and passive recovery group (PRG).

ARG Training sessions PRG

Week 1

Week 2

Week 3

Week 4

Week 5

Week 6

Week 7

2× (8 × 30 s/30 s) 100 %/50 % MAV R = 5 min 2× (12 × 30 s/30 s) 100 %/0 % MAV R = 5 min







MAV: Maximal aerobic velocity. R: Passive recovery between series. IE A: Trained group with active recovery. IEP: Trained group with passive recovery. Example: [2 × (8 × 30sIE) 100 %/50 % MAV. R = 5 min] it means that the subject had to run 2 series of 8 times 30 s/30 s composed of 30 s running at 100 % of MAV and 30 s active recovery at 50 % of MAV. The subject recovers passively 5 min between each series. Each session is repeated 3 times a week

from 4 skin-folds thickness (biceps, triceps, sub-scapular and supra-iliac), according to the method of Durnin and Rahaman [5]. Fat free mass (FFM) was calculated by subtracting total body fat from body mass. All participants performed a maximal graded test according to the procedure described by Leger and Boucher [14] until exhaustion to determine maximal oxygen uptake (VO2max) and their maximal aerobic velocity (MAV) before and after the 7-week training program. The test took place in the morning 1 h 30 min after a standardized breakfast (10 kcal/kg, 55 %, of which came from carbohydrates, 33 % from lipids and 12 % from proteins, as determined by an experienced nutritionist). The same standardized breakfast was provided to all the subjects both before and after the training period and did not contain coffee, tea, and food containing amines like banana and vanilla as it may interfere with catecholamine analysis. During the maximal graded test, respiratory gas exchange was measured breath-by-breath using a calibrated portable telemetric system (Cosmed K4b2, Rome, Italy). Heart rate (HR) was continuously monitored (Polar Electro, Kempele, Finland) with 5-s interval recording.

Blood sampling Upon arriving, before the maximal graded test, each subject lay supine on a bed and a heparinised catheter (Insyte-W, 1.1 mm o. d. × 30 mm) was inserted into an antecubital vein and thereafter the first blood sample (20 mL) was drawn. 3 other venous blood samples were drawn, immediately at the end of the graded test and after 10 and 30 min of recovery. At each extraction, the blood was collected in a vacutainer tube containing Ethylene Diamine Tetra Acetic Acid (EDTA). Plasma from the venous blood samples was separated by centrifugation at 3 000 g for 20 min (4 ° C) (ORTO ALRESA mod. Digicen.R, Spain). Aliquots were immediately frozen and stored at − 80 ° C for use in subsequent chemical analyses. To determine maximal blood lactate concentrations ([La]), arterialized capillary blood was collected from the finger at rest, 3 min after the end of the maximal graded test and after 10 min of recovery.

Biochemical analysis Lactate was determined enzymatically using a lactate analyser (Microzym, Cetrix, France). Plasma catecholamine concentrations were measured by high-performance liquid chromatography (HPLC) (Chromosystems, Thermofinnigan, France), following the method of [12]. The detection limit of catecholamines in the described method was 0.06 nmol.l − 1 and the inter-assay coefficient of variation was 5.8 %. The responsiveness of the adrenal medulla to the sympathetic nervous activity was estimated by

the ratio A/NA as used [10, 27]. All the plasma catecholamine concentrations were corrected taking into account the plasma volume variations [23].

Training program ARG and PRG participated in an intermittent training program 3 times per week (on Monday, Wednesday and Friday) during ▶ Table 2). The training 7 weeks (21 training sessions in total) (● sessions were separated by at least 48 h to allow adequate recovery. During each session, temperature, humidity and wind speed were continuously measured with an anemometer (Kestrel 3500, Nielsen-Kellerman Co. USA). The training program was exclusively composed of intermittent exercises with active recovery for ARG or passive recovery for PRG. All sessions included 3 different periods. The sessions were preceded by a standardized warm-up, which consisted of 15 min continuous jogging, followed by 5 min stretching exercises and 5 short bursts of accelerations on the track. During every training session on the athletic track (400 m) there was one subject per lane. All different distances for each athlete (running and recovery intervals) were fixed by the examiner before every session according to individual MAV. For each training session, the subjects’ pace was given by an examiner emitting sounds using a whistle and a chronograph at regular intervals up to the end of the exercise. During the 30 s active recovery, subjects of ARG had to cover a distance determined according to their own MAV. Subjects of PRG did not run and were standing waiting for the next effort. During the recovery period (ARG and PRG), a longer sound was made at mid period (15 s) to inform the subjects of the remaining time for the end of recovery. At the end of the session they cooled down for about 15 min. Progressive overload was applied by increasing the number and/or the intensity of intermittent exercises. All training sessions were supervised by 2 members of our laboratory. In the midle of the training period (on Wednesday of the fourth week), ARG and PRG performed a maximal graded test (without respiratory gas exchange measurements) to asses & MAV in order to update the training speed of each subject. It is important to note that our 2 groups ARG and PRG had the same volume (distances covered) of training, only the modes of recovery differed between their training programs. During this period CG participated in any physical activity or physical training program.

Statistics Data were expressed as mean values ± standard deviation (SD). Sigma Stat 3.10 software (SPSS, Chicago, IL, USA) was used for statistical analysis.


4 Training & Testing


[Adrenaline] (nmol/L)

1.4 1.2 1.0 0.8 0.6 0.4 0.2 0

**

[Adrenaline] (nmol/L)

**

3.5 3.0 2.5 2.0 1.5 1.0 0.5 0

*

$

£

** *

*

[Noradrenaline] (nmol/L) $

[Noradrenaline] (nmol/L) 8

**

**

**

6

8 7 6 5 4 3 2 1 0

4 2

£

**

**

*

**

*

*

Adrenaline/Noradrenaline Ratio

0

0.6 0.5 0.4 0.3 0.2 0.1 0

Adrenaline/Noradrenaline Ratio

0.5 0.4 0.3 0.2 0.1

PRG

CG

Significantly different from rest values: *: p< 0.05; **: p< 0.001. Rest

End Exe.

10 min

ARG

PRG

CG

*: Significantly different from rest values. *: p< 0.05; **: p< 0.001. $: Significantly different between ARG and PRG, p< 0.05. £: Significantly different between ARG and CG, p< 0.05.

0 ARG

£ $

**

Rest

End Exe.

10 min

30 min

30 min

Fig. 2 Plasma adrenaline, noradrenaline concentrations and the adrenaline/noradrenaline ratio determined after training at rest, at the end of maximal exercise and after 10 and 30 min recovery for active recovery group (ARG), passive recovery group (PRG) and control group (CG).

Fig. 1 Plasma adrenaline, noradrenaline concentrations and the adrenaline/noradrenaline ratio determined before training at rest, at the end of maximal exercise and after 10 and 30 min recovery for active recovery group (ARG), passive recovery group (PRG) and control group (CG).

On the basis of a power analysis (expected standard deviation of residuals = 0.9 nmol.l − 1, desired power = 0.80 and an alpha error = 0.05), we determined that a sample size of n = 6 per group would be sufficient to detect a 2.0 nmol.l − 1 increase in A, NA and La concentrations. After testing for normal distribution (Kolmogorov-Smirnov test), differences within and between the groups were analysed using a 2-way analysis of variance for repeated measurements. After confirming significant group differences over time, post-hoc Newman-Keul’s tests were performed. Linear regression analyses were used to assess the independent contribution of adrenaline, noradrenaline and lactate to incident VO2max values. Power of the correlation analyses was calculated using a Spearman’s rho test.

Results

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▶ Table 1 shows the morphological characteristics and the phys●

iological responses to the graded maximal exercise measured before and after 7 weeks of the interval-training program. The subjects of ARG and PRG were heavier than the CG subjects both before and after the training period (p < 0.05 and 0.01, respectively, for ARG and PRG). However, this training program induced no significant effects on morphological characteristics. Before the training period there were no significant differences between the 3 groups concerning MAV and VO2max. However, training induced a significant increase (p < 0.05) of these 2 parameters for ▶ Table 1). the ARG only (●

Plasma A concentrations determined at rest, at the end of the maximal graded exercise, and after 10 and 30 min of recovery, ▶ Fig. 1, 2, before and after the training period are presented in ● respectively. The maximal graded test induced a significant increase of plasma A values determined at the end of the test for the 3 groups, ARG (p < 0.01), PRG (p < 0.01) and CG (p < 0.05), both ▶ Fig. 1) and after (● ▶ Fig. 2) the training period. Before before (● training, plasma A concentrations determined at rest, at the end of the exercise and after 10 and 30 min of recovery were similar ▶ Fig. 1). However, after training, plasma between the 3 groups (● A concentrations determined immediately at the end of the maximal exercise were significantly higher in ARG compared to ▶ Fig. 2). PRG and CG (p < 0.05) (● Before and after the training period plasma NA increased significantly (p < 0.05) in all groups after the maximal graded exercise ▶ Fig. 1, 2). Plasma NA, measured immediately at the end of the (● maximal graded test, was significantly higher in ARG compared to PRG (p < 0.05) and CG (p < 0.05) only after the training period ▶ Fig. 2). (● After the training period, A/NA ratio increased significantly (p < 0.05) in response to the maximal graded test only for ARG ▶ Fig. 2). Hence, significant differences were also observed (● after this period between our 3 groups. In the present study, the elimination of A and NA was estimated by the difference between the maximal values determined at the end of the maximal exercise and those determined after 10 min of recovery (Aend-A10 and NAend-NA10). These indexes were not significantly different between groups for A (0.23 ± 0.44 nmol.L − 1 for ARG; 0.18 ± 0.54 nmol.L − 1 for PRG and 0.32 ± 0.71 nmol.L − 1 for




CG) and for NA (3.54 ± 3.84 nmol.L − 1 for ARG; 2.21 ± 2.72 nmol.L − 1 for PRG and 2.54 ± 2.77 nmol.L − 1 for CG).

Discussion

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This study shows that interval training using active recovery mode in comparison to passive recovery mode induce a significant increase of A and NA concentrations in response to maximal exercise. Hence, this type of training is also accompanied by an increase of the adrenal medulla responsiveness to the sympathetic nervous activity as shown by the significant increase of the ratio A/NA observed in ARG. The present study shows that 7 weeks of interval training induced a significant increase of MAV and VO2max only in the ARG. These results are in agreement with results of several other studies [3, 20, 24, 25]. Indeed, in recreationally active individuals a significant increase of VO2max, MAV and time to exhaustion was observed after 6–7 weeks of high-intensity interval training [3, 20]. In fact, Tabata et al. [20] observed a significant increase of VO2max (+ 7 ml.kg − 1.min − 1) in 7 moderatly trained men who performed an intermittent training programme 5 times a week for 6 weeks. This programme consisted of 7–8 sets of 20 s exercise at an intensity of about 170 % of VO2max with a 10 s rest between each bout. In the same way, Burke et al. [3] observed in 21 moderatly trained women a significant increase of VO2max (+ 5–6 %), after a 7-week intermittent training programme (30 s/30 s or 2 min/2 min at an intensity from 85 % VO2max to exhaustion (last 4 weeks) 4 times per week). Despite the fact that in these last 2 studies the recovery was passive, VO2max increased significantly which was not the case for PRG in our study. However, the intensities of their training programmes [3, 20] were higher than the intensity used in the PRG in the present study. In the present study the training programmes of ARG and PRG were exactly the same in terms of volume (e. g. relative distances covered) only the intensity of recovery differed. Therefore, the differences concerning VO2max and MAV between ARG and PRG observed in the present study can mainly be explained by the recovery mode (active vs. passive) and the intensity of the training programme. In fact, the mean intensity of the training programme with active recovery was higher than with passive recovery. The same results were also observed in highly trained runners [25] and cyclists [24]. Thus, the interval training with active recovery used in the present study is of a sufficient load (intensity, volume, and frequency of sessions, and training duration) and induces aerobic fitness improvements as outlined by other studies [4, 13]. In the present study, plasma A and NA concentrations increased markedly and significantly in response to maximal exercise in the 3 groups before and after the training period. Catecholamines are known to increase when experiencing heavy exercise, in part because of central nervous system mechanisms [27, 29]. Activation of the hypothalamic-pituitary axis and sympathetic-adrenal-medullary activation leads to A release from the adrenal medulla and NA from nerve ending into the circulation [10, 15]. The increase in sympathoadrenal activity is the most important autonomic neuroendocrine response during exercise [17]. Maximal or very intense exercise is known to induce a marked increase of plasma A and NA concentrations with respect to submaximal exercise or other stimuli [27]. Plasma A and NA concentrations measured in the present study’s 3 groups at the end of the maximal exercise are higher than

those measured in other studies in response to short sprint exercise [2] and to intermittent exercise [6]. However, the present values are lower than those measured in other studies in response to a supramaximal exercise (Wingate-test) in sprinters and endurance trained subjects [26, 27]. This is logical as the load of the graded exercise is higher than that of short sprint or intermittent exercise, but lower than that of supramaximal exercise. In this context, the load of exercise induces a doseresponse of catecholamines output [6, 29] which may explain the present results. The present study showed that ARG subjects exhibited significantly higher A and NA response (Aend and NAend) than CG and PRG after training. Such results have been previously reported when comparing endurance trained [9, 11] or sprint trained subjects [26, 27] to untrained ones. These higher catecholamine concentrations reported in ARG cannot be explained by the clearance of these hormones since the index of the elimination of A and NA measured (Aend-A10 and NAend-NA10) [26] was not significantly different between the 3 groups. Therefore, the present results can mainly be explained by a higher capacity to secrete catecholamines and argue in favour of the so-called “Sports Adrenal Medulla” previously described in endurance and sprint trained subjects [27, 29]. In fact, the only difference concerning the program training between our 2 trained groups is the recovery mode. Despite the same quantity (relative distances covered) of training performed by ARG and PRG, the intermittent exercise training with active recovery (i. e., ARG) is more intense and may induce more stress, which may lead to an increase of catecholamine secretion. On the other hand, since it is well known that the catecholamine responses are influenced by the exercise duration [29], the differences observed between ARG and PRG can also be explained by differences in the duration of the maximal graded exercise performed after the training period. However, after the training programme ARG performed only ~1 min longer during the maximal graded test than PRG and the 2 groups performed this test until exhaustion. Then, this short difference concerning the duration may not be enough to explain the catecholamine differences observed between ARG and PRG [11, 29]. Another possible explanation of the present results could also be higher adrenal medulla sensitivity to sympathetic nervous output (judged by the Aend/NAend ratio) so that adrenaline secretion is greater for a similar sympathetic nervous stimulation [9, 27]. This cannot be ruled out since ARG also exhibited a significantly higher NAend and Aend/NAend ratio with respect to the other groups. In conclusion, the present results demonstrate that interval training with active recovery in comparison to passive recovery induce a significant increase of aerobic fitness (VO2max and MAV) and A and NA concentrations in response to maximal exercise. Hence, this type of training is also accompanied by an increase of the adrenal medulla responsiveness to the sympathetic nervous activity as shown by the significant increase of the ratio A/NA only in ARG. These results can mainly be explained by the mode of recovery (active vs. passive) and/or by the longer duration performed by ARG compared to PRG of the maximal graded exercise after the training programme. Moreover, the present results also suggest that interval training with active recovery may be more efficient with respect to passive recovery to increase aerobic fitness (VO2max and MAV).


6 Training & Testing Acknowledgements

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This article is dedicated to our young colleague Dr. Délphine Thevenet who died on November 2010. Délphine participated to this study from the design to the draft of the manuscript and she conducted all the experiment on the track. The authors would like to thank all the students from the ISSEP of Tunisia for their participation and the staff of the CNMSS. Affiliations Movement, Sport and health Sciences Laboratory (M2S), UFR APS University of Rennes 2, Rennes, France 2 Movement, Sport and Heath Sciences Laboratory (M2S), Rennes 2 University – ENS Cachan, France, ENS Cachan, Rennes, France 3 CNMSS, Research Department, Tunis, Tunisia 4 Clinical Laboratory of Physiology, Medical School of Sousse, Physiology, Sousse, Tunisia 5 Laboratoire de Biochimie – Unité de recherche MSP UR 28/04 (facteurs de risque cardiovasculaire) Hopital Universitaire Sahloul, Tunisia, Madicine Faculty, Sousse, Tunisia 6 Laboratoire des adaptations cardio-circulatoires, respiratoires, métaboliques et hormonales à l’exercice musculaire, faculté de médecine Ibn El Jazzar, Sousse, Tunisia., Medicine Faculty, Sousse, Tunisia 7 Laboratoire Mouvement Sport Sante, UFR APS, Rennes, France 1

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