Search tips
Search criteria 


Logo of brjsmedBritish Journal of Sports MedicineVisit this articleSubmit a manuscriptReceive email alertsContact usBMJ
Br J Sports Med. 2007 September; 41(9): 588–591.
Published online 2007 May 14. doi:  10.1136/bjsm.2006.034264
PMCID: PMC2465394

Impact of low‐intensity isocapnic hyperpnoea on blood lactate disappearance after exhaustive arm exercise



To investigate the impact of low‐intensity isocapnic hyperpnoea (IH) on blood lactate disappearance after exhaustive arm exercise in comparison with passive and active recovery using the previously loaded muscle group.


Randomised, crossover trial.


Institute for Sports Medicine.


18 healthy non‐smoking and physically active male subjects.


Subjects performed three arm cranking tests to volitional exhaustion on 3 different days at least 48 h apart. Arm exercise was randomly followed by 30 min of passive recovery (PR), active arm cranking (AC) at 30% of peak power output or ventilatory recovery (VR) by means of IH at 30% of 12 s maximal voluntary ventilation. Blood lactate concentrations were measured every 2 min during recovery.

Main outcome measurements

Blood lactate disappearance during the three different recovery strategies.


No significant differences in blood lactate concentrations were found between interventions PR, AC and VR during the whole measurement period. Mean (SD) peak lactate concentrations were 11.09 (1.98) mmol/l for PR, 11.13 (1.44) mmol/l for AC and 11.25 (1.93) mmol/l for VR. At the end of the recovery period measured lactate concentrations were 4.35 (1.56) mmol/l for PR, 3.77 (1.60) mmol/l for AC and 4.09 (1.35) mmol/l for VR. Moreover, all other variables measured were not significantly different, with the exception of higher average recovery heart rates during AC (116 (9) bpm) and VR (111 (17) bpm) compared with PR (93 (11) bpm).


Low‐intensity IH seems not to enhance blood lactate disappearance after exhaustive arm exercise compared with passive or active recovery using the previously loaded muscle group. The magnitude of the involved muscle mass appears critical to effective active recovery.

Keywords: exercise, active recovery, lactate kinetics, respiratory muscles, training

Exhaustive, anaerobic exercise leads to a large production of lactate and hydrogen ions in the exercising muscles, causing a concomitant decrease in intracellular pH.1,2 This acidosis impairs the ability for muscle contraction and glycolytic enzyme activity, leading to reduced exercise performance.2 To regain optimal performance as soon as possible, fast lactic acid elimination is crucial for athletes, particularly if there are repeated, high‐intensity bouts of exercise within a short period of time, such as competitions in swimming, athletics or wheelchair racing.3,4

In general, blood lactate elimination is accelerated by active recovery of the previously loaded muscle group at moderate intensities.4,5,6,7,8,9,10 In practice, owing to restricted infrastructural possibilities or a densely packed schedule during a competition, active recovery is not always possible. Moreover, active recovery using the previously loaded muscle group may impair subsequent exercise performance as energy stores become additionally depleted,11 early resynthesis of muscle glycogen is compromised, and time for an optimal refilling of glycogen stores is shortened.12 This might have negative consequences for subsequent exercise performance, especially in sports or situations where it is not possible to use another muscle group for active recovery purposes (eg, leg exercise after upper body exercise) as is the case in athletes with an injured spinal cord.

Type I fibres can metabolise lactate,13,14,15 and as respiratory muscles mainly consist of type I fibres,16,17,18 we hypothesised that respiratory muscles may have the potential to enhance blood lactate elimination. If this is the case, respiratory muscles might be used as an easy to handle tool to accelerate blood lactate elimination without affecting glycogen resynthesis in previously exhausted limb muscles. This study aimed at investigating the impact of low‐intensity isocapnic hyperpnoea (IH) on blood lactate disappearance after exhaustive arm exercise and at comparing these data with results of conventional active and passive recovery protocols. An acceleration of blood lactate elimination by active recovery strategies (moderate arm cranking exercise and IH) was expected compared with that of passive recovery.

Subjects and methods


Eighteen trained, male, non‐smoking subjects participated in the study. Their average (SD) age was 30 (5) years, height 178 (7) cm, weight 72 (9) kg, weekly physical training volume 5.6 (3.3) h and peak oxygen uptake (Vo2peak) for arm cranking 42 (7) ml/min/kg. Subjects were asked to perform no strenuous exercise and eat food rich in carbohydrates the day before testing and to abstain from caffeine intake on the test days. The study was approved by the ethics committee of Canton Luzern, Switzerland. Written informed consent of the subjects was obtained before the start of the study.

Experimental procedure

Preliminary testing

Two preliminary sessions preceded the three main test trials. During the first preliminary session, standard spirometric data, including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), peak expiratory flow rate (PEF) and maximal voluntary ventilation (MVV) over 12 s were obtained by an ergospirometric device (Oxycon Alpha, Jaeger, Hoechberg, Germany). Afterwards, a familiarisation trial for IH by partial rebreathing from a bag was completed (Spirotiger, Idiag, Volketswil, Switzerland). Bag size corresponded to about one‐third of subjects' FVC. Subjects were breathing at a preset respiratory frequency to reach a target minute ventilation (see below).

The second preliminary session consisted of 30 min continuous IH at a minute ventilation corresponding to 30% MVV and ensured that subjects could sustain this load over 30 min. To assure the predetermined target ventilation, tidal volume, breathing frequency and end tidal partial pressure for carbon dioxide were monitored by means of the above‐mentioned metabolic cart. If necessary, subjects were guided to keep preset tidal volume and breathing frequency to achieve the target ventilation.

Main experiments

All three main tests started with a 2 min resting period for baseline data determination. Subjects were seated in a chair connected to an arm cranking (AC) ergometer (Ergometrics 800 SH, Ergoline, Bitz, Germany). After this resting period, subjects started AC at 20 W. Then, the workload was increased 5 W every 20 s until subjects' volitional exhaustion. Respiratory variables at rest and during the exercise tests were sampled breath by breath through a face mask by an Oxycon Pro (Jaeger, Würzburg, Germany). This device was calibrated for gas and volume according to the manufacturer's recommendations immediately before each test. The three main tests were at least 48 h apart.

During AC, the pedal axis of the ergometer was aligned with the shoulder joint axis and subjects were positioned such that the elbow was slightly flexed at maximal reach. Five minutes after the end of the test, subjects followed one of three recovery strategies in a randomised order. These strategies were passive recovery (PR), active recovery by AC or ventilatory recovery (VR) by means of IH for 30 min. While subjects sat relaxing on a chair for PR, they were either arm cranking at 30% of the previously reached maximal workload (AC) or breathing at 30% MVV with the Spirotiger device (VR) as an active recovery strategy.

Capillary blood for enzymatic lactate analysis (Super GL Ambulance, Ruhrtal Labor Technik, Möhnesee, Germany) was sampled from an earlobe at rest, immediately after cessation of the exercise test and every 2 min until the end of the recovery phase. Heart rate (HR) was determined by an HR monitor (Polar S610, Polar, Kempele, Finland) throughout the whole test and recovery period. Immediately after cessation of the AC exercise test, subjects were asked to rate their perceived exertion by means of a Borg scale, with 6 indicating “no” and 20 “maximal” exhaustion.19


Data points of the measured lactate concentrations of the three different recovery strategies were fitted to the following bi‐exponential curve, as described in detail elsewhere20:

equation image

La(t) denotes the time‐dependent lactate concentration with La(0) being the lactate concentration at the start of recovery. The form of this equation suggests that the lactate kinetics during recovery can be described by two main processes: one with a high‐velocity constant (γ1) describing the appearance (A1>0) of lactate in the bloodstream and the other, with a low‐velocity constant (γ2) describing its disappearance (A2<0).

The variables were calculated using a commercially available computer software package (SYSTAT, version 10, SPSS Inc, Richmond, California, USA) with the regression method of least mean squares.

An analysis of variance for repeated measures was applied to compare γ1 and γ2 between the different intervention strategies (PR, AC, VR). In addition, Vo2peak, peak power, rating of perceived exertion as well as maximal and average recovery HRs were analysed in the same way. If significance was found, a post hoc test with Bonferroni correction was used to locate significant differences. Results are given as mean (SD). Values were considered to be significantly different if p<0.05.

The ventilatory threshold (VT) of the exercise test preceding AC was calculated from carbon dioxide output (Vco2) and Vo2 values according to the V‐slope method.21


The mean of the subjects' FVC was 5.8 (1.1) litre (115% predicted), FEV1 4.6 (0.7) litre (109% predicted), PEF 11.4 (1.4) l/s (119% predicted) and MVV 206.8±30 l/min (140% predicted). Peak power output, Vo2peak, maximal HR and rating of perceived exertion did not differ significantly between tests (table 11).

Table thumbnail
Table 1 Values measured at the end of exhaustive arm cranking tests before starting different recovery strategies

Figure 11 shows blood lactate curves. The low‐velocity constants (γ2) describing blood lactate disappearance were 0.052 (0.031)/min, 0.072 (0.035)/min and 0.053 (0.032)/min for PR, AC and VR respectively (p = 0.138), indicating that blood lactate elimination rate constants after exhaustive arm ergometry were not significantly different among the three different recovery strategies. Average recovery HRs during AC (115.9 (9.2) bpm) and VR (111.3 (16.8) bpm) were significantly higher than the average HR during PR (92.8 (10.5) bpm).

figure sm34264.f1
Figure 1 Mean blood lactate elimination curves for different recovery strategies after an exhaustive arm cranking exercise test (AET).

Average workload during AC was 44.2 (7.3) W, corresponding to 29.9 (1.0)% of peak power output. This workload was clearly below the VT at 55.8 (14.5)% of Vo2peak, which corresponded to an absolute workload of 88.1 (30.0) W.

During VR subjects were ventilating 61.6 (9.3) l/min (29.8 (0.9)% of MVV) at an average breathing frequency of 26.2 (3.7)/min. Average end tidal partial pressure for carbon dioxide was 32.8 (5.1) mm Hg.


The main finding of this study is that there were no significant differences in blood lactate disappearance after exhaustive arm cranking exercise due to the different recovery strategies. This was surprising, as a superior impact of active recovery strategies (AC and VR) on blood lactate elimination was expected compared with PR. Different reasons may explain this observation and are discussed below.

AC for active recovery

Active recovery at moderate intensities by means of the previously loaded muscle group is known to accelerate blood lactate elimination compared with PR.4,5,6,7,8,9,10 Although AC showed a nearly 40% faster low‐velocity constant (γ2) than PR and VR, no significant differences (p = 0.138) were found between the different recovery strategies. This might be owing to the relatively large interindividual differences between subjects (fig 11)) but may be caused for other reasons discussed below.

What is already known on this topic?

Blood lactate elimination is enhanced using a previously loaded large muscle group for active recovery.

In contrast to the above mentioned studies where leg exercise was applied, we used an arm cranking exercise for recovery. Slower blood lactate kinetics for arm exercise compared with leg exercise were also reported by Thiriet et al.22 Obviously, the magnitude of the affected muscle mass is critical for effective active recovery. Arm muscle mass in a group of 29‐year‐old men was found to be only 40% (7.1 kg vs 17.7 kg) of leg muscle mass.23 Taking into account the higher proportion of type I fibres,16,24 combined with the bigger muscle mass involved during leg exercise, it seems not surprising that lactate elimination from arm muscles would be different from that of leg muscles. The large proportion of type II fibres in arm muscles16,24 limits their ability to oxidise lactate itself. In combination with the relatively small muscle mass of the arms, lactate elimination is additionally compromised compared with elimination from leg muscles.

What this study adds?

The magnitude of the affected muscle mass seems to be critical to effective active recovery as we found no significant acceleration of blood lactate elimination using either arm or respiratory muscles for active recovery.

Moreover, if the chosen intensity for AC had been too high, lactate elimination would have decelerated. However, considering the measured mean recovery HR of 116 bpm during AC compared with other active recovery HRs reported in the literature,4,7,22 it seems very unlikely that our recovery intensity of 30% of maximal power output was too high. Moreover, a recovery load of 30% of maximal power output was suggested to be within the optimal range for active recovery and has been successfully applied in the past.22,25,26 Further, the chosen recovery workload was far below the VT, which supports the assumption of an optimal active recovery intensity.

However, the present active recovery design by means of AC (instead of using previously unloaded leg muscles) was chosen, as there are situations where it is not possible to use another muscle group for active recovery purposes as is the case, for example, in athletes with an injured spinal cord.

VR for active recovery

With regard to the type of muscle fibre in the arm versus respiratory muscles, one can hypothesise that VR is better than AC and PR in accelerating blood lactate disappearance. However, this assumption was not supported by the present findings. Although respiratory muscles mainly contain type I fibres,16,17,18 the total muscle mass affected in VR is quite small and thus oxidative capacity is limited. In fact, diaphragmatic muscle mass was found to be only 262 g27 compared with the above‐mentioned 7 kg of arm muscle mass.23 Even if during VR the auxiliary respiratory muscles worked actively, this seems to be a very small active muscle mass to engage in lactate oxidation, which might be the main reason why the VR strategy failed to enhance blood lactate elimination.

A further reason might be that the chosen intensity of IH at 30% MVV was too low for a sufficient effect on lactate metabolisation over 30 min. On the other hand, a higher intensity of IH might have led to respiratory muscle fatigue, which compromises subsequent exercise performance.28,29 In fact, Martin and coworkers showed that intense IH at 66% of the mean MVV reduces subsequent running performance.29 Additionally, the possibility has to be taken into account that during upper body exercise, some of the respiratory muscles of the rib cage have to partake in non‐ventilatory functions.30 Thus, a recovery strategy like IH, integrating all respiratory muscles, should be performed at a moderate intensity, to avoid the development of rib cage muscle fatigue, which otherwise might compromise subsequent AC performance. The fact that average recovery HR during VR was close to the HR values during AC and significantly higher than during PR (table 11)) suggests that the chosen intensity of IH at 30% MVV was adequate and comparable to the intensity during AC. Hence, it is questionable if a higher intensity of IH (eg, 40–50% MVV) would provide faster lactate removal without causing respiratory muscle fatigue.

Perhaps specifically trained respiratory muscles would have provided faster blood lactate elimination. This assumption is supported by the finding of Spengler et al, who demonstrated lower blood lactate concentrations at the end of an exhaustive cycling exercise after 4 weeks of IH training.31 It was suggested by the authors that the decrease in blood lactate concentration was probably caused by enhanced lactate uptake of the trained respiratory muscles. In contrast, others observed no changes of blood lactate concentrations after respiratory muscle training.32 As the respiratory muscles of our study subjects were not specifically trained, it would be interesting to see if there were differences in the potential for lactate elimination after a respiratory training period. Further investigations are needed to answer this question.

Preliminary exercise and lactate elimination

It has been shown that the intensity of preliminary exercise influences the kinetics of subsequent lactate elimination33 and thus might falsify results. Data of the three arm cranking tests to exhaustion preceding the three recovery interventions refute this assumption for the present study. No differences were found in peak power, Vo2peak, maximal HR or peak lactate concentration between tests (table 11 and fig 11),), which implies that the preceding exhaustive exercise was comparable for each testing session.


Low‐intensity IH seems not to enhance blood lactate disappearance after exhaustive arm exercise compared with passive or active recovery with the previously loaded muscle group. The magnitude of the affected muscle mass seems to be critical to an effective active recovery as shown by the fact that AC also failed to enhance blood lactate elimination significantly.


AC - arm cranking

FVC - forced vital capacity

FEV1 - forced expiratory volume in 1 s

HR - heart rate

IH - isocapnic hyperpnoea

MVV - maximal voluntary ventilation

PEF - peak expiratory flow

PR - passive recovery

Vo2peak - peak oxygen uptake

VR - ventilatory recovery

VT - ventilatory threshold


Competing interests: None.

Some results of this study were presented at the 11th Annual Congress of the European College of Sport Science and therefore published in abstract form in Schweiz Zeitschr Sportmed Sporttraum 2006;54:69.


1. Astrand P O, Hultman E, Juhlin‐Dannfelt A. et al Disposal of lactate during and after strenuous exercise in humans. J Appl Physiol 1986. 6338–343.343 [PubMed]
2. Hermansen L. Effect of acidosis on skeletal muscle performance during maximal exercise in man. Bull Europ Physiopath Resp 1979. 15229–238.238
3. McMaster W C, Stoddard T, Duncan W. Enhancement of blood lactate clearance following maximal swimming. Effect of velocity of recovery swimming. Am J Sports Med 1989. 17472–477.477 [PubMed]
4. Monedero J, Donne B. Effect of recovery interventions on lactate removal and subsequent performance. Int J Sports Med 2000. 21593–597.597 [PubMed]
5. Ahmaidi S, Granier P, Taoutaou Z. et al Effects of active recovery on plasma lactate and anaerobic power following repeated intensive exercise. Med Sci Sports Exerc 1996. 28450–456.456 [PubMed]
6. Bond V, Adams R G, Tearney R J. et al Effects of active and passive recovery on lactate removal and subsequent isokinetic muscle function. J Sports Med Phys Fitness 1991. 31357–361.361 [PubMed]
7. Gupta S, Goswami A, Sadhukhan A K. et al Comparative study of lactate removal in short term massage of extremities, active recovery and a passive recovery period after supramaximal exercise sessions. Int J Sports Med 1996. 17106–110.110 [PubMed]
8. Hermansen L, Stensvold I. Production and removal of lactate during exercise in man. Acta Physiol Scand 1972. 86191–201.201 [PubMed]
9. Stamford B A, Weltman A, Moffatt R. et al Exercise recovery above and below anaerobic threshold following maximal work. J Appl Physiol 1981. 51840–844.844 [PubMed]
10. Weltman A, Stamford B A, Moffatt R J. et al Exercise recovery, lactate removal, and subsequent performance. Res Q 1977. 48786–796.796 [PubMed]
11. Dupont G, Blondel N, Berthoin S. Performance for short intermittent runs: active recovery vs. passive recovery. Eur J Appl Physiol 2003. 89548–554.554 [PubMed]
12. Choi D, Cole K J, Goodpaster B H. et al Effect of passive and active recovery on the resynthesis of muscle glycogen. Med Sci Sports Exerc 1994. 26992–996.996 [PubMed]
13. Brooks G A, Gaesser G A. End points of lactate and glucose metabolism after exhausting exercise. J Appl Physiol 1980. 491057–1069.1069 [PubMed]
14. Juel C. Current aspects of lactate exchange: lactate/H+ transport in human skeletal muscle. Eur J Appl Physiol 2001. 8612–16.16 [PubMed]
15. McLoughlin P, McCaffrey N, Moynihan J B. Gentle exercise with a previously inactive muscle group hastens the decline of blood lactate concentration after strenuous exercise. Eur J Appl Physiol 1991. 62274–278.278
16. Johnson M A, Polgar J, Weightman D. et al Data of the distribution of fibre types in thirty‐six human muscles. An autopsy study. J Neurol Sci 1973. 18111–129.129 [PubMed]
17. Lieberman D A, Faulkner J A, Craig A B. et al Performance and histochemical composition of guinea pig and human diaphragm. J Appl Physiol 1973. 34233–237.237 [PubMed]
18. NHLBI Workshop Summary Respiratory muscle fatigue: report of the respiratory muscle fatigue workshop group. Am Rev Respir Dis 1990. 142474–480.480 [PubMed]
19. Borg G A. Psychophysical bases of perceived exertion. Med Sci Sports Exerc 1982. 14377–381.381 [PubMed]
20. Freund H, Zouloumian P. Lactate after exercise in man: I. Evolution kinetics in arterial blood. Eur J Appl Physiol Occup Physiol 1981. 46121–133.133 [PubMed]
21. Beaver W L, Wasserman K, Whipp B J. A new method for detecting anaerobic threshold by gas exchange. J Appl Physiol 1986. 602020–2027.2027 [PubMed]
22. Thieret P, Gozal D, Wouassi D. et al The effect of various recovery modalities on subsequent performance in consecutive supramaximal exercise. J Sports Med Phys Fitness 1993. 33118–129.129 [PubMed]
23. Nindl B C, Scoville C R, Sheehan K M. et al Gender differences in regional body composition and somatotrophic influences of IGF‐I and leptin. J Appl Physiol 2002. 921611–1618.1618 [PubMed]
24. Susheela A K, Walton J N. Note on the distribution of histochemical fibre types in some normal human muscles: A study on autopsy material. J Neurol Sci 1969. 8201–207.207 [PubMed]
25. Dodd S, Powers S K, Callender T. et al Blood lactate disappearance at various intensities of recovery exercise. J Appl Physiol 1984. 571462–1465.1465 [PubMed]
26. McLellan T M, Skinner J S. Blood lactate removal during active recovery related to aerobic threshold. Int J Sports Med 1984. 3224–228.228
27. Arora N S, Rochester D F. Effect of body weight and muscularity on human diaphragm muscle mass, thickness, and area. J Appl Physiol 1982. 5264–70.70 [PubMed]
28. Mador M J, Acevedo F A. Effect of respiratory muscle fatigue on subsequent exercise performance. J Appl Physiol 1991. 702059–2065.2065 [PubMed]
29. Martin B, Heintzelman M, Chen H I. Exercise performance after ventilatory work. J Appl Physiol 1982. 521581–1585.1585 [PubMed]
30. Celli B, Criner G, Rassulo J. Ventilatory muscle recruitment during unsupported arm exercise in normal subjects. J Appl Physiol 1988. 641936–1941.1941 [PubMed]
31. Spengler C M, Roos M, Laube S M. et al Decreased exercise blood lactate concentrations after respiratory endurance training in humans. Eur J Appl Physiol 1999. 79299–305.305
32. Sonetti D A, Wetter T J, Pegelow D F. et al Effects of respiratory muscle training versus placebo on endurance exercise performance. Respir Physiol 2001. 127185–199.199 [PubMed]
33. Freund H, Oyono‐Enguelle S, Heitz A. et al Work rate‐dependent lactate kinetics after exercise in humans. J Appl Physiol 1986. 61932–939.939 [PubMed]

Articles from British Journal of Sports Medicine are provided here courtesy of BMJ Publishing Group