Effect of intensity of aerobic training on VO2max.

Gormley SE, Swain DP, High R, Spina RJ, Dowling EA, Kotipalli US, Gandrakota R.
Med Sci Sports Exerc. 2008 Jul;40(7):1336-43.

PURPOSE: To determine whether various intensities of aerobic training differentially affect aerobic capacity as well as resting HR and resting blood pressure (BP). METHODS: Sixty-one health young adult subjects were matched for sex and VO2max and were randomly assigned to a moderate- (50% VO2 reserve (VO2R), vigorous (75% VO2R), near-maximal-intensity (95% VO2R), or a nonexercising control group. Intensity during exercise was controlled by having the subjects maintain target HR based on HR reserve. Exercise volume (and thus energy expenditure) was controlled across the three training groups by varying duration and frequency. Fifty-five subjects completed a 6-wk training protocol on a stationary bicycle ergometer and pre- and posttesting. During the final 4 wk, the moderate-intensity group exercised for 60 min, 4 d.wk the vigorous-intensity group exercised for 40 min, 4 d.wk and the near-maximal-intensity group exercised 3 d.wk performing 5 min at 75% VO2R followed by five intervals of 5 min at 95% VO2R and 5 min at 50% VO2R. RESULTS: VO2max significantly increased in all exercising groups by 7.2, 4.8, and 3.4 mL.min.kg in the near-maximal-, the vigorous-, and the moderate-intensity groups, respectively. Percent increases in the near-maximal- (20.6%), the vigorous- (14.3%), and the moderate-intensity (10.0%) groups were all significantly different from each other. There were no significant changes in resting HR and BP in any group. CONCLUSION: When volume of exercise is controlled, higher intensities of exercise are more effective for improving VO2max than lower intensities of exercise in healthy, young adults.

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Only two studies have compared near-maximal intervals with lower-intensity continuous training in healthy adults, and both studies included only highly fit males as subjects (11, 16).

... groups: 1) moderate intensity (50% VO2R), 2) vigorous intensity (75% VO2R), 3) near-maximal intensity (intervals at 95% VO2R), and 4) nonexercising control.

DISCUSSION

The main finding of the study was that higher intensities of exercise elicit greater improvements in VO2max than lower intensities of exercise over a 4- to 6-wk training period in healthy, young adults. This finding is consistent with the original hypothesis. Unlike VO2max, there were no changes observed in resting HR and resting BP after training.

A study recently published by Helgerud et al. (16) examined the effects of 8 wk of aerobic endurance training at various exercise intensities in healthy, young-adult males. Groups performed running at a moderate-intensity (70% HRmax for 45 min each session), vigorous-intensity (85% HRmax for ~24 min per session), and two maximal-intensity interval training regimens that both alternated 90-95% HRmax with 70% HRmax, one using multiple 15-s intervals and one using four 4-min intervals. Both interval training groups significantly increased VO2max, whereas neither continuous training group did. Using a previously published formula, the moderate- and vigorous-intensity groups of Helgerudet al. were exercising at ~47% and ~72% HRR, respectively, which are comparable to the current study. The failure of the continuous training groups of Helgerud et al. to increase VO2max was probably due to their high baseline fitness, which averaged 58 mL/min/kg. Esfarjani and Laursen (11) recently compared interval training at VO2max with continuous training at 75% HRR in male runners. As in the study of Helgerud et al., the subjects’ baseline VO2max was greater than 50 mL/min/kg, and only the interval group increased VO2max. Both of these studies differed from the current study in the population (only males vs both males and females; high vs average fitness) and the mode of exercise (running vs cycling).

It should be noted that although interval training groups spend some of their training time at a very high intensity, a similar amount of time is spent at a lower intensity, and therefore the mean intensity of training may not be any higher than that of a continuous training program. In the current study, the interval training group used 5 min each for the work and the recovery phases of the intervals and had an average intensity of 72% HRR, which is slightly less than the 75% HRR of the vigorous group. The work–recovery periods of Helgerud et al. were 4 min at ~93% HRmax and 3 min at 70% HRmax, for a mean intensity of 83% HRmax in the interval group, whereas one of the continuous groups used 85% HRmax. Warburton et al. used 2 min at 90% HRR and 2 min at 40% HRR for the work and the recovery phases, yielding a mean intensity of 65% HRR in the interval group, and had the continuous training group use 65% HRR. Wisloff et al. used 4-min work phases at ~93% HRmax and 3-min recovery phases at 60% HRmax, for a mean intensity of 79% HRmax in the interval group, and used ~73% HRmax in the continuous training group. Despite the similarity of mean intensity between the interval and the continuous training groups, the interval groups in all of these studies experienced greater improvements in aerobic fitness after training. Therefore, although intensity is a key variable in cardiorespiratory training (as shown by comparing the two continuous training groups in this study), the mean intensity may not be as important as the highest intensity that is used for a significant portion of the training. A topic for future research is to determine what portion of training should be done at high intensities and using what work–recovery periods to obtain the greatest results.

The effect of endurance training on parameters of aerobic fitness.

Sports Med. 2000 Jun;29(6):373-86. Review.
Jones AM, Carter H.

The performance of repeated bouts of exercise over a period of time causes numerous physiological changes that result in improved performance in that exercise activity. The magnitude of the training response depends on the duration of the exercise bouts, their intensity and the frequency with which they are performed, along with the initial training status, genetic potential, age and gender of the individual. The specificity of the training stimulus is also important in terms of the type of training practised (endurance, strength or speed) and the exercise modality used. Appropriate recovery periods are required to allow adaptation to the training load: an insufficient training stimulus and/or too much recovery can lead to lack of progress or detraining while too great a training overload with insufficient recovery can lead to overtraining.

Endurance can be defined as the capacity to sustain a given velocity or power output for the longest possible time. Performance in endurance events is therefore heavily dependant upon the aerobic resynthesis of ATP; this requires an adequate delivery of oxygen from the atmosphere to cytochrome oxidase in the mitochondrial electron transport chain and the supply of fuels in the form of carbohydrates and lipids. Endurance can be crudely described through the generation of individual ‘velocity-time curves’ which relate a series of velocities (or power outputs) to the time for which these velocities or power outputs can be sustained. Endurance training causes adaptations in the pulmonary, cardiovascular and neuromuscular systems that improve the delivery of oxygen from the atmospheric air to the mitochondria and enhance the control of metabolism within the muscle cells. These adaptations shift the velocity-time curve to the right and therefore result in improved endurance exercise performance. This review will focus on the effect of endurance training on the 4 key parameters of aerobic (endurance) fitness identified by Whipp et al.: the maximal oxygen uptake (VO2max), exercise economy, the lactate/ventilatory threshold and oxygen uptake kinetics. For the purposes of this review, endurance exercise will be considered to be continuous events of approximately 5 to 240 minutes duration completed at around 65 to 100% of the VO2max. Events of shorter duration require a significant contribution from anaerobic metabolic pathways, while events of longer duration may be limited by psychological, nutritional, thermoregulatory or musculoskeletal factors rather than by ‘endurance fitness’, per se.

1. Maximal Oxygen Uptake (VO2max)

VO2max, which reflects an individual’s maximal rate of aerobic energy expenditure, has long been associated with success in endurance sports. In whole-body exercise such as running, cycling and rowing, it is widely accepted that VO2max is limited by the rate at which oxygen can be supplied to the muscles and not by the muscle’s ability to extract oxygen from the blood it receives. The VO2max appears to be strongly related to the maximal cardiac output (Qmax). The high Qmax and VO2max values commonly found in elite athletes are, in turn, related to very high maximal stroke volumes since maximal heart rates tend to be similar to those of sedentary individuals. Following training, exercising muscle may require less blood flow for the same submaximal exercise intensity because of an increase in the arterio-venous oxygen difference. The increased stroke volume resulting from increases in left ventricular size, myocardial contractility and end-diastolic volume with training, along with a decreased sensitivity to catecholamines, leads to a reduced heart rate during submaximal exercise. During maximal exercise, the greater cardiac output, along with an increased extraction of oxygen by the exercising muscle, results in a greater VO2max. In addition, the oxygen carrying capacity of the blood is increased following endurance training owing to an increased total blood haemoglobin content. There is also an increase in red cell 2,3-diphosphoglycerate which offsets the reduced haemoglobin concentration consequent to the relatively larger increase in plasma volume compared to red cell mass. The lower [Hb] following training may be advantageous in that the reduced blood viscosity may reduce the resistance of the vasculature to blood flow.

The magnitude of the increase in VO2max resulting from endurance training depends on a number of factors, notably the initial fitness status of the individual, the duration of the training programme and the intensity, duration and frequency of the individual training sessions. Since most studies of endurance training have shown some increase in VO2max with time, the optimal exercise volume and intensity for developing this parameter is not known. However, there is some evidence from the literature to suggest that a high intensity of training (approximately 80 to 100% of VO2max) may be of crucial importance provided that the minimal training volume for a particular event is covered. In a recent study, we examined the influence of 6 weeks of endurance training on parameters of aerobic fitness in 16 physical education students. Despite the relatively modest training programme (3 to 5 sessions per week of 20 to 30 minutes duration at a running speed close to the lactate threshold), we found that VO2max increased by approximately 10% (from 47.9 ± 8.4 to 52.2 ± 2.7 mg/kg/min). Other groups have also shown a 5 to 10% improvement in VO2max with short term endurance training programmes. Hickson et al. reported that VO2max increased by 23% over 9 weeks of endurance training, but the majority of this increase (14%) occurred after only 3 weeks. This rapid increase in VO2max and the similarly rapid reduction in submaximal exercise heart rate have been partly attributed to an early hypervolaemia which will increase stroke volume during exercise and also afford an increased tolerance to heat stress. There is some evidence that during longer term training programmes, VO2max will eventually stabilise, with subsequent improvements in performance resulting from continued improvements in submaximal factors such as exercise economy and lactate threshold.

2. Exercise Economy

Exercise economy has been defined as the oxygen uptake required at a given absolute exercise intensity. There is considerable interindividual variability in the oxygen cost of submaximal exercise, even in individuals of similar aerobic fitness (defined as VO2max) or similar performance capability. For example, Horowitz et al. demonstrated that elite cyclists exercising at the same power output required different rates of oxygen uptake. Interestingly, the more efficient cyclists had a greater percentage of type I fibres in the vastus lateralis, suggesting that the pattern of motor unit recruitment during exercise may be important in the determination of economy. In a classic study, Conley and Krahenbuhl reported that 10km race performance was closely related to running economy in a group of well-trained volunteers who had similarly high VO2max values. Better exercise economy (i.e. lower VO2 for a given absolute running speed or power output) can be considered to be advantageous to endurance performance because it will result in the utilisation of a lower percentage of the VO2max for any particular exercise intensity. It has been suggested that the relatively low VO2max scores that have been reported in some elite endurance athletes can be compensated for by exceptional exercise economy. Indeed, an inverse relationship between VO2max and running economy has been reported in samples of well-trained runners.

Although trained athletes are known to have better exercise economy than untrained individuals, studies that have examined the effect of endurance training on exercise economy have produced equivocal results. This may be because such training studies (typically of 6 to 12 weeks duration) are too short to produce a measurable improvement in economy, especially in individuals who are already trained. It may be speculated that good exercise economy is somehow related to the total volume of endurance training performed, since the best economy values are often found in older or more experienced athletes, or those who complete a large weekly training mileage. Furthermore, athletes’ most economical velocities or power outputs tend to be those at which they habitually train (unpublished data). This may indicate that athletes should train over a wide variety of speeds if they wish to lower the slope of the VO2-exercise intensity relationship. Only a few studies have tracked changes in exercise economy over a prolonged period of training. In one such study that measured changes in a number of physiological variables over a 5-year period in an elite female distance runner, it was reported that running economy improved appreciably with each year of training. For example, the VO2 at a running speed of 16.0 km/h decreased from 53.0 ml/kg/min in 1992 to 47.6 ml/kg/min in 1995. However, improvements in running economy can sometimes be observed even with short term training programmes. In a recent study, we found that 6 weeks of endurance running training caused a significant improvement in running economy in 16 recreationally active individuals (fig.1), with the VO2 at a representative running speed of 12.0 km/h decreasing from approximately 39 ml/kg/min to approximately 36 ml/kg/min. Franch et al. also reported that the running economy of trained volunteers could be reduced significantly following 6 weeks of high intensity distance running or long-interval training, and found that the reduction in submaximal VO2 was significantly correlated with the reduction in minute ventilation (VE).

Running economy has been associated with anthropometric (including segmental mass distribution), physiological and metabolic, and biomechanical and technical factors. Improvements in exercise economy with endurance training may result from improved muscle oxidative capacity and associated changes in motor unit recruitment patterns, reductions in exercise ventilation and heart rate for the same exercise intensity, and improved technique. These improvements may be partly offset by an increased utilisation of fat as exercise substrate following training due to the greater amount of oxygen that is required for the resynthesis of ATP from fat metabolism compared to carbohydrate metabolism. Of interest is the possibility that exercise economy is related to muscle elasticity. It has been speculated that running economy might be related to ‘fluency’ of movement and that it might therefore be improved by flexibility training. However, recent observations from our laboratory suggest that the oxygen cost of running at 16.0 km/h is negatively related to lower limb flexibility (estimated with the sit-and-reach test) in 26 international-standard male distance runners, i.e. ‘stiffer ’ runners were more economical. Similar results can be found in the literature. One explanation for these results is that stiffer muscles and tendons are better able to store elastic energy during the eccentric phase of stretch-shortening activities and that this stored energy can be released during the concentric phase of the action, thus lowering the oxygen cost of the exercise. Alternatively, inflexibility in the trunk and hip may stabilise the pelvis during the stance phase and limit the requirement for stabilising muscular activity.

It has been suggested that increasing maximal leg strength through resistance training may improve economy and endurance performance by reducing the proportion of the maximal force required for each contraction (e.g. pedal thrust) and hence delaying the recruitment of type II motor units. However, traditional resistance training programmes which involve lifting moderate to high loads at relatively slow movement speeds have, with some exceptions, been shown to be ineffective in improving endurance performance. However, of great interest is a recent study which demonstrated that ‘explosive strength training’, involving sprinting and jumping exercises and weight training using high to maximal movement speeds and low loads (0 to 40% of the 1-repetition maximum), can improve both running economy and 5km race performance. The authors suggested that the improved neuromuscular control resulting from the training could have improved running economy by allowing a tighter regulation of muscle stiffness and better utilisation of muscle elasticity. It is also possible that strength training using maximal velocity contractions may improve economy by allowing for a better recruitment of motor units or a reduced cocontraction of antagonistic muscle groups. One other study has demonstrated a similar effect of explosive strength training on the economy of cross-country skiers. Clearly, additional research is required to confirm and extend these findings.

3. Interaction Between VO2max and Economy

The locomotory velocity associated with VO2max (V-VO2max), which is a function of individual VO2max and exercise economy characteristics and which can be calculated by solving the regression equation describing the relationship between VO2 and submaximal exercise intensity for VO2max, has been shown to be an important determinant of endurance exercise performance. Morgan et al. reported that the running speed at VO2max strongly predicted 10km running performance in a group of well trained male runners with homogeneous VO2max values (approximately 65 ml/kg/min). Jones and Doust presented a comprehensive battery of physiological tests to 13 trained runners with a wide range of VO2max values (53 to 67 ml/kg/min), and reported that V-VO2max correlated more strongly with 8km running performance (r = 0.93) than any of the other measures, including VO2max (r = 0.69) and running economy (r = –0.16). Although they are closely related, the V-VO2max should not be confused with the maximal velocity reached in a fast incremental treadmill test (Vmax). Although some studies have shown that the Vmax correlates highly with endurance exercise performance, Vmax is influenced not just by VO2max and exercise economy factors but also by anaerobic capability, muscle power and neuromuscular skill in exercising at high speeds.

Several studies have shown an increased V-VO2max following endurance training. Jones reported that V-VO2max increased from 19.0 to 20.4 km/h over a 5-year period in an elite female distance runner. This improvement in V-VO2max was the result of an improved running economy because VO2max fell slightly over the same period of time. The V-VO2max is similar to the velocity that can be sustained during distance running races of 3000m (approximately 8 minutes in the elite athlete), and so this parameter may be especially important for success in middle-distance events. Billat et al. reported that only 4 weeks of normal training caused a significant improvement in running economy and V-VO2max (from 20.5 to 21.1 km/h), with no significant change in VO2max (from 71.2 to 72.7 ml/kg/min), in 8 trained males. Berthoin et al. reported that V-VO2max was significantly improved only with high intensity training in adolescent volunteers. In another study, Jones et al. found that 6 weeks of endurance training increased V-VO2max from 15.3 to 16.6 km/h in 16 volunteers, with the increased V-VO2max resulting from significant improvements in both VO2max and running economy. The V-VO2max appears to be an important and sensitive measure of endurance fitness and can be usefully measured during longitudinal work with endurance athletes. An improvement in the V-VO2max with training will mean that certain percentages of the VO2max will be associated with higher speeds after training. This may be important in the improvement of endurance race performance because athletes tend to operate at quite similar percentages of VO2max for a given duration of exercise. However, while the V-VO2max construct is practically useful, great care should be taken in its measurement. This is because VO2max may be achieved during constant-load exercise over a wide range of submaximal exercise intensities above the ‘critical power ’ because of the upward drift in oxygen uptake with time (see section 5). Therefore, for the accurate determination of V-VO2max there is a requirement both for a valid measure of VO2max and for exercise economy to be measured at several moderate intensities below the lactate threshold.

It has been suggested that the V-VO2max might represent an optimal training stimulus for improvements in endurance fitness. Hill and Rowell contend that training at V-VO2max is important because V-VO2max is the lowest speed that will elicit VO2max and it is necessary to train at VO2max to improve it. A concept that is closely related to the V-VO2max is the time for which exercise at V-VO2max can be sustained (Tmax). It has been shown that training at 100% V-VO2max allows exercise at VO2max to be sustained for the longest possible time (approximately 4 to 8 minutes). Hill and Rowell demonstrated that if interval or repetition sessions are constructed with the goal of allowing the longest possible training time at V-VO2max, then each repetition needed to be longer than 60% of Tmax. Recently, it was shown that a 4-week training programme which included 2 interval training sessions per week (6 repetitions at V-VO2max intensity for an exercise duration of 60 to 75% of the pre-training Tmax) resulted in significant improvements in VO2max, V-VO2max, Tmax and 3000m performance in trained runners. Unfortunately, this study did not have a control group, and additional studies are needed to confirm the value of using V-VO2max to set training intensity and Tmax to set training duration when the goal is to improve the V-VO2max.

4. Lactate/Ventilatory Threshold

The exercise intensity corresponding to the increase in blood lactate above resting levels (lactate threshold; LT) and the associated changes in gas exchange (ventilatory threshold; VT) are powerful predictors of endurance performance. Numerous studies also testify to the sensitivity of the LT and VT to endurance training. A rightward shift of the LT/VT to a higher power output or running speed is characteristic of successful endurance training programmes. This adaptation allows a higher absolute (running speed or power output) and relative (%VO2max) exercise intensity to be sustained without the accumulation of blood lactate after training. Endurance training is also associated with a reduction in the degree of lactacidaemia for any given absolute or relative exercise intensity. This causes the power output or running speed corresponding to arbitrary ‘blood lactate reference values’ such as 4mmol/L blood lactate to increase following a period of endurance training. Exercise above the LT is associated with a nonlinear increase in metabolic, respiratory and perceptual stress. Furthermore, exercise above the LT is associated with more rapid fatigue, either through the effects of metabolic acidosis on contractile function or through an accelerated depletion of muscle glycogen. Therefore, an improvement in the LT/VT with training is a clear marker of an enhanced endurance capacity. However, it should be noted that the LT/VT is typically found at 50 to 80% VO2max even in highly trained individuals, and it therefore occurs at a lower exercise intensity than is maintained by endurance athletes during most forms of endurance competition. The maximal lactate steady state (MLSS), which is the highest exercise intensity at which blood lactate does not accumulate over time (see section 5), may be of more importance to success in these events.

Mader proposed that the precision with which training loads can be applied may be improved through individual consideration of the LT. Several authors have hypothesised that the LT represents the optimal intensity for improvement of endurance fitness. Training at the LT should provide a high quality aerobic training stimulus without the accumulation of lactate that would compromise training duration. Anecdotally, endurance athletes and coaches feel that training at LT through the inclusion of a regular ‘threshold’ or ‘tempo’ training session is a critical component of a balanced training programme. The effect of training intensity on improvements in the LT/VT has recently been reviewed. In general, it appears that training at intensities close to or slightly above the existing LT/VT is important in eliciting significant improvements in this parameter. For example, it was reported that increasing training intensity through the use of fartlek training on 3 days per week, or adding a 20 minute run at LT speed to the weekly training programme, caused an improvement in the LT with no change in VO2max in runners. Henritze et al. reported that training at intensities above the LT may be even more effective for improving the LT, while Keith et al. have shown that continuous training at the LT or intermittent training above and below the LT are equally effective in improving LT. Collectively, these studies indicate that exercise training at an appropriately high intensity might be most effective in stimulating improvements in LT and performance.

The reduction in blood lactate for the same absolute and relative exercise intensities following endurance training may result from a reduction in the rate of lactate production (possibly consequent to a lower rate of muscle glycogen utilisation or to speeded oxygen uptake kinetics that may increase initial O2 availability/utilisation), or from an increase in the ability to exchange and remove lactate from the blood. Elite endurance athletes have a predominance of type I (‘slow-twitch’) muscle fibres in the trained musculature when compared to their sedentary peers. This is of interest because of the strong relationship that is known to exist between the percentage of type I muscle fibres and the LT. Endurance training causes a selective hypertrophy of the type I fibres and it is possible that a transformation of muscle fibre types from type IIb to type IIa, and even from type IIa to type I can eventually occur. There is also evidence that endurance training can cause an increased expression of slow myosin in type II fibres which reduces the maximal shortening speed in these fibres. Conversely, detraining and micro-gravity lead to a reduction in the expression of slow myosin in muscle fibres. The increased capillarity of skeletal muscle with endurance training has the effect of increasing both the maximal muscle blood flow capacity and the surface area available for exchange of gases, substrates and metabolites between blood and muscle. The longer mean transit time for red blood cells to pass through the muscle capillary bed will increase the time available for diffusion of oxygen from the red blood cell and increase the potential for widening the arterial-venous oxygen difference during exercise.

Endurance training results in numerous adaptations within skeletal muscle that may be significant for exercise performance, including increases in sodium-potassium pump concentration, lactate transport capacity and possibly myoglobin concentration. Endurance training also results in a marked increase in the oxidative capacity of skeletal muscle. This is due to an increase in the size and the number of mitochondria per unit area and an increase in the concentration of the enzymes of the Krebs cycle, electron transport chain and malate-aspartate shuttle. These adaptations help maintain cellular phosphorylation potential, improve the sensitivity of respiratory control and increase the capacity for aerobic ATP resynthesis during exercise in both type I and type II muscle. Muscle respiratory capacity is highly correlated with LT and these enzymatic adaptations may be important in allowing an athlete to exercise at a high percentage of VO2max for prolonged periods. It is possible that a greater oxidative enzyme complement in type I muscle fibres might delay the point at which the type II muscle fibres are recruited during exercise. Furthermore, an increase in the oxidative potential of the type II fibres might reduce their reliance on anaerobic glycolysis for ATP production. Animal studies suggest that low intensity training (approximately 50% VO2max) may be sufficient to maximise the increase in mitochondria in type I muscle, but that much higher intensities are needed to cause significant increases in mitochondrial volume in type II muscle.

The greater capacity of the Krebs cycle to accept pyruvate following training may be important in reducing the production of lactate by mass action at the onset of exercise and during high intensity exercise. However, the greater capillarity of trained muscle also allows for a greater uptake of free fatty acids from the blood and the increased activity of the enzymes involved in lipid metabolism increase the capacity for mitochondrial B-oxidation. It has been shown that there is a reduction in the rate of glycogen depletion, a decreased production and oxidation of blood-borne glucose and an increased storage and rate of utilisation of intramuscular triacylglycerol following training. The greater use of lipid during submaximal exercise, which can be documented in the lower respiratory exchange ratios found for the same absolute and relative exercise intensity following training, reduces the contribution of carbohydrate to ATP resynthesis and is therefore important in sparing muscle glycogen. This adaptation, along with evidence that endurance training increases the storage of muscle glycogen, is an important adaptation to endurance training because a depletion of muscle glycogen stores have been linked to fatigue during endurance exercise.

The hormonal response to exercise appears to change rather quickly following the onset of endurance training. For example, the catecholamine response appears to be substantially blunted for the same exercise intensity after only a few days of training. Since adrenaline is a major effector of lactate production through its modulation of muscle glycogenolysis, this may partly account for the reduction in muscle glycogen utilisation seen with endurance training. The reduced sympathetic nervous system activity may also contribute to the reduction in heart rate observed for the same exercise intensity following training.

5. Oxygen Uptake Kinetics

At the onset of ‘moderate’ exercise (that is, exercise that is below the LT) pulmonary oxygen uptake increases mono-exponentially to achieve a new steady state within 2 to 3 minutes. For constant-intensity exercise in this domain, the oxygen deficit that is incurred at the onset of exercise may cause blood lactate to rise transiently before it returns to resting levels as exercise proceeds. On the other hand, the imposition of an exercise challenge that is just above the LT causes blood lactate to rise until it attains a steady state level that is higher than the resting concentration. In this exercise domain, pulmonary VO2 will also attain a delayed steady state but the VO2 that is achieved may be higher than would be predicted based upon the relationship between VO2 and exercise intensity for moderate exercise. The MLSS can be defined as the highest running speed or power output at which blood lactate remains stable or increases only minimally (less than 1.0 mmol/L) between 10 and 30 minutes of exercise. The MLSS therefore demarcates the highest exercise intensity at which a balance exists between the appearance of lactate in the blood and the removal of lactate from the blood during long-term exercise, and is perhaps the ‘gold standard’ measure of endurance exercise capacity. In theory, the MLSS is the same as the concept of ‘critical power’ (CP) or ‘critical velocity’ that is represented by the asymptote of the hyperbolic relationship between exercise intensity and time to exhaustion. Submaximal exercise above the CP/MLSS is associated with an inexorable increase in blood lactate, pulmonary ventilation, and VO2 with time, and depending on the exercise intensity, VO2 may even rise to attain VO2max. This ‘drift’ in VO2 during constant-load exercise to values that are greater than might be expected has been termed the VO2 slow component. While the mechanisms responsible for this apparent metabolic inefficiency during high intensity submaximal exercise are not fully understood, exercise that elicits a VO2 slow component is poorly tolerated by volunteers. Therefore, training programmes that attenuate the VO2 slow component or that extend the range of exercise intensities over which the slow component does not develop will improve endurance exercise performance.

Several studies have evaluated the effects of endurance training on VO2 kinetics during cycle exercise. In general, the steady state VO2 for the same moderate intensity exercise has not been found to change following a period of endurance training, although the primary exponential increase in VO2 at the onset of exercise may be speeded. In cross-sectional studies, the VO2 on-kinetic adjustment to the same absolute or relative exercise intensity has been reported to be faster in individuals with higher VO2max values. Faster VO2 kinetics at exercise onset, resulting in a more rapid attainment of the requisite steady state oxygen uptake, might be important in reducing the initial oxygen deficit and limiting the early increase in blood lactate. A speeded VO2 on-kinetic response may facilitate the rapid establishment of an intracellular environment that allows tighter metabolic control later in exercise. Whether the primary mechanism for any speeding of the initial VO2 response to exercise is related to increased O2 delivery to muscle or to a reduced inertia of the intracellular oxidative machinery consequent to an increased muscle mitochondrial density is debated. Endurance training increases the CP, and reduces the magnitude of the VO2 slow component (defined as the increase in VO2 between 3 and 6 minutes of exercise) for the same absolute power output. Recent work in our laboratory has shown that 6 weeks of endurance running training results in a significant increase in the running speed at the MLSS, and a significant reduction in the amplitude of the VO2 slow component (from 321 to 217 ml/min on average) for the same absolute treadmill running speed (unpublished observations; fig. 3). Although the reductions in blood lactate levels, ventilation, heart rate and plasma catecholamine levels that accompany endurance training (see section 4) might partly explain the reduced O2 cost of heavy submaximal exercise after training, it appears that intramuscular changes and possibly alterations in motor unit recruitment patterns might be more important. Of interest in this respect is the suggestion that the relative contribution of the VO2 slow component to the total VO2 response to heavy exercise is negatively related to aerobic fitness (as VO2max) and/or the proportion of type I fibres in the working muscles.

6. Conclusion

Endurance exercise training results in numerous adaptations to the neuromuscular, metabolic, cardiovascular, respiratory and endocrine systems. These adaptations are reflected in improvements in the key parameters of aerobic fitness, namely the VO2max, exercise economy, the lactate/ventilatory threshold and the CP which will influence the oxygen uptake kinetics. An improvement in one or more of these parameters will result in an improvement in endurance exercise performance consequent to a rightward shift at various points on the velocity-time curve. The latter will allow an athlete to exercise for longer at the same exercise intensity or to sustain a higher speed for a given exercise duration. Although the aerobic parameters reviewed above are important determinants of endurance exercise performance, it should be borne in mind that competitive performance also depends upon psychological factors, race tactics and the prevailing environmental conditions. In addition, an athlete’s ability to generate ATP anaerobically can be important in sprint finishes between athletes whose aerobic capabilities are similar. Fukuba and Whipp have recently suggested that an athlete’s anaerobic work capacity (a derivative of the concept and computation of critical power) can determine his or her ability to initiate or respond to sections of a race that are faster than the athlete’s best average velocity for the distance.

While the parameters of aerobic fitness are interrelated, the specific emphasis placed on the training of each of these will depend upon an individual’s personal physiological ‘strengths’ and ‘weaknesses’ (which may be assessed in the sports physiology laboratory), and the duration of the event being trained for. For example, a 3000m runner may place special importance on the development of the V-VO2max and anaerobic capacity, while a marathon runner may focus on training to improve running economy and the running speed at lactate threshold. Presently, little is known about the most effective training practices for specifically improving the key parameters of aerobic fitness, or for altering different points on the velocity-time curve in order to effect a shift to the right of the velocity-time relationship. Exploration of the effect of various combinations of training volume, intensity and frequency on these determinants of endurance performance remains a fruitful area for future research.

The relationship between aerobic fitness and recovery from high intensity intermittent exercise.

Tomlin DL, Wenger HA.
Sports Med. 2001;31(1):1-11. Review.

The ability to recover quickly is critical if subsequent bouts of all-out activity are required, as in many team sports. It has been suggested that adaptations associated with endurance training should enhance recovery from high-intensity intermittent exercise, and since the theoretical basis is so compelling, coaches and athletes alike invest a great deal of time into training and maintaining aerobic fitness. As will be seen, the literature supports aerobic fitness as a means of improving recovery from high-intensity intermittent exercise.

1. Exercise Recovery

The return of the muscle to its pre-exercise state following exercise is a process known as recovery. The recovery process is biphasic, with an initial rapid phase of recovery lasting 10 seconds to a few minutes followed by a slower second recovery phase lasting anywhere from a few minutes to a number of hours. During recovery, oxygen consumption (VO2) is elevated to help restore metabolic processes to pre-exercise conditions. The post-exercise VO2 beyond that required at rest has been termed excess post-exercise oxygen consumption (EPOC).

The fast phase of recovery is marked by rapidly declining VO2 and heart rate. It is during this period that tissue stores of oxygen are quickly replenished, and most of the ATP and phosphocreatine (PCr) depleted in the muscle are restored, with 70% of the phosphagens restored within 30 seconds and 100% restored within 3 to 5 minutes. Once depleted, PCr is not restored until exercise concludes. Additionally, no replenishment of PCr occurs when the circulation is occluded, suggesting that oxygen is required for the process.

The increased metabolism marking the slow recovery period has been associated with the removal of lactate and H+, elevated body temperature, the cost of increased respiratory and cardiac functions, the effect of catecholamines and the cost of glycogen resynthesis. Recovery is not complete until metabolism has returned to pre-exercise levels.

2. Recovery from High Intensity Intermittent Exercise

The ability to perform maximally on repeated exercise bouts is influenced by the nature of both exercise and recovery periods. Generally, the more that exercise disrupts homeostasis, the greater the effect on recovery metabolism. The more complete these restorative processes, the greater the ability to generate force or maintain power on subsequent work intervals.

Although a single bout of high-intensity exercise lasting a few seconds results in decreased ATP/PCr stores, if the bout exceeds more than a few seconds anaerobic glycolysis will also be required to provide energy. The metabolic consequence of increased anaerobic glycolysis is an increase in H+ concentration and depressed pH, which may adversely affect performance by disrupting contractile processes. Following exercise, complete phosphagen recovery may require 3 to 5 minutes, but complete restoration of pH and lactate to pre-exercise levels may take an hour or more. In repeated exercise bouts, if the subsequent recovery interval is less than a few minutes long, as in many team sports, the ATP/PCr stores may be only partially restored before the onset of subsequent exercise demands, resulting in compromised performance on successive bouts. Moreover, as ATP/PCr stores are progressively depleted with subsequent high intensity work bouts, there will be increased reliance on anaerobic glycolysis. Following exercise that results in both the depletion of ATP/PCr stores and increased lactate and H+ accumulation, it will require longer to return to the pre-exercise state. Once H+ has accumulated, existing transport and metabolic pathways are less efficient, slowing the rate of recovery from exercise.

The length of the recovery interval between repeats of high-intensity bouts of exercise will also
affect recovery. Wooton and Williams found that, although power output decreased over repeated 6-second all-out sprints with either 30 or 60 seconds of recovery between sprints, power output declined less when 60 seconds of recovery was allowed. A longer recovery interval ensures more complete recovery; however, in sports requiring intermittent bursts of all-out effort the recovery periods may last only a few seconds, so performance on subsequent bouts may suffer. During brief intervals of recovery, at least some of the ATP, PCr and oxymyoglobin is restored. While restoration of the oxygen-myoglobin stores can take 10 to 80 seconds complete phosphagen recovery may require 3 to 5 or even 8 minutes. The rate of post-exercise PCr resynthesis appears to be controlled by the rate of oxidative metabolism within the muscle, and in the absence of circulation, little PCr is regenerated.

The ability to recover from exercise resulting in lactate production depends on the capacity to tolerate, buffer and/or rapidly remove H+ from working muscle. Important buffers within muscle include PCr, inorganic phosphate, protein-bound histidine residues and carnosine. Once in the blood, lactic acid is effectively buffered by sodium bicarbonate. Approximately 65% of the lactate is converted to pyruvate by lactate dehydrogenase (LDH), then undergoes aerobic degradation via the Krebs cycle and electron transport system, with the remaining 35% converted to glucose and/or glycogen, secreted in urine and sweat or converted to protein. Most of lactate oxidation occurs in skeletal muscle, particularly the slow-twitch fibres. The restoration of muscle pH is critical for optimal force production on subsequent exercise, since the rate of PCr resynthesis is influenced by the metabolic environment of muscle, especially the concentration of H+ but also the ATP concentration and the rate of oxidative phosphorylation within working muscle.

3. Possible Role of Aerobic Fitness in Enhancing Recovery

The most widely accepted measure of aerobic fitness, VO2max, represents the maximum rate at which aerobic metabolism can supply energy. Another widely used index of aerobic fitness, aerobic capacity, identifies by blood lactate or ventilatory parameters the maximal steady-state exercise speed or workload that can be sustained for extended periods of time. Increases in VO2max and aerobic capacity result from endurance training. Aerobic capacity measures have proven useful in predicting success in distance running events, with some scientists regarding it as superior to VO2max as a measure of endurance fitness.

Thoden proposes that aerobic training may enhance the ability of the muscle to recover following anaerobic exercise, suggesting that an athlete with higher aerobic fitness will tax nonoxidative sources less and thereby recover at a more rapid rate from exercise. Theoretically, an increase in aerobic fitness could enhance recovery from anaerobic performance both by supplementing anaerobic energy during the exercise and by providing aerobically derived energy at a faster rate during the recovery period. Additionally, any improvements that aid in transport to or from the muscle, such as increased blood flow, could enhance the removal of lactate, H+ and heat.

Individuals with high maximal aerobic power exhibit increased concentrations of aerobic enzymes, increased mitochondrial number, size and surface area and increased myoglobin, all contributing to improved oxygen extraction by muscle. Aerobic training also results in increased muscle blood flow, which is accomplished through elevated cardiac output, increased capillarisation of muscle tissue and an improved ability to vasodilate. Oxygen delivery in the endurance-trained athlete is further improved by increases in blood volume and total haemoglobin volume. Together, these enhancements result in an increased rate of VO2 during high intensity exercise and decreased time to reach peak VO2 during exercise, which may result in less lactic acid accumulation. In conjunction with enhanced ATP/PCr stores and elevated myokinase and creatine kinase concentrations seen in trained athletes, these adaptations should result in an ability to supply more energy through the phosphagen and aerobic systems, thus decreasing the reliance on anaerobic glycolysis and thereby stemming the rise in H+ during high intensity intermittent work. Endurance training results in lower blood and muscle lactate levels for the same absolute submaximal workload because of decreased production of lactate as a result of increased reliance on other energy systems and/or
increased lactate clearance. With reduced anaerobic glycolysis during exercise, less energy is required during the recovery period to rid the muscle of H+ and lactate, potentially hastening the recovery process.

Lactate removal from muscle is enhanced by increased buffering capacity and increased blood flow. Increased capillary density, as seen in endurance-trained individuals, provides a decreased diffusion distance between capillaries and muscle fibres, enhancing movement of oxygen and nutrients to, and the removal of H+ and lactate from, the muscle. Enhanced oxygen delivery to muscles post-exercise potentially accelerates the rate of PCr resynthesis, an
oxygen-dependent process. Tesch and Wright found a significant correlation between capillary
density and blood lactate concentration, suggesting an improved efflux of lactate as a result of increased capillary density.

Other training effects seen in aerobically trained individuals that may hasten recovery are improved temperature regulation during and after exercise, better mobilisation and utilisation of fuel substrates and increased hypertrophy of and selective recruitment of slow-twitch and fast-twitch type A muscle fibres. The increased activity of the H form of LDH associated with endurance training should also facilitate recovery by favouring the oxidation of lactate to pyruvate. This adaptation provides ready fuel, in the form of pyruvate, for aerobic metabolism and helps normalise pH by consuming H+. Thus, it appears that the metabolic and circulatory adaptations associated with high levels of aerobic power should facilitate faster recovery from high intensity exercise.

4. The Relationship Between Aerobic Fitness and Recovery from High Intensity Exercise

Numerous indicators have been used to assess recovery from exercise, including VO2, blood lactates, force or power recovery, muscle pH and muscle PCr. When relevant, research on single bouts of submaximal and maximal exercise will be presented, but it is the intention of this review to focus predominantly on the relationship between aerobic fitness and recovery from high intensity intermittent exercise.

4.1 Aerobic Response

Hamilton et al. compared the aerobic response of endurance-trained runners (VO2max 60.8 ± 4.1 ml/kg/min) and games players (VO2max 52.5 ± 4.9 ml/kg/min) during repeated all-out 6-second treadmill sprints. Although assignment to games players and endurance-trained groups was on the basis of the chosen sport rather than VO2max, VO2max was considerably different, allowing for comparisons on the basis of aerobic power. Both groups attained similar peak (mean 6 seconds) power, but endurance-trained athletes consumed significantly more oxygen during repeated intervals of all-out sprinting and demonstrated a significantly smaller percentage decrement in power over the 10 sprints than did games players. Similar results were reported by Tomlin, who examined the aerobic response of female recreational soccer players to repeated 6-second all-out cycle sprints. Grouped on the basis of VO2max, both the high (HAP) and low (LAP) aerobic power groups attained similar peak power, yet the HAP group consumed significantly more oxygen over 10 sprint-recovery cycles and displayed a smaller percentage decrement over the 10 sprints. Perhaps, consuming more oxygen during sprinting results in less reliance on anaerobic glycolysis and thus less lactic acid production, manifesting itself in less lactic acid and H+ accumulation and thus superior power maintenance.

An increase in VO2max has been associated with an increase in VO2 during repeated bouts of
supramaximal exercise. Additionally, in individuals who completed two 30-second all-out cycle sprints, Bogdanis et al. found a high correlation between VO2max and the percentage of energy contributed by aerobic metabolism on sprint 1 (r = 0.79) and sprint 2 (r = 0.87). Thus, VO2max appears to determine the magnitude of the aerobic response to repeated sprints.

Balsom et al. reported that following erythropoietin administration, individuals performing 15
× 6-second treadmill sprints showed reduced accumulations of blood lactate and the adenosine degradation product, hypoxanthine, despite performing the same amount of exercise when compared with the control condition. Additionally, Balsom et al. demonstrated that by decreasing oxygen availability via a hypobaric chamber, individuals consumed less oxygen, accumulated more lactate and experienced larger power decrements during intense intermittent exercise than under normoxic conditions. These findings suggest that increased oxygen availability, as also happens with increases in VO2max, results in increased aerobic and reduced anaerobic contribution, whereas decreased oxygen availability results in decreased aerobic and increased anaerobic contribution to sprinting.

4.2 Excess Post-Exercise Oxygen Consumption

When exercising at the same percent age of VO2 max, trained individuals consume more oxygen than untrained individuals because of their higher VO2max. Therefore, at the start of the recovery period VO2 is elevated, resulting in a greater potential magnitude for the fast EPOC. As well,
ATP/PCr stores in trained individuals tend to be
higher[39] and since PCr replenishment has been
coupled to fast EPOC,[4, 53] it is not surprising that
fast EPOC following submaximal exercise of the
same relative intensity is demonstrably higher in
endurance-trained individuals.[37,54-56] Given the same
percentage of V. O2max, trained individuals have a
larger magnitude of fast EPOC whereas total EPOC
tends to be about the same and total recovery time
shorter.[37,54-56] Hamilton et al.[48] found that fol-
lowing 10 repeated all-out treadmill sprints where
endurance-trained athletes consumed significantly
more oxygen than games players during the sprint-
recovery cycles, endurance-trained athletes appeared
to consume more oxygen immediately after exer-
cise, whereas games players consumed more oxy-
gen during the remaining 14 minutes of recovery,
resulting in a similar net EPOC, supporting similar


patterns of EPOC seen in submaximal studies. With
more oxygen consumed sooner, the fit individual
should be able to restore more ATP/PCr. The high
post-exercise V. O2 associated with higher aerobic
power may be advantageous in priming the aerobic
system to consume more oxygen immediately after
exercise which, if used to replenish ATP/PCr stores,
should be advantageous for repeated exercise, es-
pecially when subsequent exercise is primarily de-
pendent on PCr breakdown. This may at least par-
tially explain why the endurance-trained athletes
were more successful in maintaining initial power
output throughout the 10 repeats. Although the
endurance-trained athletes and games players av-
eraged similar power over the 10 sprints (612 vs
603W, respectively), and the games players gen-
erated higher power outputs on the initial 4 sprints,
the endurance-trained athletes’ power output on the
final 6 sprints exceeded that of the games players.
LeMasurier[57] investigated the relationship be-
tween V. O2max and 3 minute EPOC following high
intensity intermittent cycle sprints with 21 active
males. He failed to find a significant correlation
between relative VO2max and 3-minute EPOC fol-
lowing 12 × 5-second sprints (r = 0.19),
but confi r med moder at e rel at i onshi ps bet ween
V. O2max and EPOC following 6 × 10-second sprints
(r = 0. 47) and 3 × 20-second sprint s (r
= 0.67). With a lower volume of post-
exercise oxygen consumed following the shorter
sprints, the EPOC response of the participants may
have been more homogeneous and thereby decreas-
ed the likelihood of a significant correlation. Fur-
thermore, with 62% of the total EPOC occurring in
the first minute, a V. O2max–1-minute EPOC com-
parison may have better characterised the relation-
ship.
Bell et al.[58] investigated the relationship be-
tween recovery from high intensity intermittent ex-
ercise and 2 different measures of aerobic fitness;
aerobic capacity and VO2max. Highly trained en-
durance athletes performed 3 × 1-minute sprints at
125% VO2max, after which EPOC was measured.
Using ventilatory threshold as the measure of aer-
obic capacity, the authors failed to find a significant relationship between aerobic capacity and re-
covery or between V. O2max and recovery.
In failing to find significant relationships be-
tween aerobic fitness and EPOC (the rate of EPOC
recovery and the magnitude of EPOC) following the
sprints, Bell et al.[58] concluded that there does not
appear to be a relationship between aerobic fitness
and recovery from repeated bouts of high intensity
exercise in highly trained endurance runners. How-
ever, as conceded by the authors, the population
studied were highly trained (mean V. O2max 63.1
ml/kg/min, range 54.4 to 70.3 ml/kg/min), so even
individuals with ‘low’ aerobic power scores were
quite fit and may have had an aerobic fitness level
sufficient to result in enhanced recovery. The pos-
sibility of an aerobic fitness threshold exists, be-
yond which recovery is enhanced; however, this
hypothesis remains to be tested. Unfortunately, the
interpretation of the EPOC results may have been
hampered by an apparent lack of pre-exercise con-
trols in terms of circadian effects, previous exercise
or the thermic effect of food, all of which affect
resting V. O2 [59] and therefore net EPOC. Moreover,
conclusions on the rate of recovery were based on
the half-time recovery of EPOC, which may not be
appropriate. Although it has been shown that the
half-time EPOC recovery for submaximal exercise
improves with training,[37,60, 61] this index may be
inappropriate for cross-sectional studies. It may be
that rate of recovery is determined somewhat by
genetic factors, such as the percentage of slow ox-
idative fibres, in that while rate of recovery can be
improved, V. O2max is only one of the contributing
factors. For example, Colliander et al.[20] demon-
strated that individuals in a ‘low fast twitch’ group
were superior to a ‘high fast twitch’ group in restor-
ing force between sets of concentric contractions.
Also, the metabolic profile of muscle fibres can be
altered with endurance training through conversion
of fast glycolytic fibres to fast oxidative glycolytic
fibres,[62] thereby enhancing the oxidative capacity
of the muscle, but the enhancements do not always
translate into improvements in V. O2max.[31] Further-
more, improvements in half-time recovery may in-
dicate better recovery; however, similar half-time
recovery scores do not necessari l y suggest that
recovery rat e was the same for different i ndivi d-
u al s. If hal f-t i me EPOC recovery i s t he same for
2 individuals who differ in aerobic power, clearly
the one with higher V. O2 at the end of exercise,
which is likely to be the one with superior aerobic
power,[48,50] will utilise more oxygen in the same
period of time. Therefore, use of the half-time re-
covery rate may not accurately reflect differences
in the rate of recovery.

4.3 Lactate Removal

Since the accumulation of H+ is implicated in
fatigue, decreased accumulations create a more fa-
vourable contractile environment.[8] If, as well, lac-
tate is removed faster from muscle by an efficient
aerobic system, as hypothesised to happen in the
aerobically fit, even less lactate will accumulate,
resulting in less disruption of baseline pH levels.
Unfortunately, all of the studies examining differ-
ences in lactate response rely on measurements of
blood lactate, which only reflect muscle lactate,
providing indirect evidence about lactate produc-
tion and removal in the muscle from lactate accu-
mulation in blood. Some authors have reported en-
hanced blood lactate clearance in endurance-trained
athletes, but others have failed to find a relation-
ship between blood lactate removal and V. O2max.
When examining post-exercise blood lactate re-
sponse, methods vary, with some authors using a bi-
exponential model to describe lactate clearance[63-66]
and others using linear regression, logarithmic or
other methods.[67-69] These differences, in conjunc-
tion with the difficulties in assigning comparable
work bouts to trained and untrained, makes the com-
parison of results difficult.
It appears that aerobically fit individuals attain
peak lactate levels sooner in the post-exercise pe-
riod with passive[63, 64] and active[66] recovery, sug-
gesting a more rapid efflux of lactate from muscle
to blood in trained individuals. Some studies fail to
support a relationship between improved blood lac-
tate clearance and endurance training[68] or between
blood lactate dissipation in well-trained versus un-
trained individuals;[69] however, in both of these


studies post-exercise blood lactate was not sam-
pled until 3 minutes following the exercise bout.
This may have resulted in missing peak lactate,
especially in trained individuals,[63, 66] which is an
important variable in determining the rate of dis-
appearance of blood lactate, regardless of the mathe-
matical model used.
During passive recovery following an incre-
mental procedure to exhaustion, in which endur-
ance at hl et es worked at hi gher workloads t han
sprint-trained athletes, the endurance-trained ath-
letes also had higher blood lactate accumulations
than the sprint-trained individuals.[66] Bassett et al.[63]
demonstrated similar results, whereby trained in-
dividuals cycling for 3 minutes at 85% V. O2max work-
ed at higher workloads and accumulated more blood
lactate sooner than untrained individuals cycling at
80% V. O2max. Although both authors reported sim-
ilar rates of lactate clearance between their respec-
tive groups, it must be emphasised that since both
power output and lactate accumulation were higher
in the groups with higher aerobic fitness and there
is an inverse relationship between the rate of lac-
tate clearance and absolute work,[70] this should be
seen as superior recovery ability in the aerobically
fit. Taoutaou et al.[66] also found that when the first
20 minutes of recovery was active, post-exercise
time to peak lactate and the rate of blood lactate re-
moval was faster in the endurance-trained athletes
even though end-exercise blood lactate levels were
similar between the groups. It may be that through
active recovery some of the enhancements associ-
ated with endurance training, such as increased cap-
illary density,[34] may be reflected more readily.
Freund et al.[64] found that highly trained ath-
l etes could cl ear lactate from working muscles
faster than sedentary controls, and Oyono-Enguelle
et al.[65] suggested that aerobic training may en-
hance lactate removal following anaerobic exer-
cise. By comparing blood lactate disappearance rates
of trained versus less trained individuals from dif-
ferent studies, Bonen and Belcastro[23] also con-
cluded that trained individuals have faster lactate
disappearance rates.

4.4 Power and Force Recovery

Bogdanis et al. found that power recovery on repeated 30-second cycle sprints and resynthesis of PCr proceeds in parallel, confirming the relevance of PCr availability for power recovery. Subsequently, Bogdanis et al. analysed pre- and post-exercise
muscle biopsies from individuals who performed 2 × 30-second sprints separated by 4 minutes of passive recovery. From these results they demonstrated strong relationships between power recovery in the first 10 seconds of the second sprint and
the resynthesis of PCr (r = 0.84) and between power recovery and endurance fitness (r = 0.94), as represented by the percentage of VO2max corresponding to a blood lactate concentration of 4 mmol/L. Effectively these results link PCr resynthesis to both power recovery and endurance fitness. Unfortunately, no relationship was reported between VO2max
and power recovery or power recovery and PCr restoration.

Hakkinen and Myllyla found that power and strength athletes generated higher peak force, whereas endurance athletes were able to maintain a 60% isometric contraction for longer and exhibited better relative force recovery following a 3-minute rest period. Neither VO2max or fibre type were measured but the results imply that differences in force recovery are at least partially the result of differences in aerobic fitness, as aerobic fitness is generally superior in endurance-trained athletes. It is likely that differences in force recovery also reflect peak power differences resulting from the different training regimens of strength, power and endurance athletes.

Gaiga and Docherty found that individuals who participated in 9 weeks of interval training that successfully increased VO2max by 6 to 7% displayed increases in peak power and mean power in all 4 repeated 30-second maximal cycling sprints, with slightly greater improvements seen in the final 2 sprints. However, from the results it is difficult to establish if recovery improved or if the interval training merely enhanced the ability to generate peak power, since total work and peak power improved in all 4 repeats, with little change in the absolute power decrement from sprint 1 to sprint 4.

Caution must be exercised when comparing individuals on relative power recovery such as percentage decrement over trials, as is conventionally done, especially when peak power varies considerably between athletes. Since individuals who produce higher peak power on initial trials have the potential to display greater absolute power decrement, a power recovery index may misrepresent the data. For example, greater percentage decrement trends have been associated with more powerful initial efforts. It may be that percentage decrement is more appropriate when comparing athletes that can be matched on initial peak force; however, this is not always possible. A comparison between VO2max and percentage decrement by Tomlin was based on the results from 2 groups who generated similar peak power on the first of 10 cycle sprints; however, the group with higher aerobic power clearly demonstrated a smaller percentage decrement over the 10 sprints when compared with the LAP group.

Other researchers have investigated the relationship between VO2max and power maintenance for repeated cycle ergometer sprints. Moderate relationships have been reported between relative VO2max and percentage decrement during 6 × 6-second cycle sprints (r = –0.56), 12 × 5-second cycle sprints (r = –0.44) and 6 × all-out 40m treadmill sprints (r = –0.62).
Using a protocol with 90 seconds active recovery between 6 × 15-second sprints, McMahon and Wenger verified a significant VO2max–percentagedecrement relationship (r = –0.63). All of these studies appear to support the notion that higher aerobic power may contribute to improving power recovery over repeated intervals.

Hoffman estimated the aerobic fitness of 197 infantry soldiers on a 2000m run, then compared this to their performance on a field test of anaerobic ability, which consisted of 3 repeats of a 143m line drill sprint. He found that aerobic fitness had a low
but significant correlation with the fatigue index based on the increase in sprint times over the 3 sprints (r = – 0.33). Unfortunately, with 7 directional changes in the field test, skill may have had a larger impact on performance than the ability
to recover between sprints and this may have contributed to the low correlation coefficient. However, when the participants were divided into 5 fitness categories based on their 2000m run times, clearly the fatigue index of the low fitness group
was inferior to the fatigue index of the 3 fittest groups, supporting aerobic fitness as a contributor to power maintenance.

In a subsequent study, Hoffman et al. investigated the influence of directly measured VO2max on the ability of 20 basketball players to recover during the same 143m field test and failed to establish a significant relationship (r = 0.01, nonsignificant). It may be that the impact of skill on performance is even greater in such a small group, and that the VO2max of the basketball players was too similar (mean 50.2 ± 3.8 ml/kg/min) to show differences in recovery.

4.5 Phosphocreatine Restoration

Increased rates of PCr resynthesis following submaximal exercise have been documented in endurance-trained athletes versus individuals in a control group and in endurance-trained athletes versus sprinters, middle-distance runners and individuals in the control group.[81] Furthermore, McCully and Posner demonstrated enhanced PCr resynthesis following only 2 weeks of muscle-specific aerobic training. Unfortunately, VO2max was not measured in any of these studies, so extrapolation of the findings to VO2max is somewhat limited. Even though most endurance-trained athletes possess high levels of aerobic power, enhanced aerobic power is not necessarily the only feature associated with endurance training.

Few studies have investigated the relationship between aerobic fitness and PCr resynthesis following a single bout of high intensity exercise or high intensity intermittent exercise. 31P magnetic resonance spectroscopy (31P-MRS) was utilised
to investigate differences in PCr resynthesis in the gastrocnemius between HAP and LAP groups and between endurance-trained and sedentary individuals following single 2-minute bouts of high-intensity exercise. Neither study demonstrated differences in PCr recovery between the groups when PCr recovery was expressed as a percentage of resting levels or by using nonlinear regression model results, so it was concluded that VO2max was a poor predictor of PCr recovery. It may be more appropriate to interpret the lack of difference in the percentage PCr recovery as a better recovery rate in the endurance-trained individuals and HAP groups since they would probably have had higher initial PCr levels and would therefore have replenished more PCr in the same time. Furthermore, as a weight-bearing muscle the gastrocnemius may have been a poor choice for comparison where groups not only differed in VO2max but also in bodyweight, with the sedentary and LAP groups significantly heavier than their aerobically fit counterparts. It may also be unrealistic to expect a whole body measure of VO2max to correlate well with PCr recovery in a small muscle such as the gastrocnemius. In contrast to the results from Petersen and Cooke and Cooke et al., Takahashi et al. found VO2max to be significantly correlated to the rate of PCr recovery in the quadriceps muscle following exhaustive exercise in endurance-trained and untrained individuals.

It may also be that the impact of aerobic power becomes more obvious with repeated bouts of high-intensity exercise. Using 31P-MRS to examine PCr resynthesis following 4 repeats of 2 minutes of moderately high intensity exercise, Yoshida and Watari clearly demonstrated that endurance-trained individuals (VO2max 73.6 ml/kg/min) had significantly faster PCr recovery than control individuals (VO2max 46.6 ml/kg/min), which became increasingly apparent after the first bout of exercise.

5. Conclusion

The literature suggests that aerobic fitness probably enhances recovery from high intensity intermittent exercise through enhanced aerobic contribution, increased post-exercise VO2, and possibly by increased lactate removal and increased PCr restoration, which has been linked to improved power recovery. Now the challenge is to determine which of these relationships are cause and effect and which variables are coincidental.

Relationship between aerobic fitness and metabolic recovery from intermittent exercise in endurance athletes.

Bell GJ, Snydmiller GD, Davies DS, Quinney HA.
Can J Appl Physiol. 1997 Feb;22(1):78-85.

This investigation examined the relationship between several different aerobic fitness test results and measurements of metabolic recovery from intermittent, high-intensity exercise in 16 male cyclists. No significant correlations were found between maximal oxygen consumption, ventilation threshold, various submaximal endurance measures and the rate of metabolic recovery, net excess postexercise oxygen consumption, or blood lactate removal after intermittent high-intensity exercise except for submaximal heart rate (r = .66, p < .05). These data indicate that aerobic fitness assessments do not indicate the ability to recover after intermittent, high-intensity exercise in endurance-trained cyclists.

The ‘slow component’ of VO2 – understand it to go faster!

Link

Many athletes and coaches structure training sessions on the assumption that oxygen consumption during exercise remains constant for any given training intensity. But as Andy Jones explains, thanks to the ‘slow component’ of oxygen uptake, this assumption is not only physiologically flawed, but can also lead to inappropriate training prescriptions.

Imagine that you begin walking at a very comfortable pace on a treadmill and every few minutes the speed of the treadmill belt is progressively increased so that you need to break into a slow jog, then a faster jog, then a run, and finally a sprint. Although the walking or running speed might have increased in a linear fashion, your perception of the difficulty of the exercise challenge would almost certainly not be linear; there will come a point at which the exercise will quickly switch from feeling quite manageable, to not feeling sustainable for very much longer, and then to feeling intolerable. This is well known, but what is the physiological explanation?

To answer this question, we must first appreciate what is meant by the term ‘exercise intensity’. The intensity at which exercise is performed has traditionally been described in terms of the fraction of the maximal oxygen uptake (VO2max) that the exercise requires in the ‘steady state’. Here, the steady state refers to the plateau in oxygen uptake that is reached following a few minutes of exercise.

For example, running at a speed of 12km/h might require only 50% of the VO2max of a well-trained distance runner but as much as 75% of the VO2max of a recreational games player. However, there are two implicit assumptions in the practice of using the fraction of VO2max to describe (and also to prescribe) exercise intensity.

The first assumption is that a steady state in oxygen uptake is always attained irrespective of the speed at which an individual is walking or running, cycling, etc. The second is that two individuals who are exercising at the same fraction of their VO2max are experiencing a physiological strain that is essentially the same and are also perceiving the exercise to be equally easy (or difficult). As we shall see, these assumptions are untenable, but to understand why, it’s necessary to describe the various exercise intensity domains that have been identified and the physiological ‘thresholds’ which separate them.

Exercise intensity domains

For most individuals, walking on a treadmill at a leisurely pace will be comfortable. If, after a few minutes of walking, a small blood sample is taken and the concentration of blood lactate is measured (blood [lactate]), it is likely that it will be very similar to the value measured at rest (approximately 1 millimole per litre or 1mM). This means that the exercise is being performed below the so-called ‘lactate threshold’ (LT).

However, at some specific higher speed (which will vary from individual to individual), the blood [lactate] will be elevated above the value measured at rest, indicating that the exercise is now being performed above the LT (see figure 1).

As the walking or running speed becomes increasingly faster, the blood [lactate] will increase more and more steeply. Blood [lactate] tends to increase quite slowly until a value of about 3-4mM is reached but, thereafter, the accumulation of lactate seems to accelerate (see figure 1). This point of transition from slow to much faster accumulation of blood lactate has been termed the ‘lactate turnpoint’ (LTP).

Depending on the training status of the individual and the type of exercise being performed, the LT often occurs somewhere between 50% and 80% of the VO2max, whereas the LTP is higher and usually lies between 70% and 90% of the VO2max. The LT has been shown to be a good predictor of performance in long-distance events taking two or more hours such as the marathon, while the LTP (which, incidentally, is roughly equivalent to the so-called ‘maximal lactate steady state’, MLSS) is more closely associated with shorter endurance events such as the 10K run(1).

The pattern of blood lactate accumulation during so-called incremental exercise tests such as that described above is often used to assess changes in fitness resulting from participation in a training programme, or indeed to recommend certain types of training which might bring about specific training effects. It is interesting, therefore, to examine what happens both to blood [lactate] and to other physiological variables such as oxygen uptake when an individual exercises for quite a long period of time at a constant speed that is:

1. Below the LT;
   
2. Between the LT and the LTP;
   
3. Above the LTP.

1. During prolonged exercise at a speed below LT, blood [lactate] is maintained at very close to the resting value (apart from, possibly, a very small and short-lived rise over the first 1-2 minutes) and oxygen uptake rises rapidly following the onset of exercise to reach a steady state within about 2-3 minutes (see figure 2). This exercise intensity ‘domain’ (ie, below the LT) has been termed ‘moderate’.
2. A constant speed above the LT but still below the LTP: In this case, blood [lactate] rises above the resting value and only levels off after some 10-20 minutes. Interestingly, oxygen uptake follows a similar overall time course (see figure 2). Compared to exercise below the LT, oxygen uptake rises relatively slowly, and the achievement of a steady state is delayed. Furthermore, the eventual steady state value is higher than might have been predicted suggesting that exercise efficiency has been impaired. The exercise intensity domain lying between the LT and the LTP has been described as ‘heavy’.
3. A constant speed above the LTP: In this situation, blood [lactate] increases steeply following the onset of exercise and continues to increase until the individual becomes exhausted and has to slow down or stop. By definition, blood [lactate] can never stabilise during exercise performed above the LTP, and the higher the speed above the LTP, the more rapidly blood [lactate] will increase. The important point, however, again is that the pattern of response of oxygen uptake is very similar to that of the blood [lactate]. Oxygen uptake initially rises towards the predicted steady state but then continues to rise with time, showing no sign of abating, until the exercise is stopped (see figure 2). This exercise intensity domain has been termed ‘severe’.

The VO2 ‘slow component’

The continued increase in oxygen uptake as time progresses both in the heavy exercise intensity domain (where oxygen uptake will eventually stabilise at a higher than expected level) and in the severe exercise intensity domain (where it will not stabilise) is known as the ‘VO2 slow component’(2).

The VO2 slow component is particularly interesting to exercise physiologists because it indicates that the efficiency with which the body uses oxygen to produce energy is progressively lost while exercise continues at exactly the same speed. In fact, it has been shown that if exercise is continued for long enough the VO2max can be attained even though the exercise was predicted to be, and started out being, sub-maximal(3)!

What does this mean in practice? Let’s assume that an athlete completes an incremental treadmill test and her LTP occurs at 13km/h, corresponding to approximately 75% VO2max. If the athlete subsequently performs a continuous run at 14 km/h, she might expect her oxygen uptake to stabilise at perhaps 80% of her VO2max after a few minutes. In other words, the running speed she has chosen should be sub-maximal.

However, what will actually happen is that her oxygen uptake (and, indeed, her heart rate [HR]) will continue to increase with time as she maintains the same ‘sub-maximal’ running speed until she reaches her VO2max (and her maximal heart rate, HR max).

Once VO2max and HR max are reached, the only way that the exercise can be continued is if the additional energy that is required is supplied by anaerobic mechanisms. These mechanisms have limited capacity and, thus, once the VO2 slow component brings the oxygen uptake up to the VO2max, exercise can only be sustained for a very short period of time. In plain English, a run which should have been sub-maximal has actually turned out to be maximal (and exhausting)!

The importance of the VO2 slow component – an example

If two athletes are exercising at the same fraction of their VO2max, then it has been conventionally assumed that they are experiencing the same physiological strain, will perceive the exercise to be similarly difficult (or easy), and should benefit equally from continued exposure to the same training stimulus. But is this second assumption, for the description and prescription of exercise intensity using fractions of the VO2max, valid?

The answer to the question depends upon where the LT and LTP lie in relation to the VO2max for each of the athletes. For example, let’s say that athlete A’s LT occurs at 65% of his VO2max and his LTP occurs at 85% of his VO2max, while athlete B’s LT occurs at 55% of his VO2max and his LTP occurs at 75% of his VO2max.

If both athletes perform a continuous running session at the same speed, which corresponds to 60% of their VO2max, athlete A will be exercising below his LT while athlete B will be exercising above his LT. Athlete A will therefore be exercising in the ‘moderate’ domain (in which blood [lactate] will remain close to the resting value and an early steady state in oxygen uptake will be attained) whereas athlete B will be exercising in the ‘heavy’ domain (in which blood [lactate] will be elevated above baseline and a steady state in oxygen uptake will be delayed).

Similarly, if both athletes complete a continuous run at 80% of their VO2max, athlete A will be exercising below his LTP while athlete B will be exercising above his LTP. Athlete A will be exercising in the ‘heavy’ domain such that blood [lactate] and oxygen uptake will attain delayed steady state values, whereas athlete B will be exercising in the ‘severe’ domain in which blood [lactate] will rise inexorably throughout exercise and the VO2 slow component will drive oxygen uptake to its maximum.

For athlete A, this latter training session will be tough but manageable but, for athlete B, it will be seem very hard and might not even be sustainable beyond 20-30 minutes. It can be seen from the above that although the two hypothetical athletes were training at the same fraction of VO2max (at least at the beginning of the two training sessions), the physiological and perceptual responses to the exercise would have been very different. Athlete B would have been training much harder than athlete A in both sessions and, while this might lead to more rapid short-term fitness gains, it might also result in chronic overtraining.

This illustration reinforces the importance for athletes and coaches to understand the physiological significance of the exercise intensity domains that are bounded by the LT and LTP and to appreciate the impact that the VO2 slow component will have on the prescription of exercise intensity.

The existence of the VO2 slow component means that the assumption that a steady state in oxygen uptake will always be attained irrespective of the speed at which an individual is exercising is untenable. Rather, for any individual, there will be a wide range of exercise speeds for which a steady state in oxygen uptake or HR cannot be attained.

This obviously has important implications for the design of training sessions. For example, if a coach asks an athlete to perform a continuous exercise session at a constant speed and at a HR corresponding to, say, 90% of the maximum, it will not be possible for the athlete to satisfy both requests. If the athlete maintains the desired exercise speed, then the HR will increase over time from 90% early in the session towards the maximum as the session proceeds. Alternatively, if the athlete sticks rigidly to the prescribed HR, then he or she would have to gradually reduce the exercising speed during the training session.

While there is no question that either of these two outcomes might still produce positive training effects, the point being made here is that coaches and athletes need to appreciate the limitations that the existence of the VO2 slow component will place upon their performance during exercise above the LTP.

What causes the VO2 ‘slow component’?

The physiological mechanism responsible for the loss of muscle efficiency, which is reflected in the VO2 slow component phenomenon, is obscure (4). However, one theory is that it is related to the progressive recruitment of fast-twitch (or type II) muscle fibres during fatiguing high-intensity exercise.

At the onset of exercise, the central nervous system might activate a certain number of motor units (groups of muscle fibres), which it calculates should be sufficient to sustain the desired exercise speed. However, as high-intensity exercise continues and the initially recruited muscle fibres begin to fatigue, the central nervous system activates additional fresh motor units to ensure that the desired speed can be maintained.

The motor units that are recruited later in exercise will tend to be larger and to contain more fast-twitch muscle fibres, which although powerful, have relatively poor efficiency. This means that they have to consume more oxygen to produce the same amount of force as slow-twitch fibres.

Hence, during high-intensity exercise, as more and more fast-twitch fibres are recruited to enable the same speed to be maintained, the rate of oxygen uptake has to increase. At the same time, the muscle fibres that became fatigued earlier in exercise might continue to consume oxygen as they recover and this might also reduce efficiency and contribute to the VO2 slow component (4)

The VO2 ‘slow component’ and exercise performance

The VO2 slow component is intimately linked to the process of fatigue. For this reason, the higher the speed that can be sustained in the absence of the VO2 slow component, the better the prospects for endurance performance are.

As you may have already surmised, the most effective way to reduce or eliminate the VO2 slow component for any given exercise speed is through endurance training. This will increase the LT and LTP and therefore shift the various exercise intensity domains to higher speeds (5). In this way, a speed that was initially ‘severe’ might become ‘heavy’ or even ‘moderate’ following training.

It has been repeatedly demonstrated that a general programme of endurance training can reduce the VO2 slow component (see figure 3). Quite possibly, the increase in the number of mitochondria (the ‘power-houses’ which use oxygen to produce energy) in the muscle cells resulting from endurance training will delay or reduce the activation of the ‘fast-twitch’ muscle fibres during high-intensity exercise. It is not yet known whether there is a specific type of training that is most effective for reducing the VO2 slow component but regular training in each of the three domains (moderate, heavy, and severe) should prove to be effective (6,7).

One other, more acute, way to reduce the impact of the VO2 slow component and thus enhance exercise performance is to complete a thorough warm-up before competition or hard training sessions. Evidence suggests that the warm-up should include several minutes of quite high-intensity exercise, which appears to increase the distribution of blood flow throughout the active muscles, pre-activate the metabolic pathways, and favourably alter the pattern of motor unit activation(8). As a consequence, the fatigue process is slowed down, the recruitment of fast-twitch muscle fibres is delayed, and the VO2 slow component can be minimised.

Summary

The existence of the VO2 slow component undermines both of the assumptions inherent in the traditional description (and prescription) of ‘exercise intensity’ using the fraction of VO2max expected to be required, namely that: 1) a steady state in oxygen uptake is always attained irrespective of the speed; and, 2) a given fraction of the VO2max represents the same physiological stress in different individuals. Clearly, in creating training programmes, coaches and athletes need to be aware of the exercise intensity ‘domains’ and the very different physiological responses to exercise that which pertain within them.

Andrew M Jones PhD is professor of applied physiology at the University of Exeter

References

1. Med Sci Sports Exerc 1998 Aug; 30(8):1304-13
   
2. J Appl Physiol 1972 Sep; 33(3):351-6
   
3. Ergonomics 1988 Sep; 31(9):1265-79
   
4. Med Sci Sports Exerc 2005 Sep; 37(9):1542-50
   
5. Sports Med 2000 Jun; 29(6):373-86
   
6. J Appl Physiol 2000 Nov; 89(5):1744-52
   
7. Med Sci Sports Exerc 2006 Mar; 38(3):504-12
   
8. Sports Med 2003; 33(13):949-71