Helen Carter

The Effect of Endurance Training on Parameters of Aerobic Fitness

AbstractEndurance exercise training results in profound adaptations of the cardiorespiratory and neuromuscular systems that enhance the delivery of oxygen from the atmosphere to the mitochondria and enable a tighter regulation of muscle metabolism. These adaptations effect an improvement in endurance performance that is manifest as a rightward shift in the ‘velocity-time curve’. This shift enables athletes to exercise for longer at a given absolute exercise intensity, or to exercise at a higher exercise intensity for a given duration. There are 4 key parameters of aerobic fitness that affect the nature of the velocity-time curve that can be measured in the human athlete. These are the maximal oxygen uptake (V̇O2max), exercise economy, the lactate/ventilatory threshold and oxygen uptake kinetics. Other parameters that may help determine endurance performance, and that are related to the other 4 parameters, are the velocity at V̇O2max (V-V̇O2max) and the maximal lactate steady state or critical power. This review considers the effect of endurance training on the key parameters of aerobic (endurance) fitness and attempts to relate these changes to the adaptations seen in the body’s physiological systems with training. The importance of improvements in the aerobic fitness parameters to the enhancement of endurance performance is highlighted, as are the training methods that may be considered optimal for facilitating such improvements.

Effects of prior exercise and recovery duration on oxygen uptake kinetics during heavy exercise in humans

Prior heavy exercise (above the lactate threshold, LT) reduces the amplitude of the pulmonary oxygen uptake (V̇O2) slow component during heavy exercise, yet the precise effect of prior heavy exercise on the phase II V̇O2 response remains to be established. This study was designed to test the hypotheses that (1) prior heavy exercise increases the amplitude of the phase II V̇O2 response independently of changes in the baseline V̇O2 value and (2) the effect of prior exercise depends on the amount of external work done during prior exercise, irrespective of the intensity of the prior exercise. Nine subjects performed two 6 min bouts of heavy cycling exercise separated by 6 min baseline pedalling recovery (A), two 6 min heavy exercise bouts separated by 12 min recovery (6 min rest and 6 min baseline pedalling, B), and a bout of moderate exercise (below the LT) in which the same amount of external work was performed as during the prior heavy exercise, followed by 6 min heavy exercise (C). In both tests A and B, prior heavy exercise significantly increased the absolute V̇O2 amplitude at the end of phase II (by ∼150 ml min−1), and reduced the amplitude of the V̇O2 slow component by a similar amount. Following 12 min of recovery (B), baseline V̇O2, but not blood [lactate], had returned to pre‐exercise levels, indicating that these effects occurred independently of changes in baseline V̇O2. Prior moderate exercise (C) had no effect on either the V̇O2 or blood [lactate] responses to subsequent heavy exercise. The V̇O2 response to heavy exercise was therefore dependent on the intensity of prior exercise, and the effects on the amplitudes of the phase II and slow V̇O2 components persisted for at least 12 min following prior heavy exercise.

Effect of incremental test protocol on the lactate minimum speed

PURPOSE The purpose of this study was to investigate the effect of altering the initial running speed (RS) in the incremental portion of the lactate minimum test on the lactate minimum speed (LMS). METHODS Eight well-trained endurance runners (mean +/- SD age 29.0 +/- 5.4 yr, body mass 72.0 +/- 5.6 kg, VO2max 63.1 +/- 3.8 mL x kg(-1) min(-1)) completed a standard incremental treadmill test for the assessment of the lactate threshold (LT) and VO2max, and eight lactate minimum tests. Following a period of supramaximal exercise, subjects were allowed 8 min of recovery to allow blood [lactate] to peak. Subjects then undertook eight randomly-assigned incremental treadmill tests from different initial running speeds (3.0, 2.5, 2.0, 1.5, 1.0, and 0.5 km x h(-1) below the predetermined RS-LT, at the RS-LT, and at 1.0 km x h(-1) above the RS-LT) with RS increased by 1.0 km x h(-1) every 5 min until volitional fatigue. Blood samples for the determination of blood [lactate] were taken at the end of each stage and the LMS was determined by fitting a spline function to the data. RESULTS No LMS could be determined for the two highest initial RS conditions. For the other conditions, the LMS was significantly affected by the initial RS used in the incremental test and varied from 13.8 +/- 0.7 km x h(-1) with an initial RS of 3.0 km x h(-1) below the RS-LT, to 15.8 +/- 0.8 km x h(-1) with an initial RS of 0.5 km x h(-1) below the RS-LT. The LMS was significantly different from the RS-LT (15.4 +/- 0.8 km x h(-1)) (P < 0.05), except when the incremental test started at 1.0 or 1.5 km x h(-1) below the RS-LT. CONCLUSIONS These results suggest that the LMS test is not a valid method for estimation of the LT since it is profoundly influenced by the starting speed selected for the incremental portion of the test.

Effect of 6 weeks of endurance training on the lactate minimum speed

The aim of this study was to assess the sensitivity of the lactate minimum speed test to changes in endurance fitness resulting from a 6 week training intervention. Sixteen participants (mean +/- s: age 23+/-4 years; body mass 69.7+/-9.1 kg) completed 6 weeks of endurance training. Another eight participants (age 23+/-4 years; body mass 72.7+/-12.5 kg) acted as non-training controls. Before and after the training intervention, all participants completed: (1) a standard multi-stage treadmill test for the assessment of VO2max, running speed at the lactate threshold and running speed at a reference blood lactate concentration of 3 mmol x l(-1); and (2) the lactate minimum speed test, which involved two supramaximal exercise bouts and an 8 min walking recovery period to increase blood lactate concentration before the completion of an incremental treadmill test. Additionally, a subgroup of eight participants from the training intervention completed a series of constant-speed runs for determination of running speed at the maximal lactate steady state. The test protocols were identical before and after the 6 week intervention. The control group showed no significant changes in VO2max, running speed at the lactate threshold, running speed at a blood lactate concentration of 3 mmol x l(-1) or the lactate minimum speed. In the training group, there was a significant increase in VO2max (from 47.9+/-8.4 to 52.2+/-2.7 ml x kg(-1) x min(-1)), running speed at the maximal lactate steady state (from 13.3+/-1.7 to 13.9+/-1.6 km x h(-1)), running speed at the lactate threshold (from 11.2+/-1.8 to 11.9+/-1.8 km x h(-1)) and running speed at a blood lactate concentration of 3 mmol x l(-1) (from 12.5+/-2.2 to 13.2+/-2.1 km x h(-1)) (all P < 0.05). Despite these clear improvements in aerobic fitness, there was no significant difference in lactate minimum speed after the training intervention (from 11.0+/-0.7 to 10.9+/-1.7 km x h(-1)). The results demonstrate that the lactate minimum speed, when assessed using the same exercise protocol before and after 6 weeks of aerobic exercise training, is not sensitive to changes in endurance capacity.

Maximal lactate steady state as a training stimulus

The present study examined the use of the maximal lactate steady state (MLSS) as an exercise training stimulus in moderately trained runners. Fourteen healthy individuals (12 male, 2 female; age 25 +/- 6 years, height 1.76 +/- 0.05 m, body mass 76 +/- 8 kg mean +/- SD) took part in the study. Following determination of the lactate threshold (LT), VO2max, running velocity at MLSS (vMLSS) and a control period of 4 weeks, participants were pair matched and split into two cohorts performing either continuous (CONT: 2 sessions/week at vMLSS) or intermittent treadmill running (INT: 2 sessions/week, 3-min repetitions 0.5 km . h (-1) above and below vMLSS). vMLSS increased in CONT by 8 % from 12.3 +/- 1.5 to 13.4 +/- 1.6 km . h (-1) (p < 0.05) and in INT by 5 % from 12.2 +/- 1.9 km . h (-1) to 12.9 +/- 1.9 km . h (-1) (p < 0.05). Running speed at the LT increased by 7 % in the CONT group (p < 0.05) and by 9 % in the INT group (p < 0.05). VO2max increased by 10 % in the CONT group (p < 0.05) and by 6 % in INT (p < 0.05). Two sessions per week at vMLSS are capable of eliciting improvements in the physiological responses at LT, MLSS, and VO2max in moderately trained runners.

A disproportionate increase in VO2 coincident with lactate threshold during treadmill exercise.

PURPOSE The purpose of this study was to assess the relationship between pulmonary VO2 and running speed over a range of exercise intensities. During constant-load cycle exercise above the lactate threshold (Tlac), it has been shown that VO2 does not attain a steady state within 3 min but continues to rise until either a delayed but elevated steady-state VO2 is attained or exhaustion occurs. Since this greater oxygen cost of exercise (V02 slow component) has only been demonstrated at discrete exercise intensities above Tlac, it was hypothesised that the onset of the VO2 slow component would coincide with Tlac during an incremental test if the stage durations were of sufficient length. METHODS Five male subjects (mean +/- SD age 31 +/- 2 yr: VO2peak 60.1 +/- 5.8 mL x kg(-1) x min(-1)) performed four identical treadmill tests within an 8-d period. The tests involved the completion of six stages of 7-min duration. Running speed was increased by 0.5 km x h(-1) between stages. In the first test, fingertip capillary blood was sampled at the end of each stage for determination of Tlac. For all tests expired air was collected into Douglas bags from 3.0 to 3.75 min and from 6.0 to 6.75 min of each stage to determine any increase in V02 (deltaVO2) over the duration of the stage. RESULTS The mean deltaVO2 for each stage over the four tests was determined for each subject. Repeated measures ANOVA with post-hoc Tukey tests revealed a significant increase in deltaVO2 at running speeds above, but not below, Tlac. CONCLUSIONS The results of this study confirm the close association between the VO2 slow component and the onset of lactic acidosis and demonstrate alinearity in the VO2-exercise intensity relationship above Tlac for incremental treadmill exercise.

The Effects of Training on Gross Efficiency in Cycling: A Review

There has been much debate in the recent scientific literature regarding the possible ability to increase gross efficiency in cycling via training. Using cross-sectional study designs, researchers have demonstrated no significant differences in gross efficiency between trained and untrained cyclists. Reviewing this literature provides evidence to suggest that methodological inadequacies may have played a crucial role in the conclusions drawn from the majority of these studies. We present an overview of these studies and their relative shortcomings and conclude that in well-controlled and rigorously designed studies, training has a positive influence upon gross efficiency. Putative mechanisms for the increase in gross efficiency as a result of training include, muscle fibre type transformation, changes to muscle fibre shortening velocities and changes within the mitochondria. However, the specific mechanisms by which training improves gross efficiency and their impact on cycling performance remain to be determined.

The effect of variable gradients on pacing in cycling time-trials.

It has been reported that performance in cycling time-trials is enhanced when power is varied in response to gradient although such a mechanical pacing strategy has never been confirmed experimentally in the field. The aim of this study was, therefore, to assess the efficacy of mechanical pacing by comparing a constant power strategy of 255 W with a variable power strategy that averaged to 255 W over an undulating time-trial course. 20 experienced cyclists completed 4 trials over a 4 km course with 2 trials at an average constant power of 253 W and 2 trials where power was varied in response to gradient and averaged 260 W. Time normalised to 255 W was 411±31.1 s for the constant power output trials and 399±29.5 s for the variable power output trials. The variable power output strategy therefore reduced completion time by 12±8 s (2.9%) which was significant ( P<0.001). Participants experienced difficulty in applying a constant power strategy over an undulating course which acted to reduce their time gain. It is concluded that a variable power strategy can improve cycling performance in a field time-trial where the gradient is not constant.

Changes in blood lactate and pyruvate concentrations and the lactate-to-pyruvate ratio during the lactate minimum speed test.

The aim of this study was to assess the responses of blood lactate and pyruvate during the lactate minimum speed test. Ten participants (5 males, 5 females; mean +/- s: age 27.1 +/- 6.7 years, VO 2max 52.0 +/- 7.9 ml kg -1 min -1 ) completed: (1) the lactate minimum speed test, which involved supramaximal sprint exercise to invoke a metabolic acidosis before the completion of an incremental treadmill test (this results in a ‘U-shaped’ blood lactate profile with the lactate minimum speed being defined as the minimum point on the curve); (2) a standard incremental exercise test without prior sprint exercise for determination of the lactate threshold; and (3) the sprint exercise followed by a passive recovery. The lactate minimum speed (12.0 +/- 1.4 km h -1 ) was significantly slower than running speed at the lactate threshold (12.4 +/- 1.7 km h -1 ) (P < 0.05), but there were no significant differences in VO 2 , heart rate or blood lactate concentration between the lactate minimum speed and running speed at the lactate threshold. During the standard incremental test, blood lactate and the lactate-topyruvate ratio increased above baseline values at the same time, with pyruvate increasing above baseline at a higher running speed. The rate of lactate, but not pyruvate, disappearance was increased during exercising recovery (early stages of the lactate minimum speed incremental test) compared with passive recovery. This caused the lactate-to-pyruvate ratio to fall during the early stages of the lactate minimum speed test, to reach a minimum point at a running speed that coincided with the lactate minimum speed and that was similar to the point at which the lactate-to-pyruvate ratio increased above baseline in the standard incremental test. Although these results suggest that the mechanism for blood lactate accumulation at the lactate minimum speed and the lactate threshold may be the same, disruption to normal submaximal exercise metabolism as a result of the preceding sprint exercise, including a three- to five-fold elevation of plasma pyruvate concentration, makes it difficult to interpret the blood lactate response to the lactate minimum speed test. Caution should be exercised in the use of this test for the assessment of endurance capacity.

The critical power concept in all-out isokinetic exercise

UNLABELLED The critical power concept has been applied to constant-load exhaustive exercise and recently validated for 3-min all-out exercise. OBJECTIVES To test the application of critical power to a 3-min all-out isokinetic cycling exercise. DESIGN Single-group, experimental, comparative design. METHOD Nine participants performed a 3-min all-out isokinetic test and 4-5 constant-load exhaustive trials, at 60 and 100 rpm, on an electrically-braked cycle. The linear P-t-1 relationship was modelled using a 2-parameter model (slope: critical power; intercept: Anaerobic Work Capacity). End power and accumulated work done above EP were calculated from the 3-min tests. RESULTS No significant difference and a significant correlation was found between end power and critical power (60 rpm: 259 ± 40 W vs. 245 ± 38 W, P > 0.05; r = 0.85, P<0.01; 100 rpm: 227 ± 57 W vs. 212 ± 44 W, P > 0.05; r = 0.86, P<0.01). The Bias ± 95% limits of agreement were 14 ± 42 W at 60 rpm and 15 ± 57 W at 100 rpm. Work done above EP (60 rpm: 14.7 ± 3.0 kJ; 100 rpm: 17.3 ± 3.1 kJ) was not significantly different to the anaerobic work capacity (60 rpm: 16.2 ± 3.2 kJ; 100 rpm: 20.6 ± 6.4 kJ; P>0.05) but with only a significant correlation at 60 rpm (r = -0.71, P<0.05). CONCLUSIONS The 2-parameter model underpinning the critical power construct can be applied to a 3-min all-out isokinetic test. End power does not differ and correlates with critical power. However, a further insight into levels of agreement leads to some scepticism concerning the use of the two variables interchangeably. The great intra-subject differences between work done above EP and the intercept of the P-t-1 relationship should also be considered.