Renza Perini

The benefits that physical exercise confers on cardiovascular health are well known, whereas the notion that physical exercise can also improve cognitive performance has only recently begun to be explored and has thus far yielded only controversial results. In the present study, we used a sample of young male subjects to test the effects that a single bout of aerobic exercise has on learning. Two tasks were run: the first was an orientation discrimination task involving the primary visual cortex, and the second was a simple thumb abduction motor task that relies on the primary motor cortex. Forty-four and forty volunteers participated in the first and second experiments, respectively. We found that a single bout of aerobic exercise can significantly facilitate learning mechanisms within visual and motor domains and that these positive effects can persist for at least 30 minutes following exercise. This finding suggests that physical activity, at least of moderate intensity, might promote brain plasticity. By combining physical activity–induced plasticity with specific cognitive training–induced plasticity, we favour a gradual up-regulation of a functional network due to a steady increase in synaptic strength, promoting associative Hebbian-like plasticity. How often have we heard, " Mens sana in corpore sano " , i.e., " a sound mind in a sound body " , which suggests that only a healthy body can sustain a healthy mind. Nevertheless, although this adage has been widely used for some time, its foundational notions must still be substantiated. While the benefits that physical activity confers on car-diovascular health are well known, the idea that exercise can also increase brain " performance " has only recently begun to be investigated by neuroscientists. Thus, whether and how physical exercise makes us cognitively more resourceful has been only partially explored. Several recent studies have shown that regular aerobic physical exercise might improve cognitive functions by helping functional recovery after brain injury and by preventing cognitive decline in normal ageing (for a review see 1). Moreover, many observational studies have noted good cognitive performance in subjects who report practicing regularly physical activity 2,3. Consistent with these observations, there are also structural imaging studies confirming an association between physical activity and increased grey matter volume in subjects that exercise regularly in comparison with sedentary people 4–6. Nevertheless, some of these studies have been criticized because of the presence of other direct causal links between physical activity and cognitive performance; for instance, high cognitive abilities are more likely to be associated with higher educational levels, which are, in turn, often associated with a more health-conscious life style. To overcome these problems, other studies have concentrated on the benefits of the acute effects of physical activity on cognitive processing, irrespective of the previous fitness of tested subjects. These studies compared the subjects' cognitive performance immediately before and after a single bout of aerobic exercise (for a review see 7), and some found an improvement in attention, visuospatial functions, memory, language and executive functions e.g. 2,8–11. However, many studies have reported no significant improvement in cognitive performance after physical activity, as shown in a recent review of more than 30 studies 12. Evidence from animal studies suggest that neurotrophic factors (i.e., brain-derived neurotrophic factor-BDNF) might play a key role in such effects 13,14 , and this evidence has also been confirmed in research on humans 15–17. These studies have shown a relevant and constant increase of BDNF concentration up to 60 minutes following aerobic exercise. Specific work on BDNF has shown that this factor plays a pivotal role in the induction of activity-dependent neuroplasticity 18. Thus, it can be inferred that the advantage of physical exercise may involve directly affecting synaptic plasticity by favouring the strengthening of network structures, supporting neurogenesis and favouring

Cardiovascular responses during resting apnoea include three phases: (1) a dynamic phase of rapid changes, lasting at most 30 s; (2) a subsequent steady phase; and (3) a further dynamic phase, with a continuous decrease in heart rate (HR) and an increase in blood pressure. The interpretation was that the end of the steady phase corresponds to the physiological apnoea breaking point. This being so, during exercise apnoeas, the steady phase would be shorter, and the rate of cardiovascular changes in the subsequent unsteady phase would be faster than at rest. To test these hypotheses, we measured beat-by-beat systolic (SBP), diastolic, and mean blood pressures (MBP), HR, and stroke volume (SV) in six divers during dry resting (duration 239.4 ± 51.6 s) and exercise (30 W on cycle ergometer, duration 88.2 ± 20.9 s) maximal apnoeas, and we computed cardiac output ([Formula: see text]) and total peripheral resistance (TPR). Compared to control, at the beginning of resting (R1) and exercising (E1) apnoeas, SBP and MBP decreased and HR increased. SV and [Formula: see text] fell, so that TPR remained unchanged. At rest, HR, SV, [Formula: see text], and SBP were stable during the subsequent phase; this steady phase was missing in exercise apnoeas. Subsequently, at rest (R3) and at exercise (E2), HR decreased and SBP increased continuously. SV returned to control values. Since [Formula: see text] remained unchanged, TPR grew. The lack of steady phase during exercise apnoeas suggests that the conditions determining R3 were already attained at the end of E1. This being so, E2 would correspond to R3.

Oxygen uptake (VO2) at steady state, heart rate and perceived exertion were determined on nine subjects (six men and three women) while walking (3-7 km.h-1) or running (7-14 km.h-1) on sand or on a firm surface. The women performed the walking tests only. The energy cost of locomotion per unit of distance (C) was then calculated from the ratio of VO2 to speed and expressed in J.kg-1.m-1 assuming an energy equivalent of 20.9 J.ml O2-1. At the highest speeds C was adjusted for the measured lactate contribution (which ranged from approximately 2% to approximately 11% of the total). It was found that, when walking on sand, C increased linearly with speed from 3.1 J.kg-1.m-1 at 3 km.h-1 to 5.5 J.kg-1.m-1 at 7 km.h-1, whereas on a firm surface C attained a minimum of 2.3 J.kg-1.m-1 at 4.5 km.h-1 being greater at lower or higher speeds. On average, when walking at speeds greater than 3 km.h-1, C was about 1.8 times greater on sand than on compact terrain. When running on sand C was approximately independent of the speed, amounting to 5.3 J.kg-1.m-1, i.e. about 1.2 times greater than on compact terrain. These findings could be attributed to a reduced recovery of potential and kinetic energy at each stride when walking on sand (approximately 45% to be compared to approximately 65% on a firm surface) and to a reduced recovery of elastic energy when running on sand.

The sound (SMG) generated by the biceps muscle during isometric exercise at 20, 40, 60, and 80% of maximum voluntary contraction (MVC) up to exhaustion has been recorded by a contact transducer and integrated (iSMG), together with the surface electromyogram (EMG) in eight young untrained men. At the onset of exercise, iSMG and integrated surface EMG (iEMG) amplitude increased linearly with exercise. iSMG remained constant for 253 +/- 73 (SD), 45 +/- 16, 21 +/- 5, and 0 s at the four levels of contraction. Then iSMG increased linearly at 20% MVC, fluctuated at 40% MVC, and decreased exponentially at 60 and 80% MVC. iSMG exhaustion-to-onset ratio was 5.0 at 20%, 1.0 at 40%, and 0.2 at 60 and 80% MVC. On the contrary, independently of exercise intensity, iEMG increased with time, being 1.4 higher at exhaustion than at the onset. The nonunivocal iSMG changes with time and effort of exercise suggest that the sound may be a useful tool to acquire different information to EMG and output force during muscle contraction up to fatigue.

The activated muscle generates a low frequency rumbling noise, which is known as the Sound-MyoGram (SMG). Spectral analysis of the SMG is carried out in this work, in order to: (i) check the adequacy of both the Fast Fourier Transform (FFT) and the Maximum Entropy Spectrum Estimation (MESE). Because it is a well known technique, the FFT method is only briefly described, while the philosophy of the MESE method is given in more detail and completed with a description of the recursive algorithm; (ii) select a frequency parameter suitable to describe the SMG. For this purpose two well-defined physiological conditions (20% and 80% Maximal Voluntary Contraction) have been adopted in order to provide a safe reference for the interpretation of the findings. The results show that: (a) both FFT and MESE are adequate to estimate the SMG Power Spectrum; (b) both the mean and the median frequency are suitable parameters, the mean frequency being the more favourable one; (c) the SMG Power Spectrum is a promising tool to study the muscle activation modalities.

Cardiovascular responses during resting apnoea include three phases: (1) a dynamic phase of rapid changes, lasting at most 30 s; (2) a subsequent steady phase; and (3) a further dynamic phase, with a continuous decrease in heart rate (HR) and an increase in blood pressure. The interpretation was that the end of the steady phase corresponds to the physiological apnoea breaking point. This being so, during exercise apnoeas, the steady phase would be shorter, and the rate of cardiovascular changes in the subsequent unsteady phase would be faster than at rest. To test these hypotheses, we measured beat-by-beat systolic (SBP), diastolic, and mean blood pressures (MBP), HR, and stroke volume (SV) in six divers during dry resting (duration 239.4 ± 51.6 s) and exercise (30 W on cycle ergometer, duration 88.2 ± 20.9 s) maximal apnoeas, and we computed cardiac output ([Formula: see text]) and total peripheral resistance (TPR). Compared to control, at the beginning of resting (R1) and exercising (E1) apnoeas, SBP and MBP decreased and HR increased. SV and [Formula: see text] fell, so that TPR remained unchanged. At rest, HR, SV, [Formula: see text], and SBP were stable during the subsequent phase; this steady phase was missing in exercise apnoeas. Subsequently, at rest (R3) and at exercise (E2), HR decreased and SBP increased continuously. SV returned to control values. Since [Formula: see text] remained unchanged, TPR grew. The lack of steady phase during exercise apnoeas suggests that the conditions determining R3 were already attained at the end of E1. This being so, E2 would correspond to R3.

... TIME AND FREQUENCY DOMAIN ANALYSIS Claudio Orizio, Renza Perini, Arsenio Veicsteinas ... This confirms that by the SMG analysis the mean MUS firing frequency is retrivable by a non invasive methods. REFERENCES 1) Gordon G, Holbourn AHS J Physiol 1948, 107: ...

The power-spectral analysis of heart-rate variability (HRV) is used to compare situations of different muscular exercise in nine sedentary males (n=9) and eight professional cyclists. The changes of low-frequency (LF) and high-frequency (HF) spectral peaks, together with the weight of the very low frequencies (VLF), are described. Their relationship to changes in autonomic activation is discussed. The importance of the

The effects of an intense 8-wk aerobic training program on cardiovascular responses at rest and during exercise, including heart rate variability (HRV) as an expression of autonomic modulation, were evaluated in subjects over 70 yr (mean: 73.9 +/- 3.5 yr). Before and after training in 7 men and 8 women: a) heart rate (HR), blood pressures (BPs), pulse pressure (PP), and oxygen uptake were measured at rest, during, and after exhausting incremental exercise; b) HRV power spectra were calculated at rest in supine and sitting, and during and after two submaximal constant loads (5 min). Power in low-frequency (LF, 0.04-0.15 Hz) and high-frequency (HF, >0.15 Hz) bands were expressed as a percent of total power minus power < 0.04 Hz. After training: a) at rest HR and HRV parameters (in both body positions) were unchanged, whereas BPs decreased; b) peak cycle resistance and oxygen consumption increased by 25% and 18%, respectively, but no change in maximal HR and BPs were found; c) during submaximal loads HR was unchanged at the same metabolic demand, whereas SBP and DBP were lower than before at low loads whereas PP was unchanged. LF power decreased and HF increased at oxygen uptakes above about 0.7 L.min-1 similarly before and after training; and d) recovery of all parameters was similar to pretraining and complete after 10 min The increase in exercise capacity without changes in cardiovascular parameters suggests that 8 wk of aerobic training augmented peripheral gas exchange but not delivery to muscle. The lack of effect on HRV indicates that the improvements in aerobic power and cardiac autonomic modulation, at least in subjects over 70 yr, are dissociated. Moreover, the metabolic demand seems to be the main factor for the changes in HRV power spectra that occur during exercise.

The contracting muscle generates a low frequency sound detectable at the belly surface, ranging from 11 to 40 Hz. To study the relationship between the muscular sound and the intensity of the contraction a sound myogram (SMG) was recorded by a contact sensor from the biceps brachii of seven young healthy males performing 4-s isometric contractions from 10% to 100% of the maximal voluntary contraction (MVC), in 10% steps. Simultaneously, the electromyogram (EMG) was recorded as an index of muscle activity. SMG and EMG were integrated by conventional methods (iSMG and iEMG). The relationship between iSMG and iEMG vs MVC% is described by parabolic functions up to 80% and 100% MVC respectively. Beyond 80% MVC the iSMG decreases, being about half of its maximal value at 100% MVC. Our results indicate that the motor unit recruitment and firing rate affect the iSMG and iEMG in the same way up to 80% MVC. From 80% to 100% MVC the high motor units' discharge rate and the muscular stiffness together limit the pressure waves generated by the dimensional changes of the active fibres. The muscular sound seems to reflect the intramuscular visco-elastic characteristics and the motor unit activation pattern of a contracting muscle.

The time course of heart rate (HR) and venous blood norepinephrine concentration [NE], as an expression of the sympathetic nervous activity (SNA), was studied in six sedentary young men during recovery from three periods of cycle ergometer exercise at 21% +/- 2.8%, 43% +/- 2.1% and 65% +/- 2.3% of VO2max respectively (mean +/- SE). The HR decreased mono-exponentially with tau values of 13.6 +/- 1.6 s, 32.7 +/- 5.6 s and 55.8 +/- 8.1 s respectively in the three periods of exercise. At the low exercise level no change in [NE] was found. At medium and high exercise intensity: (a) [NE] increased significantly at the 5th min of exercise (delta [NE] = 207.7 +/- 22.5 pg.ml-1 and 521.3 +/- 58.3 pg.ml-1 respectively); (b) after a time lag of 1 min [NE] decreased exponentially (tau = 87 s and 101 s respectively); (c) in the 1st min HR decreased about 35 beats.min-1; (d) from the 2nd to 5th min of recovery HR and [NE] were linearly related (100 pg.ml-1 delta [NE] congruent to 5 beats.min-1). In the 1st min of recovery, independent of the exercise intensity, the adjustment of HR appears to have been due mainly to the prompt restoration of vagal tone. The further decrease in HR toward the resting value could then be attributed to the return of SNA to the pre-exercise level.

The changes in the soundmyogram (SMG) and electromyogram (EMG) frequency content during exhausting contractions at 20%, 40%, 60% and 80% of the maximal voluntary contraction (MVC) were investigated by the spectral analysis of the SMG and EMG detected from the biceps brachii muscles of 13 healthy men. The root mean squares (rms) of the two signals were also calculated. Throughout contraction the EMG rms always increased while this was true only at 20% MVC for the SMG. A marked decrease was detected at 60% and 80% MVC. With fatigue the EMG spectra presented a compression towards the lower frequencies at all exercise intensities. The SMG showed a more complex behaviour with a transient increase in its frequency content, followed by a continuous compression of the spectra, at 60% and 80% MVC, and a nearly stable frequency content at lower contraction intensities. This study suggested that different aspects of the changes in the motor unit's activation strategy at different levels of exhausting contractions can be monitored by SMG and EMG signals.

To elucidate the role of factors other than the nervous system in heart rate (fc) control during exercise, the kinetics of fc and plasma catecholamine concentrations were studied in ten heart transplant recipients during and after 10-min cycle ergometer exercise at 50 W. The fc did not increase at the beginning of the exercise for about 60 s. Then in the eight subjects who completed the exercise it increased following an exponential kinetic with a mean time constant of 210 (SEM 22) s. The two other subjects were exhausted after 5 and 8 min of exercise during which fc increased linearly. At the cessation of the exercise, fc remained unchanged for about 50 s and then decreased exponentially with a time constant which was unchanged from that at the beginning of exercise. In the group of eight subjects plasma noradrenaline concentration ([NA]) increased after 30 s to a mean value above resting of 547 (SEM 124) pg.ml-1, showing a tendency to a plateau, while adrenaline concentration ([A]) did not increase significantly. In the two subjects who became exhausted an almost linear increase in [NA] occurred up to about 1,300 pg.ml-1 coupled with a significant increase in [A]. During recovery an immediate decrease in [NA] was observed towards resting values. The values of the fc increase above resting levels determined at the time of blood collection were linearly related with [NA] increments both at the beginning and end of exercise with a similar slope, i.e. about 2.5 beats.min-1 per 100 pg.ml-1 of [NA] change.(ABSTRACT TRUNCATED AT 250 WORDS)

Oxygen uptake (VO2) at steady state, heart rate and perceived exertion were determined on nine subjects (six men and three women) while walking (3-7 km.h-1) or running (7-14 km.h-1) on sand or on a firm surface. The women performed the walking tests only. The energy cost of locomotion per unit of distance (C) was then calculated from the ratio of VO2 to speed and expressed in J.kg-1.m-1 assuming an energy equivalent of 20.9 J.ml O2-1. At the highest speeds C was adjusted for the measured lactate contribution (which ranged from approximately 2% to approximately 11% of the total). It was found that, when walking on sand, C increased linearly with speed from 3.1 J.kg-1.m-1 at 3 km.h-1 to 5.5 J.kg-1.m-1 at 7 km.h-1, whereas on a firm surface C attained a minimum of 2.3 J.kg-1.m-1 at 4.5 km.h-1 being greater at lower or higher speeds. On average, when walking at speeds greater than 3 km.h-1, C was about 1.8 times greater on sand than on compact terrain. When running on sand C was approximately independent of the speed, amounting to 5.3 J.kg-1.m-1, i.e. about 1.2 times greater than on compact terrain. These findings could be attributed to a reduced recovery of potential and kinetic energy at each stride when walking on sand (approximately 45% to be compared to approximately 65% on a firm surface) and to a reduced recovery of elastic energy when running on sand.

To define the dynamics of cardiovascular adjustments to apnoea, beat-to-beat heart rate (HR) and blood pressure and arterial oxygen saturation (SaO(2)) were recorded during prolonged breath-holding in air in 20 divers. Apnoea had a mean duration of 210 +/- 70 s. In all subjects, HR attained a value 14 beats min(-1) lower than control within the initial 30 s (phase I). HR did not change for the following 2-2.5 min (phase II). Then, nine subjects interrupted the apnoea (group A), whereas 11 subjects (group B) could prolong the breath-holding for about 100 s, during which HR continuously decreased (phase III). In both groups, mean blood pressure was 8 mmHg above control at the end of phase I; it then further increased by additional 12 mmHg at the end of the apnoea. In both groups, SaO(2) did not change in the initial 100-140 s of apnoea; then, it decreased to 95% at the end of phase II. In group B, SaO(2) further diminished to 84% at the end of phase III. A typical pattern of cardiovascular readjustments was identified during dry apnoea. This pattern was not compatible with a role for baroreflexes in phase I and phase II. Further readjustment in group B may imply a role for both baroreflexes and chemoreflexes. Hypothesis has been made that the end of phase II corresponds to physiological breakpoint.

It has been proposed that cardiac control is altered in the elderly. Power spectral analysis of heart rate variability (HRV) was performed on 12 male and 11 female elderly subjects (mean age 74 years) while at rest in supine and sitting positions, and at steady states during 5 min of exercise (35-95% peak oxygen consumption, VO2peak). There were no differences in power, measured as a percentage of the total of the high frequency peak (HF, centred at about 0.25 Hz; 13% in males vs 12% in females), low frequency peak (LF, centred at 0.09 Hz; 25% in males and 22% in females), and very low frequency component (VLF, at 0.03 Hz; 66% in males and 69% in females) between body positions at rest. There was no difference in spectral power between male and female subjects. Total power decreased as a function of oxygen consumption during exercise, LF% did not change up to about 14 ml x kg(-1) x min(-1) (40% and 80% VO2peak in males and females, respectively), then decreased towards minimal values in both genders. HF% power and central frequency increased linearly with metabolic demand, reaching higher values in male subjects than in female subjects at VO2peak, while VLF% remained unchanged. Thus, the power spectra components of HRV did not reflect the changes in autonomic activity that occur at increasing exercise intensities, confirming previous findings in young subjects, and indicated similar responses in both genders.

To evaluate if changes in athletes' physical fitness due to seasonal training are associated with changes in cardiovascular autonomic control, nine swimmers (three males and six females; aged 14-18 years) were evaluated before and after 5 months of training and competitions. Maximal oxygen consumption (VO2max) and ventilatory threshold were determined during a maximal test; heart rate (HR) and blood pressure (BP) variabilities' power spectra were calculated at rest (supine and sitting positions) and in the recovery of two exercises at 25 and 80% pre-training VO2max. At the end of the season: (a) VO2max and ventilatory threshold increased respectively by 12 and 34% (P<0.05); (b) at rest, HR decreased by 9 b min(-1) in both body positions, whereas BP decreased in supine position only by 17%. No change in low frequency (LF, 0.04-0.15 Hz) and high frequency (HF, 0.15-1.5 Hz) normalized powers and in LF/HF ratio of HR variability and in LF power of systolic BP variability was observed. In contrast, a significant increase in HF alpha-index (about 12 ms mmHg(-1)) was found; (c) during recovery no change in any parameter was observed. Seasonal training improved exercise capacity and decreased resting cardiovascular parameters, but did not modify vagal and sympathetic spectral markers. The increase in alpha-index observed at rest after the season and expression of augmented baroreflex sensibility indicated however that HR vagal control could have been enhanced by seasonal training. These findings suggested that autonomic system might have played a role in short-term adaptation to training.

Power spectrum analysis of heart-rate variability was made in seven men [mean age 22 (SEM 1) years] in head-out water immersion (W) and in air (A, control) at rest and during steady-state cycling to maximal intensity (maximum oxygen uptake, VO2max). At rest W resulted in a trebled increase in the total power (P < 0.05), coupled with minimal changes in the power (as a percentage of the total) of the high frequency peak (HF, centred at 0.26 Hz; 18% vs 28%) and of the low frequency peak (LF, 0.1 Hz; 24% vs 32%). A third peak at about 0.03 Hz (very low frequency, VLF) represented the remaining power both in W and A. These changes as a whole indicated that immersion caused a vagal dominance in cardiac autonomic interaction, due to the central pooling of blood and/or the pressure of water on the trunk. Exercise caused a decrease in the total power in W and A. The LF% did not change up to about 50% V02max, thereafter decreasing towards nil in both conditions. The HF% decreased in similar ways in W and A to about half at 55%-60% VO2max and then increased to reach 1.5 times the resting values at VO2max. The central frequency of HF increased linearly with oxygen uptake, showing a tendency to be higher in W than in A at medium to high intensities. The VLF% remained unchanged. The lack of differences in the LF peak between W and A during exercise would suggest that blood distribution had no effect on the readjustments in control mechanisms of arterial pressure. On the other hand, the findings of similar HF powers and the very similar values for ventilation in W and A confirmed the direct effect of the respiratory activity in heart rate modulation during exercise.

To define the dynamics of cardiovascular adjustments to apnoea during immersion, beat-to-beat heart rate (HR) and systolic (SBP) and diastolic (DBP) blood pressures were recorded in six divers during and after prolonged apnoeas while resting fully immersed in 27 degrees C water. Apnoeas lasted 215 +/- 35 s. Compared to control values, HR decreased by 20 beats min(-1) and SBP and DBP increased by 23 and 17 mmHg, respectively, in the initial 20 +/- 3 s (phase I). Both HR and BP remained stable during the following 92 +/- 15 s (phase II). Subsequently, during the final 103 +/- 29 s, SBP and DBP increased linearly to values about 60% higher than control, whereas HR remained unchanged (phase III). Cardiac output (Q') decreased by 35% in phase I and did not further change in phases II and III. Compared to control, total peripheral resistances were twice and three times higher than control, respectively, at the end of phases I and III. After resumption of breathing, HR and BP returned to control values in 5 and 30 s, respectively. The time courses of cardiovascular adjustments to immersed breath-holding indicated that cardiac response took place only at the beginning of apnoea. In contrast, vascular responses showed two distinct adjustments. This pattern suggests that the chronotropic control via the baroreflex is modified during apnoea. These cardiovascular changes during immersed static apnoea are in agreement with those already reported for static dry apnoeas.

The aim of this study was to test the hypothesis that the self selected speed in running (vss) is dependent upon the same factors that determine maximal speed in endurance events (e. g. the anaerobic threshold). Experiments were carried out on 8 recreational long distance runners (42.1 +/- 8.6 years of age, 70.1 +/- 10.6 kg of body mass, 1.74 +/- 0.06 m of body height) while they were participating in a 14 day relay race. During the "race" the subjects were not requested to perform maximally but only to cover their running turn (1 hour per day) at their preferred pace. The relationships between heart rate (HR), perceived exertion (RPE), blood lactate concentration ([La]b) and speed (v) were determined in each subject, before the race, during an incremental running test. From these relationships the speed corresponding to a 4 mM concentration of lactate in blood (v4mM) was calculated and found to be 14.3 +/- 1.8 km x h(-1) (n = 8). At this speed the RPE and HR values were 13.6 +/- 1.4 and 156.4 +/- 12.8 bpm, respectively. The average values of speed (vss, 13.4 +/- 0.6 km x h(-1)), RPE (13.5 +/- 1.4) and HR (154.4 +/- 7.6 bpm) measured during the race (n = 47) were not significantly different from those measured at the lactate threshold (v4mM, RPE4mM and v4mM). However, vss and the average HR during the race showed significantly lower variances than v4mM and HR4mM suggesting that, besides the need of avoiding lactate accumulation in blood, other factors must be involved in the choice of speed in running.