The intensity and spatial distribution of functional activation in the left precentral and postcentral gyri during actual motor performance (MP) and mental representation [motor imagery (MI)] of self-paced finger-to-thumb opposition movements of the dominant hand were investigated in fourteen right-handed volunteers by functional magnetic resonance imaging (fMRI) techniques. Significant increases in mean normalized fMRI signal intensities over values obtained during the control (visual imagery) tasks were found in a region including the anterior bank and crown of the central sulcus, the presumed site of the primary motor cortex, during both MP (mean percentage increase, 2.1%) and MI (0.8%). In the anterior portion of the precentral gyrus and the postcentral gyrus, mean functional activity levels were also increased during both conditions (MP, 1.7 and 1.2%; MI, 0.6 and 0.4%, respectively). To locate activated foci during MI, MP, or both conditions, the time course of the signal intensities of pixels lying in the precentral or postcentral gyrus was plotted against single-step or double-step waveforms, where the steps of the waveform corresponded to different tasks. Pixels significantly (r > 0.7) activated during both MP and MI were identified in each region in the majority of subjects; percentage increases in signal intensity during MI were on average 30% as great as increases during MP. The pixels activated during both MP and MI appear to represent a large fraction of the whole population activated during MP. These results support the hypothesis that MI and MP involve overlapping neural networks in perirolandic cortical areas.

Temporal and intensity coding of pain in human cortex. J. Neurophysiol. 80:3312-3320, 1998. We used a high-resolution functional magnetic resonance imaging (fMRI) technique in healthy right-handed volunteers to demonstrate cortical areas displaying changes of activity significantly related to the time profile of the perceived intensity of experimental somatic pain over the course of several minutes. Twenty-four subjects (ascorbic acid group) received a subcutaneous injection of a dilute ascorbic acid solution into the dorsum of one foot, inducing prolonged burning pain (peak pain intensity on a 0-100 scale: 48 +/- 3, mean +/- SE; duration: 11.9 +/- 0.8 min). fMRI data sets were continuously acquired for approximately 20 min, beginning 5 min before and lasting 15 min after the onset of stimulation, from two sagittal planes on the medial hemispheric wall contralateral to the stimulated site, including the cingulate cortex and the putative foot representation area of the primary somatosensory cortex (SI). Neural clusters whose fMRI signal time courses were positively or negatively correlated (P < 0.0005) with the individual pain intensity curve were identified by cross-correlation statistics in all 24 volunteers. The spatial extent of the identified clusters was linearly related (P < 0.0001) to peak pain intensity. Regional analyses showed that positively correlated clusters were present in the majority of subjects in SI, cingulate, motor, and premotor cortex. Negative correlations were found predominantly in medial parietal, perigenual cingulate, and medial prefrontal regions. To test whether these neural changes were due to aspecific arousal or emotional reactions, related either to anticipation or presence of pain, fMRI experiments were performed with the same protocol in two additional groups of volunteers, subjected either to subcutaneous saline injection (saline: n = 16), inducing mild short-lasting pain (peak pain intensity 23 +/- 4; duration 2.8 +/- 0.6 min) or to nonnoxious mechanical stimulation of the skin (controls: n = 16) at the same body site. Subjects did not know in advance which stimulus would occur. The spatial extent of neural clusters whose signal time courses were positively or negatively correlated with the mean pain intensity curve of subjects injected with ascorbic acid was significantly larger (P < 0.001) in the ascorbic acid group than both saline and controls, suggesting that the observed responses were specifically related to pain intensity and duration. These findings reveal distributed cortical systems, including parietal areas as well as cingulate and frontal regions, involved in dynamic encoding of pain intensity over time, a process of great biological and clinical relevance.

The energy cost of internal work and its relationships with lower limb mass and pedalling frequency were studied in four male subjects [age 22.2 (SD 1.5) years, body mass 81.0 (SD 5.1) kg, maximal O2 uptake (VO2max) above resting 3.06 (SD 0.4) l.min-1]. The subjects cycled at 40, 60, 80 and 100 rpm and at five different exercise intensities for every pedalling frequency (unloaded condition, UL); the same exercises were repeated after having increased the lower limbs' masses by 40% (loaded condition, L). The exercise intensities were chosen so that the oxygen consumption (VO2) did not exceed 75% of VO2max. For all the subjects and all the conditions, the rate of VO2 above resting increased linearly with the mechanical power (W). The y-intercepts of the linear regressions of VO2 on W, normalised per kilogram of overall lower limbs mass were the same in both UL and L and increased with the 4.165 power of pedalling frequency (fp). These intercepts were taken to represent the metabolic counterpart of the internal power dissipation in cycling; they amounted to 0.78, 0.34, 3.29 and 10.30 W.kg-1 for pedalling frequencies of 40, 60, 80 and 100 rpm respectively. The slope of the regression lines (delta W/delta VO2) represents the delta efficiency of cycle ergometer exercise; this was also affected by fp, ranging, on average, from 22.9% to 32.0%. These data allowed us to obtain a comprehensive description of the effects of fp (per minute), exercise intensity (W, watts) and lower limbs' mass with or without added loads (mL, kg), on VO2 (ml.min-1) during cycling: VO2 = [mL.(4.3.10(-8).fp4.165/0.35)] + (1/[(3.594.10(-5).fp2 - 0.003.fp + 0.326).0.35]).W. The mean percentage error between the VO2 predicted from this equation and the actual value was 12.6%. This equation showed that the fraction of the overall VO2 due to internal work, for a normal 70-kg subject pedalling at 60 rpm and 100 W was of the order of 0.2.

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To investigate whether motor imagery involves ipsilateral cortical regions, we studied haemodynamic changes in portions of the motor cortex of 14 right-handed volunteers during actual motor performance (MP) and kinesthetic motor imagery (MI) of simple sequences of unilateral left or right finger movements, using functional magnetic resonance imaging (fMRI). Increases in mean normalized fMRI signal intensities over values obtained during the control (visual imagery) task were found during both MP and MI in the posterior part of the precentral gyrus and supplementary motor area, both on the contralateral and ipsilateral hemispheres. In the left lateral premotor cortex, fMRI signals were increased during imagery of either left or right finger movements. Ipsilateral cortical clusters displaying fMRI signal changes during both MP and MI were identified by correlation analyses in 10 out of 14 subjects; their extent was larger in the left hemisphere. A larger cortical population involved during both contralateral MP and MI was found in all subjects. The overall spatial extent of both the contralateral and the ipsilateral MP + MI clusters was approximately 90% of the whole cortical volume activated during MP. These results suggest that overlapping neural networks in motor and premotor cortex of the contralateral and ipsilateral hemispheres are involved during imagery and execution of simple motor tasks.

The energy cost of level walking (C,) was measured from the ratio of O2 consumption to speed (from 0.1 to 1.2 m-s-') in hemiplegic patients (n=20) and in a control group of healthy subjects (n=17). Average age and body mass were 58, 54 years and 73, 78 kg, respectively. In hemiplegic patients C, was higher than in control subjects (average value at 1 .O m-s-' =3.6 and 3.3 J.m-'.kg-', respectively) and this difference increased at lower speeds (from 5.1% at 1.2 m-s-' to 28.7% at 0.1 m.s-').

Energy costs and energy sources in karate (wado style) were studied in eight male practitioners (age 23.8 years, mass 72.3 kg, maximal oxygen consumption (VO2max) 36.8 ml.min-1.kg-1) performing six katas (formal, organized movement sequences) of increasing duration (from approximately 10 s to approximately 80 s). Oxygen consumption (VO2) was determined during pre-exercise rest, the exercise period and the first 270 s of recovery in five consecutive expired gas collections. A blood sample for lactate (la-) analysis was taken 5 min after the end of exercise. The overall amount of O2 consumed during the exercise and in the following recovery increased linearly with the duration of exercise (t) from approximately 1.51 (for t equal to 10.5 s (SD 1.6)) to approximately 5.8 l, for t equal to 81.5 s (SD 1.0). The energy release from la- production (VO2la-) calculated assuming that an increase of 1 mmol.l-1 la- corresponded to a VO2 of 3 mlO2.kg-1 was negligible for t equal to or less than 20 s and increased to 17.3 ml.kg-1 (la- = 5.8 mmol.l-1 above resting values) for t equal approximately to 80 s. The overall energy requirement (VO2eq) as given by the sum of VO2 and VO2la- was described by VO2eq = 0.87 + 0.071.t (n = 64; r2 = 0.91), where VO2eq is in litres and t in seconds. This equation shows that the metabolic power (VO2eq.t-1) for this karate style is very high: from approximately 9.5 l.min-1 for t equal to 10 s to approximately 4.9 l.min-1 for t equal to 80 s, i.e. from 3.5 to 1.8 times the subjects' VO2max. The fraction of VO2eq derived from the amount of O2 consumed during the exercise increased from 11% for t equal to 10 s to 41% for t equal to 80 s whereas VO2la- was negligible for t equal to or less than 20 s and increased to 13% for t equal to 80 s. The remaining fraction (from 90% for t equal to 10 s to 46% for t equal to 80 s), corresponding to the amount of O2 consumed in the recovery after exercise, is derived from anaerobic alactic sources, i.e. from net splitting of high energy phosphates during the exercise.

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