Abstract: To determine the differences between rock-climbers and controls in finger flexor (FF) motor units (MUs) features and activation strategy, eleven climbers and ten controls volunteered for the study. After maximal voluntary contraction (MVC) assessment, five levels of isometric contractions at 20, 40, 60, 80 and 100% MVC were performed. During contractions, electromyogram (EMG) and mechanomyogram (MMG) were recorded, from which the root mean square (RMS) and mean frequency (MF) were calculated. Climbers showed significantly higher MVC. EMG RMS was statistically higher in climbers than in controls from 60 to 100% MVC. In climbers MMG RMS increased up to 80% MVC, whereas in controls it increased only up to 60% MVC. MMG MF was higher in climbers than in controls from 60 to 100% MVC (P < 0.05). EMG-MMG combined analysis revealed significant differences in MU activation strategy between the two groups. The results are compatible with a shift of climbers' muscles toward faster MUs.

Abstract: PONs are a small family of antioxidant enzymes, whose antiatherogenic activity is well known. Aim of the present study was the evaluation of the effects of moderate aerobic training on their expression, using a rat model. In order to discriminate between PON1 and PON3 enzymatic activity, we took advantage of some differences in their substrate preferences. PON1 and PON3 enzymatic activities and their protein level were analyzed in plasma and in liver microsomes, their mRNA level in the liver. Exercise training did not affect PON1 expression or enzymatic activity, but increased PON3 mRNA, protein levels and enzymatic activity. Training also induced variations in plasma membrane composition, including an increase in polyunsaturated and a decrease in mono- and di-unsaturated fatty acids. On the other hand, acute exercise inhibited PON activities, while increasing PON3 protein content in liver microsomes and reversing the relative composition in mono- di- and poly-unsaturated fatty acids, thus suggesting that physical stress, by altering membrane composition, may impair PON release from liver membranes. In conclusion, we documented for the first time the presence of PON3 in rat serum, and, notably, found that the upregulation of PON3 rather than PON1 appears to be associated with physical training.

Abstract: AIM: Disabled persons are frequently affected by nutritional status impairment, consequent to quantitative and qualitative inadequacy of diet and physical inactivity, resulting in a significant reduction of fat-free mass and bone mineral density (BMD), and an over-expression of fat mass and an increased number of biochemical risk factors for chronic degenerative diseases. The aim of this study was to analyse the applicability and the efficacy of a nutritional counselling intervention in order to improve dietary intake and nutritional status in disabled people. METHODS: Thirty-seven disabled subjects (24 with physical disability and 13 with both mental retardation and physical disability; age 33.5+/-9.2 years) underwent an assessment of nutritional status, and an intervention with nutritional counselling was proposed to each patient for one year. Anthropometric measurements, indirect calorimetry, dual-energy X-ray absorptiometry, dietary intake, and biochemical analysis at baseline (T0) and after one year (T1) of counselling intervention were performed. RESULTS: Sixty-five percent of patients dropped out. Overall, no significant improvement in cardiovascular risk factors, body composition and dietary patterns was reported at T1 in completer subjects. Six subjects who were obese or overweight at T0, reported significant weight and fat mass (FM) reduction at T1 (P=0.01 and P=0.00, respectively). CONCLUSION: Nutritional counselling seems to be ineffective and poorly applicable to disabled people. Further studies should be directed towards a treatment program associated with careful screening, motivation analysis, and follow-up in this patient population.

Abstract: Enhanced angiogenesis, or capillary growth, has a prominent role among the various beneficial effects of exercise training on the myocardium. The aim of the present study is to assess if training-induced increases in capillarity and vascularization persist after 4 weeks of detraining. Adult male rats were trained to run on a treadmill for 10 weeks at approximately 60% VO2max, which did not induce cardiac hypertrophy, but increased (P < 0.05) the soleus/body weight ratio, left ventricle capillarity and von Willebrand-positive cell density (n = 6). In another group of animals (n = 6) subjected to training followed by 4-week detraining, the soleus/body weight ratio returned to normal, with only partial reversal of left ventricle capillarity and von Willebrand-positive cell density. Markers of angiogenesis (VEGF, KDR/VEGF-R2 and HIF-1alpha mRNA, studied by real-time RT-PCR) were upregulated at the end of training, and returned to baseline value after detraining. Electron microscopy highlighted some morphological features in trained hearts (endothelial cell sprouting and bridges and pericyte detachment), suggestive of endothelial cell proliferation and capillary growth that were absent in untrained and detrained hearts. We conclude that the training-induced increase in cardiac capillarity and vascularization are retained for some time upon cessation of the training program even in the absence of angiogenic stimuli.

Abstract: The purpose of the study was to provide practical suggestions on the effect of stretching on the maximal anaerobic power preceded by active or passive warm-up. To this aim, 15 relatively fit male subjects (age 23 +/- 0.2 years, height 177 +/- 2 cm, body mass 74 +/- 2 kg; [mean +/- SE]) randomly performed a series of squat jumps (SJ) and countermovement jumps (CMJ). Jumps were preceded alternatively by: i) passive stretching of lower limbs muscles; ii) active warm-up (AWU); iii) passive warm up (PWU); and iv) the joining of stretching with either active warm-up (AWU+S) or passive warm-up (PWU+S). In control conditions (C) only jumps were required. For the 2 jumps the flight time (Ft), the peak force (Pf), and the maximal power (Wpmax) were calculated. It resulted that Ft, Pf, and Wmax values were significantly higher: i) after AWU than after PWU and PWU+S in CMJ; and ii) in AWU as compared to those of other protocols of SJ. Stretching did not negatively affect the maximal anaerobic power, per se, but seems to inhibit the effect of AWU.The results suggested that AWU seemed to increase vertical jump performance when compared to PWU, presumably due to an increase in metabolic activity as a consequence of AWU, which did not occur in PWU, despite the same skin temperature. Passive stretching alone seemed not to negatively influence vertical jump performance, whereas, if added after AWU, could reduce the power output.

Abstract: It is still unclear whether the low-frequency oscillation in heart rate is generated by an endogenous neural oscillator or by a baroreflex resonance. Our aim was to investigate this issue by analyzing blood pressure and heart rate variability and the baroreflex function in paraplegic subjects with spinal cord injury below the fourth thoracic vertebra. These subjects were selected because they represent a model of intact central neural drive to the heart, with a partially impaired autonomic control of the vessels. In our study, arterial blood pressure and ECG were recorded in 33 able-bodied controls and in 33 subjects with spinal cord lesions between the fifth thoracic and the fourth lumbar vertebra 1) during supine rest (lowest sympathetic activation), 2) sitting on a wheelchair (light sympathetic activation), and 3) during exercise (moderate sympathetic activation). Blood pressure and heart rate spectra, coherence, and baroreflex function (sequence technique) were estimated in each condition. Compared with controls, paraplegic subjects showed a reduction of the low-frequency power of blood pressure and heart rate, and, unlike controls, a 0.1-Hz peak did not appear in their spectra. Sympathetic activation increased the 0.1-Hz peak of blood pressure and heart rate and the coherence at 0.1 Hz in controls only. Paraplegic subjects also had significantly lower baroreflex effectiveness and greater blood pressure variability. In conclusion, the disappearance of the 10-s oscillation of heart rate and blood pressure in subjects with spinal cord lesion supports the hypothesis of the baroreflex nature of this phenomenon.

Abstract: To improve current knowledge of the molecular mechanisms underlying exercise-induced cardioprotection in a rat model of mild exercise training, Sprague-Dawley rats were trained to run on a treadmill up to 55% of their maximal oxygen uptake for 1 h/day, 3 days/week, 14 weeks, with age-matched sedentary controls (n = 20/group). Rats were sacrificed 48 h after the last training session. Despite lack of cardiac hypertrophy, training decreased blood hemoglobin (7.94 +/- 0.21 mM vs. 8.78 +/- 0.23 mM, mean +/- SE, P = 0.01) and increased both plasma malondialdehyde (0.139 +/- 0.005 mM vs. 0.085 +/- 0.009 mM, P = 0.05) and the activity of Mn-superoxide dismutase (11.6 +/- 0.6 vs. 16.5 +/- 1.6 mU/microg, P = 0.01), whereas total superoxide dismutase activity was unaffected. When subjected to 30-min ischemia followed by 90-min reperfusion, hearts from trained rats (n = 5) displayed reduced infarct size as compared to controls (37.26 +/- 0.92% vs. 49.09 +/- 2.11% of risk area, P = 0.04). The biochemical analyses in the myocardium, which included gene expression profiles, real-time PCR, Western blot and determination of enzymatic activity, showed training-induced upregulation of the following mRNAs and/or proteins: growth-arrest and DNA-damage induced 153 (GADD153/CHOP), heme-oxygenase-1 (HO-1), cyclooxygenase-2 (Cox-2), heat-shock protein 70/72 (HSP70/72), whereas heat-shock protein 60 (HSP60) and glucose-regulated protein 75 (GRP75) were decreased. As a whole, these data indicate that mild exercise training activates a second window of myocardial protection against ischemia/reperfusion by upregulating a number of protective genes, thereby warranting further investigation in man.

Abstract: BACKGROUND AND AIM: Obesity, cardiovascular diseases, diabetes and osteoporosis are the most frequent pathologies among people with a severe reduction of physical activity. The impairment in nutritional status, consequent to quantitative and qualitative inadequacy of diet, could be one of the first steps in the development of co-morbidities in disabled subjects. In order to evaluate this hypothesis we investigated the nutritional status and the food intake in patients with physical or mental disabilities. METHODS AND RESULTS: Thirty-seven disabled subjects (24 with exclusively physical inactivity and 13 with mental retardation and physical inactivity) mean age 33.5+/-9.2 years and 25 healthy subjects (mean age 31.0+/-9.3 years) were enrolled. Anthropometric measurements, indirect calorimetry, dual-energy X-ray absorptiometry, dietary intake and biochemical parameters were collected for each subject. Forty percent of disabled were overweight and 14% were obese. Fat free mass (FFM) and bone mineral content (BMC) was lower and fat mass (FM) was higher than able-bodied control. Absolute resting energy expenditure (REE) was lower in disabled subjects, but this difference disappeared when REE was normalized to FFM. Dietary intake resulted unbalanced (16%, 31%, 50% of total daily energy intake derived from protein, lipid and carbohydrate respectively) with a distribution of dietary fatty acid quite far from the recommended ratio [3.1(SFA):4.1(MUFA):1.0(PUFA)] and an excessive consumption of simple carbohydrates (mean intake 17.5+/-4.9%). Insufficient intake of fibre, iron, calcium, potassium and zinc was also found. Finally, alterations in the cholesterol profile were evident in more than one third of the disabled subjects, whereas fasting glucose intolerance was evident in one fourth. CONCLUSION: This study shows a consistent nutritional status impairment in disabled patients resulting in an reduction of FFM and BMC, in an over-representation of FM and in a number of biochemical risk factors for cardiovascular disease. The altered nutritional status is counterparted by a widespread inadequacy of dietary patterns. This nutritional and dietary impairment occurs both in subjects with mental and physical diseases.

Abstract: Estimation of self-similarity is a promising tool for quantifying alterations in cardiovascular dynamics. To evaluate the as yet unexplored influence of sympathetic vascular regulation on the scaling exponent, namely on the parameter characterizing self-similarity, we studied patients with a spinal cord injury as a model of progressively impaired vascular control. We considered 24 able-bodied subjects (AB) and 23 paraplegics with increasing lesion levels: between T(12) and L(4) (n=7); T(5) and T(11) (n=9); and C(6) and T(4) (n=7). We recorded the heart rate in three conditions characterized by increasing sympathetic activation: supine (SUP), sitting (SIT) and exercise (EXE). We calculated the scaling exponent by detrended fluctuation analysis (H(DFA)). Sympathetic activation had different effects on H(DFA), depending on the lesion level. H(DFA) tended to decrease in AB from SUP (0.85+0.02; mean+SEM) and SIT (0.84+0.02) to EXE (0.79+0.02). It remained constant in the T(12)-L(4) group (0.92+0.04, 0.94+0.05 and 0.94+0.04, respectively), while it increased significantly in the T(5)-T(11) group (0.88+0.07, 0.94+0.05, 1.00+0.08) and increased even more in the C(6)-T(4) group (0.83+0.07, 0.91+0.05, 1.06+0.06). Results suggest that heart-rate self-similarity depends on vascular sympathetic control, because it is altered by spinal-cord lesions, even when cardiac neural control is intact.

Abstract: Self similarity is a promising tool for quantifying alterations in cardiovascular dynamics, although the effect of the autonomic control on the scaling structure of cardiovascular signals is still unknown. To address this issue, we studied spinal-cord injured subjects as a model of progressively impaired vascular control. We considered 24 able-bodied subjects (AB) and 23 paraplegics with lesion at different levels: between T12 and L4 (N=7); T5 and T11 (N=9); and C6 and T4 (N=7). We recorded blood pressure and heart rate in three conditions characterized by increasing sympathetic activation: supine (SUP); sitting (SIT); and exercise (EXE). We calculated the scaling exponent of mean arterial pressure, H MAP, and of R-R interval, H RRI, by detrended fluctuation analysis. The sympathetic activation had different effects on the scaling exponent, depending on the lesion level. HRRI did not change significantly from SUP to SIT and to EXE in the AB and T12 -L4 group, while it increased in the T5-T11 and C6-T4 groups. Also for H MAP sympathetic activation produced changes which depend on the level of the spinal lesion. In particular, our results suggest that heart-rate self similarity depends on the vascular sympathetic control, because it is altered by the spinal-cord lesion even when the cardiac neural control is intact.