The purpose of this study was to investigate whether the voluntary neural drive and the excitability of the reflex arc could be modulated by training, even in old age. To this aim, the effects of a 16-wk strengthening program on plantar flexor voluntary activation (VA) and on the maximum Hoffman reflex (H(max))-to-maximum M wave (M(max)) ratio were investigated in 14 elderly men (65-80 yr). After training, isometric maximum voluntary contraction (MVC) increased by 18% (P < 0.05) and weight-lifting ability by 24% (P < 0.001). Twitch contraction time decreased by 8% (P < 0.01), but no changes in half relaxation time and in peak twitch torque were observed. The VA, assessed by twitch interpolation, increased from 95 to 98% (P < 0.05). Pretraining VA, also evaluated from the expected MVC for total twitch occlusion, was 7% higher (P < 0.01) than MVC. This discrepancy persisted after training. The interpolated twitch torque-voluntary torque relationship was fitted by a nonlinear model and was found to deviate from linearity for torque levels >65% MVC. Compared with younger men (24-35 yr), the H(max)- to M(max) ratio and nerve conduction velocity (H index) of the older group were significantly lower (42%, P < 0.05; and 29%, P < 0.001, respectively) and were not modulated by training. In conclusion, older men seem to preserve a high VA of plantar flexors. However, the impaired functionality of the reflex pathway with aging and the lack of modulation with exercise suggest that the decrease in the H(max)- to M(max) ratio and H index may be related to degenerative phenomena.

Hence, hypertrophy cannot alone justify the increase in torque, and other factors, such as an increase in individual fibre-specific tension (in the case of KE), a decrease in antagonist muscles' coactivation, an improved co-ordination and an increased neural drive of the other heads of quadriceps may have contributed to the increments in strength. The significant increase in muscle power seems particularly noteworthy with respect to daily activities involving the displacement of the body over time, namely, the generation of muscle power.

Patients with mitochondrial myopathies (MM) or myophosphorylase deficiency (McArdle's disease, McA) show impaired capacity for O(2) extraction, low maximal aerobic power, and reduced exercise tolerance. Non-invasive tools are needed to quantify the metabolic impairment. Six patients with MM, 6 with McA, 25 with symptoms of metabolic myopathy but negative biopsy (patient-controls, P-CTRL) and 20 controls (CTRL) underwent an incremental cycloergometric test. Pulmonary O(2) uptake (VO(2)) and vastus lateralis oxygenation indices (by near-infrared spectroscopy, NIRS) were determined. Concentration changes of deoxygenated hemoglobin and myoglobin (Delta[deoxy(Hb + Mb)]) were considered an index of O(2) extraction. Delta[deoxy(Hb + Mb)] peak (percent limb ischemia) was lower in MM (25.3 +/- 12.0%) and McA (18.7 +/- 7.3) than in P-CTRL (62.4 +/- 3.9) and CTRL (71.3 +/- 3.9) subjects. VO(2) peak and Delta[deoxy(Hb + Mb)] peak were linearly related (r(2) = 0.83). In these patients, NIRS is a tool to detect and quantify non-invasively the metabolic impairment, which may be useful in the follow-up of patients and in the assessment of therapies and interventions.

Higher DII scores, indicating greater inflammatory potential of the diet, were directly associated with LGI, as measured by a composite score of plasma and cellular biomarkers of inflammation. These findings are consistent with the contributing role of diet-mediated inflammation in increasing risk for inflammation-related chronic diseases.

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Glioblastoma multiforme (GBM) is a severe brain tumor whose ability to mutate and adapt to therapies is at the base for the extremely poor survival rate of patients. Despite multiple efforts to develop alternative forms of treatment, advances have been disappointing and GBM remains an arduous tumor to treat. One of the leading causes for its strong resistance is the innate upregulation of DNA repair mechanisms. Since standard therapy consists of a combinatory use of ionizing radiation and alkylating drugs, which both damage DNA, targeting the DNA damage response (DDR) is proving to be a beneficial strategy to sensitize tumor cells to treatment. In this review, we will discuss how recent progress in the availability of the DDR kinase inhibitors will be key for future therapy development. Further, we will examine the principal existing DDR inhibitors, with special focus on those currently in use for GBM clinical trials.

Ageing is associated with an increased susceptibility to muscle damage but little is known on how this affects muscle recovery after exercise. Hence, this study is aiming at investigating the effects of a heavy-resistance training session of neuromuscular recovery of the calf muscles of a group of elderly men aged >65. Maximal isometric and isokinetic torque, muscle voluntary activation (VA) capacity, surface electromyographic activity (EMG), peak-to-peak amplitude of action potentials associated with twitch responses of plantar flexors were evaluated before and 5 min (post1), 24 h (post2) and 48 h (post3) after 10 sets of 10 repetitions of a calf raise exercise performed at an intensity of 70% of the individual, one repetition maximum. Blood samples were taken before and 1, 48, 96 and 144 h after the training session and assayed for serum creatine kinase (CK), lactate dehydrogenase (LDH) and myoglobin (Mb). Peak torque during eccentric and concentric (120 degrees s-1) contractions and twitch parameters were significantly reduced at post1, and recovered completely at post2. No significant changes were found in integrated EMG, M-wave amplitudes and VA throughout the entire test period. CK and LDH concentrations reached peak values 48 h after the exercise session and returned to the pre-exercise values 96 h after the training session. Serum Mb level increased by 73.2% 1 h after exercise and recovered at 48 h. The reduction in peak torque following a strength training session in an elderly population could be explained mainly by fatigue of peripheral origin. After 24 h the elders recovered completely their capacities of strength production, despite muscle damage being still evident 48 h after the strength training session.