Validity of a low-cost friction encoder for measuring velocity, force and power in flywheel exercise devices

The purpose of this study was to investigate the validity of a low-cost friction encoder against a criterion measure (strain gauge combined with a linear encoder) for assessing velocity, force and power in flywheel exercise devices. Ten young and physically active volunteers performed two sets of 14 maximal squats on a flywheel inertial device (YoYo Technology, Stockholm, Sweden) with five minutes rest between each set. Two different resistances were used (0.075 kg · m2 for the first set; 0.025 kg · m2 for the second). Mean velocity (Vrep), force (Frep) and power (Prep) for each repetition were assessed simultaneously via a friction encoder (Chronojump, Barcelona, Spain), and with a strain gauge combined with a linear encoder (MuscleLab 6000, Ergotest Technology, Porsgrunn, Norway). Results are displayed as (Mean [CI 90%]). Compared to criterion measures, mean bias for the practical measures of Vrep, Frep and Prep were moderate (-0.95 [-0.99 to -0.92]), small (0.53 [0.50 to 0.56]) and moderate (-0.68 [-0.71 to -0.65]) respectively. The typical error of estimate (TEE) was small for all three parameters; Vrep (0.23 [0.20 to 0.25]), Frep (0.20 [0.18 to 0.22]) and Prep (0.18 [0.16 to 0.20]). Correlations with MuscleLab were nearly perfect for all measures in all load configurations. Based on these findings, the friction encoder provides valid measures of velocity, force and power in flywheel exercise devices. However, as error did exist between measures, the same testing protocol should be used when assessing changes in these parameters over time, or when aiming to perform inter-individual comparisons

Prohibitins Are Required for Cancer Cell Proliferation and Adhesion

Prohibitin 1 (PHB1) is a highly conserved protein that together with its homologue prohibitin 2 (PHB2) mainly localizes to the inner mitochondrial membrane. Although it was originally identified by its ability to inhibit G1/S progression in human fibroblasts, its role as tumor suppressor is debated. To determine the function of prohibitins in maintaining cell homeostasis, we generated cancer cell lines expressing prohibitin-directed shRNAs. We show that prohibitin proteins are necessary for the proliferation of cancer cells. Down-regulation of prohibitin expression drastically reduced the rate of cell division. Furthermore, mitochondrial morphology was not affected, but loss of prohibitins did lead to the degradation of the fusion protein OPA1 and, in certain cancer cell lines, to a reduced capability to exhibit anchorage-independent growth. These cancer cells also exhibited reduced adhesion to the extracellular matrix. Taken together, these observations suggest prohibitins play a crucial role in adhesion processes in the cell and thereby sustaining cancer cell propagation and survival

How Do Human Cells React to the Absence of Mitochondrial DNA?

Mitochondrial biogenesis is under the control of two different genetic systems: the nuclear genome (nDNA) and the mitochondrial genome (mtDNA). The mtDNA is a circular genome of 16.6 kb encoding 13 of the approximately 90 subunits that form the respiratory chain, the remaining ones being encoded by the nDNA. Eukaryotic cells are able to monitor and respond to changes in mitochondrial function through alterations in nuclear gene expression, a phenomenon first defined in yeast and known as retrograde regulation. To investigate how the cellular transcriptome is modified in response to the absence of mtDNA, we used Affymetrix HG-U133A GeneChip arrays to study the gene expression profile of two human cell lines, 143BTK(-) and A549, which had been entirely depleted of mtDNA (rho(o) cells), and compared it with that of corresponding undepleted parental cells (rho(+) cells).Our data indicate that absence of mtDNA is associated with: i) a down-regulation of cell cycle control genes and a reduction of cell replication rate, ii) a down-regulation of nuclear-encoded subunits of complex III of the respiratory chain and iii) a down-regulation of a gene described as the human homolog of ELAC2 of E. coli, which encodes a protein that we show to also target to the mitochondrial compartment.Our results indicate a strong correlation between mitochondrial biogenesis and cell cycle control and suggest that some proteins could have a double role: for instance in controlling both cell cycle progression and mitochondrial functions. In addition, the finding that ELAC2 and maybe other transcripts that are located into mitochondria, are down-regulated in rho(o) cells, make them good candidates for human disorders associated with defective replication and expression of mtDNA