Relationship of critical velocity to marathon running performance

The purpose of this investigation was to evaluate the critical velocity (CV) test for prediction of marathon running performance. Twelve subjects [mean age (SD) = 29 (4) years; mean body mass = 63 (13) kg] were tested for CV and completed the 1994 New York City Marathon. The CV (m?·?s^?1) was determined from times to exhaustion at four treadmill running velocities. In addition, peak oxygen consumption ( O _{2 peak}; ml?·?kg^?1?·?min^?1) and ventilatory threshold (Th_vent) were determined from an incremental treadmill test. The Th_vent was calculated using bi-segmental linear regression and was expressed as the velocity (m?·?s^?1) at Th_vent. Separate simple linear regression analyses showed that marathon time [MT; mean (SD) = 231.9 (27.4) min] correlated more highly with CV [MT = 445.3 – 50.3 (CV); r ² = 0.76, SEE = 14.1 min] than either O_2peak [MT = 390.7 – 2.7 ( O_2peak); r ² = 0.51, SEE = 20.1 min] or Th_vent [MT = 353.5 – 30.1 (Th_vent) r ² = 0.28, SEE = 27.4 min]. A stepwise regression analysis resulted in CV (entered first) and Th_vent being included in the prediction equation [MT = 443.5 – 78.9 (CV) + 34.3 (Th_vent), R ² = 0.88, SEE = 10.7 min], while O_2peak was not included. These preliminary data indicate that the CV test may be an attractive field test for assessing marathon performance capabilities.     

Effect of an aerobic training program on physical working capacity at heart rate threshold

The purpose of this investigation was to determine the effect of an aerobic training program on physical working capacity at the heart rate threshold (PWC_HRT). A total of 19 subjects volunteered for this investigation. The control group (CG) consisted of three females and four males, while the training group (TG) included four females and eight males. All subjects were pretested and posttested for maximal oxygen consumption rate ( $\dot V$ O_2max) and PWC_HRT. The training consisted of riding a cycle ergometer for 30 min at 85% of maximal heart rate (HR) three times per week for 8 weeks. Two univariate ( $\dot V$ O_2max and PWC_HRT) 2?×?2 mixed factorial analyses of variance [group (CG, TG)?×?time (pretraining, posttraining)] were used to analyze the data. A significant (P?<?0.05) group by time interaction for PWC_HRT was followed by paired t-tests to analyze the simple main effects. The PWC_HRT for the TG increased significantly (P?<?0.05) as a result of the training program, whereas no change occurred for the CG. The $\dot V$ O_2max did not change significantly for either the TG or the CG. The results of this investigation demonstrate that PWC_HRT was sensitive to the effects of an 8-week aerobic training program.     

Human embryonic stem cell encapsulation in alginate microbeads in macroporous calcium phosphate cement for bone tissue engineering

Human embryonic stem cells (hESC) are promising for use in regenerative medicine applications because of their strong proliferative ability and multilineage differentiation capability. To date there have been no reports on hESC seeding with calcium phosphate cement (CPC). The objective of this study was to investigate hESC-derived mesenchymal stem cell (hESCd-MSC) encapsulation in hydrogel microbeads in macroporous CPC for bone tissue engineering. hESC were cultured to form embryoid bodies (EB), and the MSC were then migrated out of the EB. hESCd-MSC had surface markers characteristic of MSC, with positive alkaline phosphatase (ALP) staining when cultured in osteogenic medium. hESCd-MSC were encapsulated in alginate at a density of 1millioncellsml(-1), with an average microbead size of 207μm. CPC contained mannitol porogen to create a porosity of 64% and 218-μm macropores, with 20% absorbable fibers for additional porosity when the fibers degrade. hESCd-MSC encapsulated in microbeads in CPC had good viability from 1 to 21days. ALP gene expression at 21days was 25-fold that at 1day. Osteocalcin (OC) at 21days was two orders of magnitude of that at 1day. ALP activity in colorimetric p-nitrophenyl phosphate assay at 21days was fivefold that at 1day. Mineral synthesis by the encapsulated hESCd-MSC at 21days was sevenfold that at 1day. Potential benefits of the CPC-stem cell paste include injectability, intimate adaptation to complex-shaped bone defects, ease in contouring to achieve esthetics in maxillofacial repairs, and in situ setting ability. In conclusion, hESCd-MSC were encapsulated in alginate microbeads in macroporous CPC, showing good cell viability, osteogenic differentiation and mineral synthesis for the first time. The hESCd-MSC-encapsulating macroporous CPC construct is promising for bone regeneration in a wide range of orthopedic and maxillofacial applications.     

Umbilical cord stem cells released from alginate-fibrin microbeads inside macroporous and biofunctionalized calcium phosphate cement for bone regeneration

The need for bone repair has increased as the population ages. The objectives of this study were to (1) develop a novel biofunctionalized and macroporous calcium phosphate cement (CPC) containing alginate-fibrin microbeads encapsulating human umbilical cord mesenchymal stem cells (hUCMSC) and, for the first time, (2) investigate hUCMSC proliferation and osteogenic differentiation inside the CPC. A macroporous CPC was developed using calcium phosphate powder, chitosan, and a gas-foaming porogen. Five types of CPC were fabricated: a CPC control, CPC+0.05% fibronectin (Fn), CPC+0.1% Fn, CPC+0.1% arginine-glycine-aspartate (RGD), and CPC+0.1% Fn+0.1% RGD. Alginate-fibrin microbeads containing 10(6) hUCMSC per ml were encapsulated in the CPC paste. After the CPC had set, the degradable microbeads released hUCMSC within it. The hUCMSC proliferated inside the CPC, with the cell density after 21 days being 4-fold that on day1. CPC+0.1% RGD had the highest cell density, which was 4-fold that of the CPC control. The released cells differentiated along the osteogenic lineage and synthesized bone mineral. The hUCMSC inside the CPC+0.1% RGD construct expressed the genes alkaline phosphatase, osteocalcin and collagen I, at twice the level of the CPC control. Mineral synthesis by hUCMSC inside the CPC+0.1% RGD construct was 2-fold that in the CPC control. RGD and Fn incorporation in the CPC did not compromise its strength, which matched the reported strength of cancellous bone. In conclusion, degradable microbeads released hUCMSC which proliferated, differentiated and synthesized minerals inside the macroporous CPC. The CPC with RGD greatly enhanced cell function. The novel biofunctionalized and macroporous CPC-microbead-hUCMSC construct is promising for bone tissue engineering applications.     

High-strength, in situ-setting calcium phosphate composite with protein release

The aim of this study was to develop a mechanically-strong calcium phosphate cement (CPC) with protein release. Chitosan was used to strengthen CPC and control protein release. Mass fraction of protein release = mass of released protein/mass of total protein incorporated into the specimen. Flexural strength (mean +/- sd; n = 6) of CPC containing 100 ng/mL of protein increased from 8.0 +/- 1.4 MPa with 0% chitosan, to 19.8 +/- 1.4 MPa with 15% chitosan (p < 0.05). The latter exceeded the reported strengths of sintered porous hydroxyapatite implants and cancellous bone. When the chitosan mass fraction was increased from 0% to 10% and 15%, protein release varied from 0.60 +/- 0.03 to 0.41 +/- 0.04, and to 0.23 +/- 0.07, respectively (p < 0.05). When powder:liquid ratio increased from 2:1 to 3:1 and 4:1, protein release changed from 0.89 +/- 0.10 to 0.41 +/- 0.04, and to 0.23 +/- 0.07, respectively p < 0.05. Therefore, chitosan content and powder:liquid ratio successfully controlled the protein release. The protein release mass fraction, M, was related to CPC porosity P by: M = 16.9 P(4.5). In summary, a mechanically-strong CPC with controlled protein release was formulated. Protein release was proportional to CPC porosity. The in situ-hardening, nano-apatite composite may have potential for bone tissue engineering, especially when both mechanical strength and controlled release of therapeutic/bioactive agents are needed.     

Mean power frequency and amplitude of the mechanomyographic signal during maximal eccentric isokinetic muscle actions

The purpose of the present investigation was to examine the effects of knee angular velocity on the mean power frequency (MPF) and amplitude of the mechanomyographic (MMG) signal during maximal eccentric (ECC) isokinetic muscle actions. Eleven adult subjects performed maximal ECC muscle actions of the leg extensors on a calibrated Cybex 6000 dynamometer at knee angular velocities of 60, 120, and 180 degrees.s-1. MMG was detected by a piezoelectric crystal contact sensor placed over the vastus lateralis muscle. There were no significant (p > 0.05) velocity-related changes in ECC peak torque (PT) or MMG MPF, however, the mean MMG amplitude value at 60 degrees.s-1 was significantly less (p < 0.05) than that at 180 degrees.s-1. These results did not support our previous hypothesis that the velocity-related increase in MMG amplitude for maximal ECC isokinetic muscle actions was due to selective recruitment of fast twitch fibers and derecruitment of slow twitch fibers with increasing velocity.     

Acute injury to differentiating Clara cells in neonatal rabbits results in age-related failure of bronchiolar epithelial repair

Nonciliated bronchiolar (Clara) cells are progenitor cells during lung development. During differentiation, they have a heightened injury susceptibility to environmental toxicants bioactivated by cytochrome P450 monooxygenase. When neonatal rabbits are treated with the P450-mediated cytotoxicant 4-ipomeanol (IPO), abnormal bronchiolar epithelium results. This study establishes the impact of IPO cytotoxicity on 3 stages of rabbit Clara cell differentiation, early (2.5 and 5 days postnatal [DPN]), intermediate (7 and 9 DPN), and late (15 and 21 DPN), and relates the cytotoxicity to the extent of bronchiolar repair. Neonates received a single dose of IPO (5 mg/kg) and were assessed by qualitative pathology 48 hours later for injury or at 4 weeks for repair. IPO injured the 3 stages of Clara cell differentiation to the same degree; epithelium was swollen, exfoliated, and squamated. Epithelial repair differed among the 3 stages. Bronchioles of animals treated during early and intermediate stages had simple squamous and irregularly shaped cuboidal cells. Animals treated during late stages were similar to controls. Thus, differentiating Clara cells are susceptible to injury by the P450-mediated cytotoxicant IPO, but the extent of repair varies based on when the initial injury occurs.     

Down-regulation of specific antigen-driven cytokine production in a population with endemic Schistosoma japonicum infection

Schistosome antigen-driven cytokine responses and antischistosome antibody levels of residents of a Schistosoma japonicum endemic island in Poyang Lake, Jiangxi Province were studied before and 45 days after treatment with praziquantel. IL-4, IL-5, IL-10 and INF-gamma were all detected in the supernatants of whole-blood cultures after stimulation with schistosome soluble egg antigen (SEA) and soluble worm antigen preparation (SWAP). The percentages of subjects producing detectable amounts of each cytokine assayed were higher in the group who were negative by stool examination at the start of the study than in those who were initially stool positive. After praziquantel treatment the percentages of subjects producing both type I and type II cytokines increased. This suggests that the production of both types of cytokine was down-regulated in the presence of live, egg-laying S. japonicum adult worms but that this was reversible by treatment. In contrast, the antibody studies showed higher levels of SWAP and SEA-specific antibodies (IgE, total IgG, IgG4, IgM) in subjects who were originally stool-positive than in those who were stool-negative. After treatment specific IgE responses were elevated, but total IgG and IgG4 anti-SEA and IgM anti-SWAP antibody levels all fell significantly.     

Mechanomyographic and electromyographic amplitude and frequency responses from the superficial quadriceps femoris muscles during maximal,eccentric isokinetic muscle actions

The purposes of this study were to examine the effects of gender and muscle (vastus lateralis = VL, rectus femoris = RF, and vastus medialis = VM) on the velocity-related patterns for peak torque (PT), mean power output (MP), mechanomyographic (MMG) amplitude, electromyographic (EMG) amplitude, MMG mean power frequency (MPF), and EMG MPF during maximal, eccentric isokinetic muscle actions. Thirteen females (mean +/- SD age = 21 +/- 1 years) and eleven males (mean +/- SD age = 21 +/- 2 years) volunteered for this investigation. PT and MP were measured on a calibrated Cybex 6000 dynamometer at randomly ordered velocities of 60, 120, and 180 degrees.s-1, while MMG and EMG signals were recorded simultaneously from the VL, RF, and VM muscles. The results indicated no gender-related differences for the patterns of PT, MP, MMG amplitude, EMG amplitude, MMG MPF, or EMG MPF. Furthermore, no muscle-related differences were found for the patterns of MMG amplitude, EMG amplitude, or MMG MPF. The normalized values for MP and MMG amplitude increased from 60 to 180 degrees.s-1 (60 degrees.s-1 < 120 degrees.s-1 < 180 degrees.s-1). PT and EMG MPF remained unchanged across velocity, while EMG amplitude remained unchanged from 60 to 120 degrees.s-1, but decreased (approximately 10%) from 120 to 180 degrees.s-1. The findings indicated a close association between the patterns for MP and MMG amplitude, and a similarity between the patterns for PT, EMG amplitude, and EMG MPF across velocity. Therefore, the present findings suggested that motor unit recruitment (EMG amplitude), firing rate (MMG MPF), and muscle fiber action potential conduction velocity (EMG MPF) exhibited velocity-related patterns that were similar to PT production, while MMG amplitude was more closely associated with MP.     

Function and genetics of dystrophin and dystrophin-related proteins in muscle

The X-linked muscle-wasting disease Duchenne muscular dystrophy is caused by mutations in the gene encoding dystrophin. There is currently no effective treatment for the disease; however, the complex molecular pathology of this disorder is now being unravelled. Dystrophin is located at the muscle sarcolemma in a membrane-spanning protein complex that connects the cytoskeleton to the basal lamina. Mutations in many components of the dystrophin protein complex cause other forms of autosomally inherited muscular dystrophy, indicating the importance of this complex in normal muscle function. Although the precise function of dystrophin is unknown, the lack of protein causes membrane destabilization and the activation of multiple pathophysiological processes, many of which converge on alterations in intracellular calcium handling. Dystrophin is also the prototype of a family of dystrophin-related proteins, many of which are found in muscle. This family includes utrophin and alpha-dystrobrevin, which are involved in the maintenance of the neuromuscular junction architecture and in muscle homeostasis. New insights into the pathophysiology of dystrophic muscle, the identification of compensating proteins, and the discovery of new binding partners are paving the way for novel therapeutic strategies to treat this fatal muscle disease. This review discusses the role of the dystrophin complex and protein family in muscle and describes the physiological processes that are affected in Duchenne muscular dystrophy.