ABSTRACTBarker, LA, Harry, JR, and Mercer, JA. Relationships between countermovement jump ground reaction forces and jump height, reactive strength index, and jump time. J Strength Cond Res ...32(1)248–254, 2018—The purpose of this study was to determine the relationship between ground reaction force (GRF) variables to jump height, jump time, and the reactive strength index (RSI). Twenty-six, Division-I, male, soccer players performed 3 maximum effort countermovement jumps (CMJs) on a dual-force platform system that measured 3-dimensional kinetic data. The trial producing peak jump height was used for analysis. Vertical GRF (Fz) variables were divided into unloading, eccentric, amortization, and concentric phases and correlated with jump height, RSI (RSI = jump height/jump time), and jump time (from start to takeoff). Significant correlations were observed between jump height and RSI, concentric kinetic energy, peak power, concentric work, and concentric displacement. Significant correlations were observed between RSI and jump time, peak power, unload Fz, eccentric work, eccentric rate of force development (RFD), amortization Fz, amortization time, second Fz peak, average concentric Fz, and concentric displacement. Significant correlations were observed between jump time and unload Fz, eccentric work, eccentric RFD, amortization Fz, amortization time, average concentric Fz, and concentric work. In conclusion, jump height correlated with variables derived from the concentric phase only (work, power, and displacement), whereas Fz variables from the unloading, eccentric, amortization, and concentric phases correlated highly with RSI and jump time. These observations demonstrate the importance of countermovement Fz characteristics for time-sensitive CMJ performance measures. Researchers and practitioners should include RSI and jump time with jump height to improve their assessment of jump performance.
We investigated metabolic costs, muscle activity, and perceptual responses during forward and backward running at matched speeds at different body weight support (BWS) conditions. Participants ran ...forward and backward on a lower body positive pressure treadmill at 0%BWS, 20%BWS, and 50%BWS conditions. We measured oxygen uptake, carbon dioxide production, heart rate, muscle activity, and stride frequency. Additionally, we calculated metabolic cost of transport. Furthermore, we used rating of perceived exertion and feeling scale to investigate perceptual responses. Feeling scale during running was higher with increasing BWS (0–50%BWS), regardless of running direction (p < 0.05). Oxygen uptake, heart rate, and metabolic cost of transport were influenced by the interaction of running direction and BWS (p < 0.01). For example, metabolic cost of transport during backward running was greater than when running forward only when running at 0%BWS (i.e., 4.4 ± 1.1 and 5.8 ± 1.4 J/kg/m for forward and backward running, respectively: p < 0.001). However, rectus femoris muscle activity, stride frequency, and rating of perceived exertion during backward running were averages of 113.5%, 11.3%, and 2.8 rankings greater than when running forward, respectively, regardless of BWS (p < 0.001). We interpret our observations to indicate that environment (in the context of effective body weight) is a critical factor that determines self-selected movement patterns during forward and backward running.
•We studied influence of body weight support (BWS) and direction on movement patterns.•Backward running produced greater muscular and perceptual demands, regardless of BWS.•Influence of running direction on metabolic costs was attenuated by BWS.
DNA damage and mitochondrial dysfunction are thought to play an essential role in ageing and the energetic decline of vascular smooth muscle cells (VSMCs) essential for maintaining plaque integrity. ...We aimed to better understand VSMCs and identify potentially useful compensatory pathways that could extend their lifespan. Moreover, we wanted to assess if defects in mitochondrial respiration exist in human atherosclerotic plaques and to identify the appropriate markers that may reflect a switch in VSMC energy metabolism.
Human plaque tissue and cells were assessed for composition and evidence of DNA damage, repair capacity and mitochondrial dysfunction. Fresh plaque tissue was evaluated using high resolution oxygen respirometry to assess oxidative metabolism. Recruitment and processing of the mitochondrial regulator of autophagy Pink1 kinase was investigated in combination with transcriptional and protein markers associated with a potential switch to a more glycolytic metabolism.
Human VSMC have increased nuclear (nDNA) and mitochondrial (mtDNA) damage and reduced repair capacity. A subset of VSMCs within plaque cap had decreased oxidative phosphorylation and expression of Pink1 kinase. Plaque cells demonstrated increased glycolytic activity in response to loss of mitochondrial function. A potential compensatory glycolytic program may act as energetic switch via AMP kinase (AMPK) and hexokinase 2 (Hex2).
We have identified a subset of plaque VSMCs required for plaque stability that have increased mitochondrial dysfunction and decreased oxidative phosphorylation. Pink1 kinase may initiate a cellular response to promote a compensatory glycolytic program associated with upregulation of AMPK and Hex2.
Schematic representation of the contribution of cardiovascular risk factors to the development of mitochondrial dysfunction, accelerated aging through Pink-1 dependent intermediates that control the balance between glycolytic and oxidative metabolism. Display omitted
•Microdissection of human carotid plaques identifies defects in mitochondrial energetics.•Identification and recruitment and processing of the mitophagy regulator Pink1 kinase.•Compensatory changes associated with transcriptional and protein markers of glycolytic energetics.
Future of Smart Cardiovascular Implants Bussooa, Anubhav; Neale, Steven; Mercer, John R
Sensors (Basel, Switzerland),
06/2018, Letnik:
18, Številka:
7
Journal Article
Recenzirano
Odprti dostop
Cardiovascular disease remains the leading cause of death in Western society. Recent technological advances have opened the opportunity of developing new and innovative smart stent devices that have ...advanced electrical properties that can improve diagnosis and even treatment of previously intractable conditions, such as central line access failure, atherosclerosis and reporting on vascular grafts for renal dialysis. Here we review the latest advances in the field of cardiovascular medical implants, providing a broad overview of the application of their use in the context of cardiovascular disease rather than an in-depth analysis of the current state of the art. We cover their powering, communication and the challenges faced in their fabrication. We focus specifically on those devices required to maintain vascular access such as ones used to treat arterial disease, a major source of heart attacks and strokes. We look forward to advances in these technologies in the future and their implementation to improve the human condition.
Vascular smooth muscle cells (VSMCs) in human atherosclerosis manifest extensive DNA damage and activation of the DNA damage response, a pathway that coordinates cell cycle arrest and DNA repair, or ...can trigger apoptosis or cell senescence. Sirtuin 1 deacetylase (SIRT1) regulates cell ageing and energy metabolism and regulates the DNA damage response through multiple targets. However, the direct role of SIRT1 in atherosclerosis and how SIRT1 in VSMCs might regulate atherosclerosis are unknown.
SIRT1 expression was reduced in human atherosclerotic plaques and VSMCs both derived from plaques and undergoing replicative senescence. SIRT1 inhibition reduced DNA repair and induced apoptosis, in part, through reduced activation of the repair protein Nijmegen Breakage Syndrome-1 but not p53. Fat feeding reduced SIRT1 and induced DNA damage in VSMCs. VSMCs from mice expressing inactive truncated SIRT1 (Δex4) showed increased oxidized low-density lipoprotein-induced DNA damage and senescence. ApoE(-/-) mice expressing SIRT1(Δex4) only in smooth muscle cells demonstrated increased DNA damage response activation and apoptosis, increased atherosclerosis, reduced relative fibrous cap thickness, and medial degeneration.
SIRT1 is reduced in human atherosclerosis and is a critical regulator of the DNA damage response and survival in VSMCs. VSMC SIRT1 protects against DNA damage, medial degeneration, and atherosclerosis.
Running with body weight support (BWS) and backward running have been included in exercise programs. However, it is not known how running characteristics of forward and backward running with BWS are ...influenced by the deviation in the running speed from the preferred speed (PS). The purpose of this study was to investigate how metabolic cost, muscle activity, and perceptual responses of forward and backward running with BWS are influenced by the deviation in running speed from the PS.
Eleven participants ran forward and backward at 0%BWS, 20%BWS, and 50%BWS conditions. The running speed conditions were set to their mode-specific PS, PS+10%, and PS-10%. We measured metabolic cost, muscle activity, stride frequency, rating of perceived exertion, and feeling scale.
Metabolic cost, muscle activity (rectus femoris and gastrocnemius), and rating of perceived of exertion during running increased with increasing speed, regardless BWS and running direction (P<0.05). For example, a 10% increase in running speed from the PS produced averages of 7.1% and 7.7% increases in oxygen uptake and rectus femoris muscle activity, respectively. However, stride frequency during forward and backward running with BWS did not increase with increasing speed when running speed was manipulated around the PS (i.e., 10% increments: P>0.05), with the exception of forward running at 50%BWS.
A 10% increase in running speed from the PS may be useful for individuals who are required to increase their metabolic cost, muscle activity, and perceptual responses during running, regardless of BWS and running direction.
We investigated metabolic costs, rating of perceived exertion (RPE), stride frequency (SF), and preferred speed (PS) during forward and backward running at different levels of body weight support ...(BWS). Participants completed forward and backward running on a lower body positive pressure treadmill at their preferred speed for forward and backward running at 0%BWS, 20%BWS, and 50%BWS. Oxygen uptake (V̇O
), heart rate (HR), RPE, SF, and PS were measured. HR, RPE, and SF during forward and backward running decreased with increasing BWS (P<0.05).V̇O
during both forward and backward running at 50%BWS was significantly lower than when running at 0%BWS (P<0.01). However, PS during forward and backward running increased with increasing BWS (P<0.01). Furthermore,V̇O
was different between running directions only when running at 0%BWS (P<0.01). HR and RPE were not different between running directions (P>0.05). SF during backward running was higher than that of forward running (P<0.01). PS during backward running was lower than when running forward (P<0.001). Our observations suggest that individuals may select PS and SF during running with BWS in a way that resulted in similar metabolic costs, regardless of direction of locomotion.
Cardiovascular disease remains the commonest form of mortality and morbidity in the Western World. It accounts for more deaths than the combined incidence of all cancers. There remains an urgency to ...identify and translate therapies to reduce the effects of this disease and its associated co-morbidities. Atherosclerotic disease accounts for over two thirds of all cardiovascular related deaths. Arterial vessel wall plaques rupture and cause death due to loss of integrity of the overlaying vascular smooth muscle cell (VSMC) cap. Although plaques contain a heterogeneous pool of different cell types, it is the VSMCs that by their nature are responsible for rupture. VSMC are the primary source of extracellular matrix and collagen and it has been suggested that loss of viability and vitality of these cells contributes to plaque vulnerability and rupture. While DNA damage has long been associated with atherosclerotic plaques only relatively recently has the contribution of mitochondrial DNA damage been suggested to play a role. The mitochondrial respiratory chain is a source of ATP that the cell requires for all its energetic functions but is also a source of free radicals that produce reactive species (RS). While these RS exacerbate DNA damage and attack lipids and proteins, it is the loss of ATP that may ultimately be more detrimental. Therapeutic intervention for mitochondria dysfunction is one route on alleviating this burden. Finding alternative sources of ATP synthesis by energetic reconfiguration may also provide a vital link in delaying the kinetics of plaque rupture.
•We studied changes in stride frequency and body weight support on running mechanics.•Participants ran at their preferred stride frequency (SF) and preferred SF ± 10%.•Participants ran at 0% body ...weight support (BWS), 50%BWS, and 80%BWS.•A change in SF influenced muscle activity during running, regardless of BWS.•A change in BWS influenced muscle activity, PSF, and preferred speed during running.
Running with body weight support (BWS) has been used for physical fitness enhancement. Nevertheless, gait mechanics of running with BWS is not fully understood.
We investigated influence of stride frequency manipulation on muscle activity during running at various BWS conditions.
Nineteen participants (23.8 ± 4.1 years) ran on a lower body positive pressure treadmill at their preferred speed and preferred stride frequency (PSF) for 0%BWS, 50%BWS, and 80%BWS conditions. Preferred speed and PSF were selected for each of the BWS conditions. The stride frequency conditions consisted of running at PSF, PSF+10%, and PSF-10%. Muscle activity from the rectus femoris (RF), biceps femoris (BF), tibialis anterior (TA), and gastrocnemius (GA) were measured.
RF and BF during running at the PSF+10% were higher than when running at the PSF, regardless of BWS (P < 0.01). Additionally, RF and TA during running at the PSF-10% were higher than when running at the PSF, regardless of BWS (P < 0.05). Furthermore, RF, TA, GA, and PSF during running decreased with increasing BWS (P < 0.05), although preferred speed increased with increasing BWS (P < 0.001).
These observations suggest that manipulating stride frequency by 10% from the PSF during running produces greater RF, BF, and TA than when running at the PSF, regardless of BWS. Furthermore, it was suggested that a change in BWS influences RF, TA, GA, PSF, and preferred speed during running. Such information may be useful to enable the practitioner to refine the use of running with BWS in exercise programs.
RATIONALE:DNA damage is present in both genomic and mitochondrial DNA in atherosclerosis. However, whether DNA damage itself promotes atherosclerosis, or is simply a byproduct of the risk factors ...that promote atherosclerosis, is unknown.
OBJECTIVE:To examine the effect of DNA damage on atherosclerosis, we studied apolipoprotein (Apo)E mice that were haploinsufficient for the protein kinase ATM (ataxia telangiectasia mutated), which coordinates DNA repair.
METHODS AND RESULTS:ATM/ApoE mice developed accelerated atherosclerosis and multiple features of the metabolic syndrome, including hypertension, hypercholesterolemia, obesity, steatohepatitis, and glucose intolerance. Transplantation with ATM bone marrow attenuated atherosclerosis but not the metabolic syndrome. ATM smooth muscle cells and macrophages showed increased nuclear DNA damage and defective DNA repair signaling, growth arrest, and apoptosis. Metabolomic screening of ATM/ApoE mouse tissues identified metabolic changes compatible with mitochondrial defects, with increased β-hydroxybutyrate but reduced lactate, reduced glucose, and alterations in multiple lipid species. ATM/ApoE mouse tissues showed an increased frequency of a mouse mitochondrial “common” deletion equivalent and reduced mitochondrial oxidative phosphorylation.
CONCLUSIONS:We propose that failure of DNA repair generates defects in cell proliferation, apoptosis, and mitochondrial dysfunction. This in turn leads to ketosis, hyperlipidemia, and increased fat storage, promoting atherosclerosis and the metabolic syndrome. Prevention of mitochondrial dysfunction may represent a novel target in cardiovascular disease.
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