58 resultados para 110602 Exercise Physiology

em Deakin Research Online - Australia


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The use of instability devices and exercises to train the core musculature is an essential feature of many training centres and programs. It was the intent of this position stand to provide recommendations regarding the role of instability in resistance training programs designed to train the core musculature. The core is defined as the axial skeleton and all soft tissues with a proximal attachment originating on the axial skeleton, regardless of whether the soft tissue terminates on the axial or appendicular skeleton. Core stability can be achieved with a combination of muscle activation and intra-abdominal pressure. Abdominal bracing has been shown to be more effective than abdominal hollowing in optimizing spinal stability. When similar exercises are performed, core and limb muscle activation are reported to be higher under unstable conditions than under stable conditions. However, core muscle activation that is similar to or higher than that achieved in unstable conditions can also be achieved with ground-based free-weight exercises, such as Olympic lifts, squats, and dead lifts. Since the addition of unstable bases to resistance exercises can decrease force, power, velocity, and range of motion, they are not recommended as the primary training mode for athletic conditioning. However, the high muscle activation with the use of lower loads associated with instability resistance training suggests they can play an important role within a periodized training schedule, in rehabilitation programs, and for nonathletic individuals who prefer not to use ground-based free weights to achieve musculoskeletal health benefits.

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The goals of pre-exercise nutritional strategies are to optimise the availability of carbohydrate (CHO) and fluid. Ingestion of CHO 3-4 hr prior to exercise can increase liver and muscle glycogen stores and has been associated with enhanced endurance exercise performance. The metabolic effects of CHO ingestion persist for at least 6 hr. Although an increase in plasma insulin following CHO ingestion in the hour prior to exercise inhibits lipolysis and liver glucose output, and can lead to transient hypoglycemia during subsequent exercise, there is no convincing evidence that this is always associated with impaired exercise performance. Having said that, individual experience should inform individual practice. Interventions to increase plasma FFA availability prior to exercise have been shown to reduce CHO utilisation during exercise, but do not appear to have major ergogenic benefits. It is more difficult to hyperhydrate prior to exercise and although there has been interest in glycerol ingestion, to date research results have been equivocal. At the very least, athletes should ensure euhydration prior to exercise.

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Current bio-kinematic encoders use velocity, acceleration and angular information to encode human exercises. However, in exercise physiology there is a need to distinguish between the shape of the trajectory and its execution dynamics. In this paper we propose such a two-component model and explore how best to compute these components of an action. In particular, we show how a new spatial indexing scheme, derived directly from the underlying differential geometry of curves, provides robust estimates of the shape and dynamics compared to standard temporal indexing schemes.

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Deakin University opened its Clinical Exercise Learning Centre (CELC) in May 2011, initially staffed by four (now seven) Accredited Exercise Physiologists (AEP), and funded by the university. The main objectives of CELC are to provide (i) excellent clinical practicum learning opportunities for postgraduate students enrolled in the Master of Clinical Exercise Physiology that prepare students for subsequent external placements; (ii) learning opportunities that are vertically integrated with the preparatory components of the Masters, including pathophysiology units and pre-clinical units; (iii) learning opportunities that are also integrated with the external clinical practicum program that is embedded in the Masters; (iv) a clinical service to the community and strong referral networks with local GPs; (v) a research centre that is focussed on evaluating the efficacy of Accredited Exercise Physiology (AEP) services for a range of clinical situations, with a view to contributing to a future national evidence-based practice network supported by ESSA. Deakin University funds the CELC facility, equipment, consumables, limited car parking, practice management software and server and, most importantly, the staff. Therefore CELC runs at a loss even against fees charged and this was built into the original model. Staff include an AEP clinical practicum coordinator, two casual AEPs and several academic AEPs; the latter practise as a small part of their approved workloads. The practice model is for all AEPs to provide clinical services with referred clients who are billed as if CELC is a private practice, whilst concurrently teaching and mentoring students; the latter are expected to be active learners in CELC and have exposure to a wide range of pathologies and clinical situations. Billable hours are always provided by AEPs, not students, but students can assist. CELC provides clinical services 1:1:1 (client: AEP: student), 1:1:5 and 8:1:5. CELC was awarded national runner-up in the ESSA Exercise Physiology clinic of the year in 2011 and has grown its caseload to > 200 referrers in 2013. CELC recently designed a generic research platform and has begun to roll out research projects that are designed to translate 'traditional' research-based evidence of exercise benefits for chronic disease in order to evaluate AEP efficacy of practice in the Australian context. CELC provides a model for other universities, provided those universities see it for its learning value, and not to generate revenue or profit.

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Regular exercise stimulates numerous structural, metabolic, and morphological adaptations in skeletal muscle. These adaptations are vital to maintain human health over the life span. Exercise is therefore seen as a primary intervention to reduce the risk of chronic disease. Advances in molecular biology, biochemistry, and bioinformatics, combined with exercise physiology, have identified many key signaling pathways as well as transcriptional and translational processes responsible for exercise-induced adaptations. Noncoding RNAs, and specifically microRNAs (miRNAs), constitute a new regulatory component that may play a role in these adaptations. The short single-stranded miRNA sequences bind to the 3' untranslated region of specific messenger RNAs (mRNAs) on the basis of sequence homology. This results in the degradation of the target mRNA or the inhibition of protein translation causing repression of the corresponding protein. While tissue specificity or enrichment of certain miRNAs makes them ideal targets to manipulate and understand tissue development, function, health, and disease, other miRNAs are ubiquitously expressed; however, it is uncertain whether their mRNA/protein targets are conserved across different tissues. miRNAs are stable in plasma and serum and their altered circulating expression levels in disease conditions may provide important biomarker information. The emerging research into the role that miRNAs play in exercise-induced adaptations has predominantly focused on the miRNA species that are regulated in skeletal muscle or in circulation. This chapter provides an overview of these current research findings, highlights the strengths and weaknesses identified to date, and suggests where the exercise-miRNA field may move into the future.

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The relationship between muscle strength and bone mineral density illustrates the positive effect of mechanical loading on bone. But local and systemic factors may affect both muscle and bone tissues. This study investigated the effects of long-term tennis playing on the relationship between lean tissue mass and bone mineral content in the forearms, taking the body dimensions into account. Fifty-two tennis players (age 24.2 +/- 5.8 yrs, 16.2 +/- 6.1 yrs of practice) were recruited. Lean tissue mass (LTM), bone area, bone mineral content (BMC), and bone mineral density were measured at the forearms from a DXA whole-body scan. Grip strength was assessed with a dynamometer. A marked side-to-side difference (p < 0.0001) was found in favor of the dominant forearm in all parameters. Bone area and BMC correlated with grip strength on both sides (r = 0.81 - 0.84, p < 0.0001). The correlations were still significant after adjusting for whole-body BMC body height, or forearm length. This result reinforced the putative role of the muscles in the mechanical loading on bones. In addition, forearm BMC adjusted to LTM or grip strength was higher on the dominant side, suggesting that tennis playing exerts a direct effect on bone.

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The purpose of this study was to examine, in male adolescents, the effects of long-term endurance training on cardiac structure and function, by adopting a cross-sectional comparison with a nonathletic control group. A total of 13 endurance-trained (EX) and seven untrained (CON) male adolescents (mean ± SE, age = 15.3 ± 0.3 and 15.2 ± 0.28 yrs, respectively) underwent echocardiography at rest to determine left ventricular enddiastolic dimension (LVDd), left ventricular end-systolic dimension (LVDs), left ventricular posterior wall thickness (LVPW), stroke volume (SV), and cardiac output (CO). On separate days, incremental exercise tests were conducted on a cycle ergometer to measure peak oxygen uptake (VO2max) and anaerobic power. VO2max was greater in the endurance group (54.4 ± 1.8 mL min–1 kg–1) than in the control group (45.8 ± 1.6 mL min–1 kg–1; p < 0.05). Mean exercise time was longer in EX (12.9 ± 0.7 min) than CON (10.4 ± 0.8 min; p < 0.05). No significant differences were noted between the two groups in resting heart rate, maximal heart rate, LVDd, LVDs, LVPW, SV, SV indexed, CO, and CO indexed, or in the anaerobic strength. These data provide evidence that endurance-trained adolescent males develop superior exercise performance before the cardiac remodeling that is evident in trained adult athletes.

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Purpose: The aim of this study was to test the reliability and construct validity of a reactive agility test (RAT), designed for Australian Football (AF).

Methods: Study I tested the reliability of the RAT, with 20 elite junior AF players (17.44 ± 0.55 y) completing the test on two occasions separated by 1 wk. Study II tested its construct validity by comparing the performance of 60 participants (16.60 ± 0.50 y) spread over three aged-matched population groups: 20 athletes participating in a State Under-18 AF league who had represented their state at national competitions (elite), 20 athletes participating in the same league who had not represented their state (subelite), and 20 healthy males who did not play AF (controls).

Results:
Test-retest reliability reported a strong correlation (0.91), with no significant difference (P = .22) between the mean results (1.74 ± 0.07 s and 1.76 ± 0.07 s) obtained (split 2+3). Nonparametric tests (Kruskal-Wallis and Mann-Whitney) revealed both AF groups performed significantly faster on all measures than the control group (ranging from P = .001 to .005), with significant differences also reported between the two AF groups (ranging from P = .001 to .046). Stepwise discriminant analyses found total time discriminated between the groups, correctly classifying 75% of the participants.

Conclusions:
The RAT used within this study demonstrates evidence of reliability and construct validity. It further suggests the ability of a reactive component within agility test designs to discriminate among athletes of different competition levels, highlighting its importance within training activities.

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Ten resistance trained (RT) and 6 non-resistance trained (NRT) subjects were used to determine differences in quadriceps activation between isometric single and double knee extensions and squat contractions. Greater inactivation, as measured by the interpolated twitch technique, was recorded with single (RT: 16.5%, NRT: 17.6%) than double leg extensions (RT: 8.4%, NRT: 13.4%) or squats (RT: 4.03%, NRT: 1.7%). There was no significant difference between the maximum voluntary contraction (MVC) force of the dominant leg during single and double leg extensions. However, in NRT subjects, the contralateral or non-dominant leg during double leg extensions exhibited significantly less force than the dominant leg (715.9 vs 566.9 N). This deficit may be due to a lesser reliance on the non-dominant limb. The contractions of multiple lower body muscle groups enhanced the activation of the dominant quadriceps. Greater levels of activation may be necessary to cope with the stabilization necessary for bilateral and multi-articular contractions.

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Moderate-to vigorous-intensity physical activity has an established preventive role in cardiovascular disease, type 2 diabetes, obesity, and some cancers. However, recent epidemiologic evidence suggests that sitting time has deleterious cardiovascular and metabolic effects that are independent of whether adults meet physical activity guidelines. Evidence from “inactivity physiology” laboratory studies has identified unique mechanisms that are distinct from the biologic bases of exercising. Opportunities for sedentary behaviors are ubiquitous and are likely to increase with further innovations in technologies. We present a compelling selection of emerging evidence on the deleterious effects of sedentary behavior, as it is underpinned by the unique physiology of inactivity. It is time to consider excessive sitting a serious health hazard, with the potential for ultimately giving consideration to the inclusion of too much sitting (or too few breaks from sitting) in physical activity and health guidelines.

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Provides information on a study which examined the role of amino acids during endurance exercise and the implications for sports nutrition and performance. Description of amino acid utilization during exercise; Function of glutamine; Cardiovascular function of L-arginine.

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Several studies have demonstrated that oral glucose tolerance is impaired in the immediate postexercise period. A double-tracer technique was used to examine glucose kinetics during a 2-h oral glucose (75 g) tolerance test (OGTT) 30 min after exercise (Ex, 55 min at 71 ± 2% of peak O2 uptake) and 24 h after exercise (Rest) in endurance-trained men. The area under the plasma glucose curve was 71% greater in Ex than in Rest (P = 0.01). The higher glucose response occurred even though whole body rate of glucose disappearance was 24% higher after exercise (P = 0.04, main effect). Whole body rate of glucose appearance was 25% higher after exercise (P = 0.03, main effect). There were no differences in total (2 h) endogenous glucose appearance (RaE) or the magnitude of suppression of RaE, although RaE was higher from 15 to 30 min during the OGTT in Ex. However, the cumulative appearance of oral glucose was 30% higher in Ex (P = 0.03, main effect). There were no differences in glucose clearance rate or plasma insulin responses between the two conditions. These results suggest that adaptations in splanchnic tissues by prior exercise facilitate greater glucose output from the splanchnic region after glucose ingestion, resulting in a greater glycemic response and, consequently, a greater rate of whole body glucose uptake.

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Skeletal muscle insulin sensitivity is enhanced after acute exercise and short-term endurance training. We investigated the impact of exercise on the gene expression of key insulin-signaling proteins in humans. Seven untrained subjects (4 women and 3 men) completed 9 days of cycling at 63 ± 2% of peak O2 uptake for 60 min/day. Muscle biopsies were taken before, immediately after, and 3 h after the exercise bouts (on days 1 and 9). The gene expression of insulin receptor substrate-2 and the p85α subunit of phosphatidylinositol 3-kinase was significantly higher 3 h after a single exercise bout, although short-term training ameliorated this effect. Gene expression of insulin receptor and insulin receptor substrate-1 was not significantly altered at any time point. These results suggest that exercise may have a transitory impact on the expression of insulin receptor substrate-2 and phosphatidylinositol 3-kinase; however, the predominant actions of exercise on insulin sensitivity appear not to reside in the transcriptional activation of the genes encoding major insulin-signaling proteins.