Application of Leg, Vertical, and Joint Stiffness in Running Performance: A Literature Overview

Stiffness, the resistance to deformation due to force, has been used to model the way in which the lower body responds to landing during cyclic motions such as running and jumping. Vertical, leg, and joint stiffness provide a useful model for investigating the store and release of potential elastic energy via the musculotendinous unit in the stretch-shortening cycle and may provide insight into sport performance. This review is aimed at assessing the effect of vertical, leg, and joint stiffness on running performance as such an investigation may provide greater insight into performance during this common form of locomotion. PubMed and SPORTDiscus databases were searched resulting in 92 publications on vertical, leg, and joint stiffness and running performance. Vertical stiffness increases with running velocity and stride frequency. Higher vertical stiffness differentiated elite runners from lower-performing athletes and was also associated with a lower oxygen cost. In contrast, leg stiffness remains relatively constant with increasing velocity and is not strongly related to the aerobic demand and fatigue. Hip and knee joint stiffness are reported to increase with velocity, and a lower ankle and higher knee joint stiffness are linked to a lower oxygen cost of running; however, no relationship with performance has yet been investigated. Theoretically, there is a desired “leg-spring” stiffness value at which potential elastic energy return is maximised and this is specific to the individual. It appears that higher “leg-spring” stiffness is desirable for running performance; however, more research is needed to investigate the relationship of all three lower limb joint springs as the hip joint is often neglected. There is still no clear answer how training could affect mechanical stiffness during running. Studies including muscle activation and separate analyses of local tissues (tendons) are needed to investigate mechanical stiffness as a global variable associated with sports performance.

Sex-Based Differences in Oxygen Cost of Walking and Energy Equivalents in Minimally Disabled People with Multiple Sclerosis and Controls

Background: Elevated oxygen cost of walking and energy equivalents are reported for highly and moderately disabled people with multiple sclerosis (MS). However, less is known about minimally impaired individuals. Moreover, no sex-based data on the metabolic rates of people with MS are available. In this cross-sectional study, the metabolic rates and temporospatial parameters of gait during overground walking in minimally disabled people with MS versus matched controls were quantified and whether sex-based differences occur was examined. Methods: Sixty-nine minimally impaired adults with MS (37, relapsing-remitting MS [RRMS]; 32, clinically isolated syndrome [CIS]) and 25 matched controls completed two 6-minute walking bouts at comfortable and fast speeds. The oxygen cost of walking, energy equivalents, and respiratory exchange ratio were recorded through breath-by-breath open-circuit spirometry. Gait analysis was performed via a portable electronic walkway. Results: At comfortable but not at fast speed, men with RRMS showed higher oxygen cost of walking than men with CIS (+17.9%, P = .04) and male controls (+21.3%, P = .03). In the RRMS group, men showed higher oxygen cost of walking (+19.2%, P = .04) and energy equivalents (+19.2%, P = .02) than women. Elevated oxygen cost of walking and energy equivalents in men were paralleled by significantly larger base of support and step time asymmetry during walking. Conclusions: Metabolic demands are elevated while walking in minimally disabled people with RRMS. Furthermore, higher energy demands occur in men, probably due to increased step symmetry and base of support. Clinicians are advised to follow energy expenditure metrics collected while walking because they can indicate a decrease in fitness, even in the early phase of MS.

Oxygen Cost of Walking in People with Multiple Sclerosis and Its Association with Fatigue: A Systematic Review and Meta-analysis

Background: This systematic review and meta-analysis aimed to compare the oxygen cost of walking in people with multiple sclerosis (MS) and controls and to assess the relationship between oxygen cost of walking and fatigue in people with MS. Methods: Four databases (CINAHL, MEDLINE, ProQuest, Web of Science) were searched up to September 2020. Studies were included if they recruited adults with MS and either compared oxygen cost of walking in those with MS and a control population or determined the relationship between oxygen cost of walking and fatigue. Meta-analysis of the standardized mean difference in oxygen cost of walking between people with MS and controls was performed. Results: Nine studies were included in this review, of which seven compared oxygen cost of walking in people with MS (n = 176) and controls (n = 142) and four investigated the relationship between oxygen cost of walking and fatigue. Meta-analysis revealed that people with MS (with predominantly mild-to-moderate disability) had a significantly higher oxygen cost of walking compared with controls (standardized mean difference = 2.21, 95% CI = 0.88 to 3.54, P = .001). In addition, three studies found a significant yet weak positive association between oxygen cost of walking and fatigue. Conclusions: People with MS expend more energy when walking compared with controls. This increase in energy expenditure may contribute to the development of fatigue, as some studies found that higher oxygen costs of walking were associated with greater fatigue. Future studies should investigate whether reducing energy expenditure during movement improves fatigue.

Nitrate-Induced Improvements in Exercise Performance Is Coincident With Exuberant Changes in Metabolic Genes and the Metabolome in Zebrafish (Danio rerio) Skeletal Muscle

Objectives Dietary nitrate (NO3−) supplementation improves exercise performance by reducing the oxygen cost of exercise and enhancing skeletal muscle function. However, the mechanisms underlying the beneficial effects on exercise performance are not well understood and may be supported by changes in metabolism within the skeletal muscle. The purpose of this study was to elucidate nitrate-induced changes in skeletal muscle energy metabolism associated with improvements in exercise performance that may reflect enhanced metabolic flexibility. Methods Fish were exposed to sodium nitrate (60.7 mg/L, 303.5 mg/L, and 606.9 mg/L), or control water, for 21 days and analyzed at intervals during a strenuous exercise test. Nitrate storage in muscle was measured using chemiluminescence. We utilized nuclear magnetic resonance spectroscopy (NMR), liquid-chromatography tandem mass spectrometry (LC-MS/MS) untargeted metabolomics and real-time quantitative polymerase chain reaction (RT-qPCR) to determine changes in muscle metabolism with nitrate and exercise. Results Nitrate treatment significantly increased muscle nitrate concentrations, while muscle nitrate levels declined with increasing exercise duration, and nitrate treatment was associated with a decrease in the oxygen cost of exercise. In skeletal muscle, nitrate treatment upregulated expression of genes central to nutrient sensing (mtor), glucose (hk2) and lipid metabolism (acaca), redox signaling (nrf2a) and muscle differentiation (sox6). Nitrate treatment caused rested skeletal muscle to have significantly increased metabolites directly linked to energy production (phosphocreatine (PCr), creatine (Cr), adenosine nucleosides, purines, glycolytic, fatty acid and tricarboxylic acid cycle (TCA) intermediates) and a concomitant decrease in these metabolites after exercise, compared to rested-control fish. Conclusions Our data suggest that nitrate exposure may improve exercise performance by changing the metabolic programming of muscle prior to exercise, thus increasing the availability of energy producing metabolites required for exercise such as ATP and phosphocreatine. Funding Sources Celia Strickland and G. Kenneth Austin III Endowment and National Institutes of Health.

Nitrate-induced improvements in exercise performance are coincident with exuberant changes in metabolic genes and the metabolome in zebrafish skeletal muscle.

Dietary nitrate supplementation improves exercise performance by reducing the oxygen cost of exercise and enhancing skeletal muscle function. However, the mechanisms underlying these effects are not well understood. The purpose of this study was to assess changes in skeletal muscle energy metabolism associated with exercise performance in a zebrafish model. Fish were exposed to sodium nitrate (60.7 mg/L, 303.5 mg/L, 606.9 mg/L), or control water, for 21 days and analyzed at intervals (5, 10, 20, 30, 40 cm/sec) during a two-hour strenuous exercise test. We measured oxygen consumption during an exercise test and assessed muscle nitrate concentrations, gene expression and the muscle metabolome before, during and after exercise. Nitrate exposure reduced the oxygen cost of exercise and increased muscle nitrate concentrations at rest, which were reduced with increasing exercise duration. In skeletal muscle, nitrate treatment upregulated expression of genes central to nutrient sensing (mtor), redox signaling (nrf2a) and muscle differentiation (sox6). In rested muscle, nitrate treatment increased phosphocreatine (P = 0.002), creatine (P =0.0005), ATP (P = 0.0008), ADP (P = 0.002), and AMP (P =0.004) compared to rested-control muscle. Following the highest swimming speed, concentration of phosphocreatine (P = 8.0 x 10-5), creatine (P =6.0 x 10-7), ATP (P = 2.0 x 10-6), ADP (P = 0.0002), and AMP (P =0.004) decreased compared to rested nitrate muscle. Our data suggests nitrate exposure in zebrafish lowers the oxygen cost of exercise by changing the metabolic programming of muscle prior to exercise and increasing availability of energy-rich metabolites required for exercise.

GLUTATIONE POSTCONDITIONING ATTENUATES MYOCARDIAL ISCHEMIAREPERFUSION INJURY IN RATS VIA INHIBITION OF MPTP

The effect of post-conditioning with reduced glutathione (GSH, hepaval Italy/Ukraine) on myocardial contractility, oxygen cost, and mitochondrial factor release as a marker of mitochondrial permeability transition pore (MPTP) opening was studied in ischemia–reperfusion model at Langendorffisolated rat heart. It was found that reperfusion with KrebsHenseleit solution containing GSH provided more complete restoration of the left ventricle developed pressure (70.2 and 56% at 5th and 40th min of reperfusion against 23.6 and 30.9% in control, P < 0.05 for both), reduced oxygen cost of myocardial work (184 and 157% at 5th and 40th min of reperfusion against 413 and 216% in control, P < 0.05 for both), and decreased the value of mitochondrial factor by 3 times, indicating inhibition of MPTP. It was shown that the level of GSH in cardiac tissues was significantly increased by 1.5 times 30 min after administration of hepaval (52 mg per kg) intraperitoneally, indicating accumulation of GSH from the bloodstream. Thus, we have shown that post-conditioning with GSH had cardioprotective effect, inhibited the formation of MPTP and can be used as a tool for correction of post-ischemic disturbances of heart function.