Local vibration therapy increases oxygen re-saturation rate and maintains muscle strength following exercise-induced muscle damage.

Context: Exercise induced muscle damage (EIMD) is associated with transient reductions in strength and athletic performance. Studies conclude aetiology is due in part to muscle micro vascular damage and disruption of blood flow. Previous research on vibration therapy reports modulation in muscle blood flow, oxygenation and strength. Objective: The aim of this study was to observe if local vibration therapy (VT) alleviates the impairments and haemodynamic changes associated with EIMD. Design: Controlled laboratory study. Setting: Laboratory and public gymnasium. Patients or other participants: Ten healthy participants (6 males: 4 females; age: 38±15 yrs; height: 1.72±0.48 m; mass 72.0±10.4 kg) were randomized into experimental (VT) and control (CON) groups. Interventions: Both groups performed 10 sets of 10 eccentric wrist flexions at 70% of 1-repetition maximum to induce muscle damage. Subsequent assessment of wrist flexor strength and flexor carpus ulnaris (FCU) muscle oxygen saturation (SmO2) occurred at 1-, 24- and 48 hr-post exercise. VT group underwent 10 min of local VT (45 Hz) starting 1 hr-post exercise and applied twice daily (separated by 8 hrs) for 48 hrs during habitual waking hours. CON group received no local VT. Main outcome measure(s): Grip strength, resting muscle oxygen (SmO2), muscle oxygen de-saturation and re-saturation rate. Results: No difference in grip strength observed pre EIMD, but the VT group demonstrated greater strength at 1 hr (P=0.004), 24 hr (P=0.031) and 48 hr (P=0.021) post EIMD compared to controls. No difference in SmO2 re-saturation over time (P>0.05), but the VT group had a greater re-saturation rate compared to controls at 1 hr (P=0.007, d = 2.6), 24 hr (P=0.001 d = 3.1) and 48 hr (P=0.035, d = 1.7) post EIMD. Conclusions: Local VT successfully attenuated the effects of EIMD and increased SmO2 re-saturation in FCU muscles. Including local VT as part of a recovery protocol post-EIMD could be beneficial for rehabilitation and athletic training purposes

Segregating the Distinct Effects of Sedentary Behavior and Physical Activity on Older Adults' Cardiovascular Profile: Part 2-Isotemporal Substitution Approach.

The aim of the study was to provide an isotemporal substitution model to predict how changes in physical behavior may affect the cardiovascular parameters (CVPs) of older adults. Methods: Participants wore a thigh-mounted accelerometer for 7 days. Phenotype of the carotid, brachial, and popliteal artery was conducted using ultrasound. Isotemporal substitution was used to simulate the degree to which replacing 1 hour of physical behavior with another would affect CVP. Results: Substitution of sedentary behavior with Standing and sporadic moderate- to vigorous-intensity physical activity (MVPA accumulated in bouts <10 min) would reduce resting heart rate [−6.20 beats per minute (−12.1 to −0.22) and −3.72 beats per minute (−7.01 to −0.44), respectively]. Substitution of sedentary behavior with light-intensity physical activity would reduce carotid artery diameter [−0.54 mm (−1.00 to −0.07)]. Substitution of Standing with sporadic MVPA would increase popliteal artery diameter [1.31 mm (0.11 to 2.51)]. Conclusions: Our modeling suggests that an accumulation of MVPA bouts that are shorter than the recommended 10-minute minimum may still improve CVP, with lower intensity physical activity also influencing CVP. Our findings are a promising avenue for lifestyle interventions in older adults to reduce the aging effects on CVP for those who cannot engage or sustain sufficient MVPA

The interactions of physical activity, exercise and genetics and their associations with bone mineral density: implications for injury risk in elite athletes

Low bone mineral density (BMD) is established as a primary predictor of osteoporotic risk and can also have substantial implications for athlete health and injury risk in the elite sporting environment. BMD is a highly multi-factorial phenotype influenced by diet, hormonal characteristics and physical activity. The interrelationships between such factors, and a strong genetic component, suggested to be around 50–85% at various anatomical sites, determine skeletal health throughout life. Genome-wide association studies and case–control designs have revealed many loci associated with variation in BMD. However, a number of the candidate genes identified at these loci have no known associated biological function or have yet to be replicated in subsequent investigations. Furthermore, few investigations have considered gene–environment interactions—in particular, whether specific genes may be sensitive to mechanical loading from physical activity and the outcome of such an interaction for BMD and potential injury risk. Therefore, this review considers the importance of physical activity on BMD, genetic associations with BMD and how subsequent investigation requires consideration of the interaction between these determinants. Future research using well-defined independent cohorts such as elite athletes, who experience much greater mechanical stress than most, to study such phenotypes, can provide a greater understanding of these factors as well as the biological underpinnings of such a physiologically “extreme” population. Subsequently, modification of training, exercise or rehabilitation programmes based on genetic characteristics could have substantial implications in both the sporting and public health domains once the fundamental research has been conducted successfully

Associations of bone mineral density-related genes and marathon performance in elite European Caucasian marathon runners.

Bone mineral density (BMD) is a multi-factorial phenotype determined by factors such as physical activity, diet and a sizeable genetic component. Athletic populations tend to possess higher BMD than non-athletes due to a larger volume of exercise completed. Despite this, some endurance runners can possess low BMD and/or suffer stress fractures, which can have negative impacts on their health and performance. Therefore, we hypothesised that elite endurance runners would possess a genotype associated with enhanced BMD and a reduced risk of injury, resulting in less training interruption and greater potential success. The study compared the genotype and allele frequencies of 5 genetic variants associated with BMD (LRP5 rs3736228, TNFRSF11B rs4355801, VDR rs2228570, WNT16 rs3801387, AXIN1 rs9921222) in elite (men < 2 h 30 min, n = 110; women < 3 h 00 min, n = 98) and sub-elite (men 2 h 30 min – 2 h 45 min, n = 181; women 3 h 00 min – 3 h 15 min, n = 67) marathon runners with those of a non-athlete control population (n = 474). We also investigated whether marathon personal best time was associated with a more “advantageous” BMD genotype. Congruent with our hypothesis, the “risk” T allele for the AXIN1 rs9921222 polymorphism was 5% more frequent in the control group than in sub-elites (P = 0.030, χ2 = 4.69) but no further differences were observed for this variant (P ≥ 0.083, χ2 ≤ 4.98). WNT16 rs3801387 genotype frequency differed between athletes and controls (P = 0.002, χ2 = 12.02) and elites vs controls (P = 0.008, χ2 = 9.72), as did allele frequency. However, contrary to our hypothesis, it was the “risk” A allele that was ~5% more frequent in athletes than controls. Similarly, when combining data from all 5 variants, the athletes had a lower Total Genotype Score than controls (53.6 vs 65.7; P ≤ 0.001), again suggesting greater genetic susceptibility to bone injury in athletes. Personal best times were not associated with genotype in any comparison. These results suggest that high-level endurance runners do not benefit from genetic resistance to bone injury and a resulting ability to sustain large training volumes, contradicting our hypothesis. High-level endurance runners appear to be at a higher risk of bone injury from a genetic perspective, for as yet unexplained reasons, although large inter-individual differences in genetic risk exist

TTN genotype is associated with fascicle length and marathon running performance.

Titin provides a molecular blueprint for muscle sarcomere assembly and sarcomere length can vary according to titin isoform expression. If variations in sarcomere length influence muscle fascicle length, this may provide an advantage for running performance. Thus the aim of this study was to investigate if the titin (TTN) rs10497520 polymorphism was associated with muscle fascicle length in recreationally active men (RA; n = 137) and marathon personal best time in male marathon runners (MR; n = 141). Fascicle length of the vastus lateralis was assessed in vivo using B-mode ultrasonography at 50% of muscle length in RA. All participants provided either a whole blood, saliva or buccal cell sample, from which DNA was isolated and genotyped using real-time polymerase chain reaction. Vastus lateralis fascicle length was 10.4% longer in CC homozygotes, those carrying two copies of the C-allele, than CT heterozygotes (p = 0.003) in RA. In the absence of any TT homozygotes, reflective of the low T-allele frequency within Caucasian populations, it is unclear if fascicle length for this group would have been smaller still. No differences in genotype frequency between the RA and MR groups were observed (p = 0.500), although within the MR group the T-allele carriers demonstrated marathon personal best times 2 min 25 s faster than CC homozygotes (p = 0.020). These results suggest that the T-allele at rs10497520 in the TTN gene is associated with shorter skeletal muscle fascicle length and conveys an advantage for marathon running performance in habitually trained men. This article is protected by copyright. All rights reserved

Bone mineral density in high-level endurance runners: part B—genotype-dependent characteristics

Purpose: Inter-individual variability in bone mineral density (BMD) exists within and between endurance runners and non-athletes, probably in part due to differing genetic profiles. Certainty is lacking, however, regarding which genetic variants may contribute to BMD in endurance runners and if specific genotypes are sensitive to environmental factors, such as mechanical loading via training. Method: Ten single-nucleotide polymorphisms (SNPs) were identified from previous genome-wide and/or candidate gene association studies that have a functional effect on bone physiology. The aims of this study were to investigate (1) associations between genotype at those 10 SNPs and bone phenotypes in high-level endurance runners, and (2) interactions between genotype and athlete status on bone phenotypes. Results: Female runners with P2RX7 rs3751143 AA genotype had 4% higher total-body BMD and 5% higher leg BMD than AC + CC genotypes. Male runners with WNT16 rs3801387 AA genotype had 14% lower lumbar spine BMD than AA genotype non-athletes, whilst AG + GG genotype runners also had 5% higher leg BMD than AG + GG genotype non-athletes. Conclusion: We report novel associations between P2RX7 rs3751143 genotype and BMD in female runners, whilst differences in BMD between male runners and non-athletes with the same WNT16 rs3801387 genotype existed, highlighting a potential genetic interaction with factors common in endurance runners, such as high levels of mechanical loading. These findings contribute to our knowledge of the genetic associations with BMD and improve our understanding of why some runners have lower BMD than others

Sarcopenia, obesity, and sarcopenic obesity: Relationship with skeletal muscle phenotypes and single nucleotide polymorphisms

Obesity may aggravate the effects of sarcopenia on skeletal muscle structure and function in the elderly, but no study has attempted to identify the gene variants associated with sarcopenia in obese women. Therefore, the aims of the present study were to: (1) describe neuromuscular function in sarcopenic and non-sarcopenic women with or without obesity; (2) identify gene variants associated with sarcopenia in older obese women. In 307 Caucasian women (71 ± 6 years, 66.3 ± 11.3 kg), skeletal muscle mass was estimated using bioelectric impedance, and function was tested with a 30 s one-leg standing-balance test. Biceps brachii thickness and vastus lateralis cross-sectional area (VLACSA) were measured with B-mode ultrasonography. Handgrip strength, maximum voluntary contraction elbow flexion (MVCEF), and knee extension torque (MVCKE) were measured by dynamometry, and MVCKE/VLACSA was calculated. Genotyping was performed for 24 single-nucleotide polymorphisms (SNPs), selected based on their previous associations with muscle-related phenotypes. Based on sarcopenia and obesity thresholds, groups were classified as sarcopenic obese, non-sarcopenic obese, sarcopenic non-obese, or non-sarcopenic non-obese. A two-way analysis of covariance was used to assess the main effects of sarcopenia and obesity on muscle-related phenotypes and binary logistic regression was performed for each SNP to investigate associations with sarcopenia in obesity. There were no significant obesity * sarcopenic status interactions for any of the investigated muscle-related phenotypic parameters. Neither sarcopenia nor obesity had a significant effect on biceps brachii thickness, but sarcopenia was associated with lower VLACSA (p = 0.003). Obesity was associated with lower MVCEF (p = 0.032), MVCKE (p = 0.047), and MVCKE/VLACSA (p = 0.012) with no significant effect of sarcopenia. Adjusted for age and height, three SNPs (ACTN3 rs1815739, MTHFR rs1801131, and MTHFR rs1537516) were associated with sarcopenia in obese participants. Sarcopenia was associated with a smaller muscle size, while obesity resulted in a lower muscle quality irrespective of sarcopenia. Three gene variants (ACTN3 rs1815739, MTHFR rs1801131, and MTHFR rs1537516) suspected to affect muscle function, homocysteine metabolism, or DNA methylation, respectively, were associated with sarcopenia in obese elderly women. Understanding the skeletal muscle features affected by sarcopenia and obesity, and identification of genes related to sarcopenia in obese women, may facilitate early detection of individuals at particular risk of sarcopenic obesity

Static one-leg standing balance test as a screening tool for low muscle mass in healthy elderly women

Background: Identification of simple screening tools for detecting lower skeletal muscle mass may be beneficial for planning effective interventions in the elderly. Aims: We aimed to (1) establish a threshold for one-leg standing balance test (OLST) time for low muscle mass, and (2) test the ability of that threshold to assess muscular impairments in a poor balance group. Methods: Eyes-open OLST (maximum duration 30 s) was performed with right and left legs in 291 women (age 71 ± 6 years). OLST time was calculated as the sum of the OLST time of right and left legs. Fat-free mass (FFM), skeletal muscle mass (SMM), fat mass, biceps brachii and vastus lateralis sizes; handgrip strength (HGS), elbow flexion maximum torque (MVC ) and knee extension maximum torque (MVC ) were measured. Muscle quality was calculated as MVC /FFM and physical activity was assessed by questionnaire. Low muscle mass was defined as SMM of 22.1%, a previously established threshold for pre-sarcopenia. Results: The OLST threshold time to detect low muscle mass was 55 s (sensitivity: 0.63; specificity: 0.60). The poor balance group (OLST < 55 s) had higher fat mass (3.0%, p < 0.001), larger VL thickness (5.1%, p = 0.016), and lower HGS (− 10.2%, p < 0.001), MVC (− 8.2%, p = 0.003), MVC (− 9.5%, p = 0.012), MVC /FFM (− 11.0%, p = 0.004) and physical activity (− 8.0%, p = 0.024) compared to the normal balance group. While after adjusting age, the differences exist for HGS, fat mass and VL thickness only. Discussion: An OLST threshold of 55 s calculated as the summed score from both legs discriminated pre-sarcopenic characteristics among active, community-dwelling older women with limited potential (sensitivity 0.63, specificity 0.60). Conclusion: OLST, which can be performed easily in community settings without the need for more complex muscle mass measurement, may help identify women at risk of developing sarcopenia. EF KE KE relative EF KE K

Dietary protein requirement threshold and micronutrients profile in healthy older women based on relative skeletal muscle mass

Although multiple nutrients have shown protective effects with regard to preserving muscle function, the recommended amount of dietary protein and other nutrients profile on older adults for maintenance of high muscle mass is still debatable. The aims of this paper were to: (1) identify dietary differences between older women with low and high relative skeletal muscle mass, and (2) identify the minimal dietary protein intake associated with high relative skeletal muscle mass and test the threshold ability to determine an association with skeletal muscle phenotypes. Older women (n = 281; 70 ± 7 years, 65 ± 14 kg), with both low and high relative skeletal muscle mass groups, completed a food questionnaire. Skeletal muscle mass, fat-free mass (FFM), biceps brachii thickness, vastus lateralis anatomical cross-sectional area (VLACSA ), handgrip strength (HGS), maximum elbow flexion torque (MVCEF ), maximum knee extension torque (MVCKE ), muscle quality (HGS/Body mass), and fat mass were measured. Older women with low relative skeletal muscle mass had a lower daily intake of protein, iodine, polyunsaturated fatty acid (PUFA), Vit E, manganese, milk, fish, nuts and seeds (p < 0.05) compared to women with high relative skeletal muscle mass. The minimum required dietary protein intake for high relative skeletal muscle mass was 1.17 g/kg body mass/day (g/kg/d) (sensitivity: 0.68; specificity: 0.62). Women consuming ≥1.17 g/kg/d had a lower BMI (B = −3.9, p < 0.001) and fat mass (B = −7.8, p < 0.001), and a higher muscle quality (B = 0.06, p < 0.001). The data indicate that to maintain muscle mass and function, older women should consume ≥1.17 g/kg/d dietary protein, through a varied diet including milk, fish and nuts that also contain polyunsaturated fatty acid (PUFA) and micronutrients such as iodine, Vit E and manganese

ACTN3 R577x genotype is not associated with elite european caucasian marathon performance

Objectives A common nonsense polymorphism (R577X) in the ACTN3 (α-actinin-3 protein) has been associated with elite athlete status previously. Specifically, the X allele has been positively associated with elite endurance status, however, this remains inconclusive due to contradictory reports within the literature. Thus, the current study aimed to compare ACTN3 R577X genotype and allele frequency distributions in ‘elite’ and ‘sub-elite’ marathon runners with those of a non-athletic, control population and to determine whether marathon personal best time was associated with ACTN3 R577X genotype.Method Four hundred and eighty four elite and sub-elite European Caucasian marathon runners and 554 ethnically matched controls provided a DNA sample from which the ACTN3 R577X polymorphism was genotyped using real-time PCR. Personal best (PB) times were used to determine elite (men < 2 h 30 min, n = 111; women < 3 h 00 min, n = 105) or sub-elite (men 2 h 30 min – 2 h 45 min, n = 189; women 3 h 00 min – 3 h 15 min, n = 79) status. Genotype and allele frequencies were compared between athletes and controls using Chi-square analyses. One-way ANOVAs were implemented to identify any genotype-dependent differences in PB times for men and women, which were subject to correction for multiple comparisons.Results The X allele was ∼3% more frequent in the marathon runners than in non-athlete controls (see Table 1 and Figure 1), although this small difference did not approach statistical significance. There were no significant differences in genotype (χ2 = 3.40; P = 0.182) or allele (χ2 = 2.31; P = 0.128) frequency distributions between athletes (RR = 29.1%, RX = 50.6% XX = 20.2%; R = 54.4%, X = 45.6%) and controls. There were also no differences between elite and sub-elite genotype (P = 0.968, χ2 = 0.66) and allele frequencies (P = 0.916, χ2 = 0.11). Similarly, no differences in genotype or allele frequencies were found between either elite (P = 0.439, χ2 = 1.65; P = 0.265, χ2 = 1.24) or sub-elite (P = 0.254, χ2 = 2.74; P = 0.183, χ2 = 1.77) runners and the control group. Neither were PB times genotype-dependent for either men (P = 0.864) or women (P = 0.966).Conclusion No differences in genotype and allele frequencies were observed between athletes and controls, elite vs sub-elite, nor elite and sub-elite comparisons with the control group. Additionally, there was no genotype-dependent influence on PB time, which further emphasises that the ACTN3 R577X polymorphism does not influence elite endurance athlete status or determine marathon performance in European Caucasian runners. This is congruent with some previous findings and suggests other genetic variants or environmental factors may play a more prominent role in achieving elite endurance athlete status