Georgina K. Stebbings

Resting Arterial Diameter and Blood Flow Changes With Resistance Training and Detraining in Healthy Young Individuals

CONTEXT Disruptions to habitual training routines are commonly due to injury or illness and can often lead to detraining adaptations. The implications of such adaptations to the human vasculature in a trained, asymptomatic population are not fully understood. OBJECTIVE To determine the extent of local and systemic changes in arterial diameter and blood flow to resistance training and subsequent detraining in young adults. DESIGN Randomized controlled clinical trial. SETTING University physiology laboratory and fitness suite. PATIENTS OR OTHER PARTICIPANTS Twenty-one healthy volunteers (aged 20.0 ± 2.8 years, 11 men and 10 women). INTERVENTION(S) Eight-week lower limb resistance training period and subsequent 4-week detraining period. MAIN OUTCOME MEASURE(S) Quadriceps and hamstrings concentric torque (strength), resting heart rate, arterial diameter, and blood flow velocity in the superficial femoral and carotid arteries were measured at 0, 8, 10, and 12 weeks. RESULTS Resistance training increased quadriceps and hamstring strength (32% and 35%, respectively, P < .001), whereas strength decreased during detraining (24% and 27%, respectively, P < .05). Resting heart rate decreased after resistance training (16%, P < .01) and increased during detraining (19%, P < .001). Additionally, resistance training significantly increased superficial femoral and carotid resting arterial diameters (27% and 13%, respectively, P < .001) and mean blood flow (53% and 55%, respectively, P < .001). Detraining resulted in a significant decrease in superficial femoral and carotid resting diameter (46% and 10%, respectively, P < .001) and mean blood flow (61% and 38%, respectively, P < .05). CONCLUSIONS Resistance training initiated both local and systemic changes to arterial diameter and blood flow; these changes appeared to reverse after detraining. The local changes in response to detraining showed a worsening (beyond pretraining values) of the vascular dimensional and blood flow characteristics.

The emergence of sedentary behaviour physiology and its effects on the cardiometabolic profile in young and older adults

It has recently emerged that sedentary behaviour is independent of a lack of physical activity as individuals can be sufficiently active, based on the recommended physical activity guidelines, but also spend the majority of their waking hours engaging in sedentary behaviour. Individuals who follow this pattern of physical activity and sedentary behaviour are known as ‘active couch potatoes’. Sedentary behaviour has been found to have detrimental effects on cardiometabolic markers associated with cardiovascular disease. Since the positive effects of moderate-to-vigorous intensity physical activity do not necessarily negate the deleterious effects of sedentary behaviour on cardiometabolic markers, it is postulated that engaging in light physical activity is an intervention that will successfully reduce levels of sedentary behaviour and may hence improve health markers of quality of life. We propose that such lifestyle changes may be particularly relevant to older populations as these engage in sedentary behaviour for the majority of their waking hours, thereby adding to the negative aging effect on cardiometabolic markers.

Association of ACTN3 R577X but not ACE I/D gene variants with elite rugby union player status and playing position

We aimed to quantify the ACE I/D and ACTN3 R577X (rs1815739) genetic variants in elite rugby athletes (rugby union and league) and compare genotype frequencies to controls and between playing positions. The rugby athlete cohort consisted of 507 Caucasian men, including 431 rugby union athletes that for some analyses were divided into backs and forwards and into specific positional groups: front five, back row, half backs, centers, and back three. Controls were 710 Caucasian men and women. Real-time PCR of genomic DNA was used to determine genotypes using TaqMan probes and groups were compared using χ2 and odds ratio (OR) statistics. Correction of P values for multiple comparisons was according to Benjamini-Hochberg. There was no difference in ACE I/D genotype between groups. ACTN3 XX genotype tended to be underrepresented in rugby union backs (15.7%) compared with forwards (24.8%, P = 0.06). Interestingly, the 69 back three players (wings and full backs) in rugby union included only six XX genotype individuals (8.7%), with the R allele more common in the back three (68.8%) than controls (58.0%; χ2 = 6.672, P = 0.04; OR = 1.60) and forwards (47.5%; χ2 = 11.768, P = 0.01; OR = 2.00). Association of ACTN3 R577X with playing position in elite rugby union athletes suggests inherited fatigue resistance is more prevalent in forwards, while inherited sprint ability is more prevalent in backs, especially wings and full backs. These results also demonstrate the advantage of focusing genetic studies on a large cohort within a single sport, especially when intrasport positional differences exist, instead of combining several sports with varied demands and athlete characteristics.

Variability and distribution of muscle strength and its determinants in humans

Introduction: Inter‐individual variability in measurements of muscle strength and its determinants was identified to: (1) produce a normative data set describing the normal range and (2) determine whether some measurements are more informative than others when evaluating inter‐individual differences. Methods: Functional and morphological characteristics of the vastus lateralis were measured in 73 healthy, untrained adult men. Results: Inter‐individual variability (coefficient of variation) was greater for isometric maximal voluntary contraction (MVC) torque (18.9%) compared with fascicle force (14.6%; P = 0.025) and physiological cross‐sectional area (PCSA; 17.2%) compared with anatomical cross‐sectional area (ACSA, 13.0%; P < 0.0005). The relationship between ACSA and isometric MVC torque (r2 = 0.56) was weaker than that between PCSA and fascicle force (r2 = 0.68). Conclusions: These results provide a normative data set on inter‐individual variability in a variety of muscle strength‐related measurements and illustrate the benefit of using more stringent measures of muscle properties. Muscle Nerve 49: 879–886, 2014

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 whether 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=.003) in RA. In the absence of any TT homozygotes, reflective of the low T‐allele frequency within Caucasian populations, it is unclear whether fascicle length for this group would have been smaller still. No differences in genotype frequency between the RA and MR groups were observed (P=.500), although within the MR group, the T‐allele carriers demonstrated marathon personal best times 2 minutes 25 seconds faster than CC homozygotes (P=.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.

Fat mass and obesity associated (FTO) gene influences skeletal muscle phenotypes in non-resistance trained males and elite rugby playing position

BackgroundFTO gene variants have been associated with obesity phenotypes in sedentary and obese populations, but rarely with skeletal muscle and elite athlete phenotypes.MethodsIn 1089 participants, comprising 530 elite rugby athletes and 559 non-athletes, DNA was collected and genotyped for the FTO rs9939609 variant using real-time PCR. In a subgroup of non-resistance trained individuals (NT; n = 120), we also assessed structural and functional skeletal muscle phenotypes using dual energy x-ray absorptiometry, ultrasound and isokinetic dynamometry. In a subgroup of rugby athletes (n = 77), we assessed muscle power during a countermovement jump.ResultsIn NT, TT genotype and T allele carriers had greater total body (4.8% and 4.1%) and total appendicular lean mass (LM; 3.0% and 2.1%) compared to AA genotype, with greater arm LM (0.8%) in T allele carriers and leg LM (2.1%) for TT, compared to AA genotype. Furthermore, the T allele was more common (94%) in selected elite rugby union athletes (back three and centre players) who are most reliant on LM rather than total body mass for success, compared to other rugby athletes (82%; P = 0.01, OR = 3.34) and controls (84%; P = 0.03, OR = 2.88). Accordingly, these athletes had greater peak power relative to body mass than other rugby athletes (14%; P = 2 x 10-6).ConclusionCollectively, these results suggest that the T allele is associated with increased LM and elite athletic success. This has implications for athletic populations, as well as conditions characterised by low LM such as sarcopenia and cachexia.

Reliability and validity of the international physical activity questionnaire compared to calibrated accelerometer cut-off points in the quantification of sedentary behaviour and physical activity in older adults

Background The aim was to determine the reliability and validity of IPAQ measured sedentary behaviour (SB) and moderate–vigorous physical activity (MVPA) in older persons whilst examining any sex differences in reliability and validity results. Method 89 participants (73.7 ± 6.3 years, 54% female) completed the IPAQ. Participants were fitted with a thigh mounted triaxial accelerometer (GeneActiv Original) for seven consecutive days and subsequently completed a second IPAQ. Results IPAQ showed weak reliability qualities for Total SB (h·week-1) and 10 minute MVPA (accumulated in bouts ≥ 10 continuous minutes, h·week-1). IPAQ had poor concurrent validity qualities for Total SB, 10 minute MVPA, but not Sporadic MVPA (accumulated in bouts < 10 continuous minutes, h·week-1). IPAQ only categorised participant physical behaviour classification correctly 2% of the time. Sex differences were only present for the correlation slope of IPAQ 10 minute MVPA reliability measures. Conclusion Our data suggests that the IPAQ is not suitable for assessing older adults habitual physical behaviour.

Relationships between muscle size, strength, and physical activity in adults with muscular dystrophy: Muscle strength, size and physical activity in muscular dystrophy

Muscular dystrophy (MD) is characterized by progressive muscle wasting and weakness, yet few comparisons to non‐MD controls (CTRL) of muscle strength and size in this adult population exist. Physical activity (PA) is promoted to maintain health and muscle strength within MD; however, PA reporting in adults with MD is limited to recall data, and its impact on muscle strength is seldom explored.

18 No association between tendon-related genes and performance in elite european caucasian marathon runners

Tendons adapt to load under normal physiological conditions, however, under extreme loading conditions, such as those experienced by elite endurance athletes, incomplete adaptation may occur and cause injury. The prevalence of tendinopathies in elite endurance athletes is approximately 50%, thus variability exists in an athlete’s tolerance to extreme loading. A number of intrinsic and extrinsic factors contribute to modulating injury risk, some of which are modifiable and others, such as genetic variants, are non-modifiable. It was hypothesised that elite marathon runners would possess a genotype associated with enhanced tendon function, and thus protective against tendinopathy. Here, we compared the genotype frequencies of six genetic variants (COL1A1 rs1800012, VEGFA rs699947, TIMP2 rs4789932, MMP3 rs591058, MMP3 rs650108, MMP3 rs679620), previously associated with tendinopathy, in elite (men <2 hour 30 min, n=109, women <3 hour 00 min, n=99) and sub-elite (men 2 hour 30 min-2 h 45 min, n=189; women 3 hour 00 min-3 h 15 min, n=71) marathon runners with those of a non-athletic control group (n=564). Genotype associations with marathon personal best time in the athlete group were also investigated. All participants provided either a whole blood, saliva or buccal cell sample, from which DNA was isolated, and genotyped for all six variants using real-time PCR. Genotype frequency differed between athletes and controls for TIMP2 rs4789932 (TT=17%, CT=51%, CC=32% vs TT=22%, CT=42%, CC=36%, respectively; χ2=8.135, p=0.017) only. However, there was no clear difference in allele frequencies between groups for TIMP2 rs4789932. MMP3 rs650108 genotype frequency differed between female elite and sub-elite athletes (χ2=11.913, p=0.003) only and, as hypothesised, it was the ‘risk’ A-allele that was ~10% less frequent in the elite, than sub-elite athletes. Following combination of all genotype data into a total genotype score, no differences in score between athletes and controls were observed (t=2.93, p=0.769). Similarly, no associations between total genotype score and marathon personal best time in male and female runners were observed (r≤0.066, p≥0.394). The results suggest elite marathon runners do not possess a genotype protective against tendinopathy, at least for the tendon-related genetic variants we investigated.

4 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 hour 30 min, n=110; women <3 hour 00 min, n=98) and sub-elite (men 2 hour 30 min – 2 hour 45 min, n=181; women 3 hour 00 min – 3 hour 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.