The contribution of muscle hypertrophy to strength changes following resistance training

Purpose Whilst skeletal muscle hypertrophy is considered an important adaptation to resistance training (RT), it has not previously been found to explain the inter-individual changes in strength after RT. This study investigated the contribution of hypertrophy to individual gains in isometric, isoinertial and explosive strength after 12 weeks of elbow flexor RT. Methods Thirty-three previously untrained, healthy men (18–30 years) completed an initial 3-week period of elbow flexor RT (to facilitate neurological responses) followed by 6-week no training, and then 12-week elbow flexor RT. Unilateral elbow flexor muscle strength [isometric maximum voluntary force (iMVF), single repetition maximum (1-RM) and explosive force], muscle volume (V m), muscle fascicle pennation angle (θ p) and normalized agonist, antagonist and stabilizer sEMG were assessed pre and post 12-week RT. Results Percentage gains in V m correlated with percentage changes in iMVF (r = 0.527; P = 0.002) and 1-RM (r = 0.482; P = 0.005) but not in explosive force (r ≤ 0.243; P ≥ 0.175). Percentage changes in iMVF, 1-RM, and explosive force did not correlate with percentage changes in agonist, antagonist or stabilizer sEMG (all P > 0.05). Percentage gains in θ p inversely correlated with percentage changes in normalized explosive force at 150 ms after force onset (r = 0.362; P = 0.038). Conclusions We have shown for the first time that muscle hypertrophy explains a significant proportion of the inter-individual variability in isometric and isoinertial strength gains following 12-week elbow flexor RT in healthy young men

Whey protein does not enhance the adaptations to elbow flexor resistance training

Purpose: It is unclear whether protein supplementation augments the gains in muscle strength and size observed following resistance training (RT), as limitations to previous studies include small cohorts, imprecise measures of muscle size and strength, and no control of prior exercise or habitual protein intake (HPI). We aimed to determine whether whey protein supplementation affected RT-induced changes in elbow flexor muscle strength and size. Methods: We pair-matched 33 previously untrained, healthy young men for their HPI and strength response to 3-wk RT without nutritional supplementation (followed by 6-wk no training), and then randomly assigned them to protein (PRO; n = 17) or placebo (PLA; n = 16) groups. Participants subsequently performed elbow flexor RT 3 d/wk for 12-wk and consumed PRO or PLA immediately before and after each training session. We assessed elbow flexor muscle strength [unilateral 1-RM and isometric maximum voluntary force (MVF)] and size [total volume and maximum anatomical cross-sectional area (ACSAmax) determined with MRI] before and after the 12-wk RT. Results: PRO and PLA demonstrated similar increases in muscle volume (PRO, 17.0 ± 7.1% vs. PLA, 14.9 ± 4.6%; P = 0.32), ACSAmax (PRO, 16.2 ± 7.1% vs. PLA, 15.6 ± 4.4%; P = 0.80), 1-RM (PRO, 41.8 ± 21.2% vs. PLA, 41.4 ± 19.9%; P = 0.97) and MVF (PRO, 12.0 ± 9.9% vs. PLA, 14.5 ± 8.3%; P = 0.43). Conclusion: In the context of this study, protein supplementation did not augment elbow flexor muscle strength and size changes that occurred after 12-wk RT. Key words: Protein supplementation – strength training – muscle hypertrophy – muscle architecture – training respons

Muscle Growth, Repair and Preservation: A Mechanistic Approach

Resistance exercise, amino acid ingestion and an anabolic hormone environment all have the capacity to elevate muscle protein synthesis (MPS), while a catabolic hormone environment, such as elevated pro-inflammatory cytokines as seen during disuse, aging, and conditions such as cancer and AIDS, can cause an increase in muscle protein degradation (MPD). When the rate of MPS exceeds that of MPD there is a positive net protein balance (NPB) and over a prolonged period of time this results in accretion of contractile material and muscle growth, or hypertrophy. In contrast, when NPB is chronically negative, muscle atrophy occurs, i.e. muscle size decreases. Various signaling pathways within the muscle fiber appear to play a crucial role in the adaptive processes, and understanding how these pathways can be modulated will help the design of therapies to prevent or reverse muscle atrophy in a host of muscle wasting conditions

Do PTK2 gene polymorphisms contribute to the interindividual variability in muscle strength and the response to resistance training? A preliminary report.

The protein tyrosine kinase-2 (PTK2) gene encodes focal adhesion kinase, a structural protein involved in lateral transmission of muscle fiber force. We investigated whether single-nucleotide polymorphisms (SNPs) of the PTK2 gene were associated with various indexes of human skeletal muscle strength and the interindividual variability in the strength responses to resistance training. We determined unilateral knee extension single repetition maximum (1-RM), maximum isometric voluntary contraction (MVC) knee joint torque, and quadriceps femoris muscle specific force (maximum force per unit physiological cross-sectional area) before and after 9 wk of knee extension resistance training in 51 untrained young men. All participants were genotyped for the PTK2 intronic rs7843014 A/C and 3'-untranslated region (UTR) rs7460 A/T SNPs. There were no genotype associations with baseline measures or posttraining changes in 1-RM or MVC. Although the training-induced increase in specific force was similar for all PTK2 genotypes, baseline specific force was higher in PTK2 rs7843014 AA and rs7460 TT homozygotes than in the respective rs7843014 C- (P = 0.016) and rs7460 A-allele (P = 0.009) carriers. These associations between muscle specific force and PTK2 SNPs suggest that interindividual differences exist in the way force is transmitted from the muscle fibers to the tendon. Therefore, our results demonstrate for the first time the impact of genetic variation on the intrinsic strength of human skeletal muscle

TRIM63 (MuRF-1) Gene Polymorphism is Associated with Biomarkers of Exercise-Induced Muscle Damage

Unaccustomed strenuous exercise can lead to muscle strength loss, inflammation and delayed onset muscle soreness, which may be influenced by genetic variation. We investigated if a missense single nucleotide polymorphism (A>G, rs2275950) within the TRIM63 gene (encoding MuRF-1 and potentially affecting titin mechanical properties) was associated with the variable response to unaccustomed eccentric exercise. Sixty-five untrained, healthy participants (genotyped for rs2275950: AA, AG and GG) performed 120 maximal eccentric knee extensions (ECC) to induce muscle damage. Isometric and isokinetic maximal voluntary knee extension contractions (MVCs) and muscle soreness were assessed before, immediately after, and 48h after ECC. AA homozygotes were consistently stronger [baseline isometric MVC: 3.23±0.92 Nm/kg (AA) vs. 2.09±0.67 Nm/kg (GG); p=0.006] and demonstrated less muscle soreness over time (p=0.022) compared to GG homozygotes. This may be explained by greater titin stiffness in AA homozygotes, leading to intrinsically stronger muscle fibers that are more resistant to eccentric damaging contractions

The impact of obesity on skeletal muscle strength and structure through adolescence to old age.

Obesity is associated with functional limitations in muscle performance and increased likelihood of developing a functional disability such as mobility, strength, postural and dynamic balance limitations. The consensus is that obese individuals, regardless of age, have a greater absolute maximum muscle strength compared to non-obese persons, suggesting that increased adiposity acts as a chronic overload stimulus on the antigravity muscles (e.g., quadriceps and calf), thus increasing muscle size and strength. However, when maximum muscular strength is normalised to body mass, obese individuals appear weaker. This relative weakness may be caused by reduced mobility, neural adaptations and changes in muscle morphology. Discrepancies in the literature remain for maximal strength normalised to muscle mass (muscle quality) and can potentially be explained through accounting for the measurement protocol contributing to muscle strength capacity that need to be explored in more depth such as antagonist muscle co-activation, muscle architecture, a criterion valid measurement of muscle size and an accurate measurement of physical activity levels. Current evidence demonstrating the effect of obesity on muscle quality is limited. These factors not being recorded in some of the existing literature suggest a potential underestimation of muscle force either in terms of absolute force production or relative to muscle mass; thus the true effect of obesity upon skeletal muscle size, structure and function, including any interactions with ageing effects, remains to be elucidated

Combined effects of body composition and ageing on joint torque, muscle activation and co-contraction in sedentary women

This study aimed to establish the interplay between body mass, adiposity, ageing and determinants of skeletal muscle strength. One hundred and two untrained healthy women categorised by age into young (Y) (mean ± SD, 26.7 ± 9.4 years) vs. old (O) (65.1 ± 7.2 years) were assessed for body fat, lean mass, plantar flexion and dorsiflexion maximum voluntary isometric contraction (MVC) torque, muscle activation capacity and antagonist muscle co-contraction. MVC torque normalised to body mass in the obese group was 35 and 29 % lower (p < 0.05) in Y and 34 and 31 % lower (p < 0.05) in O, compared with underweight and normal weight individuals, respectively. Y with ≥40 % body fat had significantly lower activation than Y with <40 % body fat (88.3 vs. 94.4 %, p < 0.05), but O did not exhibit this effect. Co-contraction was affected by ageing (16.1 % in O vs. 13.8 % in Y, p < 0.05) but not body composition. There were significant associations between markers of body composition, age, strength and activation capacity, with the strongest correlation between muscle strength and total body mass (r = 0.508 in Y, p < 0.001, vs. r = 0.204 in O, p < 0.01). Furthermore, the age-related loss in plantar flexion (PF) MVC torque was exacerbated in obese compared to underweight, normal weight and overweight individuals (-0.96 vs. -0.54, -0.57 and -0.57 % per year, p < 0.05). The negative impact of adiposity on muscle performance is associated with not only muscular but also neural factors. Overall, the effects of ageing and obesity on this system are somewhat cumulative. © 2014 The Author(s)

The individual and combined influence of ACE and ACTN3 genotypes on muscle phenotypes before and after strength training

Alternative measures of muscle size, strength, and power to those used in previous studies could help resolve the controversy surrounding associations between polymorphisms of the angiotensin-I converting enzyme (ACE) and α-actinin-3 (ACTN3) genes and skeletal muscle phenotypes, and the responses to resistance training (RT). To this end, we measured quadriceps femoris muscle volume (Vm), physiological cross-sectional area (PCSA), maximum isometric force (Ft), specific force (Ft per unit PCSA), maximum isoinertial strength (1-RM), and maximum power (Wmax; n = 40) before and after 9-week knee extension RT in 51 previously untrained young men, who were genotyped for the ACE I/D and ACTN3 R577X polymorphisms. ACTN3 R-allele carriers had greater Vm, 1-RM, and Wmax than XX homozygotes at baseline (all P  0.05). Muscle phenotypes were independent of ACE genotype before (all P > 0.05) and after RT (all P > 0.01). However, people with the “optimal” ACE+ACTN3 genotype combination had greater baseline 1-RM and Wmax compared to those with the “suboptimal” profile (both P < 0.0125). We show for the first time that the ACTN3 R577X polymorphism is associated with human Vm and (independently and in combination with the ACE I/D polymorphism) influences 1-RM and Wmax

Genomics as a practical tool in sport - have we reached the starting line?

The genetic component of athletic performance approximates 50%, depending on which specific element of performance is considered. Limited genetic testing is already available commercially and genetic tests are likely to become powerful tools to improve sport performance in the future. Currently, however, selection of athletes for training squads or competition based on genomic data is premature. Larger volumes of longitudinal data within individual sports are needed to determine the efficacy of using genomic data in the management of elite athletes via manipulation of training load and diet based on personal genomic information

Training duration may not be a predisposing factor in potential maladaptations in talent development programmes that promote early specialisation in elite youth soccer

Purpose To determine whether training duration is a predisposing factor in potential maladaptations in talent development programmes that promote early specialisation in elite youth soccer. Methods Training times and type of 184 elite soccer players, from the under-9 to under-21 age groups (age 9.4 to 18.4 yrs; stature 1.38 to 1.82 m; body mass 32.2 to 76.2 kg) were recorded. Results Total training time progressively increased between the under-9 (268 ± 25 min/week) and under-14 (477 ± 19 min/week) groups with the majority of training time (96.5 ± 3.9%) consisting of soccer training and matches. Total training time then subsequently reduced from under-14 to under-15 (266 ± 77 min/week) groups, with no differences in training time between under-15 and under-21. Only under-15 to under-21 players completed resistance training; this inclusion coincided with a reduction in soccer training and match play when compared to time spent in these activities for younger groups (73.8 ± 3.2% of total training). Conclusion Data suggest that although the majority of training is focused on technical development, the training duration as a whole is unlikely to contribute to potential maladaptations in talent development programmes in elite youth soccer