Robert M. Erskine

Training-induced changes in structural and mechanical properties of the patellar tendon are related to muscle hypertrophy but not to strength gains

To obtain a better understanding of the adaptations of human tendon to chronic overloading, we examined the relationships between these adaptations and the changes in muscle structure and function. Fifteen healthy male subjects (20+/-2 yr) underwent 9 wk of knee extension resistance training. Patellar tendon stiffness and modulus were assessed with ultrasonography, and cross-sectional area (CSA) was determined along the entire length of the tendon by using magnetic resonance imaging. In the quadriceps muscles, architecture and volume measurements were combined to obtain physiological CSA (PCSA), and maximal isometric force was recorded. Following training, muscle force and PCSA increased by 31% (P<0.0001) and 7% (P<0.01), respectively. Tendon CSA increased regionally at 20-30%, 60%, and 90-100% of tendon length (5-6%; P<0.05), and tendon stiffness and modulus increased by 24% (P<0.001) and 20% (P<0.01), respectively. Although none of the tendon adaptations were related to strength gains, we observed a positive correlation between the increase in quadriceps PCSA and the increases in tendon stiffness (r=0.68; P<0.01) and modulus (r=0.75; P<0.01). Unexpectedly, the increase in muscle PCSA was inversely related to the distal and the mean increases in tendon CSA (in both cases, r=-0.64; P<0.05). These data suggest that, following short-term resistance training, changes in tendon mechanical and material properties are more closely related to the overall loading history and that tendon hypertrophy is driven by other mechanisms than those eliciting tendon stiffening.

Resistance training increases in vivo quadriceps femoris muscle specific tension in young men

Aim:  The present study investigated whether in vivo human quadriceps femoris (QF) muscle specific tension changed following strength training by systematically determining QF maximal force and physiological cross‐sectional area (PCSA).

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.

Costamere remodeling with muscle loading and unloading in healthy young men

Costameres are mechano‐sensory sites of focal adhesion in the sarcolemma that provide a structural anchor for myofibrils. Their turnover is regulated by integrin‐associated focal adhesion kinase (FAK). We hypothesized that changes in content of costamere components (beta 1 integrin, FAK, meta‐vinculin, gamma‐vinculin) with increased and reduced loading of human anti‐gravity muscle would: (i) relate to changes in muscle size and molecular parameters of muscle size regulation [p70S6K, myosin heavy chain (MHC)1 and MHCIIA]; (ii) correspond to adjustments in activity and expression of FAK, and its negative regulator, FRNK; and (iii) reflect the temporal response to reduced and increased loading. Unloading induced a progressive decline in thickness of human vastus lateralis muscle after 8 and 34 days of bedrest (−4% and −14%, respectively; n = 9), contrasting the increase in muscle thickness after 10 and 27 days of resistance training (+5% and +13%; n = 6). Changes in muscle thickness were correlated with changes in cross‐sectional area of type I muscle fibers (r = 0.66) and beta 1 integrin content (r = 0.76) at the mid‐point of altered loading. Changes in meta‐vinculin and FAK‐pY397 content were correlated (r = 0.85) and differed, together with the changes of beta 1 integrin, MHCI, MHCII and p70S6K, between the mid‐ and end‐point of resistance training. By contrast, costamere protein level changes did not differ between time points of bedrest. The findings emphasize the role of FAK‐regulated costamere turnover in the load‐dependent addition and removal of myofibrils, and argue for two phases of muscle remodeling with resistance training, which do not manifest at the macroscopic level.

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 after resistance training (RT) because limitations to previous studies include small cohorts, imprecise measures of muscle size and strength, and no control of prior exercise or habitual protein intake. 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 habitual protein intake and strength response to 3-wk RT without nutritional supplementation (followed by 6 wk of 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(-1) for 12 wk and consumed PRO or PLA immediately before and after each training session. We assessed elbow flexor muscle strength (unilateral 1-repetition maximum and isometric maximum voluntary force) and size (total volume and maximum anatomical cross-sectional area determined with magnetic resonance imaging) 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), anatomical cross-sectional area (PRO 16.2% ± 7.1% vs PLA 15.6% ± 4.4%, P = 0.80), 1-repetition maximum (PRO 41.8% ± 21.2% vs PLA 41.4% ± 19.9%, P = 0.97), and maximum voluntary force (PRO 12.0% ± 9.9% vs PLA 14.5% ± 8.3%, P = 0.43). CONCLUSIONS In the context of this study, protein supplementation did not augment elbow flexor muscle strength and size changes that occurred after 12 wk of RT.

The impact of obesity on skeletal muscle architecture in untrained young vs. old women

It is unknown whether loading of the lower limbs through additional storage of fat mass as evident in obesity would promote muscular adaptations similar to those seen with resistance exercise. It is also unclear whether ageing modulates any such adjustments. This study aimed to examine the relationships between adiposity, ageing and skeletal muscle size and architecture. A total of 100 untrained healthy women were categorised by age into young (Y) (mean ± SD: 26.7 ± 9.4 years) vs. old (O) (65.1 ± 7.2 years) and body mass index (BMI) classification (underweight, normal weight, overweight and obese). Participants were assessed for body fat using dual energy x‐ray absorptiometry, and for gastrocnemius medialis (GM) muscle architecture (skeletal muscle fascicle pennation angle and length) and size [GM muscle volume and physiological cross‐sectional area (PCSA)] using B‐mode ultrasonography. GM fascicle pennation angle (FPA) in the obese Y females was 25% greater than underweight (P = 0.001) and 25% greater than normal weight (P = 0.001) individuals, while O females had 32 and 22% greater FPA than their underweight (P = 0.008) and normal weight (P = 0.003) counterparts. Furthermore, FPA correlated with body mass in both Y and O females (Y r = 0.303; P < 0.001; O r = 0.223; P = 0.001), yet no age‐related differences in the slope or r‐values were observed (P > 0.05). Both GM muscle volume (P = 0.003) and PCSA (P = 0.004) exhibited significant age × BMI interactions. In addition, muscle volume and PCSA correlated with BMI, body mass and fat mass. Interestingly, ageing reduced both the degree of association in these correlations (P < 0.05) and the slope of the regressions (P < 0.05). Our findings partly support our hypotheses in that obesity‐associated changes in GM PCSA and volume differed between the young and old. The younger GM muscle adapted to the loading induced by high levels of body mass, adiposity and BMI by increasing its volume and increasing its pennation angle, ultimately enabling it to produce higher maximum torque. Such an adaptation to increased loading did not occur in the older GM muscle. Nonetheless, the older GM muscle FPA increased to a similar extent to that seen in young GM muscle, an effect which partly explains the relatively enhanced absolute maximum torque observed in obese older females.

What causes in vivo muscle specific tension to increase following resistance training

It is not known why in vivo muscle specific tension increases following resistance training in humans but changes in muscle fibre‐type composition, increased single‐fibre specific tension or lateral force transmission might provide explanations. Lateral force transmission would increase specific tension but decrease contraction velocity, thus not affecting maximal power per unit muscle volume. In vivo muscle specific tension, power output and muscle volume were determined in the quadriceps femoris of 42 young men, while myosin heavy chain (MyHC) isoform composition, single‐fibre (SF) specific tension, SF maximal shortening velocity (Vmax) and SF peak power (Wmax) of the vastus lateralis were established in a subsample (n= 17) before and after high‐intensity leg‐extension resistance training (3 sessions week−1 for 9 weeks). Following training, in vivo muscle specific tension increased by 17% but the power output/muscle volume ratio remained unaltered. Furthermore, there was no relationship between the training‐induced decrease in MyHC IIX and the change in specific tension in vivo. In addition, SF specific tension, Vmax and Wmax were unchanged following training. In conclusion, a change in fibre‐type composition does not explain the increased in vivo specific tension, nor does it seem likely that increased myofilament packing occurred with resistance training. However, an unchanged in vivo power per unit muscle volume is in accordance with the notion of enhanced lateral force transmission after strength training.

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), but responses to RT were independent of ACTN3 genotype (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.

Genetic variation and exercise-induced muscle damage: implications for athletic performance, injury and ageing

Prolonged unaccustomed exercise involving muscle lengthening (eccentric) actions can result in ultrastructural muscle disruption, impaired excitation–contraction coupling, inflammation and muscle protein degradation. This process is associated with delayed onset muscle soreness and is referred to as exercise-induced muscle damage. Although a certain amount of muscle damage may be necessary for adaptation to occur, excessive damage or inadequate recovery from exercise-induced muscle damage can increase injury risk, particularly in older individuals, who experience more damage and require longer to recover from muscle damaging exercise than younger adults. Furthermore, it is apparent that inter-individual variation exists in the response to exercise-induced muscle damage, and there is evidence that genetic variability may play a key role. Although this area of research is in its infancy, certain gene variations, or polymorphisms have been associated with exercise-induced muscle damage (i.e. individuals with certain genotypes experience greater muscle damage, and require longer recovery, following strenuous exercise). These polymorphisms include ACTN3 (R577X, rs1815739), TNF (−308 G>A, rs1800629), IL6 (−174 G>C, rs1800795), and IGF2 (ApaI, 17200 G>A, rs680). Knowing how someone is likely to respond to a particular type of exercise could help coaches/practitioners individualise the exercise training of their athletes/patients, thus maximising recovery and adaptation, while reducing overload-associated injury risk. The purpose of this review is to provide a critical analysis of the literature concerning gene polymorphisms associated with exercise-induced muscle damage, both in young and older individuals, and to highlight the potential mechanisms underpinning these associations, thus providing a better understanding of exercise-induced muscle damage.

Obesity decreases both whole muscle and fascicle strength in young females but only exacerbates the aging-related whole muscle level asthenia.

Obesity has previously been associated with greater muscle strength. Aging, on the other hand, reduces muscle specific force (the force per unit physiological cross‐sectional area [PCSA] of muscle). However, neither the effect of obesity on skeletal muscle specific force nor the combined effects of aging and obesity on this parameter are known. This study aimed to describe the interplay between body mass index (BMI)/adiposity, aging, and skeletal muscle specific force. Ninety‐four untrained healthy women categorized by age into young (Y; mean ± SD: 25.5 ± 9.0 years) versus old (O; 64.8 ± 7.2 years) were assessed for body composition, gastrocnemius medialis (GM) muscle volume (V), net maximum voluntary contraction (nMVC), and specific force (SF). The young obese, while demonstrating 71% and 29% (P < 0.001) higher V and nMVC compared to normal BMI individuals, were in fact 26% (P = 0.007) weaker than these, where V was used to scale nMVC (i.e., nMVC/V). The weakness associated with obesity was further exemplified in the 34% (P < 0.001) lower SF relative to normal BMI individuals. Similarly, ≥40% body fat was associated with 60% and 27% (P < 0.001) higher V and nMVC, but 11% and 25% (P < 0.01) lower nMVC/V and SF than <40% body fat. The aging‐related rates of decline in V (−2 cm3/year P < 0.05) and nMVC (−1.2 cm3/year P < 0.05) were highest in obesity defined by BMI. This effect was also seen when segregating by >40% adiposity. Interestingly, however, obesity appeared advantageous to the aging‐related changes in nMVC/V (P < 0.001) and SF (P < 0.001). Unlike previous reports of greater strength in the obese compared with leaner age‐matched counterparts, we in fact demonstrate that the young sedentary obese, are substantially weaker, where the volume of skeletal muscle is used to scale the maximal torque output, or forces are quantified at the fascicular level. The seemingly positive impact of obesity on rate of aging, however, is complex and warrants further investigations.