ACTN3 R577X polymorphism does not influence explosive leg muscle power in elite volleyball players

We examined the association of R577X polymorphism (rs1815739) in the α‐actinin‐3 (ACTN3) gene with “explosive” leg muscle power performance in a group of male and female elite volleyball players (n=66, 31 men, 35 women) and in a group of non‐athletic male and female young adults (n=334, 243 men, 91 women). We assessed power performance by means of the vertical squat and counter‐movement jump tests. We also determined whether the genotypic frequencies of the ACTN3 R577X genotypes differed between groups. We did not observe any effect of the ACTN3 R577X polymorphism on study phenotypes in both groups, regardless of gender (all P>0.05). Genotype frequencies were similar between volleyball and control groups (P=0.095). Moreover, we did not find an association between the ACTN3 R577X polymorphism and the likelihood of being an elite volleyball player using the dominant (RR vs RX+XX) and the recessive model (RR+RX vs XX). In summary, these findings suggest that the ACTN3 R577X polymorphism does not influence explosive leg muscle power in elite volleyball players.     

Association analysis of the ACTN3 R577X polymorphism with passive muscle stiffness and muscle strain injury

Passive muscle stiffness is considered to be a major factor affecting joint flexibility and is thought to relate to the occurrence of muscle strain injury. In skinned muscle fiber experiments, the R577X polymorphism of the α‐actinin‐3 gene (ACTN 3 ) has been associated with passive muscle stiffness. Our primary purpose was to clarify whether the ACTN 3 R577X polymorphism influences passive stiffness of human muscle in vivo. We also examined whether the ACTN 3 R577X polymorphism is associated with the occurrence of hamstring strain injury. Seventy‐six healthy young male subjects were genotyped for the ACTN 3 R577X (rs1815739) polymorphism. Shear modulus (an index of stiffness) of each hamstring muscle (biceps femoris, semitendinosus, and semimembranosus) was assessed using ultrasound shear wave elastography, and history of hamstring strain injury was collected via a questionnaire. The muscle shear moduli of the semitendinosus and semimembranosus were significantly higher in R‐allele (RR  + RX genotype) carriers than in XX genotype carriers, whereas the shear modulus of the biceps femoris did not differ among the ACTN 3 R577X genotypes. Frequency of past hamstring strain injury also did not differ between the 3 genotypes nor between the R‐allele and XX genotype carriers. This study indicates that RR and RX genotypes of the ACTN 3 R577X polymorphism (corresponding to the presence of α‐actinin‐3 in type II muscle fibers) are associated with increased passive muscle stiffness of the human hamstring in vivo. However, this altered mechanical property might not affect the risk of hamstring muscle strain injury.     

Adding strength to endurance training does not enhance aerobic capacity in cyclists

The molecular signaling of mitochondrial biogenesis is enhanced when resistance exercise is added to a bout of endurance exercise. The purpose of the present study was to examine if this mode of concurrent training translates into increased mitochondrial content and improved endurance performance. Moderately trained cyclists performed 8 weeks (two sessions per week) of endurance training only (E, n = 10; 60‐min cycling) or endurance training followed by strength training (ES, n = 9; 60‐min cycling + leg press). Muscle biopsies were obtained before and after the training period and analyzed for enzyme activities and protein content. Only the ES group increased in leg strength (+19%, P < 0.01), sprint peak power (+5%, P < 0.05), and short‐term endurance (+9%, P < 0.01). In contrast, only the E group increased in muscle citrate synthase activity (+11%, P = 0.06), lactate threshold intensity (+3%, P < 0.05), and long‐term endurance performance (+4%, P < 0.05). Content of mitochondrial proteins and cycling economy was not affected by training. Contrary to our hypothesis, the results demonstrate that concurrent training does not enhance muscle aerobic capacity and endurance performance in cyclists.     

Lack of β2‐AR improves exercise capacity and skeletal muscle oxidative phenotype in mice

β₂‐adrenergic receptor (β₂‐AR) agonists have been used as ergogenics by athletes involved in training for strength and power in order to increase the muscle mass. Even though anabolic effects of β₂‐AR activation are highly recognized, less is known about the impact of β₂‐AR in endurance capacity. We presently used mice lacking β₂‐AR [β₂‐knockout (β₂ KO)] to investigate the role of β₂‐AR on exercise capacity and skeletal muscle metabolism and phenotype. β₂ KO mice and their wild‐type controls (WT) were studied. Exercise tolerance, skeletal muscle fiber typing, capillary‐to‐fiber ratio, citrate synthase activity and glycogen content were evaluated. When compared with WT, β₂ KO mice displayed increased exercise capacity (61%) associated with higher percentage of oxidative fibers (21% and 129% of increase in soleus and plantaris muscles, respectively) and capillarity (31% and 20% of increase in soleus and plantaris muscles, respectively). In addition, β₂ KO mice presented increased skeletal muscle citrate synthase activity (10%) and succinate dehydrogenase staining. Likewise, glycogen content (53%) and periodic acid‐Schiff staining (glycogen staining) were also increased in β₂ KO skeletal muscle. Altogether, these data provide evidence that disruption of β₂‐AR improves oxidative metabolism in skeletal muscle of β₂ KO mice and this is associated with increased exercise capacity.     

Skeletal muscle IL‐15/IL‐15Rα and myofibrillar protein synthesis after resistance exercise

In vitro and in vivo studies described the myokine IL ‐15 and its receptor IL ‐15Rα as anabolic/anti‐atrophy agents, however, the protein expression of IL ‐15Rα has not been measured in human skeletal muscle and data regarding IL ‐15 expression remain inconclusive. The purpose of the study was to determine serum and skeletal muscle IL ‐15 and IL ‐15Rα responses to resistance exercise session and to analyze their association with myofibrillar protein synthesis (MPS ). Fourteen participants performed a bilateral leg resistance exercise composed of four sets of leg press and four sets of knee extension at 75% 1RM to task failure. Muscle biopsies were obtained at rest, 0, 4 and 24 hours post‐exercise and blood samples at rest, mid‐exercise, 0, 0.3, 1, 2, 4 and 24 hours post‐exercise. Serum IL ‐15 was increased by ~5.3‐fold immediately post‐exercise, while serum IL ‐15Rα decreased ~75% over 1 hour post‐exercise (P <.001). Skeletal muscle IL ‐15Rα mRNA and protein expression were increased at 4 hours post‐exercise by ~2‐fold (P <.001) and ~1.3‐fold above rest (P =.020), respectively. At 24 hours post‐exercise, IL ‐15 (P =.003) and IL ‐15Rα mRNA s increased by ~2‐fold (P =.002). Myofibrillar fractional synthetic rate between 0‐4 hours was associated with IL ‐15Rα mRNA at rest (r =.662, P =.019), 4 hours (r =.612, P =.029), and 24 hours post‐exercise (r =.627, P =.029). Finally, the muscle IL ‐15Rα protein up‐regulation was related to Leg press 1RM (r =.688, P =.003) and total weight lifted (r =.628, P =.009). In conclusion, IL ‐15/IL ‐15Rα signaling pathway is activated in skeletal muscle in response to a session of resistance exercise.