John K. Petrella

Potent myofiber hypertrophy during resistance training in humans is associated with satellite cell-mediated myonuclear addition: a cluster analysis.

A present debate in muscle biology is whether myonuclear addition is required during skeletal muscle hypertrophy. We utilized K-means cluster analysis to classify 66 humans after 16 wk of knee extensor resistance training as extreme (Xtr, n = 17), modest (Mod, n = 32), or nonresponders (Non, n = 17) based on myofiber hypertrophy, which averaged 58, 28, and 0%, respectively (Bamman MM, Petrella JK, Kim JS, Mayhew DL, Cross JM. J Appl Physiol 102: 2232-2239, 2007). We hypothesized that robust hypertrophy seen in Xtr was driven by superior satellite cell (SC) activation and myonuclear addition. Vastus lateralis biopsies were obtained at baseline and week 16. SCs were identified immunohistochemically by surface expression of neural cell adhesion molecule. At baseline, myofiber size did not differ among clusters; however, the SC population was greater in Xtr (P < 0.01) than both Mod and Non, suggesting superior basal myogenic potential. SC number increased robustly during training in Xtr only (117%; P < 0.001). Myonuclear addition occurred in Mod (9%; P < 0.05) and was most effectively accomplished in Xtr (26%; P < 0.001). After training, Xtr had more myonuclei per fiber than Non (23%; P < 0.05) and tended to have more than Mod (19%; P = 0.056). Both Xtr and Mod expanded the myonuclear domain to meet (Mod) or exceed (Xtr) 2,000 mum(2) per nucleus, possibly driving demand for myonuclear addition to support myofiber expansion. These findings strongly suggest myonuclear addition via SC recruitment may be required to achieve substantial myofiber hypertrophy in humans. Individuals with a greater basal presence of SCs demonstrated, with training, a remarkable ability to expand the SC pool, incorporate new nuclei, and achieve robust growth.

Does habitual dietary intake influence myofiber hypertrophy in response to resistance training? A cluster analysis

Although resistance exercise training (RT) is a common intervention to stimulate muscle protein synthesis and increase skeletal muscle mass, the optimal daily protein and total energy intakes sufficient to support RT-mediated muscle growth are as yet unclear. Further, the efficacy of RT varies widely among adults of all ages and whether this is attributable to interindividual differences in nutrition is not known. To determine if self-selected daily intake of macronutrients and specific components of dietary protein and fat are predictive of the magnitude of RT-mediated muscle growth, detailed 4-day dietary records were analyzed on 60 subjects previously clustered (K-means cluster analysis) as non-, modest, and extreme responders (non, n = 16; mod, n = 29; xtr, n = 15), based on the magnitudes of change in vastus lateralis myofiber cross-sectional area following a 16-week, 3-day-per-week, high-intensity RT. Despite the marked contrast between 60% myofiber hypertrophy in xtr and zero growth in non, we found no differences among response clusters in daily intakes of energy (mean +/- SEM: non 102 +/- 8; mod 111 +/- 6; xtr 109 +/- 5 kJ.kg-1.day-1), protein (non 0.97 +/- 0.08; mod 1.07 +/- 0.07; xtr 1.05 +/- 0.06 g.kg-1.day-1), carbohydrate (non 3.02 +/- 0.24; mod 3.18 +/- 0.20; xtr 3.14 +/- 0.17 g.kg-1.day-1), and fat (non 0.95 +/- 0.09; mod 1.05 +/- 0.08; xtr 1.03 +/- 0.08 g.kg-1.day-1), which generally met or exceeded dietary recommendations. There were no cluster differences in intakes of branched chain amino acids known to stimulate muscle protein synthesis. Using the novel K-means clustering approach, we conclude from this preliminary study that protein and energy intakes were sufficient to facilitate modest and extreme muscle growth during RT and intrinsic or extrinsic factors other than nutrient ingestion apparently impaired the anabolic response in nonresponders.

The effect of loss of visual input on muscle power in resistance trained and untrained young men and women.

Abstract Killebrew, SS, Petrella, JK, Jung, AP, and Hensarling, RW. The effect of loss of visual input on muscle power in resistance trained and untrained young men and women. J Strength Cond Res 27(2): 495–500, 2013—Visual impairment has been shown to reduce muscle power when compared with that in sighted individuals. The purpose of this study was to assess whether the loss of visual input affects lower limb muscle power production in sighted men and women who are resistance trained and untrained. Twenty-seven college-aged participants (19–23 years) performed a seated double-leg press with and without visual input (resulting from being blindfold) in 2 separate counterbalanced trials. Lower limb concentric power was calculated by measuring the distance and time a leg press footplate was displaced while lifting 60% of 1-repetition maximum as quickly as possible. Loss of visual input reduced power output by 22.8 W (−6.4%) in all participants (p < 0.01). When resistance training status was taken into account, resistance trained participants (n = 12, trained >2× per week) did not lose power output (4.4 W, −1.1%, p = 0.90), whereas untrained men and women (n = 15) had significantly less power when visual input was removed via blindfold (37.6 W, −11.7%, p < 0.01). Untrained women experienced the greatest decrease in power when blindfolded (39 W, −15.9%, p < 0.01). Muscle power decreases in the absence of vision, but a regular strength training program attenuates this occurrence in young men and women. In practical application, strength training interventions may be successful in protecting individuals from losses in muscle power when visual input is removed.

Human neuromuscular aging: Sex differences revealed at the myocellular level

&NA; Age‐related muscle loss (sarcopenia) is a major clinical problem affecting both men and women – accompanied by muscle weakness, dysfunction, disability, and impaired quality of life. Current definitions of sarcopenia do not fully encompass the age‐related changes in skeletal muscle. We therefore examined the influence of aging and sex on elements of skeletal muscle health using a thorough histopathological analysis of myocellular aging and assessments of neuromuscular performance. Two‐hundred and twenty‐one untrained males and females were separated into four age cohorts [mean age 25 y (n = 47), 37 y (n = 79), 61 y (n = 51), and 72 y (n = 44)]. Total (−12%), leg (−17%), and arm (−21%) lean mass were lower in both 61 y and 72 y than in 25 y or 37 y (P < 0.05). Knee extensor strength (−34%) and power (−43%) were lower (P < 0.05) in the older two groups, and explosive sit‐to‐stand power was lower by 37 y (P < 0.05). At the histological/myocellular level, type IIx atrophy was noted by 37 y and type IIa atrophy by 61 y (P < 0.05). These effects were driven by females, noted by substantial and progressive type IIa and IIx atrophy across age. Aged female muscle displayed greater within‐type myofiber size heterogeneity and marked type I myofiber grouping (˜5‐fold greater) compared to males. These findings suggest the predominant mechanisms leading to whole muscle atrophy differ between aging males and females: myofiber atrophy in females vs. myofiber loss in males. Future studies will be important to better understand the mechanisms underlying sex differences in myocellular aging and optimize exercise prescriptions and adjunctive treatments to mitigate or reverse age‐related changes.