Catecholamines have been implicated in the regulation of cardiac hypertrophy. The serial injection of a catecholamine (epinephrine, norepinephrine or isoproterenol) will increase cardiac muscle mass. In a canine model of left ventricular hypertrophy secondary to aortic coarctation, the endogen

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Osteopontin (OPN) expression increases in the heart during hypertrophy and heart failure. Here, we studied the role of OPN in pressure overload-induced hypertrophy and analyzed the signaling pathways involved in hypertrophy. Aortic banding (AB) was performed in a group of wild-type (WT) and OPN knockout (KO) mice to induce pressure overload. Left ventricular (LV) structural and functional remodeling was studied 1 month after AB. AB increased OPN and β1 integrin (a receptor for OPN) protein expression in WT-AB group. Hypertrophic response as measured by increased heart weight-to-body weight ratio and myocyte cross-sectional area was significantly increased in WT-AB and KO-AB groups when compared with their respective shams. However, the increase was significantly higher in WT-AB. Re-expression of atrial natriuretic factor was only detected in WT-AB group. LV end-diastolic pressure-volume curve obtained using Langendorff perfusion analysis exhibited a leftward shift in WT-AB group, not in KO-AB. LV-developed pressures measured over a range of LV volumes were significantly increased in WT-AB, not in KO-AB mice. Increased phosphorylation of c-Jun N-terminal kinases, p38 kinase, Akt, and glycogen synthase kinase-3β was significantly higher in WT-AB when compared with KO-AB group. Increased OPN expression may play an essential role in modulating compensatory cardiac hypertrophy in response to chronic pressure overload.

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Resistance exercise training (RET) is a well-known stimulus for muscle protein synthesis. Protein supplementation, in conjunction with RET, has been shown to yield greater accretion of lean body mass than RET alone. Few studies have compared two multi-ingredient, isonitrogenous supplements of differing quality protein. Therefore, the purpose of the current study was to determine whether there was an augmented effect of a high-quality whey protein multi-ingredient nutritional supplement on hypertrophy in young adults following a RET program. We hypothesized that the multi-ingredient supplement would induce hypertrophy to a greater extent than the control supplement in young adults. Twenty-six (13 male, 13 female) healthy young adults (22 ± 2 years [mean ± SD]) were randomly assigned to either the multi-ingredient nutritional supplement (SUPP, n=12: 20g whey protein, 2g leucine, 2.5g creatine monohydrate, 300mg calcium citrate, 1000IU vitamin D) or control beverage (CON, n=12: 20g collagen protein, 1.4g alanine, 0.6g glycine) groups, ingesting their respective supplements twice daily. Measurements were obtained prior to and after a 10-week linear RET program. Dual-energy X-ray absorptiometry (DXA), ultrasound, one-rep maximum (1RM), and biopsies from the vastus lateralis muscle were performed. A 2-way ANOVA (time by supplement) revealed significantly larger increases in lean body mass (LBM), as assessed via DXA, from the active supplement compared to the control (SUPP: +4.1 ± 1.3kg CON: +2.8 ± 1.7kg, p=0.004). We conclude that the consumption of a multi-ingredient nutritional supplement increased lean body mass to a greater extent than to that observed in the CON group in healthy young adults. / Thesis / Master of Science in Kinesiology / Resistance exercise training (RET) is known to augment muscle size, a process known as hypertrophy. Several factors may affect hypertrophy, such as supplementation with protein and amino acids, increasing an individual’s potential to maximize muscle hypertrophy beyond RET-induced gains. However, little is known regarding the effectiveness of multi-ingredient supplements and the synergistic effects they may exhibit on hypertrophy and strength gains. The present thesis shows the effect of a specific multi-ingredient supplement that contained: whey protein, creatine, calcium, vitamin D, and leucine, compared to a low-quality collagen-based supplement, on measures of hypertrophy and strength in young adults. Interestingly, the active supplement (SUPP) induced greater gains in lean body mass (LBM), type II muscle fibre CSA, and bicep CSA and thickness compared to the control (CON), but not strength. These findings provide insight into a novel formulation of ingredients on exercise-induced increases in hypertrophy in young adults.

Training is preparation for what is expected to come through utilization of the plastic and resistive features of nature, known as adaptation. As such, training in humans may have a number of desired goals. These are typically related to sports performance or education. Whatever the goal, a plan needs to be made for reaching it. One needs to identify or select which activities and environments constitute the event or events to which adaptation is sought. Adaptations occurs by imposing something similar to said environment and practicing the selected activities in preparation for the events that can ultimately lead to goal fulfillment. One quite common goal of physical training is to achieve a more lean and muscular physique, be it for reasons of performance or esthetics. A leaner and more muscular physique can have many advantages for health and quality of life. If we are to prepare the body’s physical capabilities and properties, they should be utilized in the preparation. By proper design and execution of a program for physical preparation, we set out on the path to achieve the goal. A factor that is often highlighted as an important key to building muscle in the human body is the steroid hormone testosterone. According to the hormone hypothesis, increases in muscle mass are achieved through transient elevations in anabolic hormones, such as testosterone and IGF1, induced by physical training. To achieve hypertrophy of the muscles through physical training, one must ensure sure that the muscles get the correct signal, the growth signal, as a result of the training. The work presented in this thesis is, in part, an examination of the hormone hypothesis, with both empirical and theoretical elements. The empirical foundations are results of an experiment in which a group of young men were subjected to a program of physical training, designed for all intents and purposes in accordance with contemporary knowledge, to result in muscular hypertrophy in the subjects. The goal was achieved, with an average 4.6% increase in lean body mass in the subjects after the training program. However, there was no evidence that anabolic hormones were elevated at any time during the measurement period. The major part of this thesis details a model for explaining the collected observations. It is not intended to merely provide a guide for achieving a leaner more muscular physique but rather is aimed at formulating the problem of inducing the desired adaptations and difficulties involved in approaching the problem. For reasons discussed in this thesis, I do not claim that this is the full and final word on the matter. However, it goes some way toward explaining why, and perhaps how, desired goals should be formulated so that the muscles may understand them.

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Long bone lengthening occurs at the growth plate (GP) by well-regulated chondrocyte proliferation, hypertrophy and terminal matrix deposition. GP chondrocyte (GPC) hypertrophy has been implicated to be the main determinant of bone growth rate; however the mechanism is poorly understood. The work of this thesis examined some of the cellular process that drives the chondrocyte swelling or hypertrophy particularly in a mammalian post natal GPs using living in situ GPC and fixed GP tissues. Confocal scanning microscopy (CLSM) was used to determine living in situ GPC volume and dimension changes in proliferative zone (PZ) through to hypertrophic zone (HZ) chondrocytes of different GPs of various bones. While PZ cells showed similar volumes and dimensions, HZ cells varied in different GPs, even within the same long bone but at opposite ends. However, the hypertrophic cell volume measured at a single post natal age (day 7) was independent of the corresponding bone length. This could reflect a complex interplay between local and systemic factors in different GPs, which occurs throughout the active phase of bone growth. Maintaining GPC morphology was critical in studying GPC hypertrophy using fixed tissues. This work highlighted a problem caused by conventional fixative solutions, which caused up to 44% hypertrophic GPC shrinkage following GP fixation. This artifact appeared to be associated with the hyperosmotic nature of the fixatives used and could be abolished by adjusting the fixative osmolarity close to physiological level (280 mOsm), or could be significantly reduced by bisecting bone tissues prior to tissue fixation. This thesis proposed roles for plasma membrane transporter(s) in mediating GPC hypertrophy. This hypothesis was tested by examining roles of sodium-hydrogen exchanger (NHE) and anion exchanger (AE) in GPC hypertrophy using an ex vivo bone growth inhibition model. Inhibition of bone growth by inhibitors of NHE (EIPA) and AE (DIDS) respectively was shown to be dose-dependent. The histology of bones demonstrated that the late HZ width was significantly reduced in GPs treated with EIPA or DIDS. Although in situ GPC volumes in the PZ and HZ were not notably different in DIDS-treated GP, the cell volumes in both zones were significantly reduced by EIPA treatment. Fluorescence immunohistochemistry revealed distinctive cellular localisations of NHE1 and AE2 in the PZ and early HZ. These results suggest a possible role of AE in mediating GPC volume increase in PZ chondrocytes and those in the early stages of cell hypertrophy, whereas NHE could possibly maintain intracellular pH of GPC throughout all GP zones. This thesis has characterized various changes in volume and dimensions of living in situ GPC from PZ through to HZ of different GPs of postnatal rats. This work emphasized the importance of fixative osmolarity in order to accurately preserve the normal volume/morphology of cells within tissues. Most importantly, this thesis confirmed a potential role of the plasma membrane transporters, AE and NHE in GPC hypertrophy of growing bones.