For decades, most scientists and practitioners have agreed that muscle hypertrophy also induces strength gains. However, a recent publication "The Problem of Muscle Hypertrophy: Revisited," questioned the mechanistic role that exercise-induced increases in muscle size have on the exercise-induced increases in strength (of force production), as well as the influence that exercise-induced increases in strength have on sports performance. Such suggestions undermine the important of certain aspects of strength and conditioning for sport. Specifically, if not acting as a mechanism for strength adaptation, it is unclear if there is a sports-related benefit to skeletal muscle hypertrophy. In addition, the authors argued that if strength has little impact on sports performance, strength and conditioning programs may be doing little more than delaying recovery from practicing the actual sport. This contention also indicates that hypertrophy should be avoided in nearly all scenarios because increased muscle size would be additional mass that must be overcome. The purpose of this special discussion is to allow for an in-depth scientific discussion of the experimental evidence for and against the position of Buckner et al. That exercise-induced increases in muscle size have little relevance on the exercise-induced increases in strength and thus, sport performance.

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<p>Sarcopenia is the age-associated loss of muscle mass and strength. Studies have shown that combining resistance training with high protein intake increases muscle mass and strength in older adults. Women are at higher risk than men of sarcopenia. Thus, it is essential to find interventions to lessen women’s risk of losing muscle mass with aging. However, limited studies combine a specific higher-protein diet and a resistance training program in older women to determine skeletal muscle responses. This study aimed to assess the impact of a 12-week resistance training program with a high protein lean beef diet on skeletal muscle mass, strength, and quality in older women compared to a normal protein diet or a high protein diet composed of a lesser amount of beef. </p> <p>The study included three diets; a USDA recommended protein diet (0.8 g/kg/day), a high protein lean beef diet (1.4 g/kg/day), and a high protein diet composed of lesser beef (1.4 g/kg/day). Sixteen subjects were included in the study. The resistance training program consisted of leg extension, leg press, leg curl, chest press, and seated row. Muscle strength was determined by one-repetition maximum assessment at weeks one, six, and twelve. In addition, subjects underwent an MRI pre- and post-intervention to assess quadriceps volume and intermuscular adipose tissue (IMAT). Muscle quality was defined as the leg extension one-repetition maximum over the quadriceps volume. </p> <p>Muscle strength, muscle quality, and quadriceps volume increased with training in all three diet groups (P<0.05, main effect of time). No difference in muscle strength, quality, or quadriceps volume was found between the diet groups. IMAT decreased in all diet groups (P<0.05, main effect of time), but no differences were seen between the diet groups. These findings suggest that the 12-weeks of resistance training increased skeletal muscle strength, quality, and mass, independent of the normal protein or high protein diet and the source of protein in the diet.</p>

It has been hypothesized that an increase in the ratio of plasma tryptophan (TRP) to branched-chain amino acid (BCAA) concentrations may mediate an increase in cerebral serotonin synthesis, through an increased cerebral tryptophan uptake. It is postulated that the increased brain serotonin content may induce central fatigue during prolonged exercise. Until present, this postulate had not been subject to rigorous scientific testing during prolonged exercise. Therefore the aim of this study was to investigate whether ingesting a BCAA supplement during prolonged exercise improves physical performance and central fatigue. The use of such a supplement during prolonged exercise could then be expected to have a large effect on performance. Eight trained cyclists (VO₂ max= 61.9 ± 4.3 ml 02/kg/min) ingested, in random order, a drink containing either 10% carbohydrate (CHO), 10% CHO and 0.16% branched-chain amino acid (BCAA) or 0.16% BCAA. Every hour, for the duration of the exercise (4 hours, 55% VO₂ max) blood samples were analysed for amino acids, ammonia, free fatty acids, glycerol, glucose and insulin concentrations. Urine was analysed for urea and creatinine concentrations. Heart rate, oxygen consumption (VO₂), respiratory exchange ratio (RER) and rating of perceived exertion were also analysed. Thereafter, subject's 40km time trial performance and RPE was assessed on a Velodyne windtrainer. Central fatigue following the time trial was quantified using the Sternberg reaction-time paradigm. The serum concentration of the BCAA's declined as a result of the exercise, in the BCAA only trial. Tryptophan concentration, however, did not change during the exercise. The serum TRP:BCAA ratio increased (0.16 ± 0.06 to 0.20 ± 0.10; p≤0.05) in the CHO trial only. The BCAA trial differed from the two trials in which CHO was ingested because plasma ammonia and glucose concentrations did not increase, while free fatty acids (FF A's) and glycerol concentrations increased significantly (p≤0.05). The lower RER in the BCAA trials suggests a higher proportion of fat was oxidised in these trials, compared to the other two trials. Cycling performance, over a 40km time trial, (CHO= 68.59 ± 6.02; CHO+ BCAA = 68.00 ± 3.01; BCAA = 69.43 ± 5.35 min/sec), ratings of perceived exertion, submaximal or maximal heart rates, and mental performance were not different between trials. Data from this study appears to refute the thesis hypothesis that an increase in serum TRP:BCAA decreases physical performance and central fatigue, during prolonged exercise.

<p>Skeletal muscle is dependent upon its microvasculature to deliver oxygen and substrates to support the metabolic demands of muscle contraction. Skeletal muscle capillary density is determined by a variety of factors including muscle fiber metabolic phenotype and mitochondrial volume as well as prior exercise training status. Additionally, muscle microvascular density and function can diminish with age, contributing to several age-related muscle dysfunctions. Skeletal muscle fibers regulate their surrounding microvasculature through the release of angiogenic and angiostatic signaling factors. A robust increase in angiogenic signaling from skeletal muscle facilitates increases in muscle capillarization following endurance exercise. Extracellular vesicles (EV) are membrane bound signaling factors secreted by every cell type. Skeletal muscle-derived EVs (SkM-EVs) may help facilitate numerous signaling functions of skeletal muscle including between skeletal muscle and its microvasculature.</p> <p>The primary aim of my dissertation research was to determine the signaling roles that SkM-EVs in regulating endothelial cell homeostasis and angiogenesis in states of aging and health. Chapter 1 provides an overview of the relevant literature. Chapter 2 represents an investigation into how age-related cellular senescence impacts the angiogenic potential of skeletal muscle progenitor cells. We found that stress-induced senescence increases release of small EVs and has pro-senescent and angiostatic effects on culture endothelial cells. In Chapter 3 we compared the release, contents, and angiogenic potential of SkM-EVs collected from primarily oxidative or primarily glycolytic skeletal muscle tissue in mice. We found that oxidative muscle tissue secretes more EVs than glycolytic muscle tissue, and the miR contents of EVs differ greatly between the two phenotypes. Additionally, EVs from oxidative tissue enhanced endothelial cell migration and tube formation compared to glycolytic tissue EVs, in a potentially nitric oxide mediated fashion. In Chapter 4, we tested how PGC-1α overexpression effected myotube EV release and angiogenic potential. We found that PGC-1α overexpression did not impact myotube EV release, but increased the angiogenic signaling potential of SkM-EVs. Chapter 5 is a brief summary of the results and limitations of the projects presented in Chapters 2-4, with a short discussion of potential future research directions.</p>

Impedance cardiography is an important tool in determining a person's hemodynamic properties. The makers obtained through thoracic impedance have been shown to be of great importance when monitoring critical care patients. Technological developments have made this process noninvasive and ambulatory, opening up new possibilities for potential use. A study was conducted by remotely monitoring healthy subjects (n=5), who performed an 8-minute mild-to-moderate aerobic exercise protocol, followed up by a four minute cognitive stress test. Testing was conducted onsite at Kennedy Space Center in association with the National Aeronautics and Space Administration using the MW1000A (MindWare Technologies LTD, Gahanna, OH) ambulatory impedance cardiography monitoring (ICG) device. The current study was conducted in order to establish the test-retest reliability of the ICG during aerobic exercise and cognitive stress across a 2 week period. For the purpose of this study Heart Rate (HR), Left Ventricular Ejection Time (LVET) Stroke Volume (SV), Cardiac Output (CO), and Pre-Ejection Period (PEP) were acquired and analyzed during three phases. The phases were, walking on a level treadmill, walking at incline, and an at rest mental arithmetic stress test. Testing has shown that the MW1000A device can provide accurate ambulatory impedance cardiography monitoring with no significant difference between testing intervals. The simple application of electrodes makes this device easy to use and requires little training. Its non-invasive properties render employing ICG both a simple and effective means of determining the hemodynamic properties of a subject.

The mammalian/mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway appears to be the primary regulator of protein synthesis and growth. While resistance exercise paradigms are often divided into hypertrophy (HYP) and strength (STR) protocols, it is unknown whether these protocols differentially stimulate mTORC1 signaling. The purpose of this study was to examine mTORC1 signaling in conjunction with circulating hormone concentrations following a typical lower-body HYP and STR resistance exercise protocol. Ten resistance-trained men (24.7±3.4y; 90.1±11.3kg; 176.0±4.9cm) performed each resistance exercise protocol in a random, counterbalanced order. Blood samples were obtained at baseline (BL), immediately (IP), 30 minutes (30P), 1 hour (1H), 2 hours (2H), and 5 hours (5H) post-exercise. Fine needle muscle biopsies were completed at BL, 1H, and 5H. Electromyography of the vastus lateralis was also recorded during each protocol. HYP and STR produced a similar magnitude of muscle activation across sets. Myoglobin and lactate dehydrogenase concentrations were significantly greater following STR compared to HYP (p=0.01-0.02), whereas the lactate response was significantly higher following HYP compared to STR (p=0.003). The GH, cortisol, and insulin responses were significantly greater following HYP compared to STR (p=0.0001-0.04). No significant differences between protocols were observed for the IGF-1 or testosterone response. Intramuscular anabolic signaling analysis revealed a significantly greater (p=0.03) phosphorylation of IGF-1 receptor at 1H following HYP compared to STR. Phosphorylation status of all other signaling proteins including mTOR (mammalian target of rapamycin), p70S6k (ribosomal S6 kinase 1), and RPS6 (ribosomal protein S6) were not significantly different between trials. Despite significant differences in markers of muscle damage and the endocrine response following STR and HYP, both protocols appeared to elicit similar mTORC1 activation in resistance-trained men.