Bioenergetics

The molecular mechanisms of synaptic function and development have been studied extensively, but little is known about the energy requirements of synapses, or the mechanisms that coordinate their energy production with their metabolic demands. These are oversights, as synapses with high energy demands are more susceptible to degeneration and degrade in the early stages of diseases such as amyotrophic lateral sclerosis, spinal muscle atrophy and Parkinson’s disease. Here, in a structure-function study at Drosophila motor neuron terminals, a neurophysiological model was generated to investigate how power (ATP/s) supply is integrated to satisfy the power demand of presynaptic terminals. Power demands were estimated from six nerve terminals through direct measurements of neurotransmitter release and Ca2+ entry, as well as theoretical estimation of Na+ entry and power demands at rest (cost of housekeeping). The data was leveraged with a computational model that simulated the power demands of the terminals during their physiological activity, revealing high volatility in which power demands can increase 15-fold within milliseconds as neurons transition from rest to activity. Another computational model was generated that simulated ATP production scenarios regarding feedback to the power supply machinery (Oxphos and glycolysis) through changes in nucleotide concentrations, showing that feedback from nucleotides alone fail to stimulate power supply to match the power demands of each terminal. Failure of feedback models invokes the need for feed forward mechanisms (such as Ca2+) to stimulate power supply machinery to match power demands. We also quantified mitochondrial volume, density, number and size in each nerve terminal, revealing all four features positively correlate with the terminals power demands. This suggests the terminals enhance their oxidative capacity by increasing mitochondrial content to satisfy their power demands. And lastly, we demonstrate that abolishing an ATP buffering system (the phosphagen system) does not impair neurotransmission in the nerve terminals, suggesting motor nerve terminals are capable of satisfying their power demands without the ATP buffering system.

The purpose of this study was to examine the acute and temporal response of CK- MM and FGF-21 to 3-day/wk. different repetition-range, volume-equated resistance training programs over 8-weeks in previously trained males. Sixteen trained, college- aged males were counterbalanced into high (DUP-HR) or low (DUP-LR) repetition groups. Subjects performed the squat and bench press 3x/wk. for 8 weeks. Blood samples were collected at various intervals throughout the study. Trained individuals did not elicit significant acute or chronic changes in CK-MM or FGF-21 following training and the lack of change was present in both groups. Additionally, neither biomarker correlated with changes in 1RM strength. There was a very strong correlation between acute mean (r=0.95) and acute percentage change (r=0.97) increase from pre training to post training in week #1. Additionally, a moderate correlation in percentage change was observed (r=0.59) of both biomarkers from pre training to 48 hours post training in week #2.

The purpose of this study was to determine if resistance exercise altered
peripheral BDNF concentration. Eighteen trained male subjects were split into two
groups performing varied repetition ranges. DUP-HR and DUP-LR groups trained
3x/week for 8 weeks, and were equated for total volume (repetitions X sets X intensity).
Plasma BDNF and interleukin-6 (IL-6) levels were measured prior to and immediately
following the first exercise session of weeks 1, 2, 4 and 6. Pre-exercise levels were also
assessed prior to the second and third sessions of week 1 and 6. Lastly, resting levels
were measured before and after training intervention. No group differences (p>0.05) were detected for either biomarker. An acute BDNF elevation (p=0.018) was detected only in the final week of training. IL-6 elevations were detected at all acute measurements (p<0.01). BDNF and IL-6 percentage change correlated significantly (p<0.05) in week-1. No chronic alterations were observed (p>0.05).

Since its inception, the domestic corn ethanol industry in the United States has been dependant on federal subsidies and trade restrictions to keep afloat. Although this political support has allowed the industry to grow, there have been a number of negative externalities as a result, namely the growing demand for corn causing significant increases in the prices of many consumer goods. Despite the fact that consumers are facing rising prices in agricultural and energy markets, ethanol still maintains a level of support around the general American populace that is counterintuitive given its economic reality. In this paper, I contend that much of ethanol's support is maintained through the intentional manipulation of the product's public perception on behalf of politicians and industrial superpowers. I will demonstrate this phenomenon through the use of both Stigler's (1971) and Pelzman's (1976) model of iso-majority.