Enhancing and Extending Biological Performance and Resilience

Abstract

Human performance, endurance, and resilience have biological limits that are genetically and epigenetically predetermined but perhaps not yet optimized. There are few systematic, rigorous studies on how to raise these limits and reach the true maxima. Achieving this goal might accelerate translation of the theoretical concepts of conditioning, hormesis, and stress adaptation into technological advancements. In 2017, an Air Force-sponsored conference was held at the University of Massachusetts for discipline experts to display data showing that the amplitude and duration of biological performance might be magnified and to discuss whether there might be harmful consequences of exceeding typical maxima. The charge of the workshop was “to examine and discuss and, if possible, recommend approaches to control and exploit endogenous defense mechanisms to enhance the structure and function of biological tissues.” The goal of this white paper is to fulfill and extend this workshop charge. First, a few of the established methods to exploit endogenous defense mechanisms are described, based on workshop presentations. Next, the white paper accomplishes the following goals to provide: (1) synthesis and critical analysis of concepts across some of the published work on endogenous defenses, (2) generation of new ideas on augmenting biological performance and resilience, and (3) specific recommendations for researchers to not only examine a wider range of stimulus doses but to also systematically modify the temporal dimension in stimulus inputs (timing, number, frequency, and duration of exposures) and in measurement outputs (interval until assay end point, and lifespan). Thus, a path forward is proposed for researchers hoping to optimize protocols that support human health and longevity, whether in civilians, soldiers, athletes, or the elderly patients. The long-term goal of these specific recommendations is to accelerate the discovery of practical methods to conquer what were once considered intractable constraints on performance maxima.

Healthspan Maintenance and Prevention of Parkinson’s-like Phenotypes with Hydroxytyrosol and Oleuropein Aglycone in C. elegans

“…Another possible background mechanism for the observed effects could be hormesis, already considered in the case of the effect of tyrosol in C. elegans [58]. Several studies indicate that different stressors extend lifespan in C. elegans in a hormetic-like manner [110][111][112] and suggest that hormetic effects could be exploited to prevent the onset of various diseases [13,113,114], including neurodegenerative disorders, and to slow down the ageing process [115,116].…”

Long weekend sleep is linked to stronger academic performance in male but not female pharmacy students

“…Nightly sleep durations considerably shorter or longer than 7 hours have been correlated with morbidity and the acceleration of death in a U-shaped pattern. 29 This observation and a large body of work on the preponderance of U-shaped dose-response curves in biology 30 might be construed to assume that long sleep durations cause poor health. However, those who are sick also tend to sleep more, and regularly forcing the infirm awake in an attempt to shorten their sleep durations to seven hours/night might worsen their health status and hasten an early death, as suggested by studies of intensive care unit delirium, the risk of which is reduced by the simple measure of using earplugs.…”

Hydrogen Sulfide and Carnosine: Modulation of Oxidative Stress and Inflammation in Kidney and Brain Axis

“…In line with this observation, Nrf2 encodes the vitagene antioxidant pathway which exists to counteract different forms of stress (e.g., oxidative, environmental, and mitochondrial stress). Vitagenes include heat shock protein 70 (Hsp70), heme oxygenase 1 (HO-1), γ-glutamylcysteine synthetase (γ-GCs), thioredoxin (Trx), and sirtuins (SIRTs) ( Figure 3 ) [ 1 , 233 , 234 , 235 ] as biomarkers for stress adaptation, cross-tolerance, and resilience underlying hormesis or preconditioning [ 236 ] ( Figure 3 ).…”