Understanding of physiological responses of organisms is typically based on data collected during an isolated event. Although many fundamental insights have been gained from these studies, evaluating the response to a single event ignores the fact that each individual has experienced a unique set of events throughout its life that may have altered its physiology. The idea that prior experiences can influence subsequent performance is known as a carry-over effect. Carry-over effects may explain much of the variation in performance found among individuals. For example, high physical activity has been shown to improve mitochondrial respiratory function and biogenesis and reduce oxidative stress, and has been linked to improved health and longevity. In this study, we asked whether the bioenergetic differences between active and inactive individuals carry over to impact performance in a subsequent reproductive event and alter a female's reproductive outcome. Female mice that had access to a running wheel for a month before mating gave birth to a larger litter and weaned a heavier litter, indicating that high physical activity had a positive carry-over effect to reproduction. Mice that ran also displayed higher mitochondrial respiration and biogenesis with no changes in endogenous antioxidant enzymes. These results provide a mechanistic framework for how the conditions that animals experience before breeding can impact reproductive outcomes.
It has been proposed that mitochondria display a biphasic response to reactive oxygen species (ROS) accumulation referred to as mitohormesis. Under mitohormesis, low levels of ROS stimulate protection against oxidative damage, whereas high levels result in the accumulation of oxidative damage. The mechanisms that underlie improved function following low levels of ROS production are poorly understood. We evaluated the changes in mitochondrial performance in house mice following X‐irradiation, which induces ROS production. Eight mice were maintained as unexposed controls and 8 mice were assigned to each of 5 groups that varied in time between x‐ray exposure and mitochondrial isolation, including 1 hour, 1, 4, 7, and 10 days after x‐ray. We measured mitochondrial respiratory function (RCR), ROS production (H2O2), and oxidative lipid damage (4‐HNE) in the liver and the skeletal muscle from both hind legs and liver. In liver, RCR showed a right skewed U‐shape curve in which day 1 and day 4 mice had significantly lower RCR than both non‐irradiation control, and all other x‐rayed mice. H2O2 and 4‐HNE in liver displayed inverse U‐shaped curves, with both peaking on day 4. Similar trends that were not significant were observe for RCR, H2O2 and 4‐HNE levels in muscle. These data provide evidence that mitochondria become damaged in response to x‐ray, but recover within one week of exposure. This represents the protective effect that ROS exposure has on mitochondrial function. Ongoing measurements of oxidative damage repair, mitophagy, mitochondrial apoptosis, and biogenesis will provide more comprehensive understanding of the mitohormetic response. The value of x‐ray in inducing oxidative damage in experimental studies will be discussed.Support or Funding InformationThis research was funded by US National Science Foundation grant 1453784
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