As animals get smaller, their ability to generate usable work from muscle contraction is decreased by the muscle’s force–velocity properties, thereby reducing their effective jump height. Very small animals use a spring-actuated system, which prevents velocity effects from reducing available energy. Since force–velocity properties reduce the usable work in even larger animals, why don’t larger animals use spring-actuated jumping systems as well? We will show that muscle length–tension properties limit spring-actuated systems to generating a maximum one-third of the possible work that a muscle could produce—greatly restricting the jumping height of spring-actuated jumpers. Thus a spring-actuated jumping animal has a jumping height that is one-third of the maximum possible jump height achievable were 100% of the possible muscle work available. Larger animals, which could theoretically use all of the available muscle energy, have a maximum jumping height that asymptotically approaches a value that is about three times higher than that of spring-actuated jumpers. Furthermore, a size related “crossover point” is evident for these two jumping mechanisms: animals smaller than this point can jump higher with a spring-actuated mechanism, while animals larger than this point can jump higher with a muscle-actuated mechanism. We demonstrate how this limit on energy storage is a consequence of the interaction between length–tension properties of muscles and spring stiffness. We indicate where this crossover point occurs based on modeling and then use jumping data from the literature to validate that larger jumping animals generate greater jump heights with muscle-actuated systems than spring-actuated systems.

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T his chapter is a call for consequential education research that has transformative potential: intellectually, educationally, and socially. It is about learning to see differently. It is an argument about seeing our work with youth and communities in ways that can help education researchers see ingenuity instead of ineptness and inability, to see resilience instead of deficit, and to imagine futures with youth from nondominant communities instead of imposing failure. We use the notion of "learning to see" both metaphorically and as a theoretical lens and methodological guide to illustrate how rigorous and consequential education research can help us imagine and design new forms of learning and schooling. We argue that rupturing educational inequality also involves new forms of inquiry that help reconceptualize what it means to work with nondominant communities.

Spontaneous Ca2+ signaling from the InsP3R intracellular Ca2+ release channel to mitochondria is essential for optimal oxidative phosphorylation (OXPHOS) and ATP production. In cells with defective OXPHOS, reductive carboxylation replaces oxidative metabolism to maintain amounts of reducing equivalents and metabolic precursors. To investigate the role of mitochondrial Ca2+ uptake in regulating bioenergetics in these cells, we used OXPHOS-competent and OXPHOS-defective cells. Inhibition of InsP3R activity or mitochondrial Ca2+ uptake increased α-ketoglutarate (αKG) abundance and the NAD+/NADH ratio, indicating that constitutive endoplasmic reticulum (ER)–to–mitochondria Ca2+ transfer promoted optimal αKG dehydrogenase (αKGDH) activity. Reducing mitochondrial Ca2+ inhibited αKGDH activity and increased NAD+, which induced SIRT1-dependent autophagy in both OXPHOS-competent and OXPHOS-defective cells. Whereas autophagic flux in OXPHOS-competent cells promoted cell survival, it was impaired in OXPHOS-defective cells because of inhibition of autophagosome-lysosome fusion. Inhibition of αKGDH and impaired autophagic flux in OXPHOS-defective cells resulted in pronounced cell death in response to interruption of constitutive flux of Ca2+ from ER to mitochondria. These results demonstrate that mitochondria play a fundamental role in maintaining bioenergetic homeostasis of both OXPHOS-competent and OXPHOS-defective cells, with Ca2+ regulation of αKGDH activity playing a pivotal role. Inhibition of ER-to-mitochondria Ca2+ transfer may represent a general therapeutic strategy against cancer cells regardless of their OXPHOS status.