Declutter and Focus: Empirically Evaluating Design Guidelines for Effective Data Communication.

Data visualization design has a powerful effect on which patterns we see as salient and how quickly we see them. The visualization practitioner community prescribes two popular guidelines for creating clear and efficient visualizations: declutter and focus. The declutter guidelines suggest removing non-critical gridlines, excessive labeling of data values, and color variability to improve aesthetics and to maximize the emphasis on the data relative to the design itself. The focus guidelines for explanatory communication recommend including a clear headline that describes the relevant data pattern, highlighting a subset of relevant data values with a unique color, and connecting those values to written annotations that contextualize them in a broader argument. We evaluated how these recommendations impact recall of the depicted information across cluttered, decluttered, and decluttered+focused designs of six graph topics. Undergraduate students were asked to redraw previously seen visualizations, to recall their topics and main conclusions, and to rate the varied designs on aesthetics, clarity, professionalism, and trustworthiness. Decluttering designs led to higher ratings on professionalism, and adding focus to the design led to higher ratings on aesthetics and clarity. They also showed better memory for the highlighted pattern in the data, as reflected across redrawings of the original visualization and typed free-response conclusions, though we do not know whether these results would generalize beyond our memory-based tasks. The results largely empirically validate the intuitions of visualization designers and practitioners. The stimuli, data, analysis code, and Supplementary Materials are available at https://osf.io/wes9u/.

Control of glycolysis in contracting skeletal muscle. I. Turning it on.

Why does the onset of glycolytic flux in muscle lag the start of exercise? We tested the hypothesis that both elevated metabolite levels and muscle activity are required for flux to begin. Glycolytic flux was determined from changes in muscle pH, phosphocreatine concentration, and P(i) concentration ([P(i)]) as measured by 31P magnetic resonance spectroscopy. Eight subjects performed rapid ankle dorsiflexions to approximately 45% of maximal voluntary contraction force under ischemia at a rate of 1 contraction/s. Subjects completed two bouts of exercise separated by 1 min of ischemic rest. Glycolytic flux was activated by 27 s in the first bout, ceased during the ischemic rest period, and was activated more quickly in the second bout. Because the onset in both bouts occurred at approximately the same [P(i)], ADP concentration, and AMP concentration, the activation of glycolysis appears to be related to the elevation of these metabolite concentrations. However, because no glycolytic flux occurred at rest, even when metabolite levels were high, both muscle activity and elevated metabolites are needed to turn on this pathway. We conclude that the delayed onset of glycolytic flux during exercise reflects the time needed to raise metabolites to flux-activating levels.

Control of glycolysis in contracting skeletal muscle. II. Turning it off.

Glycolytic flux in muscle declines rapidly after exercise stops, indicating that muscle activation is a key controller of glycolysis. The mechanism underlying this control could be 1) a Ca(2+)-mediated modulation of glycogenolysis, which supplies substrate (hexose phosphates, HP) to the glycolytic pathway, or 2) a direct effect on glycolytic enzymes. To distinguish between these possibilities, HP levels were raised by voluntary 1-Hz exercise, and glycolytic flux was measured after the exercise ceased. Glycolytic H(+) and ATP production were quantified from changes in muscle pH, phosphocreatine concentration, and P(i) concentration as measured by 31P magnetic resonance spectroscopy. Substrate (HP) and metabolite (P(i), ADP, and AMP) levels remained high when exercise stopped because of the occlusion of blood flow with a pressure cuff. Glycolytic flux declined to basal levels within approximately 20 s of the end of exercise despite elevated levels of HP and metabolites. Therefore, this flux does not subside because of insufficient HP substrate; rather, glycolysis is controlled independently of glycogenolytic HP production. We conclude that the inactivation of glycolysis after exercise reflects the cessation of contractile activity and is mediated within the glycolytic pathway rather than via the control of glycogen breakdown.