Our observation of greater acute and chronic reductions in plasma triglycerides with moderate compared with vigorous exercise (19) supports this hypothesis.
In agreement with this hypothesis, physical exercise is known to increase dendritic complexity, spine density, and synaptic plasticity [ 43, 215, 216].
To test this hypothesis, we exercised wild-type mice that transgenically express the fluorescent autophagy marker GFP-LC3 on a treadmill, using a running protocol with increasing speed at defined intervals.
To test this hypothesis, an endurance exercise training study was performed in muscle-specific JNK1/2 knockout (mJNKKO; Mapk8LoxP/LoxP Mapk9LoxP/LoxP MCK-Cre−/+) mice and wild-type (WT; MCK-Cre−/+) controls.
The recent study by LeMoine et al [24] in the muscle of exercising zebrafish would seem to support this hypothesis.
To test this hypothesis, we examined whether exercising voluntary control over SMA and PHC after neurofeedback training caused specific performance changes in a motor reaction time task and in a word memory task, respectively (Fig. 1).
Rather than treating GO enrichment as a definitive result, we approached this analysis as an exercise in hypothesis generation.
This hypothesis is, however, primarily based on exercise-induced hyperlactatemia.
The rationale for this hypothesis was that fitter individuals usually reach higher symptom scores during exercise compared to individuals less accustomed to the uncomfortable sensations of exercise [24].
This hypothesis is supported by consistent reports of reduced airway inflammation following exercise training [ 34].
To test this hypothesis, we compared the protective effect of caffeine on oculomotor control post-exercise to that of a norepinephrine-dopamine reuptake inhibitor.
