Fructose was first discovered in fruit, hence the name, but forms one-half of a molecule of sucrose—table sugar—which is a glucose molecule and a fructose molecule bonded together. Fructose has a noticeably sweeter taste than glucose, and is responsible for much of the sweetness of table sugar.
Glucose in the bloodstream can be intensely damaging, so insulin is mobilized to drive it into the muscles for use and the fat tissue for storage. Every cell in the body can metabolize glucose.
Fructose can be metabolized only in the liver, and it is is dealt with by the same pathway as handles ethanol. This means that fructose in quantity—either too much over the long term, or more than the liver can handle in the short term—causes the same liver damage as ethyl alcohol. Fructose also affects the dopamine receptors in the brain in the same way as alcohol, and so it is just as addictive. It lacks only the short-term toxicity of alcohol.
Explosive performance is provided by glucose, not fructose, since the muscles cannot metabolize fructose, and glycogen cannot be shared between cells. Excessive glycogen in the liver is part of what makes the liver insulin-resistant, along with the fat droplets created by an excess of fructose in the liver. This means that fructose directly, not indirectly, causes insulin-resistance.
The glucose used in the muscles of a keto-adapted athlete for explosive performance was manufactured by the liver from dietary protein and shared as glucose. Liver glycogen (as I understand it, anyway) gets metabolized in the liver—once carbohydrate intake drops low enough to permit it.
The fructose in sucrose and the fructose in high-fructose corn syrup is the same molecule. I believe that the only difference between sucrose and HFCS is that the fructose and the glucose are not bonded together in HFCS, and of course the percentage of fructose is 55%, not 50%.
This lecture details the metabolism of fructose in the liver: