An abstract from the Journal of General Physiology
During excitation, muscle cells gain Na+ and lose K+, leading to a rise in extracellular K+ ([K+]o), depolarization, and loss of excitability. Recent studies support the idea that these events are important causes of muscle fatigue and that full use of the Na+,K+-ATPase (also known as the Na+,K+ pump) is often essential for adequate clearance of extracellular K+. As a result of their electrogenic action, Na+,K+ pumps also help reverse depolarization arising during excitation, hyperkalemia, and anoxia, or from cell damage resulting from exercise, rhabdomyolysis, or muscle diseases. The ability to evaluate Na+,K+-pump function and the capacity of the Na+,K+ pumps to fill these needs require quantification of the total content of Na+,K+ pumps in skeletal muscle. Inhibition of Na+,K+-pump activity, or a decrease in their content, reduces muscle contractility. Conversely, stimulation of the Na+,K+-pump transport rate or increasing the content of Na+,K+ pumps enhances muscle excitability and contractility. Measurements of [3H]ouabain binding to skeletal muscle in vivo or in vitro have enabled the reproducible quantification of the total content of Na+,K+ pumps in molar units in various animal species, and in both healthy people and individuals with various diseases. In contrast, measurements of 3-O-methylfluorescein phosphatase activity associated with the Na+,K+-ATPase may show inconsistent results. Measurements of Na+ and K+ fluxes in intact isolated muscles show that, after Na+ loading or intense excitation, all the Na+,K+ pumps are functional, allowing calculation of the maximum Na+,K+-pumping capacity, expressed in molar units/g muscle/min. The activity and content of Na+,K+ pumps are regulated by exercise, inactivity, K+ deficiency, fasting, age, and several hormones and pharmaceuticals. Studies on the α-subunit isoforms of the Na+,K+-ATPase have detected a relative increase in their number in response to exercise and the glucocorticoid dexamethasone but have not involved their quantification in molar units. Determination of ATPase activity in homogenates and plasma membranes obtained from muscle has shown ouabain-suppressible stimulatory effects of Na+ and K+.
The above information is a bit overwhelming in its language, so I'll do my best to explain it. As we know, muscle function is controlled by the sodium potassium pump. During exercise, potassium leaves the muscles, shifting into the bloodstream. Once the exercise ceases, potassium is pumped out of the bloodstream back into the muscle cells. Someone with Hyperkalemic Periodic Paralysis would experience depolarization and loss of muscle function during muscle activity, thus exercise being a trigger of attacks, while someone with Hypokalemic Periodic Paralysis would experience paralysis following muscle activity, thus "rest after exercise" being the trigger.
As Periodic Paralysis experts have noted on many occasions, the functions of the sodium potassium pump isn't felt by people who are well. It is those who have conditions of the muscle - in our case an ion channelopathy - who experience chaos from these shifts as our voltage gate allows incorrect ratios of sodium and potassium to flow in and out of the muscles. To put it bluntly, our bodies short circuit. Depending on the type of Periodic Paralysis, our sodium potassium pump will be either regulated or triggered by "exercise, inactivity, K+ deficiency, fasting, age, and several hormones and pharmaceuticals". There are other regulators and triggers as well, and again, it very much depends on the type of PP.
I believe this explains why physical activity is a trigger (or ultimately leads to a trigger) in all types of Periodic Paralysis. This is my assessment of the article, but if I am completely off-base (see my disclaimer in the sidebar), feel free to share in comments.