Yes, what you say makes sense, thank you for clarifying that. So although the body is able to take absorb glucose more readily, in the window stage, it is not because of increased insulin production, but because of increased cellular sensitivity to glucose as a result of exercise.

So unless there is a feedback loop that is directed my insulin receptors there would not be more or less insulin in the blood because the insulin feedback loop is proportional to glucose levels. So it remains that insulin levels will act as they always do but exercise will make the cell more receptive to glucose increasing uptake, and not as a result of more insulin than would normally be present.

I checked my libraries data base and could not find much. I will keep on looking.

Here is an abstract that concurs with what Enthalpic has said

Postprandial blood glucose and insulin levels are both risk factors for developing obesity, type-2 diabetes, and coronary heart diseases. To date, research has shown that a single bout of moderate-to high-intensity aerobic exercise performed <=24 hours before a carbohydrate ingestion has a positive effect on the postprandial glucose and insulin response, but the reports on the effect of a single bout of resistance exercise are scarce. The purpose of this study was to examine if a bout of resistance exercise performed 14 hours before ingestion of a carbohydrate-rich meal might reduce the postprandial increment in blood glucose and plasma insulin concentration. Ten healthy, strength-trained, young men participated in a meal and resistance exercise experiment. All subjects ingested a carbohydrate-rich meal (1 g carbohydrate per kg body weight) after fasting for 12 hours either with no exercise the preceding 3 days or after a bout of resistance exercise performed 14 hours earlier. Blood glucose and plasma insulin were measured every 15 and 30 minutes, respectively, for 2 hours. The postprandial blood glucose response measured as the peak value, the slope (from time 0 to peak value), and the incremental area under the curve 0-60 min (IAUC0-60 min) was significantly (p <= 0.05) reduced 14 hours after the resistance exercise compared with the control experiment (no exercise). However, total IAUC was not significantly influenced by a bout of previous resistance exercise. Also, the plasma insulin response did not differ between the 2 experiments. From the present study it would appear that a bout of resistance exercise can reduce the post-prandial glucose elevation for at least 14 hours.

From:
ANDERSEN, EIVIND 1; HOSTMARK, ARNE T. 1,2 EFFECT OF A SINGLE BOUT OF RESISTANCE EXERCISE ON POSTPRANDIAL GLUCOSE AND INSULIN RESPONSE THE NEXT DAY IN HEALTHY, STRENGTH-TRAINED MEN. Journal of Strength & Conditioning Research. 21(2):487-491, May 2007.



And another one


Individuals with insulin resistance are characterized by impaired insulin action on whole-body glucose uptake, in part due to impaired insulin-stimulated glucose uptake into skeletal muscle. A single bout of exercise increases skeletal muscle glucose uptake via an insulin-independent mechanism that bypasses the typical insulin signalling defects associated with these conditions. However, this 'insulin sensitizing' effect is short-lived and disappears after ~48 h. In contrast, repeated physical activity (i.e. exercise training) results in a persistent increase in insulin action in skeletal muscle from obese and insulin-resistant individuals. The molecular mechanism(s) for the enhanced glucose uptake with exercise training have been attributed to the increased expression and/or activity of key signalling proteins involved in the regulation of glucose uptake and metabolism in skeletal muscle. Evidence now suggests that the improvements in insulin sensitivity associated with exercise training are also related to changes in the expression and/or activity of proteins involved in insulin signal transduction in skeletal muscle such as the AMP-activated protein kinase (AMPK) and the protein kinase B (Akt) substrate AS160. In addition, increased lipid oxidation and/or turnover is likely to be another mechanism by which exercise improves insulin sensitivity: exercise training results in an increase in the oxidative capacity of skeletal muscle by up-regulating lipid oxidation and the expression of proteins involved in mitochondrial biogenesis. Determination of the underlying biological mechanisms that result from exercise training is essential in order to define the precise variations in physical activity that result in the most desired effects on targeted risk factors, and to aid in the development of such interventions.

From:

Hawley, J. A.; Lessard, S. J. Exercise training-induced improvements in insulin action. Acta Physiologica. 192(1):127-135, January 2008.

Although the above is not conclusive it suggests that insulin secretion is normal after exercise, but the effects of exercise on glucose sensitivity contribute to the increased glucose uptake, and not that there is more insulin present than normally would be with the same blood glucose levels, without exercise.