Several studies, some older, others relatively recent, have scientifically demonstrated the benefits of exercise. Apart from the molecular mechanisms involved, the main, and most widely accepted, effect of exercise on glucose metabolism is represented by the marked enhancement of insulin sensitivity [25, 26], even in diabetic subjects [27, 28].

Most of the studies on exercise and glucose metabolism have focused on the chronic effect of exercise. On one hand, exercise seems to improve the action of insulin [29], while plasma insulin response to a given hyperglycemic stimulus is decreased [30], suggesting an improvement in insulin action. However, few data are available on the acute effect of exercise on glucose metabolism. Furthermore, mainly due to the differences in the metabolic tests used to assess insulin response, the type of exercise performed, and the population studied, in depth knowledge as to how physical exercise impacts insulin production is still lacking.

Our study demonstrated a significant reduction in both fasting and 1-hour glucose levels following OGTT, suggesting a more effective insulin secretion, after a single bout of light aerobic exercise. We also observed that a single 30-minute bout of aerobic exercise in young and healthy, untrained subjects, improved insulin sensitivity with a concomitant improvement in glucose levels and a positive trend in beta cell secretory response [31, 32].

It is rather difficult to accurately distinguish between improved insulin sensitivity and improved insulin responsiveness in vivo. However, some studies have attempted to verify the underlying mechanisms in muscles perfused or incubated in vitro with different insulin concentrations, demonstrating that exercise improves both the sensitivity and responsiveness of skeletal muscle to insulin [33]. The increase in muscle insulin sensitivity after a single bout of exercise occurs as the acute insulin-independent stimulation of glucose transport by the exercise wears off. Animal models have shown that the increase in muscle insulin sensitivity persists as long as muscle glycogen supercompensation does not occur [34].

In a 1985 study, Arciero et al. showed that compared to a short-term low calorie diet (no more than 10 days), short-term exercise is more effective in enhancing insulin action in adult individuals with abnormal glucose tolerance (impaired glucose tolerance or type 2 diabetes) [35].

Another study compared the effects of aerobic and resistance training on several metabolic risk factors, concluding that both types of training improve metabolic features in type 2 diabetic patients in a similar way and that improved glucose control was mainly driven by an enhanced insulin sensitivity, with no significant changes in beta cell function [36].

Conversely, Dela et al. demonstrated that aerobic training in trained subjects with type 2 diabetes may lead to an enhanced beta cell function, even though the effect of training depends on the remaining beta cell secretory capacity, i.e. training improves beta cell insulin secretion only on condition of moderate secretory capacity. In contrast, in diabetics with low secretory capacity, training showed no effects on beta cell function [37].

On the other hand, Dunstan et al. found that short-term circuit training (3 days/week for 8 weeks) in metabolically well-controlled type 2 diabetes subjects, did not improve insulin area under the curve after oral glucose load [38], thus suggesting the presence of other mechanisms behind the modification of beta cell secretory capacity after exercise or, at least, a more effective secretion of insulin (same amount of released insulin, better peripheral effect on insulin-dependent tissues).

Although in daily clinical practice 2-hour post-load glycaemia is used for clinical reasons (diagnosis of alterations of glucose tolerance/metabolism), growing evidence has highlighted the importance of evaluating glycaemia after 1 h. In fact, it has been suggested that higher 1 h glucose level at OGTT is a strong predictor of future risk of type 2 diabetes [16]. Moreover, levels of 1-hour post-load plasma glucose higher than 155 mg/dl have been associated with different types of subclinical organ damage, such as chronic kidney disease and carotid atherosclerosis [39,40,41], well known independent predictors of increased cardiovascular mortality. Thus, improvement in 1-hour post-load plasma glucose following a single session of aerobic physical activity suggests that exercise could have a direct effect on T2D risk and cardiovascular risk.

To date, few studies have evaluated the effect of a single bout of aerobic physical exercise on glucose and insulin metabolism in healthy subjects. Shambrook et al. [11] demonstrated that short bouts (10 min) of exercise after each meal are better than a single 30-minute bout to minimize post-meal glucose elevation. Similarly, Kao and colleagues [42] examined the effects of a single bout of short-duration, high-intensity exercise and long duration, low intensity exercise on insulin sensitivity and the adiponectin/leptin ratio in individuals with different body mass indices (BMIs) who did not exercise regularly; they found that HOMA - IR improved significantly for both exercise patterns in the normal weight group and for the high intensity pattern in the obese group. However, no other insulin resistance indexes or insulin secretion parameters were analyzed.

Another study investigated the effect of a single bout of aerobic exercise on short-term high fat diet-induced postprandial glucose and incretin metabolism during an oral glucose tolerance test. They found that although exercise did not improve postprandial glucose and insulin metabolism during the OGTT, it did however normalize the increased postprandial GLP-1 levels induced by the high fat diet [43].

Engeroff et al. [44] found that, after a meal mimicking a typical Western breakfast and a sedentary period of 4 h, regular short exercise breaks, but not exercise prior to sitting, could lower blood insulin levels in premenopausal, healthy, female participants. Given these conflicting results, due to the heterogeneity of the population enrolled, duration of exercise and concomitant diet, we decided to enroll healthy, normal weight, untrained volunteers, in order to perform our metabolic assessment.

We metabolically studied all enrolled subjects before and after performing a single bout of aerobic exercise monitored using a metabolic holter. After the single bout of physical activity, we found an improvement in glycemic values, particularly those measured at fasting state and 1 h post-oral glucose load.

Insulinemic values mirrored this trend, given that 1 h post-load levels were also significantly reduced. Moreover, assessing the surrogate indices of insulin sensitivity and insulin secretion, we found that secretion improved after exercise, although this improvement did not reach statistical significance. This seems to be due to increased peripheral sensitivity to insulin, as evidenced by the statistically significant improvement in all the indices of insulin resistance considered [45, 46]. Specifically, we found an improvement in both whole-body insulin sensitivity, assessed by Matsuda index and confirmed by the OGIS index, and in hepatic insulin sensitivity considering HOMA - IR and QUICKI indexes (obtained only from fasting glucose and insulin levels).

Even though we have still not reached a complete understanding of the effect of physical exercise on insulin production, mainly due to the differences in the metabolic tests used to assess insulin response, the type of exercise and the population studied, our study demonstrated the acute improvement of insulin sensitivity after exercise, primarily influenced by the improved capacity of beta cells to produce insulin.

Our study had some limitations: the sample size was limited, and C-peptide values, which would have allowed us to improve our understanding of insulin secretion, were not measured.

Despite these potential limitations, the strengths of our study include the enrollment of young, healthy, untrained subjects, who represent an ideal model in which to verify the pathophysiology of insulin secretion and sensitivity. Furthermore, the use of the armband allowed the precise monitoring of physical activity and the normalization of the results for energy expenditure.