Home Medicine Towards optimizing exercise prescription for type 2 diabetes: modulating exercise parameters to strategically improve glucose control
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Towards optimizing exercise prescription for type 2 diabetes: modulating exercise parameters to strategically improve glucose control

  • Alexis Marcotte-Chénard and Jonathan P. Little EMAIL logo
Published/Copyright: March 25, 2024
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Translational Exercise Biomedicine
From the journal Translational Exercise Biomedicine Volume 1 Issue 1

Abstract

Type 2 diabetes (T2D) is a complex and multifaceted condition clinically characterized by high blood glucose. The management of T2D requires a holistic approach, typically involving a combination of pharmacological interventions as well as lifestyle changes, such as incorporating regular exercise, within an overall patient-centred approach. However, several condition-specific and contextual factors can modulate the glucoregulatory response to acute or chronic exercise. In an era of precision medicine, optimizing exercise prescription in an effort to maximize glucose lowering effects holds promise for reducing the risk of T2D complications and improving the overall quality of life of individuals living with this condition. Reflecting on the main pathophysiological features of T2D, we review the evidence to highlight how factors related to exercise prescription can be modulated to target improved glucose control in T2D, including the frequency, intensity, total volume, and timing (e.g., pre- vs. post-prandial) of exercise, as well as exercise modality (e.g., aerobic vs. resistance training). We also propose a step-by-step, general framework for clinicians and practitioners on how to personalize exercise prescription to optimize glycemic control in individuals living with T2D.

Keywords: physical activity; HIIT; MICT; timing; intensity; frequency

Introduction

The prevalence of type 2 diabetes (T2D) has increased dramatically in recent years with 451 million estimated cases worldwide [1]. Among individuals living with T2D in Canada, only half reach the glycemic control target of having a hemoglobin A1c≤7 % [2] with similar achievement of the A1c target in the United States, Europe, and other countries [3]. The combined high prevalence and non-optimal management of this condition results in a direct cost of more than $966 billion USD in 2021 [4]. At a more personal level, individuals with T2D face an elevated risk of developing additional comorbidities, which can diminish quality of life and increase the likelihood of premature mortality [5, 6]. Strategies to optimize T2D management, specifically focusing on improving glycemic control, are therefore crucial to address the associated costs and improve overall health of people living with this condition.

Figure 1: Graphical representation of the study. Key points: 1) Prioritize a patient-centered approach based on the individuals’ preferences, condition and goals; 2) Gradually increasing exercise volume towards physical activity guidelines while adjusting intensity to achieve similar improvements efficiently and increasing frequency to every other day can improve glucose control in individuals living with T2D; 3) Exercising in the morning may offer superior benefits, yet the timing should be tailored to individual preferences and conditions, with postprandial exercise presenting a practical option for managing hyperglycemia; 4) Combining resistance and aerobic training is optimal for reducing body fat, while high-intensity interval training may provide additional advantages in targeting visceral fat. Figure created with BioRender.
Figure 1:

Graphical representation of the study. Key points: 1) Prioritize a patient-centered approach based on the individuals’ preferences, condition and goals; 2) Gradually increasing exercise volume towards physical activity guidelines while adjusting intensity to achieve similar improvements efficiently and increasing frequency to every other day can improve glucose control in individuals living with T2D; 3) Exercising in the morning may offer superior benefits, yet the timing should be tailored to individual preferences and conditions, with postprandial exercise presenting a practical option for managing hyperglycemia; 4) Combining resistance and aerobic training is optimal for reducing body fat, while high-intensity interval training may provide additional advantages in targeting visceral fat. Figure created with BioRender.

Over the past 30 years, exercise has emerged as a pivotal element in the prevention and management of T2D [7], primarily due to the ability of exercise to acutely lower blood glucose concentration and enhance insulin sensitivity [8], [9], [10]. In addition to these effects on glucoregulation, engaging in physical activity provides a plethora of other health benefits, such as reducing the risk of cardiovascular disease [11, 12], improving cardiorespiratory fitness [13], helping to maintain weight loss [14], and improving quality of life for individuals living with T2D [15]. The current physical activity guideline for individuals living with T2D recommend at least 150 min per week of moderate to vigorous intensity aerobic exercise with no more than two consecutive days without exercising [16, 17]. In addition to aerobic training (AT), persons with T2D should undertake moderate to vigorous resistance training (RT) at least 2 days per week [16, 17]. While these guidelines offer a general framework to improve glycemic control, recent advancements in our understanding of this complex condition may facilitate more personalized and optimal exercise prescriptions.

T2D is a heterogenous and multifaceted condition with pathophysiology involving interactions between several key organs and organ systems with the end result being dysregulation of glucose control [18, 19]. Hence, it seems plausible that adjusting various exercise parameters, including modalities (e.g., AT vs. RT), intensity (e.g., moderate vs. high intensity), and timing (e.g., morning vs. evening, before vs. after a meal), may result in distinct impacts on these organ systems (and their interactions) to influence an individual’s glycemic response. In the age of precision medicine, it may be possible to tailor exercise interventions to maximize benefits for individuals living with T2D (Figure 1).

The purpose of the present narrative review is to bridge the gap between the complex and heterogeneous pathophysiology of T2D and exercise prescription variables with the goal of optimizing improvements in glucose control. More specifically, we will provide a brief overview of the pathophysiology of T2D focusing on insulin resistance, beta cell function, and obesity to set the stage for discussion on 1) the impact of standard exercise prescription variables (e.g., frequency, volume, type, and intensity) on glucose control, 2) the timing of exercise (e.g., morning vs. afternoon; pre- vs. postprandial), 3) the impact of high-intensity exercise on adipose tissue; and 4) practical guidelines for exercise specialists and healthcare providers.

Pathophysiological basis of type 2 diabetes

T2D is a metabolic disorder that ultimately results in impaired regulation of blood glucose. Glycemic control is primarily regulated by the interplay between insulin action on insulin responsive tissues (e.g., liver, skeletal muscle, adipose) and insulin production capacity from pancreatic beta cells [20]. The development of T2D is a complex process that typically manifests over several years and involves both environmental (e.g., education, family environment, access to a healthy diet) and individual factors (e.g., genetics, aging, lifestyle) [21, 22]. Although T2D can present as several different proposed phenotypes [23, 24] and is not always associated with clinical obesity, it is generally accepted that excess accumulation of fat within key metabolic tissues (liver, skeletal muscle, and pancreas) – perhaps related to a “personal fat threshold” [25] and highly correlated with overall adiposity – contributes to insulin resistance and insufficient insulin secretion, resulting in impaired ability to control blood glucose. In the present review, we will briefly summarize these main pathophysiological features of T2D (i.e., insulin resistance, β-cell dysfunction, and excessive fat accumulation) before focusing on how one might be able to strategically apply exercise to target T2D pathophysiology and improve glycemic control.

Insulin resistance

Under normal physiological conditions, insulin binds with the extracellular α-subunits of insulin receptors located on the cell membrane, causing phosphorylation of the β-subunit which initiates a sequence of cellular processes that facilitate the transport and metabolism of glucose within the cell [23, 26]. Insulin resistance (IR) refers to the reduced capacity of different cells/tissues to respond adequately to normal concentrations of insulin, typically focused on reduced ability to increase glucose uptake and utilization [27, 28]. As elegantly reviewed by Petersen and Shulman [23], several mechanisms contribute to IR in various tissues, many of which are driven by nutrient oversupply [23]. Indeed, an increase in nutrient-derived metabolites such as diacylglycerol (DAG), ceramide, and branched-chain amino acids have all been shown to contribute to the development of IR. Along those lines, an overabundance of macronutrients may also propagate an inflammatory environment and promote the formation of free radicals, which collectively contribute to the exacerbation of IR [23]. Although the exact molecular mechanisms (and their interactions) have not been fully elucidated, impairments in insulin signaling appear to occur at both the receptor itself and at the post-receptor level [23, 29], [30], [31]. Within the context of exercise, research has tended to focus on skeletal muscle insulin resistance, although impacts of exercise on liver [32] and adipose [33] insulin sensitivity also cannot be overlooked.

Beta-cell dysfunction

The pancreas is a sophisticated endocrine organ made up of several thousands of islets, each containing β-cells, α-cells, and δ-cells [34]. The β-cells are responsible for the production and release of insulin into the circulation, with the primary function to keep plasma glucose levels within a narrow concentration on a minute-by-minute basis. However, in the presence of IR, the β-cells exhibit a compensatory response synthesizing and secreting a higher amount of insulin in attempts to overcome the reduction in tissue insulin action [35]. It has been calculated that in lean individuals, only 0.5 units of insulin would be needed to dispose of a 75 g load of glucose after 2 h compared to individuals living with T2D, where 45 units may be needed to dispose of the same load [36]. This compensatory mechanism has historically been seen as the major factor leading to β-cell “exhaustion” and the subsequent development of hyperglycemia [35]. However, based on the literature, both IR and β-cell dysfunction are usually present in the early development of T2D [37], suggesting that the traditional view of β-cell exhaustion due to excess insulin demand is likely too simplistic. Indeed, at the point of diagnosing T2D, it is observed that the individual has already experienced a reduction of more than 80 % in their β-cell function [18], and inappropriate insulin secretion for the level of IR is one of the greatest predictors of future development of T2D [37].

Obesity

The prevalence of obesity, which can be defined as having a body mass index (BMI) over 30 kg/m2 (a surrogate for excess adiposity [38]) and/or the presence of abnormal or excess adiposity that impairs health [39], has increased dramatically in recent years [40]. Despite the known limitations of BMI, this anthropometric index remains a valid populational and clinical tool to assess adiposity [41] and has been epidemiologically and mechanistically associated with T2D [42, 43].

Adipose tissue is a metabolically active organ that synthesizes a wide variety of active messengers (e.g., leptin, adiponectin, IL-6, TNF-alpha, etc.) that regulate whole-body homeostasis [44]. However, in the presence of IR, the ability of insulin to inhibit lipolysis is impaired, resulting in a sustained increase in plasma free fatty acid (FFA) [45]. This persistent increase in FFA availability contributes to the increase in glucose production by the liver via stimulation of gluconeogenesis [46, 47], can induce hepatic and skeletal muscle IR through accumulation of ectopic lipids [23, 48] and promotes β-cell dysfunction [49, 50]. As the adipose tissue enlarges, the distance between the capillaries and adipocyte core increases, which appears to trigger adipocyte hypoxia and activation of a pro-inflammatory response via recruitment of macrophages and other immune cells [51]. The spillover of pro-inflammatory cytokines originated from macrophage-infiltrated adipose tissue in the circulation (e.g., TNF-alpha; IL-1beta), contributes to chronic low-grade inflammation and is mechanistically linked to the development of IR and T2D [52]. It should also be noted that the location of the adipose tissue may be of particular importance. Indeed, analysis from the Framingham Heart Study has shown that visceral adipose tissue (VAT) measured with computed tomography was more correlated with IR compared to subcutaneous adipose tissue [53]. These adipose tissue depot-specific effects are likely due to more direct anatomical proximity to the liver [54], along with differences in lipolytic capacity and cell composition [55, 56].

This brief overview emphasizes that the progression of T2D is a multifaceted process involving various contributing factors, notably IR and β-cell dysfunction, which both may be caused by excessive accumulation of adipose tissue and ectopic fat. Therefore, therapeutic approaches focusing on counteracting IR, improving β-cell function, and reducing (particularly visceral) fat would be hypothesized to improve glycemic control in people living with T2D. The next section will address how one might use this information in attempts to optimize exercise prescription to enhance insulin sensitivity, β-cell function, and adiposity management.

Exercise and type 2 diabetes

Exercise, glucose tolerance, and insulin resistance

For several decades now, exercise has been recognized as a primary therapeutic approach in the management of T2D. This was primarily the case because exercise is known to acutely improve glycemic control in individuals with [57] and without T2D [9, 58]. Indeed, muscle contraction triggers translocation of GLUT4 to the sarcolemma via a non-insulin-dependent pathway [59]. Classic studies [60], [61], [62] demonstrate that the pool of intracellular GLUT4 transporters existed that responded to muscle contraction (exercise) was different than the insulin-responsive GLUT4 transporter pool and that the effects of muscle contraction and insulin on myocellular glucose uptake were additive [63]. This work has been extended in vivo in humans living with T2D where an acute bout of moderate exercise is known to induce GLUT4 translocation to the sarcolemma reducing blood glucose concentration [61, 64]. Therefore, even in the presence of IR, performing exercise (muscle contractions) can promote the entry and utilization of glucose in the muscle without the need for insulin. A single session of moderate-intensity aerobic exercise has also been shown to improve insulin sensitivity and glucose tolerance in the hours after [65], with effects lasting up to 48 h [9]. It is therefore not surprising that a single bout of exercise can lower 24 h glucose values assessed by continuous glucose monitoring when compared to a non-exercise day [10]. Mechanistically, several factors could modulate this glucose lowering response following exercise such as IL-6 release [66] which potentialized the insulin sensitivity [67, 68] and upregulation of specific key proteins within the insulin signaling pathway (IRS-1, PI3K, and AMPK complexes) that increase GLUT4 translocation [69, 70]. The cycle of glycogen depletion and repletion in response to acute exercise also likely to play a significant role in enhancing post-exercise glucose uptake and insulin sensitivity [71]. However, recent meta-analysis using individual participant data (n=106) demonstrated no discernible relationship between glycogen depletion and the improvement of glycemic control in the hours following exercise cessation. The authors posit that the enhancement of glycemic control post-exercise (i.e., insulin-stimulated muscle glucose uptake) is likely regulated by cellular mechanisms that elevate the “set point” for muscle glycogen storage [72]. Nonetheless, the repeated increases in glucose uptake and insulin sensitivity in response to acute bouts of exercise over a prolonged period of regular training appears sufficient to lead to an improvement in A1c [16, 17], the clinical marker of diabetes management representing average blood glucose concentration over the past 2–3 months. In addition to the cumulative effect of these repeated exercise bouts, other chronic adaptations could also contribute to the improvement in glucose control. Indeed, an increase in muscle capillary density [73, 74], a reduction in intra-muscular DAG and ceramides content [75, 76], reduction in chronic inflammation [77], GLUT4 protein content and mitochondrial biogenesis [71] could all represent adaptations that contribute to the improvement in glycemic control (e.g., A1c) following prolonged exercise interventions. Altogether, the combination of the acute effect of each individual bout of exercise and chronic adaptations to exercise training contribute to the improvement in glucose tolerance and insulin sensitivity, reiterating the important of regular exercise and increased overall physical activity in the management of T2D.

Exercise and β-cell function

In addition to the improvement in insulin sensitivity, exercise has also been shown to improve β-cell mass and function (for review see: [78]). However, considering the invasive nature of assessing β-cell proliferation, apoptosis, and cell viability, which are all proxies of β-cell mass, there is limited direct evidence of β-cell adaptation to exercise in humans. Therefore, most of our knowledge relies on the evidence gathered in animal models. Briefly, the improvement in β-cell mass following exercise could be explained by the increase in cell proliferation and viability as well as reducing cell apoptosis [79, 80]. Similarly, several direct mechanisms related to β-cell function can mostly be studied in isolated islets obtained from animal models. Exercise has been shown to attenuate the reduction of GLUT2 (the main glucose transporter in β-cells) in diabetic rats [80]. Prolonged exercise in rodents has also been shown to increase islet insulin content [79]. Considering the scope of the present review, which primarily focuses on human studies, we invite the reader to consult Curran and colleagues’ [78] review for a deeper understanding of the effect of exercise on the β-cell mass and function.

In contrast to direct measures of β-cell mass and function, in vivo insulin secretion (and its dynamics) can be measured in humans and allows researchers to explore how exercise might impact metrics of β-cell function in humans. Filho and colleagues reported in their systematic review that exercise interventions can improve beta-cell-related outcomes [81]. Nonetheless, as highlighted by Curran et al. [78], it is essential to take into consideration the simultaneous improvement in insulin sensitivity when assessing peripheral blood insulin following an exercise intervention. Indeed, a smaller amount of insulin may be needed to achieve a comparable glucose lowering effect, which in turn may lead to an underestimation of the improvement in β-cell function. In this context, Michishita and colleagues [82] have shown that a 12-week intervention of ∼180 min per week of aerobic exercise can improve some metrics of β-cell function (e.g., insulinogenic index) in individuals with impaired glucose tolerance and T2D. Similar results were also obtained by Backx et al. [83], where a 12-week aerobic exercise intervention (60 min × 5 per week including moderate to vigorous intensity; 60–90 % HR reserve) improved β-cell responsiveness calculated with a mathematical model using c-peptide and glucose level in newly diagnosed T2D. Altogether, rodent and human studies show that exercise has the potential to improve β-cell mass and function, however there are fewer studies in humans living with T2D that assess β-cell when compared to insulin sensitivity or overall glucose control.

Exercise and adiposity

Finally, considering the close physiological relationship between the development of T2D and obesity, it is of interest to assess the impact of exercise on the reduction of fat mass. Several meta-analyses have shown that various exercise modalities (i.e., HIIT, MICT, resistance training, and combined exercise) can reduce fat mass in individuals livings with T2D [13, 84], [85], [86], [87], [88], [89]. Interestingly, a recently published meta-analysis including 21 studies (1,034 individuals living with T2D), showed that the reduction in body fat mass following an exercise intervention was associated with a decrease in A1c [90]. Specifically, for every kilogram of fat mass, a concomitant decrease of 0.2 % in A1c is expected, reinforcing weight/fat loss as an outcome of interest in the management of T2D. Regarding the mechanisms explaining weight loss following exercise interventions, it is likely overly simplistic to solely attribute it to an increase in energy expenditure associated with exercise. On the other hand, the interaction between energy expenditure and food intake is modulated by different physiological, psychological, and behavioral mechanisms [91, 92]. However, it is evident that exercise has the potential to reduce adipose tissue and this effect is likely associated with improvement in several cardiometabolic markers beyond glucose control (e.g., inflammation, lipid profile, etc. [93]).

As outlined in these previous sections, exercise can improve glucose control via multiple inter-related mechanisms including improvements in insulin sensitivity, glucose tolerance, β-cell function, and reduced adiposity. Figure 2 offers a visual representation of the interplay between the mechanisms and consequences of IR, β-cell dysfunction and excess adipose tissue along with the potential mitigating effects of exercise on these pathophysiological features of T2D. In an era of precision medicine and with the advancement in knowledge in the field of exercise physiology, there are several parameters that healthcare providers and exercise specialists could manipulate to optimize the health benefits provided by exercise.

Figure 2: Key mechanisms in type 2 diabetes pathophysiology and the role of exercise. This illustration provides a concise overview of various mechanisms, with a focus on β-cell dysfunction, insulin resistance, and adipose tissue. While we recognize the significance of other factors in the development of T2D [18], we selected these particular aspects based on the current literature availability. *Despite originating from adipose tissue, the negative impact of DAG and ceramides is primarily observed when they accumulate in tissues such as skeletal muscle and liver. FFA, free fatty acids; DAG, diacylglycerol; GLUT4, glucose transporter protein type-4; IRS-1, insulin receptor substrate 1; PI3K, phosphoinositide 3-kinases; TNF-α, tumor necrosis factor-alpha; IL-6, interleukin 6. Figure created with BioRender.
Figure 2:

Key mechanisms in type 2 diabetes pathophysiology and the role of exercise. This illustration provides a concise overview of various mechanisms, with a focus on β-cell dysfunction, insulin resistance, and adipose tissue. While we recognize the significance of other factors in the development of T2D [18], we selected these particular aspects based on the current literature availability. *Despite originating from adipose tissue, the negative impact of DAG and ceramides is primarily observed when they accumulate in tissues such as skeletal muscle and liver. FFA, free fatty acids; DAG, diacylglycerol; GLUT4, glucose transporter protein type-4; IRS-1, insulin receptor substrate 1; PI3K, phosphoinositide 3-kinases; TNF-α, tumor necrosis factor-alpha; IL-6, interleukin 6. Figure created with BioRender.

Impact of exercise parameters on glycemic control

As previously mentioned, the current exercise guidelines for individuals living with T2D is to exercise for at least 150 min at moderate to vigorous intensity and to perform two resistance training sessions per week [16, 17]. These guidelines are based on high-quality randomized controlled trial evidence and are similar to those for the general population with the added context that individuals living with diabetes should “take no more than 2 days off between exercise bouts”, which emphasizes the insulin-sensitizing properties of each bout of acute exercise. However, these broad guidelines serve as a general tool, but within these recommendations, there remains scope for several exercise-related parameters to be modulated. The American College of Sports Medicine has elaborated a general guide for practitioners for individualized exercise prescription incorporating the following aspects: Frequency, Intensity, Time, Type, Volume, Pattern, and Progression [94]. It is important to bear in mind when interpreting the results of some studies that there is an interplay between different exercise parameters, making the isolation of specific factors difficult. For example, increasing exercise frequency could consequently increase the total exercise volume performed if the exercise duration and intensity are not modulated. Considering the available literature, our focus will be on the effect of frequency, volume, type as well as intensity of exercise on glycemic control in individuals living with T2D.

Frequency

Knowing that exercise acutely increases insulin sensitivity [8, 9], exercise frequency (i.e., number of sessions per week) has been proposed to be an important mediator in glycemic control. This was confirmed in Umpierre et colleagues’ meta-analysis where the authors showed that exercise frequency was correlated with the improvement in A1c (r=−0.64 [95]). However, it is difficult to isolate the effect of exercise frequency and total volume performed as the latter is modulated by the duration, intensity as well as the frequency of exercise. Therefore, the result observed by Umpierre et al. could be related to the total volume of exercise performed rather than the frequency per se. However, Van Dijk and colleagues [96] have shown that either 30 min performed daily, or 60 min performed every other day of cycling at 50 % maximal workload capacity, reduces the prevalence of hyperglycemia in a similar fashion in older individuals with T2D. Therefore, it could be speculated that as long as exercise is performed every other day (in line with the guidelines caveat noted above), individuals living with T2D should benefit from the glucose lowering effect of exercise of different frequencies if the total volume is similar.

Volume

Epidemiological studies and meta-analyses have shown that increased overall physical activity levels could play an important role in improving glycemic control (i.e., A1c [2, 97]) while even small amounts of physical activity and reducing sedentary behaviour can be of benefit [98, 99]. A recently published meta-analysis has shown a J-shape non-linear dose-response between physical activity level and A1c with as little as 150 MET min/week shown to help improve glucose control (i.e., A1c) in individuals with uncontrolled diabetes [97]. This analyses also demonstrated that higher exercise volume could result in greater improvement in A1c with the optimal dose being around 1,100 MET min/week in most individuals with T2D. Similarly, Jayedi and colleagues [99] have shown that as little as 30 min of moderate to vigorous aerobic training per week could improve glycemic control (i.e., reduction of 0.22 % A1c) and that higher volume generally results in greater improvement. Therefore, it seems that performing a total weekly exercise volume that is below the current physical activity guidelines could provide benefits on glycemic control, while a higher volume can generate even greater improvements. It is to be noted that this dose-response relationship between total exercise volume and glycemic control is not unanimously accepted in the scientific community with some recent evidence showing no association between the amount of exercise and decrease in A1c [100].

Type

The most commonly used exercise types in the clinical setting as well as in the scientific literature are AT and RT or a combination of both. Larger scale randomized controlled trials have shown that both aerobic (45 min at 75 % HR max) and resistance training (2–3 sets of seven exercise at ∼ 80 % 1RM) could improve A1c over a 22-week intervention, while the combination of both appears to generate greater improvement [101]. Similar results were observed in the HART-D study, where combined exercise for 9 months showed a significant improvement in A1c (−0.34 %) while aerobic and resistance training alone did not (−0.24 and −0.16 % respectively [102]). These observations were confirmed in more recent network meta-analyses where combined supervised exercise was more potent in improving glycemic control (i.e., A1c), compared to supervised aerobic and supervised resistance training alone [103, 104]. Unsurprisingly, Pan and colleagues have shown in their meta-analysis that unsupervised aerobic and unsupervised resistance training were less efficacious in decreasing A1c compared to when the exercise sessions were supervised [104]. Therefore, based on the overall literature, both supervised aerobic and resistance can be effective in improving glycemic control in individuals with T2D, while combining both seems to be the best approach.

Intensity

In one of the first meta-analyses examining the impact of exercise in individuals with T2D, it was proposed that the intensity of exercise, rather than volume, better predicted improvements in A1c levels following an intervention [105]. Building on these findings, the popularity of more vigorous exercise modalities, such as high-intensity interval training (HIIT), has increased with several studies comparing the efficacy of HIIT to the more traditionally prescribed moderate-intensity continuous training (MICT) for improving various aspects of glucoregulation and T2D pathophysiology. To date, several meta-analyses have compared HIIT and MICT on glycemic control (i.e., A1c) in individuals with T2D [13, 85, 106], [107], [108], [109]. Despite the large number of publications having compared these two training modalities, the results are mixed within different studies and meta-analyses, which make it difficult to discern whether HIIT or MICT is likely to result in greater improvement in glycemic control. Three meta-analyses report that there is no significant difference between HIIT and MICT regarding the improvement in A1c [85, 106, 107], while Liu and colleagues support the idea that HIIT may be superior to MICT (−0.37 % [−0.55 to −0.19] p<0.0001 [13]). Liubaoerjijin et al. [108] also point out that increasing intensity could lead to greater improvement in glycemic control, confirming the results of a meta-regression that investigated the effect of exercise on glycemic control [105]. This discrepancy between meta-analyses results may stem from heterogeneity within the included studies, such as the HIIT modalities varying in volume, duration, intensity, and frequency, along with differences in the characteristics of the studied populations or the management of confounding variables including diet, non-exercise-related energy expenditure, or medication. Considered as a whole and based on recent data [106], it seems most appropriate to conclude that HIIT generates similar improvement in glycemic control compared to MICT in a more time-efficient manner. This finding was also observed acutely, with a meta-analysis indicating no discernible distinction between MICT and HIIT modalities in 24 h CGM derived glucose control in individuals living with T2D [10]. Therefore, both HIIT and MICT are most likely to improve glycemic control following an acute bout of exercise (e.g., measured via CGM) or following an intervention (i.e., lowering of A1c), but the total volume performed might be an important contributor of this response [95]. As for resistance training, the intensity (e.g., percentage of 1 repetition maximum; 1RM) is also a parameter that needs to be considered. A recently published meta-analysis has shown that both medium-low intensity as well as high-intensity resistance training could improve A1c in individuals living with T2D [110]. However, despite not being significant, the improvement in A1c following higher intensity resistance training tended to be clinically superior compared to medium-low intensity (−0.49 vs. −0.33 % respectively).

Overall, combining exercises (aerobic and resistance training) while progressively increasing volume and performing exercise regularly (at least every other day) appear to have the most evidence for eliciting the largest improvement in glycemic control in individuals living with T2D. Aiming to perform some training sessions at a higher intensity, for example by incorporating HIIT, may have some additional benefit and/or elicit similar benefits in less time. However, it should be emphasized that these conclusions are focused on the impact of exercise on glycemic control (e.g., A1c), which is only one variable of importance to T2D management. Although glycemic control is typically used to guide clinical treatment of T2D it would be short-sighted to make it the only priority when programming an exercise intervention. The exercise program that optimizes glucose control may not be the same as the exercise program to elicit the largest increase in cardiorespiratory fitness, maximal strength, functional mobility, or quality of life, which healthcare providers, exercise specialists, and individuals living with T2D may deem more important. Accordingly, the optimal exercise prescription should also consider the personal goals and preferences of each person. For example, for individuals presenting clinical manifestations of sarcopenia (e.g., low muscle mass and strength), resistance training might be the most highly recommended option as it could improve glycemic control while simultaneously prioritizing gains in muscle mass and strength [111].

Timing of exercise

With the growing interest in chronobiology, research exploring how the timing of exercise influences physiological and clinical outcomes has become a hot topic. In the context of T2D management, studies on the timing of exercise have tended to focus on physical activity performed in the morning vs. in the evening as well as before (pre-prandial) or after (post-prandial) meals.

Morning vs. afternoon exercise

Teo and colleagues [112] investigated the effect of a 12-week multimodal training intervention (i.e., 30 min walking at 60–70 % VO2 peak and at three sets of four resistance training exercise at ∼55 % 1RM) performed either in the morning or the afternoon in older adults with and without T2D. A main effect of time was observed for all glycemic outcomes (e.g., A1c) independently of the allocations. However, when analyzing individuals with T2D only, a greater effect size was observed for A1c and fasting glucose in the morning group compared to the afternoon group [112]. This finding was confirmed in our previous meta-analysis, which revealed that performing exercise during the morning, as opposed to the afternoon, had the potential to decrease 24 h glucose levels in individuals with T2D (−0.6 vs. −0.1 mmol/L [113]). In contrast, Savikj and colleagues have shown that afternoon HIIT (i.e., 6 × 1 min at ≥220 W) may reduce 24 h continuous glucose monitoring (CGM) more than morning HIIT in 11 older males with T2D [114]. This discrepancy could be explained by a multitude of factors, such as the smaller sample size, inconsistencies in dietary control, as well as the free-living nature of the study. Another study comparing different timing of exercise has shown that a 50 min walk at 5 km/h performed in the morning, in the afternoon, or the evening does not differently modulate 24 h CGM responses under controlled dietary conditions in older adults living with T2D [113]. Interestingly, fasting glucose was lower in the morning following the morning exercise condition compared to when the participant performed the afternoon exercise condition (−0.4 mmol/L [113]). A recent study with a larger sample size (n=139 individuals living with metabolic syndrome) demonstrated that a 16-week intervention of aerobic training (i.e., 4 × 4 min intervals at 90 % of HR max) was more effective in improving plasma fasting insulin and insulin resistance when exercise was performed in the morning compared to the afternoon [115]. Contrarily, sub-analyses from a 12-week intervention study in individuals at risk or with T2D reported that exercising (i.e., 2 × 30 min at 70 % W max per week and 1 × resistance training per week) in the afternoon may elicit greater improvement in different cardiometabolic outcomes [116]. Clearly, the data are mixed on whether morning vs. afternoon exercise is superior for improving glucose control and cardiometabolic health markers in T2D. Overall, considering the interaction between exercise, food intake, and subsequent compensatory movement behaviour [92], further well-controlled lab-based studies are required to properly elucidate how the timing of exercise may influence glycemic control. It is most likely that different phenotypes of T2D may respond differently to different timing of exercise such as individuals experiencing the dawn phenomenon who may benefit to a greater extent from evening exercise, as it increases insulin sensitivity and glucose tolerance throughout the night. Along those lines, considering the preference of the individual based on their chronotype may also be important [117]. The chronotype, which refers to the circadian rhythmicity of an individual (i.e., “early bird” vs. “night owl” [118], could influence the development and management of T2D. Indeed, evening-type persons have a 2.5-fold increased risk of developing T2D even when controlling for sleep quality and duration [119] and was also associated with less optimal glycemic control in individuals currently living with the condition [120]. Concomitantly, Hensone et al. demonstrates that in individuals with T2D, the evening chronotype had higher sedentary time and lower moderate to vigorous physical activity time compared to the morning chronotype [121]. Therefore, in individuals with evening chronotypes, performing exercise in the morning may induce a realignment toward a more morning-like chronotype [122], which may have a beneficial impact on glycemic control. Another interesting concept, capitalizing on the wider availability of modern CGM technology, might be to time exercise in relation to peak glucose, as demonstrated in a recent pilot trial in individuals living with T2D [123]. Overall, more research is needed to verify how much exercise timing matters in individuals living with T2D before an optimal exercise time of day might be suggested. Similar to the conclusions provided for different exercise parameters described above, it would seem most pragmatic for an individual living with T2D to perform exercise at a time of day that works with their personal goals, preferences and schedule rather than concerning themselves with what time of day might elicit (slightly) greater metabolic benefits (if any).

Fasted vs. post-meal exercise

While the results regarding the distinct benefit of a morning or afternoon exercise on glycemic control remain inconclusive, the timing of exercise in relation to dietary intake is more consistent. Previous meta-analysis including 12 studies (135 participants with T2D) have shown that post-prandial aerobic exercise could reduce glucose area under the curve and the prevalence of hyperglycemia for the next 24 h [124]. In another meta-analysis, Teo and colleagues reported that post-meal exercise tends to produce a more consistent improvement in glycemic control-related outcomes compared to pre-meal exercise [125]. The comparison of pre- and post-meal exercise on glycemic control relies mostly on indirect comparisons and using different exercise modalities and volumes [125], thereby limiting our confidence in drawing definitive conclusions. However, Pahra et al. [126] have demonstrated that compared to 45 min of brisk walking pre-meal (i.e., 4.8 km/h), 15 min of walking at the same pace after each meal (i.e., breakfast, lunch, and dinner) reduces to a greater extent fasting glucose as well as A1c after a 60-day intervention. Along those lines, DiPietro and colleagues [127] elegantly demonstrated that 15 min of post-meal exercise (i.e., 3 METS) performed three times a day was more potent than 45 min of continuous walking at the same intensity to control post-prandial glycemia. Building on these results, other groups have investigated the timing of exercise in the post-prandial state. Huang et al. [128] have investigated the effect of exercising (HIIT; 6 × 1 min at 85 % W max) 30, 60 or 90 min post-breakfast compared to metformin alone on glucose control-related outcomes [128]. Compared to metformin alone, exercising at 30, 60 or 90 min post breakfast improves glucose levels, with seemingly greater improvement in the 30 min post-meal compared to 90 min post-meal conditions (i.e., 90 min; p=0.04 [128]). These results are in line with [129] where linear regression showed that exercise performed less than 2 h after a meal generated a greater reduction in capillary blood glucose concentration compared to more than 2 h [129]. In one of the most convincing and pragmatic RCTs on post-meal exercise in individuals living with T2D (n=41), Reynolds and colleagues demonstrated that advice to walk 10 min after meals led to significantly greater improvements in CGM-derived glucose metrics (postprandial incremental area under the curve) across a 14-day intervention period when compared to control (no exercise) or general advice to walk for 30 min per day [130]. However, it is worth noting that Terada and colleagues have observed that performing HIIT (i.e., 15 × 1 min at 100 % VO2 peak with 3 min of rest at 40 % VO2 peak) and MICT (i.e., 55 % of VO2 peak) in the fasted state improve to a greater extent postprandial glucose excursions compared to post-breakfast exercise [131].

From a physiological standpoint, exercise induces non-insulin dependent translocation of GLUT4 to the sarcolemma and increased intramuscular glucose utilization, which combined with the higher plasma concentrations of glucose and insulin following a meal, creates a favorable environment to increase glucose clearance and limit post-prandial hyperglycemia. Considering that post-prandial hyperglycemia has been linked to an increased risk of cardiovascular diseases [132], targeting postprandial glucose spikes through strategically-timed exercise may have clinical significance. Based on the previously discussed evidence, exercising in the post-prandial state, approximately 30 min after meal ingestion, may be a valuable and practical option to reduce post-prandial glucose excursions. Such a strategy may be particularly impactful following carbohydrate-rich meals [130], however glucose-lowering effects of post-meal walking has also been shown in the context of low-carbohydrate diets [133]. In this context, integrating other forms of exercise or physical activity strategically in the postprandial period (e.g., walking breaks, resistance-band exercises, exercise “snacks”) represent avenues for future study in the field [134], [135], [136]. Although the data are promising, most studies are acute (single day) or short-term (weeks) in this area. Further long-term studies are needed to assess the glucose-lowering and clinical impact of emergent exercise strategies performed in the postprandial period in individuals living with T2D.

Weight loss: targeting visceral adipose tissue

As previously discussed, obesity (particularly visceral adiposity) plays a pivotal role in the pathophysiology of T2D. In this context, exercise interventions that contribute to a significant weight loss, more precisely, a reduction in total or visceral fat mass, maybe a crucial aspect to consider in the management of T2D. Many studies have investigated the effect of different exercise modalities on the improvement of body composition in individuals living with T2D [90, 104, 137]. The network meta-analysis from [103] has shown that both supervised aerobic and resistance exercise training were associated with a decrease in BMI and waist circumference compared to no exercise in individuals with T2D [103]. In support, O’Donoghue et al. [138] have shown that the exercise intervention with the most likelihood of decreasing body fat percentage in individuals living with obesity (but not T2D) was a combination of high-intensity aerobic training and high-load resistance training.

A popular area of recent research has been comparing HIIT with MICT on body composition outcomes. Several studies report that both exercise modalities generate similar reductions in BMI, waist-to-hip ratio and circumference, and total fat mass [85, 139, 140], while other evidence suggests that HIIT may yield superior results in improvement body composition related outcomes [13, 141]. Discrepancies in findings can likely be explained by several confounding factors such as the duration of the intervention, the total volume of exercise performed, and the inclusion of different HIIT protocols. Of potential interest, Wewege et al. [142] reported that, in individuals living with obesity, both HIIT and MICT generate greater weight loss when exercise is performed on a treadmill compared to a cycle ergometer [142]. Although more work is required and the mechanisms are unclear, it is possible that higher muscle recruitment while running compared to cycling results in greater energy expenditure [143].

In addition to total body fat or surrogate measures (e.g., waist circumference), there is also interest in the impact of different exercise training strategies on body fat distribution and visceral adipose tissue. Although diet-induced weight loss is a more potent intervention compared to physical activity alone for fat/weight loss, a reduction in visceral adipose tissue, even in the absence of weight loss [144], following exercise training is a consistent finding. The meta-analysis from Sabag et al. [88] investigated the effect of exercise on ectopic fat in 24 studies (1,383 individuals with T2D [88]). A significant reduction in VAT was observed when exercise was compared to a control group [88]. Interestingly, this decrease in VAT was only observed in aerobic exercise interventions and not in resistance training interventions. Along those lines, a recent meta-analysis reported that exercise could reduce VAT, but this effect seems to be driven by the intensity of the exercise [145]. The greater reduction in VAT with higher intensity exercise interventions (e.g., HIIT vs. MICT) has also been observed in randomized trials in individuals with [146, 147] and without [148] T2D.

Altogether, the prescription of exercise with the goal of improving weight/fat loss-related outcomes can be achieved via different exercise modalities, including both aerobic or resistance training. However, considering the greater energy expenditure generated following aerobic exercise [149], one should consider performing aerobic training for at least 150 min per week to achieve the current physical activity guidelines and preferably, combining both aerobic and resistance training for maximizing benefits. Higher-intensity exercise, often implemented as HIIT, seems to promote a greater reduction in VAT, which could help target this key pathophysiological feature of T2D.

Practical application

Bridging the gap between physiological and clinical research in real-world settings and applying this knowledge to help guide an exercise prescription for persons living with T2D remains a difficult task. Figure 3 provides general guidelines on how one might go about optimizing and personalizing an exercise prescription in individuals living with T2D. While these guidelines are based on our experience and interpretation of the available literature – and might be optimal to improve cardiometabolic-related outcomes, specifically glycemic control – we stress that a patient-centered approach should be used in practice. Indeed, using a bio-psycho-social perspective putting the patient first and acknowledging their preferences, goals, values, and circumstances rather than a medical, disease-centred approach is in line with most clinical practice guidelines for lifestyle therapy in chronic conditions. Previous meta-analyses report that compared to standard care, which often has a disease-centered approach, patient-centered care improves glycemic control to a greater extent [150]. Therefore, the first step for exercise specialists and clinicians would be to adopt a patient-centered approach, while finding ways to increase physical activity levels based on preferences, goals, and personal circumstances (Figure 3; Phase 1).

Figure 3: Optimizing exercise prescription to improve glycemic control in individuals with T2D. This figure provides a proposed framework on how one might go about optimizing glycemic control with exercise and physical activity in individuals with T2D. We recommend using these guidelines from left to right as a starting point but following a patient-centered approach based on individual needs and contextual factors may require approaching priorities in a different manner; MVPA, moderate to vigorous physical activity; SB, sedentary behaviour; RT, resistance training; AT, aerobic training; VAT, visceral adipose tissue; HIIT, high-intensity intervals training; IS, insulin sensitivity; *, evidence regarding the timing of exercise (i.e., morning vs. afternoon) is still controversial and further studies are needed to properly evaluate this matter. Figure created with BioRender.
Figure 3:

Optimizing exercise prescription to improve glycemic control in individuals with T2D. This figure provides a proposed framework on how one might go about optimizing glycemic control with exercise and physical activity in individuals with T2D. We recommend using these guidelines from left to right as a starting point but following a patient-centered approach based on individual needs and contextual factors may require approaching priorities in a different manner; MVPA, moderate to vigorous physical activity; SB, sedentary behaviour; RT, resistance training; AT, aerobic training; VAT, visceral adipose tissue; HIIT, high-intensity intervals training; IS, insulin sensitivity; *, evidence regarding the timing of exercise (i.e., morning vs. afternoon) is still controversial and further studies are needed to properly evaluate this matter. Figure created with BioRender.

Once the patient has adopted a more active lifestyle, modulating different exercise parameters could then help maximize the exercise-related health benefits. Considering that both resistance training and aerobic training could generate similar benefits on glycemic control [103, 104], progressively increasing the total volume towards the current physical activity guidelines may be the next valuable option. If applicable and achievable, increasing the total volume of exercise may then lead to a more substantial improvement in glycemic control [97, 99]. Based on the previously discussed evidence, increasing exercise intensity (e.g., by incorporating HIIT) may not provide additional benefits on glycemic control, but may provide a more time-efficient way to exercise. However, exercise intensity plays a crucial role in the improvement of cardiorespiratory fitness [106] and there is some evidence that higher-intensity aerobic exercise may lead to greater reductions in VAT (see below). Perhaps most importantly, ensuring that exercise is performed regularly (at least every other day) will maximize the glucose-lowering and insulin-sensitizing effects of a training program (Figure 3; Phase 2).

Another emerging aspect to consider when optimizing or personalizing exercise prescription for T2D could be the timing of exercise. Indeed, based on the previously discussed studies, exercising the in morning might generate more consistent improvement in glucose control in individuals living with T2D. These results are not unanimous and future higher-quality studies are needed in this area. Nonetheless, exercising in the postprandial state seems to be a practical and evidence-based strategy to mitigate post-meal glucose spikes and reduce overall hyperglycemia. Therefore, healthcare providers can select the timing of exercise based on patient’s preferences while considering the recommendation to engage in post-prandial exercise (e.g., short post-meal walks of ∼15 min), particularly for individuals experiencing high glucose excursions after eating (Figure 3; Phase 3).

Finally, some individuals living with T2D may benefit from a reduction in fat mass, especially VAT. Evidence has shown that several exercise modalities can generate improvements in body composition, while aerobic exercise may generate a greater energy expenditure which could, in the long run, favor a greater weight loss. Exercise intensity also seems to have an important impact on VAT. Therefore, exercise modalities that elicit greater energy expenditure, along with HIIT, may have additional benefits for individuals with higher abdominal obesity, a proxy for excessive VAT accumulation (Figure 3; Phase 4).

This general framework could help the improvement of glycemic control in individuals living with T2D but can be personalized based on various contextual factors. Indeed, while increasing exercise volume to reach the current physical activity guideline might be considered for many healthcare providers as a priority, some people experiencing large post-prandial glucose spikes might benefit to a greater extent from strategically dispersing their exercise after each meal instead of increasing the overall volume. It is also important to consider the inherent variability in exercise responses and how this may affect health outcomes if the ultimate goal is to better optimize personalized exercise prescriptions [151]. Indeed, the present review mostly discussed the extrinsic factors that could influence the exercise response (e.g., exercise type/intensity, timing, etc.) while a plethora of intrinsic factors such as age, biological sex, race and ethnicity, hormonal status and genetics are clearly important for understanding individualized responses to exercise. For example, biological sex influences several clinical features in T2D [152] and previous meta-analysis has shown that females consistently engaged in less MVPA compared to males across lifespan [153]. However, the exercise response following an intervention (e.g., improving glycemia, insulin profiles and cardiovascular risk factors) does not seem to be influenced by biological sex [154]. Nevertheless, given the historical predominance of males as participants in exercise physiology studies, it is essential to conduct further well-designed studies to assess sex-based differences in responses to exercise. In this regard, we encourage readers to consult the recently published article by Noone and colleagues [151] which thoroughly discusses the variation in exercise response based on extrinsic and intrinsic factors.

Behavioral factors and emergent approaches

The objective of this review was to facilitate the translation of research findings into practical insights for clinicians and healthcare providers, specifically regarding the physiological impact of different exercise parameters on glucose control in individuals with T2D. Nevertheless, it is essential to understand how behavioral and psychological components may affect adherence to exercise, which in turn may improve the overall management of this condition. Several barriers and facilitators, some of which are sex and gender dependent, could influence exercise participation in individuals living with T2D [155, 156]. These include perceived physiological barriers (e.g., higher perceived RPE), psychological (e.g., self-efficacy, motivation, mental health), social and cultural (e.g., walkability, socioeconomic status, built environment, colonialism) as well as environmental (e.g., climate change [156]). Therefore, it is crucial to address both barriers and facilitators when intervening with this population and ensuring that the exercise intervention is tailored according to the patient’s characteristics, goals, and needs. Our goal is that the physiological knowledge presented in the present manuscript can be used by clinicians within a patient-centric approach to maximize exercise-related benefits for individuals living with T2D.

Healthcare providers and kinesiologists could also consider other emergent approaches when prescribing exercise. For example, blood flow restriction may be a valuable alternative to regular resistance training in frail individuals presenting clinical manifestation of sarcopenia [157], particularly considering its common co-occurrence with T2D [111]. Along those lines, incorporating different exercise modalities that could impact enjoyment or engagement such as exergaming [158] could be valuable strategy to reduce hyperglycemia and glycemic execution after a meal [159] and improve exercise adherence [160], but further studies are needed in individuals living with T2D [161]. Finally, implementing technology-assisted exercise modalities such as mobile app-assisted self-care might also be a valuable approach to improve glucose control in individuals living with T2D [162].

Limitation, challenges and future directions

The general framework (Figure 3) suggested in this article must be interpreted and used in light of its limitations. This narrative review offers a broad overview of the currently existing knowledge while incorporating evidence from systematic reviews and meta-analyses but itself is not a systematic review and is therefore susceptible to bias. Furthermore, our primarily focus was on exercise interventions that could have a beneficial effect on glucose control, which may not capture the myriad of other health benefits that physical activity can provide. Nonetheless, this review proposes a framework on how to integrate physiological and clinical knowledge into real-world settings and how exercise specialists, clinicians, and knowledge users might go about optimizing exercise prescriptions in individuals living with T2D.

One of the foremost challenges in the field of exercise physiology is understanding the substantial heterogeneity observed in exercise response. The response to exercise interventions may be influenced by various factors, such as the parameters of the intervention (e.g., duration, intensity, volume), characteristics of the population (e.g., age, sex, ethnicity, time since diagnosis, socioeconomic status), but also external factors including medication, dietary habits, motivation, sleep quality, stressors, mental health, season differences, among others. While we acknowledge the impossibility of controlling all these variables, precision and comprehensive reporting of these factors, particularly the intervention itself, are crucial to help the research community understand this variability. Consequently, we strongly recommend that researchers in the field of exercise physiology adhere to best practices in reporting and conduct of intervention trials [e.g., CONSORT – [163]; TIDIER – [164]] with specific emphasis on exercise-specific guidelines, such as CERT (Consensus on Exercise Reporting Template [165]) to help mitigate bias and improve reproducibility among studies. With respect to explicitly optimizing exercise prescription for T2D, further larger scale RCTs investigating the effect of different exercise modalities, doses, intensities, and timing on various glucose-homeostasis-related outcomes (e.g., A1c, fasting glucose, oral glucose tolerance test, insulin sensitivity, etc.) in individuals with T2D are still needed before definitive conclusions can be drawn. Furthermore, it will be of interest to explore how exercise might interact with diabetes (and other) medications that are commonly prescribed in individuals living with T2D.

Conclusions

T2D is a complex condition with heterogeneous pathophysiological features resulting in metabolic disruption and chronic hyperglycemia. Exercise plays a fundamental role in blood glucose control, and tailoring specific exercise parameters may help enhance the benefits for individuals living with T2D. In light of the recent literature, healthcare professionals can adjust several factors, including exercise types, overall volume, frequency, intensity, and timing, based on the preferences and needs of their clients to maximize glucose control. The ability to customize exercise regimens has the potential to improve T2D management, consequently reducing the associated risk of comorbidities and improving the quality of life for individuals living with this condition.

Corresponding author: Jonathan P. Little, PhD, School of Health and Exercise Sciences, The University of British Columbia, Okanagan Campus, 1147 Research Rd, V1V 1V7 Kelowna, BC, Canada, Phone: 250.807.9876, E-mail:

Acknowledgments

Figures were made with Biorender.com.

  1. Research ethics: Not applicable.

  2. Informed consent: Not applicable.

  3. Author contributions: The authors has accepted responsibility for the entire content of this manuscript and approved its submission.

  4. Competing interests: The authors state no conflict of interest.

  5. Research funding: AMC was supported by the Canadian Institutes of Health Research (CIHR) – Frederick Banting Charles Best doctoral scholarship. JPL is supported by a Killam Accelerator Research Fellowship.

  6. Data availability: Not applicable.

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Received: 2024-02-03
Accepted: 2024-03-06
Published Online: 2024-03-25

© 2024 the author(s), published by De Gruyter on behalf of Shangai Jiao Tong University and Guangzhou Sport University

This work is licensed under the Creative Commons Attribution 4.0 International License.

Articles in the same Issue

  1. Frontmatter
  2. Editorial
  3. Translational exercise biomedicine – where do we go?
  4. Perspective
  5. Toward an integrative approach to translational exercise biomedicine
  6. Review Article
  7. Metabolomic and proteomic applications to exercise biomedicine
  8. Research Articles
  9. Effects of 12 weeks of power-oriented resistance training plus high-intensity interval training on metabolic syndrome factors in older people with COPD
  10. The effect of breaking sitting time with physical activity breaks on cognitive performance in young people with cerebral palsy: an exposure response cross-over feasibility design
  11. Menopausal transition alters female skeletal muscle transcriptome
  12. Acute effects of transcranial direct current stimulation on cycling performance in trained male athletes
  13. Review Article
  14. Towards optimizing exercise prescription for type 2 diabetes: modulating exercise parameters to strategically improve glucose control
  15. Research Article
  16. Therapeutic resistance training: proposal for an algorithm-based approach
https://doi.org/10.1515/teb-2024-2007
Keywords for this article
physical activity; HIIT; MICT; timing; intensity; frequency
Creative Commons
BY 4.0

Articles in the same Issue

  1. Frontmatter
  2. Editorial
  3. Translational exercise biomedicine – where do we go?
  4. Perspective
  5. Toward an integrative approach to translational exercise biomedicine
  6. Review Article
  7. Metabolomic and proteomic applications to exercise biomedicine
  8. Research Articles
  9. Effects of 12 weeks of power-oriented resistance training plus high-intensity interval training on metabolic syndrome factors in older people with COPD
  10. The effect of breaking sitting time with physical activity breaks on cognitive performance in young people with cerebral palsy: an exposure response cross-over feasibility design
  11. Menopausal transition alters female skeletal muscle transcriptome
  12. Acute effects of transcranial direct current stimulation on cycling performance in trained male athletes
  13. Review Article
  14. Towards optimizing exercise prescription for type 2 diabetes: modulating exercise parameters to strategically improve glucose control
  15. Research Article
  16. Therapeutic resistance training: proposal for an algorithm-based approach
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