Toward Individualized High-Intensity Interval Training in Type 1 Diabetes: A Framework for Safe Implementation †
Abstract
1. Introduction
2. Materials and Methods
3. Results
4. Discussion
5. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Acknowledgments
Conflicts of Interest
References
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| Population Characteristics | HIIT Protocol Parameters | Reported Outcomes and Effects | Control and Safety Criteria |
|---|---|---|---|
| Number of Participants. Age, Sex. Duration of type 1 diabetes diagnosis. Type of insulin therapy (multiple daily injections vs. insulin pump). | Warm-up: intensity and duration. Protocol format: interval and recovery duration. Exercise intensity (expressed as %VO2max, %HRmax, or relative workload). Weekly frequency and total duration of the intervention. | Physical fitness responses (VO2max, aerobic power, strength). Metabolic, physiological and neurological effects. Adverse events. Other reported outcomes. | Pre- and post-exercise blood glucose monitoring. Hypoglycemia prevention strategies. Training supervision. |
| Study | Total Time (Weeks) | Weekly Freq. | Session Time (min) | Warm-Up (min/Intensity) | HIIT Bouts | Effort Phase (sec/Intensity) | Recovery Phase (sec/Intensity) | Cooldown (min) |
|---|---|---|---|---|---|---|---|---|
| Harmer et al. (2008) [8] | 7 | 3 | 25–35 | NR | 4-6-8-10 | 30 All-out | 240/ passive | NR |
| Tonoli et al. (2015) [9] | Acute (1 day) | 1 | 22 | 2/100 W | 10 | 60–90% VO2max | 60/50 W | NR |
| Rooijackers et al. (2017) [10] | Acute (1 day) | 1 | 15 | 4/50 W | 3 | 30-All-out (Borg > 15) | 240/50 W | NR |
| Wiegers et al. (2017) [11] | Acute (1 day) | 1 | 15 | 4/50 W | 3 | 30 All-out | 240/50 W | NR |
| Farinha et al. (2017) [12] | 10 | 3 | 25 | 3/50 W | 10 | 60–90% HRmax | 60/50 W | 2/ 50 W |
| Riddell et al. (2019) [5] | Acute (4 sessions) | 1 | 25 | 0.5/50% VO2peak | 10 | 100–130% PPO | 30/50% VO2peak | 0.5 |
| Scott et al. (2019) [1] | 6 | 3 | 15–23 | 3/low-intensity | 6-8-10 * | 60–100% VO2peak | 60/50 W | NR |
| Boff et al. (2019) [13] | 8 | 3 | 40 | 5/60% HRmax | 6 | 60–85% HRmax | 240/50% HRmax | 5 |
| Farinha et al. (2019) [14] | 10 | 3 | 25 | 3/50 W | 10 | 60–≥90% HRmax | 60/50 W | NR |
| Scott et al. (2019) [15] | 12 | 3 | 12–20 | 2/Jogging | 6-8-10 * | 60–85% HRmax | 60/ Passive | NR |
| Lee et al. (2020) [16] | 12 | 3 | 33 | 5/60% HRpeak | 4 | 240–85–95% HRpeak | 180/50–70% HRpeak | 3 |
| Lee et al. (2020) [7] | Acute (4 sessions) | Variable | 33 | 5/60% HRpeak | 4 | 240– High intensity | 180 | 3 |
| Minnebeck et al. (2020) [17] | 4 | 2 | 16–20 | 5/20 W | 4 to 6 | 60-All-out (≥95% HRmax) | 60/ Passive | 3 |
| Alarcón-Gómez et al. (2021) [2] | 6 | 3 | 28–40 | 5/50 W | 12-16-20 * | 30–85% PPO | 60/ 40% PPO | 5/ 50 W |
| Alarcón-Gómez et al. (2021) [18] | 6 | 3 | 28–40 | 5/50 W | 12-16-20 * | 30–85% PPO | 60/ 40% PPO | 5/ 50 W |
| Mascarenhas et al. (2022) [19] | Acute (1 day) | 1 | 30 | NR | 5 | 10– Max intensity | 300/60% VO2max | NR |
| Farrell et al. (2024) [20] | 4 | 3 | 20 | 5/gentle cycling | 4 | 30–≥90% HRpeak | 120/ Active | 5 |
| Scoubeau et al. (2024) [21] | 12 | 3 | 35 | 3 | 8 | 120–90% HRmax | 120/ Active (VT1) | NR |
| Study | n | Age (Years) | Outcomes | Other Effects | ||
|---|---|---|---|---|---|---|
| Physical Fitness | Metabolics | Physiological/Neurological | ||||
| Harmer et al. (2008) [8] | 8 | 21–29 | NR | ↑ Exercise-induced plasma glucose (acute exercise) ↔ HbA1c ↔ Resting plasma glucose | ↓ Exercise-induced hyperglycemia (post-exercise), ↓ Exercise-induced lactate accumulation (post-exercise) | ↓ VCO2peak ↓ VEpeak (post-training), ↔ Acid–base status within physiological range No hypoglycemia reported during exercise |
| Tonoli et al. (2015) [9] | 10 | 18–44 | NR | ↓ post-blood glucose levels | ↑ BDNF ↑ IGF-1 postexercise; improves executive function | Serum-free insulin, and blood glucose serum was correlated with serum BDNF and negatively correlated to serum IGF-1 |
| Rooijackers et al. (2017) [10] | 30 (10 NAH, 10 IAH, 10 healthy) | 19–37 | NR | ↑ blood glucose (normal range), ↑ Blood Lactate ↓ pH | ↓ Awareness of hypoglycemia ↑ adrenaline ↑ noradrenaline ↑ GH ↑ Cortisol (remains ↑ IAH) | HIIT mitigates cognitive impairment during hypoglycemia in NAH |
| Wiegers et al. (2017) [11] | 18 (6 IAH, 6 NAH, 6 healthy) | 19–30 | NR | ↑ Brain Lactate, most pronounced increase in IAH, ↓↓ Brain lactate in hypoglycemic phase (IAH); identical lactate decay rate (all groups) | ↓ Adrenaline response to hypoglycemia (IAH < NAH/Healthy) | ↑ cerebral lactate transport/oxidation in IAH. |
| Farinha et al. (2017) [12] | 9 | 18–40 | ↑ Strength and cardiopulmonary fitness, ↑ VO2peak, ↑ FFM | ↓ HbA1c and ↓ Fasting glucose. ↑ Antioxidants (TAC, CAT, SOD) ↓ sRAGE (↓ inflammation ↓ vascular damage) | ↑ iHSP70 protein (cell protection biomarker) | ST+HIIT ↓ insulin dose ↑ adherence to exercise |
| Riddell et al. (2019) [5] | 16 | 24–44 | NR | ↑ Plasma glucose (post-exercise hyperglycemia), ↑ Lactate, ↓ Ketone bodies, ↓ Free fatty acids, ↑ Serum insulin | ↑ HR (≈HRmax) ↑ Oxygen uptake (≈VO2peak). ↑ Catecholamines, ↑ GH, ↑ RPE (near-maximal) | Similar inter-subject glycemic, hormonal, and lactate responses No hypoglycemia risk (fasted HIIT) |
| Scott et al. (2019) [1] | 7 | 26–32 | ↑ VO2peak, ↑ Wmax | ↔ glucose during HIIT (fed state); ↑ Nocturnal hyperglycemia. | ↓ aPWV; ↔ CHO ↔ TG | HIIT prevents acute intra-session glucose drops |
| Boff et al. (2019) [13] | 9 | 19–33 | ↑ VO2peak | ↔ Glycemic control (HbA1c/Glucose) | ↑ FMD, superior to MCT | Improvement in FMD and VO2peak are positively correlated |
| Farinha et al. (2019) [14] | 9 | 18–40 | NR | ↓ blood glucose | ↓ HbA1c ↓ RoCE | - |
| Scott et al. (2019) [15] | 11 | 27–33 | ↑ VO2peak, ↑ Perceived physical fitness | ↔ Glycemic stability (during and 1 h post-exercise), ↔ BMI | No Severe hypoglycemia ↔ Nocturnal glucose levels | ↓ Short-acting insulin dose ↑ Adherence and compliance ↓ Perceived barriers (time constraints, fear of hypoglycemia) |
| Lee et al. (2020) [16] | 24 | 30–50 | ↑ Maximal treadmill exercise test time, ↑ Leg strength | ↓ Mean glucose, ↔ Body weight, ↔ Lipid profile | ↓ HbA1c, ↑ Leptin | ↔ Total daily insulin dose, ↔ Adiponectin, ↔ Hypoglycemia incidence, ↔ Glycemic safety (24 h) (with appropriate self-management) |
| Lee et al. (2020) [7] | 12 | 44 ± 10 | ↑ Strength (Leg) ↑ VO2peak and time on Bruce protocol | ↓ Mean 24h glucose, ↑ total body lean mass | ↓ HbA1c in subgroup with ≥50% adherence ↑ Leptin | ↑ Adherence and compliance severe hypoglycemic (1 event) Targeted at a high-risk population |
| Minnebeck et al. (2020) [17] | 22 (11 Overweight, 11 Normal Weight) | 26–57 | ↑ VO2peak ↑ maximal exercise capacity ↑ physical fitness | ↓ Daily basal and bolus insulin requirements post-HIIT | HbA1c: downward trend in overweight subgroup; ↓ LDL ↓ UA | ↑ HRQoL (physical role limitations) |
| Alarcón-Gómez et al. (2021) [2] | 11 | 33–43 | ↑ VO2max; ↑ FFM, 3.4%), ↓ FM (6.4%). | ↓ Fasting Glucose (7.8%). Low rate of mild hypoglycemia (1.5%). | Improves HRV ↑ HRQoL (physical and social domains) and sleep quality | No severe hypoglycemia; HIIT is safe and efficient for ↓ CV risk. ↑Adherence |
| Alarcón-Gómez et al. (2021) [18] | 11 | 33–43 | NR | Low incidence of mild hypoglycemia No severe hyperglycemias. No increase in nocturnal hyperglycemia. | ↑ HRQoL (physical and social domains), ↑ SQ | ↑ exercise enjoyment, ↑ motivation (intrinsic and identified regulation) HIIT is safe for improving well-being |
| Mascarenhas et al. (2022) [19] | 31 | 10–15 | NR | ↓ RoCE (Lower reduction in blood glucose during exercise). Better recovery (RoCR) in the 30 min post-exercise | Reduces the risk of hypoglycemia | NR |
| Farrell et al. (2024) [20] | 18 | 20–54 | NR | ↓ hypoglycemia ↑ plasma glucagon during hypoglycemia | improvements CCR ↑ response to hypoglycemia Improved glucagon and norepinephrine response | Maintained hypoglycemia symptom awareness (total/autonomic)/HIIT is safe in IAH |
| Scoubeau et al. (2024) [21] | 10 | 30–56 | ↑ VO2peak, ↑ VT1, ↑ Maximal O2pulse | ↔ HbA1c ↔ Lipid profile | NR | NR |
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García, M.S.; Víscido, M.P.; Escobar, F.E.; Gerez, G.D.; Farfán, F.D.; Cano, L.A. Toward Individualized High-Intensity Interval Training in Type 1 Diabetes: A Framework for Safe Implementation. Med. Sci. Forum 2026, 44, 2. https://doi.org/10.3390/msf2026044002
García MS, Víscido MP, Escobar FE, Gerez GD, Farfán FD, Cano LA. Toward Individualized High-Intensity Interval Training in Type 1 Diabetes: A Framework for Safe Implementation. Medical Sciences Forum. 2026; 44(1):2. https://doi.org/10.3390/msf2026044002
Chicago/Turabian StyleGarcía, María Soledad, Manuel Parajón Víscido, Francisco Esteban Escobar, Gonzalo Daniel Gerez, Fernando Daniel Farfán, and Leonardo Ariel Cano. 2026. "Toward Individualized High-Intensity Interval Training in Type 1 Diabetes: A Framework for Safe Implementation" Medical Sciences Forum 44, no. 1: 2. https://doi.org/10.3390/msf2026044002
APA StyleGarcía, M. S., Víscido, M. P., Escobar, F. E., Gerez, G. D., Farfán, F. D., & Cano, L. A. (2026). Toward Individualized High-Intensity Interval Training in Type 1 Diabetes: A Framework for Safe Implementation. Medical Sciences Forum, 44(1), 2. https://doi.org/10.3390/msf2026044002

