Table 1.
Clinical studies evaluating the effects of different patterns of PA on β-cell function and glucose homeostasis.
| Refs. | Year | Population | Intervention |
Duration
(Weeks) |
Frequency
(Sessions/Week) |
Intensity
(min/Session) |
Dietary
Intervention |
Effects on
β-Cell Function |
Additional Effects on
Glucose Homeostasis |
| Solomon [8] | 2010 | NGT obese subjects | AT | 12 | 5 | 60 | ✔️ | ↓ OGTT-derived IS (not significant when corrected for IR) |
- |
| T2DM obese subjects | AT | 12 | 5 | 60 | ✔️ | ↑ OGTT-derived IS | - | ||
| Dela [9] | 2004 | T2DM subjects | AT vs. no exercise |
12 | 5 | 30–40 | ✕ | ↑ β-cell secretory capacity in subjects with preserved β-cell function at baseline | - |
| Bloem [30] | 2008 | IGT overweight/obese subjects | AT | 1 | 7 | 60 | ✕ | ↓ AIRg ↑ DI |
↑ Insulin sensitivity |
| Croymans [31] | 2013 | Non-diabetic overweight/obese subjects |
RT | 12 | 3 | 60 | ✕ | ↑ DI | ↑ Insulin sensitivity (OGTT-derived mISI) ↓ glucose AUCOGTT ↓ insulin AUCOGTT |
| Dela [32] | 2010 | Normal weight or overweight first-degree relatives of T2DM subjects | AT (endurance) |
12 | 6 | 45 | ✕ | =glucose-stimulated IS | ↑ glucose-mediated GU |
| Control group | AT (endurance) |
12 | 6 | 45 | ✕ | =glucose-stimulated IS | ↑ insulin-mediated GU ↑ glucose-mediated GU |
||
| Hordern [33] | 2008 | T2DM overweight/obese subjects | AT + RT | 4 | 3 | 80–85 | ✕ | =HOMA-β | Baseline glucose and HbA1c were predictors of ↓ blood glucose after intervention |
| Boulè [34] | 2005 | Non-diabetic overweight/obese subjects |
AT (endurance) |
20 | 3 | 30–50 | ✕ | ↑ AIRg (in the quartile with the worst baseline GT) ↓ AIRg (in the quartile with the better baseline GT) |
- |
| Solomon [35] | 2013 | IGT and T2DM overweight/obese subjects |
AT | 12-16 | 4–5 | 60 | ✕ | ↑ 1st and 2nd-phase DI | - |
| He [36] | 2016 | Prediabetic normal weight and overweight subjects |
AT vs. RT vs. control |
93 | 3 | 50–60 | ✕ | ↓ HOMA-β (in both groups vs control) Baseline HOMA-β, HbA1c and BMI were predictors of positive β-cell response to training |
↓ glucose levels ↓ HbA1c ↓ HOMA-IR (in both groups vs control) |
| Malin [37] | 2013 | Prediabetic obese subjects | AT | 12 | 5 | 60 | ✔️ | ↑ 1st and 2nd-phase DI (related to exercise-dose) |
- |
| Bacchi [38] | 2012 | Overweight T2DM patients | AT + RT | 16 | 3 | 60 | ✔️ | No major effects | Baseline HbA1c was predictor of changes in HbA1c after intervention |
| Lee [39] | 2012 | Non-diabetic obese adolescent subjects | AT vs. RT vs. no-exercise |
12 | 3 | 60 | ✕ | =IS at hyperglycemic clamp =DI at hyperglycemic clamp |
↑ Insulin sensitivity only in RT group =GT |
| Slentz [40] | 2009 | Non-diabetic overweight/obese subjects | AT (at different amount/intensity) vs. no exercise |
32 | Variable | Variable | ✕ | ↑ DI (moderate-intensity group displayed major improvements in the DI) |
- |
| AbouAssi [41] | 2015 | Non-diabetic overweight/obese subjects | AT vs. RT vs. AT + RT |
32 | Variable | Variable | ✕ | ↑ DI ↑ glucose effectiveness (in the AT + AR group compared to AT and AR groups alone) |
- |
| Madsen [42] | 2015 | T2DM overweight/obese subjects | HIIT | 8 | 3 | 30 | ✕ | ↑ DI ↓ HOMA-β |
↓ glucose levels ↓ HbA1c ↓ HOMA-IR |
| Non-diabetic subjects | HIIT | 8 | 3 | 30 | ✕ | - | - | ||
| Nieuwoudt [43] | 2017 | T2DM subjects |
F-HIT | 6 | 3 | 10–20 | ✕ | ↑ DI =1st and 2nd-phase IS |
- |
Key and abbreviations: ↑: increased; ↓: decreased; =: no changes; ✔️: yes; ✕: no; AT: aerobic training; RT: resistance training; HIIT: high-intensity interval training; F-HIT: functional high-intensity training; NGT: normal glucose-tolerant; T2DM: type 2 diabetes mellitus; IGT: impaired glucose-tolerant; IS: insulin secretion; OGTT: oral glucose tolerance test; AIRg: acute insulin response to glucose; DI: disposition index; mISI: muscle insulin sensitivity index; AUCOGTT: OGTT-derived area under the curve; GU: glucose uptake; GT: glucose tolerance; HbA1c: glycosylated hemoglobin; HOMA-IR: homeostatic model assessment for insulin resistance; HOMA- β: homeostatic model assessment for β-cell function.