IntroductionType 2 diabetes (T2D) in elderly patients is associated with accelerated loss of skeletal muscle mass and strength. However, there are few meta-analysis reviews which investigate the effects of resistance training (RT) on glycemic control and skeletal muscle in the patients.MethodsThree electronic databases were searched (from the earliest date available to November 2016). Studies were included according to the inclusion criteria: T2D patients at least 60 years old, fasting plasma glucose of at least 7.0, and at least 8 weeks of RT.ResultsFifteen cohorts of eight studies (360 patients, average age 66 years) met the inclusion criteria. RT groups lowered glycosylated hemoglobin (HbA1c) (mean ES = −0.37, 95% CI = −0.55 to −0.20, P < 0.01) but did not result in a significant effect on lean body mass (LBM) (mean ES = 0.08, 95% CI = −0.15 to 0.30, P = 0.50). Homogeneity was shown between studies regarding HbA1c and LBM (Q = 15.70, df = 9, P = 0.07 and Q = 0.12, df = 4, P = 0.998, respectively). High-intensity subgroups showed a slight tendency to improve (rather than duration, frequency, and weekly volume) and to decrease HbA1c levels more than low-intensity subgroups (P = 0.37). RT increased muscular strength (mean ES = 1.05, 95% CI = 0.26–1.84, P = 0.01). No training components explained the heterogeneity between studies with changes in muscle strength.ConclusionRT improves glycemic control and muscle strength in elderly patients with T2D. RT with high intensity can be a strategy to treat patients with T2D and sarcopenia associated with aging.

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Studies have shown that early-stage type 1 diabetes mellitus (T1DM) leads to an exaggerated reflex pressor response to both static muscle contraction and tendon stretch. However, whether similar responses are present during dynamic exercise (i.e., intermittent contraction) is not known. Therefore, the purpose of this study was to determine whether T1DM leads to an exaggerated reflex pressor response to intermittent muscle contraction. We measured the exercise pressor reflex in unanesthetized, decerebrated T1DM (Streptozotocin 50 mg/kg; STZ) and healthy control (CTL) Sprague Dawley rats by intermittently contracting the hindlimb muscles for 30 s while measuring mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and heart rate (HR). Intermittently contracting the hindlimb muscles evoked exaggerated mean RSNA (STZ: Δ109 ± 21%, n=4; CTL: Δ61 ± 8%, n=5, p<0.05), peak MAP (STZ: Δ32 ± 2 mmHg, n=9; CTL: Δ12 ± 2 mmHg, n=6, p<0.05), blood pressure index (STZ: Δ625 ± 60 mmHg·s, n=9; CTL: Δ241 ± 46 mmHg·s, n=6, p<0.05), and HR (STZ: Δ24 ± 3 bpm, n=9; CTL: Δ9 ± 3 bpm, n=6, p<0.05) responses to similar developed tensions (p>0.05) in T1DM compared to CTL rats. T1DM rats also exhibited exaggerated early-onset sympathetic (onset: 1 s) and pressor (onset: 5 s) responses. These data show that early-stage T1DM leads to an exaggerated pressor reflex evoked by intermittent muscle contraction. The early onset and greater blood pressure index suggest that cardiovascular strain during dynamic exercise may be significantly higher in individuals with T1DM.

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