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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Type 2 diabetes is associated with neuropathic symptoms, including development of peripheral neuropathy and an exaggerated exercise pressor reflex, both of which have been demonstrated in UC Davis Type 2 diabetes mellitus (UCD‐T2DM) rats. This novel animal model more closely mimics the human disease state than traditional T2DM rodent models. Several studies have demonstrated changes in nerve growth factor (NGF) in diabetic patients, with some showing increases and others decreases, and this has been proposed as a potential driver of the development of peripheral neuropathy. Additionally, increased expression of purinergic 2X3 (P2X3) receptors has been suggested as a potential mechanism underlying peripheral nerve sensitization. However, interactions between these factors during diabetes progression are not fully understood. Therefore, the objective of this study was to investigate the relations between NGF, P2X3, and peripheral neuropathy during diabetes progression in UCD‐T2DM rats. We hypothesized that NGF levels would be correlated with traditional indexes of diabetes (glucose and HbA1c) as well as P2X3 expression and mechanical allodynia as measured by paw withdrawal threshold. Methods Blood was collected monthly from the tail vein of male UCD‐T2DM rats from 4 to 8 months of age. Serum levels of NGF, leptin, and insulin were measured by ELISA. Development of mechanical allodynia was tracked monthly using Von Frey filaments to measure paw withdrawal threshold. At 8 months of age, L4‐5 dorsal root ganglia were harvested and P2X3 receptor protein levels were quantified using the Jess automated western blotting platform. Pearson correlations were calculated using Graphpad Prism 9. Results Consistent with wasting and loss of pancreatic beta cell function during diabetes progression, glucose and HbA1c increased significantly over time whereas body weight, insulin, and leptin levels decreased. Circulating NGF concentration was negatively correlated with glucose (r=‐0.61, P<0.01) and HbA1c (r=‐0.79, p<0.01) demonstrating that NGF decreased with the progression of diabetes. Circulating NGF concentration was positively correlated with body weight (r=0.61, p<0.01), insulin (r=0.77, p<0.01), and leptin (r=0.82, p<0.01) thereby showing the same decreasing trend with diabetes progression. Interestingly, NGF was negatively correlated with P2X3 receptor expression (r=‐0.81, p=0.03) and neither NGF nor P2X3 were significantly associated with mechanical allodynia (NGF: r=0.14, p=0.45; P2X3: r= 0.15, p=0.75). Conclusion Circulating NGF is significantly associated with several indexes of diabetes progression in UCD‐T2DM rats, including glucose, HbA1c, leptin, and insulin levels. Though decreasing concentrations of NGF are associated with increases in P2X3 receptor protein expression, neither NGF nor P2X3 appear to be associated with the development of mechanical allodynia.

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We previously determined that the exercise pressor reflex and mechanoreflex are exaggerated during the progression of type 2 diabetes mellitus (T2DM) in UCD‐T2DM rats. For this first study T2DM onset was determined using a non‐fasting glucose threshold of 200 mg/dL. Importantly, aging, which may also be associated with autonomic modulation changes, was not investigated during this previous study. Therefore, the objective of the current study was to determine if these changes in the exercise pressor reflex during T2DM progression occur independent of aging. We hypothesized that the exercise pressor reflex and mechanoreflex would remain exaggerated during the progression of T2DM when compared against age‐matched healthy controls. Methods Studies were conducted in fasted, unanesthetized, decerebrated UCD‐T2DM rats, using a fasting glucose of 140 mg/dL as diagnostic criteria, at 4 different time points of disease progression (pre‐onset: before developing diabetes; early‐onset: 3‐7 wks after onset; established: 23‐28 wks after onset; and chronic: 39‐44 wks after onset). Healthy, age‐matched Sprague Dawley rats were used as controls (CTL). The exercise pressor reflex was evoked by statically and intermittently contracting the hindlimb for 30 s, and the mechanoreflex was evoked by stretching the Achilles tendon for 30 s. Peak changes in mean arterial pressure (MAP) and developed tension were measured and compared across all groups (one‐way ANOVA followed by Holm Sidak's post hoc analysis). Results We found that fasting blood glucose was significantly higher after the onset of T2DM and remained above the diagnostic threshold (140 mg/dL) during the progression of the disease (p<0.05). Static hindlimb muscle contraction significantly increased peak pressor response in early‐onset UCD‐T2DM rats, but not in other stages of T2DM, compared to age‐matched healthy controls (CTL: 10 ± 1 mmHg, n=7; T2DM: 24 ± 5 mmHg, n=6, p<0.05) with similar developed tensions, p>0.05. Likewise, intermittent hindlimb muscle contraction significantly increased peak pressor response in early‐onset UCD‐T2DM rats, but not later stages of T2DM, compared to their age‐matched healthy controls (CTL: 9 ± 1 mmHg, n=6; T2DM: 36 ± 7 mmHg, n=4, p<0.05) with similar developed tensions, p>0.05. Similarly, passive tendon stretch significantly increased peak pressor response in early‐onset UCD‐T2DM rats, but not later stages of T2DM, compared to their age‐matched healthy controls (CTL: 12 ± 5 mmHg, n=6; T2DM: 36 ± 8 mmHg, n=7, p<0.05) with similar developed tensions, p>0.05. Conclusion These findings suggest that the exercise pressor reflex and mechanoreflex are exaggerated at the onset of T2DM, as diagnosed by fasted glucose of 140mg/dL, but not later in the disease, and this change occurs independent of aging.