This study evaluated the effect of 4 weeks of low-load resistance exercise with blood flow restriction (BFRE) on increasing strength in comparison with high-load resistance exercise (HLE), and assessed changes in blood, vascular and neural function. Healthy adults performed leg extension BFRE or HLE 3 days/week at 30% and 80% of strength, respectively. During BFRE, a cuff on the upper leg was inflated to 30% above systolic blood pressure. Strength, pulse-wave velocity (PWV), ankle-brachial index (ABI), prothrombin time (PT) and nerve conduction (NC) were measured before and after training. Markers of coagulation (fibrinogen and D-dimer), fibrinolysis [tissue plasminogen activator (tPA)] and inflammation [high sensitivity C-reactive protein (hsCRP)] were measured in response to the first and last exercise bouts. Strength increased 8% with BFRE and 13% with HLE (P < 0.01). No changes in PWV, ABI, PT or NC were observed following training for either group (P > 0.05). tPA antigen increased 30–40% immediately following acute bouts of BFRE and HLE (P = 0.01). No changes were observed in fibrinogen, D-dimer or hsCRP (P > 0.05). These findings indicate that both protocols increase the strength without altering nerve or vascular function, and that a single bout of both protocols increases fibrinolytic activity without altering selected markers of coagulation or inflammation in healthy individuals.

This pilot study indicates that a customized print-based intervention shows promise in improving physical activity levels and health and function in women with multiple sclerosis.

In Brief Patients with type 1 or type 2 diabetes are two times more likely to experience depression than their peers without diabetes. Comorbid depression results in deleterious effects on glycemic control, worsened diabetes complications, functional disability, and premature mortality. Once identified, depression can be effectively treated with antidepressant medications, psychotherapy, or a combination of both. Patients and providers should monitor depressive symptoms to identify their recurrence and work collaboratively to address barriers to care that exist in both urban and rural areas.

Depression affects one in four people with diabetes and significantly affects diabetes health. Earlier studies of the treatment of depression have documented that cognitive behavioral therapy (CBT) and exercise have each been found to be effective in treating depression in people with and without diabetes in the context of medical settings. Individuals in rural areas lack regular access to medical centers and require treatment options that may be adapted for local communities. To date, no studies have combined CBT and exercise for people with diabetes. This article presents a translational behavioral depression intervention study designed for individuals with type 2 diabetes in a rural Appalachian region as a model of an interdisciplinary approach to the treatment of depression in diabetes.

Cold exposure in conjunction with aerobic exercise stimulates gene expression of PGC-1α, the master regulator of mitochondrial biogenesis. PGC-1α can be expressed as multiple isoforms due to alternative splicing mechanisms. Among these isoforms is NT-PGC-1α, which produces a truncated form of the PGC-1α protein, as well as isoforms derived from the first exon of the transcript, PGC-1α-a, PGC-1α-b, and PGC-1α-c. Relatively little is known about the individual responses of these isoforms to exercise and environmental temperature. Therefore, we determined the expression of PGC-1α isoforms following an acute bout of cycling in cold (C) and room temperature (RT) conditions. Nine male participants cycled for 1h at 65% Wmax at −2 °C and 20 °C. A muscle biopsy was taken from the vastus lateralis before and 3h post-exercise. RT-qPCR was used to analyze gene expression of PGC-1α isoforms. Gene expression of all PGC-1α isoforms increased due to the exercise intervention (p < 0.05). Exercise and cold exposure induced a greater increase in gene expression for total PGC-1α (p = 0.028) and its truncated isoform, NT-PGC-1α (p = 0.034), but there was no temperature-dependent response in the other PGC-1α isoforms measured. It appears that NT-PGC-1α may have a significant contribution to the reported alterations in the exercise- and temperature-induced PGC-1α response.