Hypertension is a very prevalent cardiovascular (CV) disease risk factor in developed countries. All current treatment guidelines emphasise the role of nonpharmacological interventions, including physical activity, in the treatment of hypertension. Since our most recent review of the effects of exercise training on patients with hypertension, 15 studies have been published in the English literature. These results continue to indicate that exercise training decreases blood pressure (BP) in approximately 75% of individuals with hypertension, with systolic and diastolic BP reductions averaging approximately 11 and 8mm Hg, respectively. Women may reduce BP more with exercise training than men, and middle-aged people with hypertension may obtain greater benefits than young or older people. Low to moderate intensity training appears to be as, if not more, beneficial as higher intensity training for reducing BP in individuals with hypertension. BP reductions are rapidly evident although, at least for systolic BP, there is a tendency for greater reductions with more prolonged training. However, sustained BP reductions are evident during the 24 hours following a single bout of exercise in patients with hypertension. Asian and Pacific Island patients with hypertension reduce BP, especially systolic BP, more and more consistently than Caucasian patients. The minimal data also indicate that African-American patients reduce BP with exercise training. Some evidence indicates that common genetic variations may identify individuals with hypertension likely to reduce BP with exercise training. Patients with hypertension also improve plasma lipoprotein-lipid profiles and improve insulin sensitivity to the same degree as normotensive individuals with exercise training. Some evidence also indicates that exercise training in hypertensive patients may result in regression of pathological left ventricular hypertrophy. These results continue to support the recommendation that exercise training is an important initial or adjunctive step that is highly efficacious in the treatment of individuals with mild to moderate elevations in BP.

Obesity is associated with insulin resistance in skeletal muscle; accordingly, weight loss dramatically improves insulin action. We sought to identify molecular remodeling of muscle commensurate with weight loss that could explain improvements in insulin action. Muscle from morbidly obese women was studied before and after gastric bypass surgery. Gastric bypass surgery significantly reduced body mass by approximately 45% and improved insulin action. We then assessed mRNA profiles using a stringent statistical analysis (statistical concordance with three probe set algorithms), with validation in a cross-sectional study of lean (n = 8) vs. morbidly obese (n = 8) muscle. Growth factor receptor-bound protein 14 (GRB14), glycerol-3-phosphate dehydrogenase 1 (GPD1), and growth differentiation factor 8 (GDF8; myostatin) significantly decreased approximately 2.4-, 2.2-, and 2.4-fold, respectively, after weight loss (gastric bypass). Increased expression of these transcripts was associated with increased obesity in the cross-sectional group (lean vs. morbidly obese muscle). Each transcript was validated by real-time quantitative RT-PCR assays in both study groups. Using Ingenuity Pathway Analysis, we show that all three transcripts are involved in the same regulatory network including AKT1, IGF1, TNF, PPARG, and INS. These results suggest that GRB14, GPD1, and GDF8 are weight loss-responsive genes in skeletal muscle and that the observed transcriptional modulation of these would be expected to improve insulin signaling, decrease triglyceride synthesis, and increase muscle mass, respectively, with weight loss. Thus our data provide a possible regulatory pathway involved in the development of insulin resistance in the morbidly obese state, and improvement of insulin resistance with weight loss.

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