The objective of this study was to evaluate effects of genistein and moderate intensity exercise on Achilles tendon collagen and cross-linking in intact and ovariectomized (OVX) female Sprague-Dawley rats. Rats were separated into eight groups (n=9 per group): intact or OVX, treadmill exercised or sedentary, genistein-treated (300 mg•kg−1•day−1) or vehicle. After 6-weeks, tendons were assayed for the collagen-specific amino acid hydroxyproline and hydroxylyslpyridinoline (HP). Collagen content was not influenced by exercise (p=0.40) but was lower (p<0.001) in OVX vehicle rats compared to intact vehicle rats (OVX: 894±35 µg collagen/mg dry weight, intact: 1185±72 µg collagen/mg dry weight). In contrast, collagen content in OVX rats treated with genistein was greater (p=0.010, 1198±121 µg collagen/mg dry weight) when compared to untreated rats and not different from intact rats (p=0.89). HP content was lower in OVX genistein-treated when compared to intact genistein-treated rats, but only within the sedentary animals (p=0.05, intact-treated: 232±39mmol/mol collagen, OVX-treated: 144±21mmol/mol collagen). Our findings suggest that ovariectomy leads to a reduction in tendon collagen, which is prevented by genistein. HP content, however, may not have increased in proportion to the addition of collagen. Genistein may be useful for improving tendon collagen content in conditions of estrogen deficiency.

This study evaluated the activity and content of cyclooxygenase (COX)-1 and -2 in response to acute resistance exercise (RE) in human skeletal muscle. Previous work suggests that COX-1, but not COX-2, is the primary COX isoform elevated with resistance exercise in human skeletal muscle. COX activity, however, has not been assessed after resistance exercise in humans. It was hypothesized that RE would increase COX-1 but not COX-2 activity. Muscle biopsies were taken from the vastus lateralis of nine young men (25 ± 1 yr) at baseline (preexercise), 4, and 24 h after a single bout of knee extensor RE (three sets of 10 repetitions at 70% of maximum). Tissue lysate was assayed for COX-1 and COX-2 activity. COX-1 and COX-2 protein levels were measured via Western blot analysis. COX-1 activity increased at 4 h ( P < 0.05) compared with preexercise, but returned to baseline at 24 h (PRE: 60 ± 10, 4 h: 106 ± 22, 24 h: 72 ± 8 nmol PGH2·g total protein−1·min−1). COX-2 activity was elevated at 4 and 24 h after RE ( P < 0.05, PRE: 51 ± 7, 4 h: 100 ± 19, 24 h: 98 ± 14 nmol PGH2·g total protein−1·min−1). The protein level of COX-1 was not altered ( P > 0.05) with acute RE. In contrast, COX-2 protein levels were nearly 3-fold greater ( P > 0.05) at 4 h and 5-fold greater ( P = 0.06) at 24 h, compared with preexercise. In conclusion, COX-1 activity increases transiently with exercise independent of COX-1 protein levels. In contrast, both COX-2 activity and protein levels were elevated with exercise, and this elevation persisted to at least 24 h after RE.

Heart failure with preserved ejection fraction (HFpEF) is a complex clinical condition. Initially called diastolic heart failure, it soon became clear that this condition is more than the opposite side of systolic heart failure. It is increasingly prevalent and lethal. Currently, HFpEF represents more than 50% of heart failure cases and shares a 90-day mortality and readmission rate similar to heart failure with reduced ejection fraction. Heart failure with preserved ejection fraction is best considered to be a systemic disease. From a cardiovascular standpoint, it is not just a stiff ventricle. A stiff ventricle combined with a stiff arterial and venous system account for the clinical manifestations of flash pulmonary edema and the marked changes in renal function or systemic blood pressure with minor changes in fluid volume status. No effective pharmacologic treatments are available for patients with HFpEF, but an approach to the musculoskeletal system has merit: the functional limitations and exercise intolerance that patients experience are largely due to abnormalities of peripheral vascular function and skeletal muscle dysfunction. Regular exercise training has strong objective evidence to support its use to improve quality of life and functional capacity for patients with HFpEF. This clinical review summarizes the current evidence on the pathophysiologic aspects, diagnosis, and management of HFpEF.

The purpose of this study was to evaluate cyclooxygenase (COX)‐1 and ‐2 activation in response to an acute bout of resistance exercise (RE) in human skeletal muscle. Before, 4, and 24 hours after a bout of unilateral knee extensor RE (3 sets of 10 repetitions at 70% of maximum) muscle biopsies were taken from the vastus lateralis of seven young males (25±0.4 y). Biopsy samples were assayed for COX‐1 and COX‐2 activity (700200, Cayman Chemical). COX‐1 activity was not increased with RE (PRE: 5.0±1.0, 4 hrs: 6.5±1.1, 24 hrs: 7.7±1.9 nmol PGH2·g muscle−1·min−1) while COX‐2 activity was elevated at 24 (p<0.05) but not four hours after exercise (PRE: 4.5±1.1, 4 hrs: 5.8±1.1, 24 hrs: 8.9±1.4 nmol PGH2·g muscle−1·min−1). Prostaglandin (PG) production due to COX‐1 and COX‐2 was similar (COX‐1/COX‐2 ratio: 1.1±0.3) before RE. This ratio (0.8±0.3) decreased at 24 hours indicating a greater proportion of PG production from COX‐2. COX activity has been implicated as a necessary component of a RE‐induced increase in skeletal muscle protein synthesis. Muscle protein synthesis is elevated as early as 1–4 hours after RE. Thus our data suggest that an elevation in COX‐1 or COX‐2 activity may not be necessary for the RE‐induced increase in protein synthesis. Our findings also support the general consensus that COX‐2 is inducible and that COX‐2 enzyme activity is present in resting skeletal muscle.Funding: MWU Start‐Up Funds, and MWU College of Health Sciences

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