The influence of acute resistance exercise on cyclooxygenase-1 and -2 activity and protein levels in human skeletal muscle

Abstract

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.

Reduced large elastic artery stiffness with regular aerobic exercise in middle-aged and older adults

“…However, analogous assessments are experimentally challenging in humans, and future studies are needed to examine the contribution of any structural changes to reduced arterial stiffness with exercise in humans. In addition, exercise may also induce functional changes to the vasculature via mechanisms other than reduced NFkB signalling, such as alterations in the sympathetic nervous system [27], TNF-α [28], endothelin-1 [29] signalling or the COX 1/2 pathway [30]. …”

Oral Supplementation of Melatonin Protects against Fibromyalgia-Related Skeletal Muscle Alterations in Reserpine-Induced Myalgia Rats

“…Regarding this hypothesis, cyclooxygenase-1 (COX-1) seems to be a key enzyme. COX-1 is a constitutive enzymatic isoform involved, at skeletal muscle level, in the regulation of microcirculation, basal turnover and in various stages of myogenesis [ 15 ] and so it may also be involved in fibromyalgic pathogenesis. Furthermore, the decrease in mitochondrial mass and the rise in production of mitochondria derived radical oxygen species (ROS) have recently been proposed as relevant events in the fibromyalgia-related alterations [ 16 ].…”

Human inflammatory and resolving lipid mediator responses to resistance exercise and ibuprofen treatment

“…1). Both COX-1 and COX-2 enzymatic activities are elevated in human skeletal muscle tissue 4 h postresistance exercise (17), suggesting that PG biosynthesis may be heightened acutely and mediate inflammatory processes during early postexercise recovery. However, the eicosanoid response during early postexercise recovery and effect of exercise on the wider lipid mediator metabolome remains uncharacterized.…”