The aging process is associated with loss of muscle mass and strength and decline in physical functioning. The term sarcopenia is primarily defined as low level of muscle mass resulting from age-related muscle loss, but its definition is often broadened to include the underlying cellular processes involved in skeletal muscle loss as well as their clinical manifestations. The underlying cellular changes involve weakening of factors promoting muscle anabolism and increased expression of inflammatory factors and other agents which contribute to skeletal muscle catabolism. At the cellular level, these molecular processes are manifested in a loss of muscle fiber cross-sectional area, loss of innervation, and adaptive changes in the proportions of slow and fast motor units in muscle tissue. Ultimately, these alterations translate to bulk changes in muscle mass, strength, and function which lead to reduced physical performance, disability, increased risk of fall-related injury, and, often, frailty. In this review, we summarize current understanding of the mechanisms underlying sarcopenia and age-related changes in muscle tissue morphology and function. We also discuss the resulting long-term outcomes in terms of loss of function, which causes increased risk of musculoskeletal injuries and other morbidities, leading to frailty and loss of independence.

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Chronic overload of a skeletal muscle by removing its synergists produces hypertrophy and marked changes in its metabolic and biochemical properties. In this study alterations in the contractile properties of the plantaris 12-14 wk after bilateral removal of the soleus and gastrocnemius were investigated. In situ isometric and isotonic contractile properties of overloaded plantaris (OP), normal plantaris (NP), and normal soleus (NS) were tested at 33 +/- 1 degree C. Op were 97% heavier than NP and produced 43 and 46% higher twitch (Pt) and tetanic (Po) tensions. However, NP produced more tension per cross-sectional area than OP (mean 26.2 vs. 21.6 N/cm2; P less than 0.001). Isometric twitch time to peak tension (TPT) and half-relaxation time (1/2RT) were significantly longer in OP (mean 36.4 vs. 32.5 ms and 23.9 vs. 18.4 ms). Mean maximum shortening velocity (Vmax, mm/s per 1,000 sarcomeres) were 34.1 for NP and 18.1 for OP (P less than 0.001). The degree of conversion toward the Vmax of NS was 74% compared with only 19 and 14% for TPT and 1/2RT. OP produced a higher proportion of Po at a given stimulation frequency than NP and showed less fatigue than NP after repetitive stimulation. Chronic overload of the fast plantaris modified to varying degrees the contractile properties studied toward that resembling a slow muscle. Although the maximum tension of OP was markedly enhanced it was not in proportion to the increase in muscle mass.

Background: Nurses have an essential role in implementing evidence-based practices (EBP) that contribute to high-quality outcomes. It remains unknown how healthcare facilities can increase nurse engagement in EBP.

Active salmonids maintain myocardial contractility at temperatures that are cardioplegic for mammals. We postulated that myofibrillar Ca2+ sensitivity in the trout heart might 1) exhibit lower temperature dependence and/or 2) be greater over the range of physiological temperatures. Temperature-induced changes in intracellular pH may also play a role as alkalosis typically increases calcium affinity of myofibrillar adenosinetriphosphatase (ATPase). Ca2+ sensitivities of ventricular myofibrillar ATPase were determined in rats and in rainbow trout (Oncorhynchus mykiss) over a physiological range of pH and temperatures. Maximal myofibrillar ATPase activities of each species were similar and equally affected by temperature. Trout myofibrillar ATPase lost Ca2+ dependence at 37 degrees C. At constant pH, reduced temperature decreased calcium affinity more in trout (0.35 pCa/10 degrees C) than in rat (0.08-0.16 pCa/10 degrees C). Under alpha-stat conditions, the effects of temperature were reduced in both trout (0.2 pCa/10 degrees C) and rat (no significant effect). Over trout physiological temperatures, Ca2+ sensitivity was greater than rat at 37 degrees C. Qualitatively similar results were observed in studies measuring tension in skinned trout ventricular fibers. One mechanism by which the trout heart is able to maintain contractility at low temperatures is through the inherent higher Ca2+ sensitivity of the contractile element compared with mammalian species.

Hypertension (HTN) is a common complication of recombinant erythropoietin (EPO) therapy, but the mechanism of the EPO-associated HTN is uncertain. In the present study we examined the effects of EPO and the vehicle alone on rat caudal artery contractile response and basal and thrombin-stimulated platelet cytosolic Ca2+ concentration ([Ca2+]i) in vitro and on blood pressure (BP) and heart rate in vivo. At high concentrations (200 U/ml) EPO caused a small but consistent contraction in the caudal artery rings (P < 0.01) without affecting the response to either angiotensin II (ANG II) or the alpha 1-agonist methoxamine. Incubation with EPO significantly increased basal platelet [Ca2+]i (P < 0.01) and augmented the thrombin-induced rise of [Ca2+]i in Ca(2+)-free medium (P < 0.05). Long-term EPO administration led to a significant elevation of BP within 2 wk regardless of whether the hematocrit was allowed to rise or was kept constant by dietary iron deficiency. In contrast, single intravenous administration of high-dose EPO (400 and 5,000 U/kg), estimated to yield plasma concentrations comparable with those employed in vitro, failed to either alter BP or modify the BP response to ANG II during a 60-min observation period. This was associated with a significant rise in plasma guanosine 3',5'-cyclic monophosphate but no discernible change in plasma atrial natriuretic peptide, suggesting enhanced nitric oxide (NO) release. Thus, at high concentrations, EPO appears to possess a fast-acting pressor effect in vitro but not in vivo. The observed discrepancy may be due to enhanced NO release with EPO administration in vivo. However, HTN does occur with repeated EPO administration in a time-dependent and hematocrit-independent manner. This suggest that expression of the hypertensive effect of EPO in vivo involves a gradual conditioning process.

Although endurance training has been shown to profoundly affect the oxidative capacity of skeletal muscle, little information is available concerning the impact of endurance training on skeletal muscle isomyosin expression across a variety of muscle fiber types. Therefore, a 10-wk running program (1 h/day, 5 days/wk, 20% grade, 1 mile/h) was conducted to ascertain the effects of endurance training on isomyosin expression in the soleus, vastus intermedius (VI), plantaris (PLAN), red and white medial gastrocnemius (RMG and WMG), and red and white vastus lateralis muscles (RVL and WVL). Evidences of training were noted by the presence of a resting and a submaximal exercise bradycardia, as well as an enhancement in peak O2 consumption in the trained rodents relative to the nontrained controls. No evidence for skeletal muscle hypertrophy was observed subsequent to training when muscle weight was normalized to body weight. Shifts in the isomyosin profile of the trained VI, RMG, RVL, and PLAN were seen relative to the nontrained controls. Specifically, training affected the slow myosin (SM) composition of the VI by decreasing the relative content of the SM2 isoform by 14% while increasing that of the SM1 isoform (P less than 0.05). In addition, training elicited various degrees of a fast to slower myosin transformation in the RMG, RVL, and PLAN. All three muscles showed a significant reduction in the fast myosin 2 isoform (P less than 0.05), with significant increases in intermediate myosin in the RVL and PLAN along with elevations in SM2 in the RMG and PLAN (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The objective of this study was to estimate the limitations imposed by the kinetics of activation and relaxation on the ability of slow skeletal muscle to produce mechanical work. These estimates were made by the following methods: 1) using the work loop technique and measuring the actual mechanical work (WA) produced by rat soleus muscles (n = 6) at four different frequencies (0.5, 1, 2, and 4 Hz) and seven different amplitudes of length change (1, 2, 3, 4, 5, 6, and 7 mm); 2) determining the force-velocity relationships of the soleus muscles and using this data to quantify the theoretical mechanical work (WT) that could be produced under the work loop conditions described above; and 3) subtracting WA from WT. The difference between WT and WA was interpreted to represent limitations imposed by activation and relaxation. Under certain conditions (high frequency, small strain), factors controlling the kinetics of activation and relaxation reduced the mechanical work of the soleus muscle by approximately 60%. Hence, activation and relaxation collectively represent important factors limiting the production of mechanical work by slow skeletal muscle.