Blood flow capacity in skeletal muscle declines with age. Reduced blood flow capacity may be related to decline in the maximal vasodilatory capacity of the resistance vasculature. This study tested the hypothesis that aging results in impaired vasodilatory capacity of first-order (1A) arterioles isolated from rat-hindlimb locomotory muscle: 1A arterioles (90–220 μm) from gastrocnemius and soleus muscles of young (4 mo) and aged (24 mo) Fischer-144 rats were isolated, cannulated, and pressurized via hydrostatic reservoirs. Vasodilatory responses to increasing concentrations of ACh (10−9 to 10−4 M), adenosine (ADO, 10−10 to 10−4 M), and sodium nitroprusside (SNP, 10−10 to 10−4 M) were evaluated at a constant intraluminal pressure of 60 cmH2O in the absence of flow. Flow-induced vasodilation was also evaluated in the absence of pressure changes. Responses to ADO and SNP were not altered by age. Endothelium-dependent vasodilation induced by flow was significantly reduced in arterioles from both gastrocnemius and soleus muscles. In contrast, endothelium-dependent vasodilation to ACh was reduced only in soleus muscle arterioles. These results indicate that aging impairs vasodilatory responses mediated through the endothelium of resistance arterioles from locomotory muscle, whereas smooth muscle vasodilatory responses remain intact with aging. Additionally, ACh-induced vasodilation was altered by age only in soleus muscle arterioles, suggesting that the mechanism of age-related endothelial impairment differs in arterioles from soleus and gastrocnemius muscles.

Ageingreducesendothelium-dependentvasodilatationinhumansandanimals,andinhumans, exercise training reverses the ageing-associated reduction in endothelium-dependent vasodilatation. The purpose of this study was to determine the mechanism(s) by which 10-12 weeks of treadmill exercise enhances endothelium-dependent vasodilatation in muscles of differing fibre composition from young and old rats. Three-and 22-month-old male Fischer 344 rats were assigned to young sedentary, young exercise-trained, old sedentary, or old exercisetrained groups. Arterioles were isolated from the soleus and gastrocnemius muscles; luminal diameter changes were determined in response to the endothelium-dependent vasodilator acetylcholine (ACh, 10 −9 -10 −4 mol l −1 ) alone and in the presence of the nitric oxide synthase (NOS) inhibitor L-NAME (10 −5 mol l −1 ) or the combination of L-NAME and the cyclooxygenase inhibitor indomethacin (10 −5 mol l −1 ). Training ameliorated the ageing-induced reduction in endothelium-dependent vasodilatation in soleus muscle arterioles. Treatment with L-NAME alone and in combination with indomethacin abolished differences in ACh vasodilatation occurring with ageing and training. Expression of endothelial NOS (eNOS) mRNA in soleus arterioles was unaltered by ageing, whereas eNOS protein was increased with age; training elevated both eNOS mRNA and protein. In gastrocnemius muscle arterioles, ageing did not alter maximal vasodilatation, but ageing and training increased maximal arteriolar diameter. These results demonstrate that ageing-induced reductions and training-induced enhancement of endothelial vasodilatation both occur through the nitric oxide signalling mechanism in highly oxidative skeletal muscle, but ageing and training do not appear to act on the same portion of the signalling cascade.

Purpose:To investigate the relationship between maximum strength and differences in jump height during weighted and unweighted (body weight) static (SJ) and countermovement jumps (CMJ).Methods:Sixty-three collegiate athletes (mean ± SD; age= 19.9 ± 1.3 y; body mass = 72.9 ± 19.6 kg; height = 172.8 ± 7.7 cm) performed two trials of the SJ and CMJ with 0 kg and 20 kg on a force plate; and two trials of mid-thigh isometric clean pulls in a custom rack over a force plate (1000-Hz sampling). Jump height (JH) was calculated from fight time. Force-time curve analyses determined the following: isometric peak force (IPF), isometric force (IF) at 50, 90, and 250 ms, and isometric rates of force development (IRFD). Absolute and allometric scaled forces, [absolute force/(body mass0.67)], were used in correlations.Results:IPF, IRFD, F50a, F50, F90, and F250 showed moderate/strong correlations with SJ and CMJ height percent decrease from 0 to 20 kg. IPFa and F250a showed weak/moderate correlations with percent height decrease. Comparing strongest (n = 6) to weakest (n = 6): t tests revealed that stronger athletes (IPFa) performed superior to weaker athletes.Conclusion:Data indicate the ability to produce higher peak and instantaneous forces and IRFD is related to JH and to smaller differences between weighted and unweighted jump heights. Stronger athletes jump higher and show smaller decrements in JH with load. A weighted jump may be a practical method of assessing relative strength levels.

We determined whether aging diminishes bone blood flow and impairs endothelium-dependent vasodilation. Femoral perfusion was lower in old animals, as well as endothelium-dependent vasodilation and NO bioavailability. These effects could contribute to old age-related bone loss and the increased risk of fracture.Introduction: Aging has been shown to diminish bone blood flow in rats and humans. The purpose of this study was to determine whether blood flow to regions of the femur perfused primarily through the principal nutrient artery (PNA) are diminished with aging and whether this putative reduction in flow is associated with impaired endothelium-dependent vasodilation. Materials and Methods: Blood flow was measured in conscious young adult (4-6 mo old) and aged (24-26 mo old) male Fischer-344 rats using radiolabeled microspheres. Endothelium-dependent vasodilation of the PNA was assessed in vitro using acetylcholine (ACh), whereas the contribution of the NO synthase (NOS) and cyclooxygenase (COX) signaling pathways to endothelium-dependent vasodilation was determined using the NOS and COX inhibitors L-NAME and indomethacin, respectively. Results: Femoral blood flow in the aged rats was 21% and 28% lower in the proximal and distal metaphyses, respectively, and 45% lower in the diaphyseal marrow. Endothelium-dependent vasodilation was reduced with old age (young: 83 ± 6% maximal relaxation; aged: 62 ± 5% maximal relaxation), whereas endotheliumindependent vasodilation (sodium nitroprusside) was unaffected by age. The reduction in endotheliumdependent vasodilation was mediated through impairment of the NOS signaling pathway, which resulted in lower NO bioavailability (young: 168 ± 56 nM; aged: 50 ± 7 nM). Conclusions: These data show that reductions in metaphyseal bone and diaphyseal marrow perfusion with old age are associated with diminished endothelium-dependent vasodilation through an impairment of the NOS mechanism. Such age-related changes in bone perfusion and vascular NO signaling could impact clinical bone loss, increase risk of fracture, and impair fracture healing in the elderly.

Context:The metabolic syndrome, characterized by central obesity with dyslipidemia, hypertension, and hyperglycemia, identifies people at high risk for type 2 diabetes.Objective: Our objective was to determine how the insulin resistance of the metabolic syndrome is related to muscle fiber composition.Design: Thirty-nine sedentary men and women (including 22 with the metabolic syndrome) had insulin responsiveness quantified using euglycemic clamps and underwent biopsies of the vastus lateralis muscle. Expression of insulin receptors, insulin receptor substrate-1, glucose transporter 4, and ATP synthase were quantified with immunoblots and immunohistochemistry.Participants and Setting: Participants were nondiabetic, metabolic syndrome volunteers and sedentary control subjects studied at an outpatient clinic. Main Outcome Measures:Insulin responsiveness during an insulin clamp and the fiber composition of a muscle biopsy specimen were evaluated.Results: There were fewer type I fibers and more mixed (type IIa) fibers in metabolic syndrome subjects. Insulin responsiveness and maximal oxygen uptake correlated with the proportion of type I fibers. Insulin receptor, insulin receptor substrate-1, and glucose transporter 4 expression were not different in whole muscle but all were significantly less in the type I fibers of metabolic syndrome subjects when adjusted for fiber proportion and fiber size. Fat oxidation and muscle mitochondrial expression were not different in the metabolic syndrome subjects. Conclusion:Lower proportion of type I fibers in metabolic syndrome muscle correlated with the severity of insulin resistance. Even though whole muscle content was normal, key elements of insulin action were consistently less in type I muscle fibers, suggesting their distribution was important in mediating insulin effects. ) has more than doubled since 1980 (1). Because of obesity-related illness, the average life expectancy in the United States may soon decline for the first time (2). The metabolic syndrome is a precursor to the development of overt diabetes (3). Insulin resistance and hyperinsulinemia are key elements of the metabolic syndrome that is characterized by visceral obesity, hypertension, hyperlipidemia, hyperglycemia, coronary heart disease, and increased mortality (4). The severity of insulin re- Abbreviations: BMI, body mass index; GIR, glucose infusion rate; GLUT4, glucose transporter 4; IRS-1, insulin receptor substrate-1; SSGIR, steady-state glucose infusion rate; VO 2 max, maximal oxygen consumption.