Regional muscle glucose uptake remains elevated one week after cessation of resistance training independent of altered insulin sensitivity response in older adults with type 2 diabetes.

BACKGROUND: Aging is associated with a decline in skeletal muscle size.Muscle is critical both for mobility and glucose disposal. While resistance exercise (RE) increases muscle mass and function in the elderly, its role in improving glucose utilization is less clear. AIMS: To investigate whether muscle size was linked with insulin sensitivity (IS) in elders with diabetes following RE and if regional muscle glucose uptake differed from systemic glucose utilization. METHODS: Seven (68.4 ± 5.9 yr) adults with diabetes participated. After 16 weeks of RE, within 24 h (post 1) and after 1 week of no exercise (post 2), lean tissue cross-sectional area (CSA) and IS via glucose infusion rate (GIR) were assessed along with a standardized 18-F fluorodeoxyglucose (FDG)-positron emission tomography uptake value (SUV). RESULTS: CSA increased between pre-test (108.5 ± 35.3 cm2) and post 1 (116.8 ± 40.9 cm2), p=0.02 and did not differ at post 2 (116.0 ± 39.3 cm2). GIR during the 40 mU/m2/min insulin clamp differed between pretest (22.0 ± 15.8 mg/kg/min) and post 1 (67.9 ± 72.8 mg/kg/min), and post 1 and post 2 (25.0 ± 27.2 mg/kg/min) but not between pre-test and post 2. GIR results during the 200 mU/m2/min insulin clamps also differed between pre-test and post 1, and post 1 and post 2 but not between pre-test and post 2. FDG-SUV increased between pre-test (1.1 ± 0.2) and post 1 (1.4 ± 0.3), and remained stable between post 1 and post 2 (1.4 ± 0.4). CONCLUSION: RE that increased muscle size and FDG-SUV improved IS 24 h but not 1 week after exercise training.

The effect of basic training on aerobic capacity and body fat in New Zealand army recruits.

Physical fitness levels were assessed in 50 males recruits at the beginning, the middle and the end of ten weeks basic army training. Aerobic capacity was predicted indirectly from a timed 2.4 km run. Body fat levels were estimated from three skinfold measurements. Estimated VO2 max increased from 48.7 ml.kg-1 min-1 to 56.6 ml.kg-1 min-1, ie, 16.2 percent rise. Accompanying this increase was a decline in percent body fat from 12.4 percent to 10.2 percent, with no change in total body weight. It was concluded that the level of training intensity at 58 ml.kg-1 min-1, was effective in reducing body fat and increasing aerobic capacity.

Effects of membrane potential on sodium-dependent calcium uptake by sarcolemma-enriched preparations from canine ventricle.

The effect of membrane potential on sodium-dependent calcium uptake by vesicles in an isolated cardiac sarcolemma preparation was examined. Initial time course studies showed that the reaction deviated from initial velocity conditions within minutes. This appeared to be due, in part, to loss of the sodium gradient. Assays carried out to 10 sec revealed a linear component of uptake (2 to 10 sec) and a faster component (complete by 2 sec). The latter was eliminated by loading the preparation with ethyleneglycol-bis-(beta-aminoethyl ether)N,N'-tetraacetic acid (EGTA). This maneuver did not affect the slow component, and subsequent studies used preparations containing EGTA. Potassium Nernst potentials (EK), established by potassium gradients in the presence of valinomycin, were varied from -100 to +30 mV by changing [K+]o from 1.18 to 153.7 mM ([K+]i = 50 mM). The initial velocity of sodium-dependent calcium uptake was stimulated twofold by changing EK from -100 to 0 mV and another twofold by raising EK from 0 to +30 mV. For the total range of EK and [K+]o, 32 to 36% of the increase appeared to reflect stimulation by extravesicular potassium. The remainder appeared to be due to membrane potential. The profile of sodium-dependent calcium uptake versus EK suggested that calcium influx through electrogenic sodium/calcium exchange may be much more affected by the positive region of the cardiac action potential than by the negative region.

Relationship between steady-state depression of calcium-dependent action potentials and competition for binding sites by nifedipine, nitrendipine, and PY 108-068.

The objective of the present study was to determine the time-courses for depression and recovery of calcium-mediated action potentials in canine Purkinje fibers following exposure to dihydropyridine (DHP) calcium channel antagonists and to determine if the reported discrepancy (up to 1,000 X) between I50 values for inducing physiologic effects in isolated tissues and the dissociation constant (Kd) for [3H]nitrendipine binding to membrane sites could be reduced when physiologic measurements were made under experimentally determined steady-state conditions. Changes in dV/dtmax of slow calcium-mediated action potentials (20 mM KCl, 10(-6) M isoproterenol) were recorded at 10-min intervals during exposure (2-4 h) to nifedipine, nitrendipine, and PY 108-068 (10(-9) M-4 X 10(-8) M). Time to steady state was slow, with half-life t1/2 values of 40 min (nifedipine), 84 min (nitrendipine), and 81 min (PY 108-068). Steady state I50 values for depressing dV/dtmax were 12.08 (nifedipine), 5.74 (nitrendipine), and 4.88 nM (PY 108-068). In isolated cardiac sarcolemma preparations (37 degrees C), these compounds competed for [3H]nitrendipine binding sites with Ki values of 8.1, 1.3, and 4.9 nM, respectively. These results show that attainment of steady-state depression of calcium channel function can be slow, but that the discrepancy between the physiologic data and the binding data is reduced significantly (less than 5 X) when physiologic measurements are made at steady state and binding studies are performed at 37 degrees C.