Neuromuscular responses of the plantar flexors to whole-body vibration.

Enhanced physical performance following whole-body vibration (WBV) has been attributed to increased muscle activity; however, few studies have measured the mechanisms underlying these changes. The objective of this study was to measure the responsiveness of the Ia pathway as well as contractile properties in 16 young adults (24±2 years, eight men, eight women) following repeated bouts of acute WBV (45 Hz, 2 mm). Hoffman reflexes (H-reflex), compound muscle action potentials (M-wave), and twitch contractile properties were measured prior to and immediately following five 1-minute WBV exposures, and at 3, 5, 10, and 20 minute post-WBV. M-wave and H-reflex amplitudes decreased by 8% (P<.001) and by 46% (P<.05), respectively, whereas peak twitch torque decreased by 9% (P<.01) and rate of twitch torque development slowed 8% (P<.05). Percent voluntary activation and maximal plantar flexor torque were unchanged as a consequence of WBV (P>.05). In response to acute WBV, the root mean square of the soleus electromyography signal (EMGRMS ) increased by 8%, while the EMGRMS of the lateral gastrocnemius increased by 3% (P<.05). These data indicate that the responsiveness of the Ia pathway is diminished and contractile function is impaired immediately following WBV, and that the neural mechanisms underlying improved performance following WBV lie in alternative hypotheses possibly involving spindle disfacilitation or Golgi afferent modulation.

The effects of a 2 week modified high intensity interval training program on the homeostatic model of insulin resistance (HOMA-IR) in adults with type 2 diabetes.

AIM: High intensity interval training (HIIT) induces similar metabolic adaptations to traditional steady state aerobic exercise training. Until recently, most HIIT studies have examined maximum efforts in healthy populations. The current study aimed to examine the effects of a 2 week modified HIIT program on the homeostatic model of insulin resistance (HOMA-IR) in individuals with type 2 diabetes (T2D). It was hypothesized that HIIT would improve HOMA-IR. METHODS: Nine individuals with T2D (age=40.2±9.7 y; BMI=33.9±5.3; fasting plasma glucose [FPG]=8.7±2.9 mmol/L; HbA1C=7.3±1.2%; [mean±SD]) performed 6 individualized training sessions of HIIT (4x30 seconds at 100% of estimated maximum workload followed by 4 minutes of active rest) over 2 weeks. HOMA-IR was calculated from FPG and serum insulin and compared against a prior 2 week baseline period. RESULTS: Blood glucose was reduced immediately after each HIIT session (P<0.05). Anthropometrics, FPG, serum insulin, and HOMA-IR were unchanged after training. However, 6 of the 9 individuals exhibited reduced HOMA-IR values after the training period and there was a significant negative correlation between HOMA-IR value prior to training and change in HOMA-IR after HIIT. CONCLUSION: These observations tend to support the positive health benefits of HITT for individuals with T2D reported in recently published data using a modified HIIT protocol. However, they suggest that the magnitude of the disease should be assessed when examining the effects of exercise interventions in individuals with T2D.

Myocardial stretch alters twitch characteristics and Ca2+ loading of sarcoplasmic reticulum in rat ventricular muscle.

OBJECTIVE: The aim was to determine the influence of diastolic muscle length on force development and timing parameters of cardiac muscle twitch contraction and to determine whether a length dependency exists for the calcium loading capacity of the sarcoplasmic reticulum. METHODS: Right ventricular papillary muscles and trabeculae were isolated from hearts of female Wistar rats weighing 220-280 g. Papillary muscles were stretched to diastolic lengths of 90, 95, and 100% Lmax and paced at 1.0 Hz. Individual twitch profiles were characterised by their peak force and the maximum rate (dF/dt) of the positive and negative force changes. Intrinsic timing was identified through waveform analysis that divided the twitch profile into time domains for the ascending limb (T0-T1; T1-T2) and the descending limb (T2-T3; T3-T4). Each domain was compared at three muscle lengths. The sarcoplasmic reticular calcium content at short (1.88 microns) and long (2.11 microns) sarcomere lengths was characterised by rapid cooling contractures after 1 s and 60 s of diastolic rest. RESULTS: Peak developed force and the maximum rate of positive and negative force development decreased as diastolic muscle length was reduced from Lmax to 90% Lmax. The intrinsic timing for the segment that reflects the relaxation phase of the twitch (T1-T4) was shortened as muscle length was reduced. The time domain that reflects the combined effects of calcium release and the early phase of contraction (T0-T1) was insensitive to diastolic muscle length. The fractional release of sarcoplasmic reticular calcium at different muscle lengths was approximately 32-35% of the total sarcoplasmic reticulum calcium pool. CONCLUSIONS: The data on the intrinsic timing of the twitch characteristics coupled with rapid cooling contracture analysis suggests a fractional calcium release that is approximately 32-35% of the total sarcoplasmic reticular capacity at either long or short muscle lengths. However, the loading capacity of the sarcoplasmic reticulum is greater when the muscle operates at a shorter diastolic length. This can be interpreted as meaning that diastolic muscle length differentially influences sarcoplasmic reticular calcium storage and release processes.

Inotropic interventions and myocardial force-interval relation: a quantitative approach.

OBJECTIVES: To analyze inotropic influence on the early and late phases of cardiac sarcoplasmic reticulum calcium loading. DESIGN: Papillary muscles with parallel edges and no evidence of tissue branching were selected from the heart. Only muscle preparations that maintained stable passive diastolic and developed forces were used for analysis. Muscles were stretched to their maximum length and stimulated at 0.2 Hz. The early and late phases of sarcoplasmic reticulum calcium loading were evaluated quantitatively by mathematical fitting of the force-interval relation. Increasing the extracellular calcium or decreasing the extracellular sodium was used to increase the inotropic state. ANIMALS: Right ventricular papillary muscles were isolated from female Wistar rats weighing 200 to 220 g. Electrical stimulation and data acquisition were controlled through a microcomputer. MAIN RESULTS: Increasing the extracellular calcium concentration from 0.5 to 1.0 mM produced a 90% increase in developed tension. This was accounted for by a 41% increase in the early phase of sarcoplasmic reticulum loading and a 29% increase in the late phase. A 20% reduction in the extracellular sodium concentration increased contractile force 100% and shifted the force-interval curve to the left. This was accounted for through an increase in both early and late phases of sarcoplasmic reticulum loading. CONCLUSION: These results are consistent with the current model of excitation-contraction coupling and clearly indicate that various positive inotropic interventions have selective effects on each process of the force-interval relation that cooperatively interact with each other. Mathematical fitting of data clearly improves the quantitative aspect of the force-interval response.

Distribution of cyclic AMP phosphodiesterase in adipose tissue from trained rats.

Fat cells were isolated from sedentary and exercise trained female Sprague-Dawley rats and cyclic AMP phosphodiesterase (cyclic AMP-PDE) activities were determined from crude homogenates of the fat cells in the whole homogenate, P5, P48, and S48 fractions. Exercise training resulted in a significant increase in the mean specific activity of cyclic AMP-PDE (pmol X min-1 X mg-1) from the whole homogenate and S48 fraction at cyclic AMP concentrations of 4, 8, and 16 microM and in the P48 fraction at 8 and 16 microM cyclic AMP. Cyclic AMP-PDE kinetic plots according to Lineweaver-Burk for the calculation of Michaelis constants (Km) and maximum enzyme velocities (Vmax) were nonlinear, indicating both a low and high enzyme form. The Michaelis constants were significantly lower in trained rats than those of its control for the high Km form of cyclic AMP-PDE in the whole and soluble fractions and for the low Km form of the P5 particulate fraction. The Vmax of the high Km form of the P48 particulate fraction from trained animals was also significantly higher than that found in its control. Phosphodiesterase inhibition by methylxanthines in the various fractions was similar in both trained and sedentary animals. These changes in specific activity, Michaelis constants, and Vmax of cyclic AMP-PDE from crude homogenates of isolated fat cells from exercise trained animals may account for the decreased intracellular levels of cyclic AMP following catecholamine stimulation of isolated fat cells from trained rats.

Lipolysis in isolated myocardial cells from diabetic rat hearts.

Diabetes in rats was induced with streptozotocin (100 mg/kg); myocardial cells (myocytes) were isolated from the hearts 3-4 days later. Diabetic myocytes were characterized as having the same viability and ATP content as control myocytes, but the yield was reduced. The triacylglycerol content of diabetic myocytes was elevated by 3.7-fold; this resulted in an increased rate of glycerol output during subsequent incubations. There was a stoichiometric relationship between the decline in the cellular triacylglycerol content and the release of glycerol into the incubation medium. Isoproterenol stimulated the output of glycerol from control myocytes by about twofold, but the stimulation of glycerol output from diabetic myocytes by isoproterenol was markedly less. The combination of 1-methyl-3-isobutylxanthine with isoproterenol or 8-(4-chlorophenylthio)-adenosine 3',5'-cyclic monophosphate also failed to produce the same lipolytic response in diabetic myocytes as in control myocytes. Triacylglycerol-loaded myocytes from control rats, prepared by including palmitate in the isolation buffers, were also characterized as having increased basal rates of glycerol output and a reduced lipolytic response to isoproterenol. The level of free fatty acids in diabetic myocytes was 2.8-fold greater than in myocytes from control hearts. The intracellular accumulation of free fatty acids in these quiescent populations of diabetic myocytes may limit the ability of catecholamines to produce a further stimulation of lipolysis.

Serum lipoproteins of the Zucker rat in response to an endurance running program.

Previous studies have concluded that exercise training has resulted in increases in cholesterol associated with high-density lipoprotein (HDL). However, data regarding alterations in triglyceride, cholesterol, and the protein associated with the three major lipoproteins in a hyperlipoproteinemic state in response to exercise training are not available. Serum lipoprotein levels from normal and hyperlipoproteinemic Zucker rats were studied following 9 and 18 wk of treadmill running to determine the extent that the three major serum lipoprotein classes were affected. Nine weeks of treadmill running reduced serum triglyceride content in obese rats (sedentary, 294 +/- 19 [SE]; trained, 128 +/- 40 mg X dl-1) but did not affect total serum cholesterol (sedentary, 85 +/- 6; trained, 90 +/- 6 mg X dl-1). Serum very low-density lipoprotein from the trained obese rats contained lower levels of triglyceride (57%), cholesterol (46%), and protein (61%). HDL cholesterol (sedentary, 61 +/- 4; trained, 73 +/- 4 mg X dl-1) was increased by 14% in the obese rat. In the lean rat, HDL cholesterol was the only lipoprotein fraction altered following 9 wk of treadmill running. The data from this study indicate that hypertriglyceridemia can be reduced in the obese rat and that HDL cholesterol can be increased by physical activity requiring about 70% maximal aerobic capacity.

Stimulation of lipolysis in rat heart myocytes by isoproterenol.

Calcium-tolerant myocytes were isolated from rat hearts. Isoproterenol produced a dose-dependent increase in glycerol output (lipolysis) that could be blocked by propranolol. The presence of glucose in the incubation medium enhanced the release of glycerol from myocytes but had no effect on the decline in triacylglycerol content. No incorporation of radioactivity from [U-14C]glucose into glycerol could be detected. In incubations with isoproterenol, there was a stoichiometric relationship between the glycerol output and the decrease in triacylglycerol levels. The addition of the phosphodiesterase inhibitor 1-methyl-3-isobutylxanthine resulted in an increase in the basal glycerol output and an enhancement of the isoproterenol-stimulated lipolytic rate. Forskolin and 8-(4-chlorophenylthio)adenosine 3',5'-cyclic monophosphate also produced a concentration-dependent stimulation of lipolysis in myocytes. Therefore, lipolysis in isolated myocytes must be regulated by adenosine 3',5'-cyclic monophosphate-dependent mechanisms. These results demonstrate that lipolysis can be observed in myocardial cells and that the lipolytic response to isoproterenol cannot be secondary to a physiological (inotropic) response since these myocyte preparations are quiescent.

Regulation of rates of lipolysis in isolated myocardial cells from rat heart.

Rates of lipolysis in isolated myocardial cells (myocytes) from rat heart, as measured by the release of glycerol and a reduction in endogenous triacylglycerols, can be stimulated by isoproterenol. Myocyte preparations were calcium-tolerant and were quiescent, even in the presence of isoproterenol, so the stimulation of lipolysis by isoproterenol cannot be secondary to a physiological (inotropic) response. N6-Phenylisopropyladenosine did not reduce isoproterenol-stimulated rates of lipolysis. Increasing the calcium concentration in the incubation medium from 0.75 to 3 mM did not increase the basal output of glycerol. Furthermore, incubation of calcium-tolerant myocytes in the absence of calcium had no effect on either basal or isoproterenol-stimulated rates of lipolysis. Therefore, calcium ions must not influence the lipolytic process directly, and so the calcium dependency for lipolysis observed with perfused heart preparations must reflect the effect of calcium on the contractile performance of the heart, which only secondarily produced a change in rates of lipolysis.

Attenuation of blood pressure increases in Dahl salt-sensitive rats by exercise.

Systolic blood pressure was determined weekly to assess the development of hypertension in sedentary and active Dahl salt-sensitive (S) rats that were exercised by running at 20 m/min, 60 min/day, 5 days/wk. The marked rise in blood pressure that occurred with feeding 8% NaCl (wt/wt) diet in Dahl S rats could be attenuated by chronically practiced endurance running, but only if exercise at 20 m/min was started at the beginning of salt feeding. Under the same dietary feeding conditions, running at 27 m/min resulted in incomplete attenuation of hypertension. Further, running for 30 min/day was not as beneficial as running 60 min/day at 20 m/min. Delaying the start of exercise for 6 wk after the beginning of salt feeding did not result in reduction of hypertension in the S rat. These experiments indicate that increases in blood pressure can be prevented in Dahl S rats for 12 wk if running is initiated concomitantly with salt feeding. Blood pressure is not reduced if hypertension due to salt feeding has been continued for 6 wk. The results also indicate that there is an optimal exercise intensity, duration, or both, for controlling hypertension in Dahl rats.