Strategies of adaptation of small arteries in diaphragm and gastrocnemius muscle to aerobic exercise training

Aerobic exercise training is associated with adaptive changes in skeletal muscles and their vascular bed; such changes in individual muscles may vary depending on their characteristics and recruitment. This study was aimed at comparing the effects of eight-week treadmill training on the locomotor and respiratory muscles in rats. The training course increased the aerobic performance in rats, which was evidenced by an increase in maximum O₂ consumption and a decrease in the blood lactate concentration in ramp test. The succinate dehydrogenase activity was increased in the red portion of the gastrocnemius muscle, but not in the diaphragm of trained rats. Arterial segments were isolated from feed arteries and studied by wire myography. The relaxation in response to acetylcholine in gastrocnemius arteries in trained animals was higher as compared with controls (due to higher NO production), while contractile responses to noradrenaline (in the presence of propranolol) were not changed. On the contrary, the endothelial function of diaphragm arteries was not affected by training, but contractile responses to activation of α-adrenoceptors were markedly increased. Thus, aerobic training may increase the blood supply rate to both locomotor and respiratory muscles, but the underlying regulatory mechanisms are different. The results obtained allow us to reveal the physiological mechanisms that determine the physical performance of the body under conditions of compromised functioning of the respiratory system.     

Endurance training reduces the magnitude of exercise-induced hyperammonemia in humans

The purpose of this study was to determine the influence of endurance-type exercise training on alterations of the ammonia content of blood in exercising humans. Seven females and four males trained 6 days/wk for 7 wk alternating days of continuous cycling (40 min) and interval running (five 5-min bouts). The NH3 content of blood was determined before and during cycle ergometer (CE) exercise (4 min) at power outputs (PO) of 119, 172, and 241 W pretraining and of 163, 230, and 271 W posttraining. These PO for each occasion represent relative work loads of approximately 65, 90, and 115% of peak CE maximum O2 uptake (PCE VO2), respectively. Training increased (P less than 0.05) PCE VO2 approximately 32% (2.72 +/- 0.25 to 3.56 +/- 0.29 l/min or 38.5 +/- 1.9 to 51.2 +/- 2.3 ml X kg-1 X min-1). Both pre- and posttraining the NH3 content of blood increased (P less than 0.05) with increasing intensity of exercise. Training did not influence the measure of these responses during exercise at the same relative intensity. During exercise at the same absolute PO, approximately 168 or 235 W, however, increases in blood NH3 were less (P less than 0.05) after training. The results indicate that the magnitude of increase in blood NH3 during exercise is determined by the energy requirement of the absolute work load, relative to an individual's aerobic power.     

Effect of aerobic training on the plasma ACTH response to exercise

The purpose of this study was to reexamine the effect of training on plasma adrenocorticotropin (ACTH) levels during exercise. Ten adult volunteers were split into a control and an experimental group. The experimental group participated in a 12-wk training program that resulted in a significant 11% increase in their mean maximal O2 uptake. The plasma ACTH response to a 150-W work rate was measured in both groups before and after the training program. The experimental group demonstrated a significant reduction in the ACTH response (11 vs. 4 pg/ml) to the work rate, whereas the control group demonstrated an unchanged response (16 vs. 13 pg/ml) over the course of the study. These data suggest that the ACTH response to an absolute submaximal work rate is blunted after training.     

Modulation of extracellular matrix using adenovirus vectors

Metabolism of the extracellular matrix (ECM) is a complex process that becomes disregulated in disease states characterized by chronic inflammation of joints, as is seen in rheumatoid arthritis or fibrosis of the lung. The participation of certain cytokines in this process is generally accepted (transforming growth factor-beta induces fibrosis), while the roles of other cytokines are less clear. Oncostatin M (OSM) is a member of the interleukin-6/leukaemia inhibitory factor (or gp130) cytokine family, and its participation in inflammation and the regulation of ECM metabolism is supported by a number of activities identified in vitro, including regulation of matrix metalloproteinase-1 and tissue inhibitor of metalloproteinases-1. Local overexpression of transforming growth factor-beta has been shown to be fibrogenic in mouse lung, whereas local OSM overexpression via intra-articular administration has been shown to induce a pannus-like inflammatory response in the synovium of mouse knee joints. Here we examine the effects of OSM in the context of those of transforming growth factor-beta using an established adenovirus vector that expresses mOSM (AdmOSM). We administered the virus intra-nasally into Balb/C mice to achieve high expression of OSM in the lung, and examined the effects at various time points. AdmOSM resulted in a vigorous inflammatory response by day 7 which was characterized by an elevation of neutrophil and mononuclear cell numbers and a marked increase in collagen deposition. These data support the use of such systems to study the ECM in vivo, and indicate a potential role for OSM in inflammatory responses that can modulate steady-state ECM deposition in Balb/C mice.     

Metformin inhibits mitochondrial adaptations to aerobic exercise training in older adults

Metformin and exercise independently improve insulin sensitivity and decrease the risk of diabetes. Metformin was also recently proposed as a potential therapy to slow aging. However, recent evidence indicates that adding metformin to exercise antagonizes the exercise‐induced improvement in insulin sensitivity and cardiorespiratory fitness. The purpose of this study was to test the hypothesis that metformin diminishes the improvement in insulin sensitivity and cardiorespiratory fitness after aerobic exercise training (AET) by inhibiting skeletal muscle mitochondrial respiration and protein synthesis in older adults (62 ± 1 years). In a double‐blinded fashion, participants were randomized to placebo (n = 26) or metformin (n = 27) treatment during 12 weeks of AET. Independent of treatment, AET decreased fat mass, HbA1c, fasting plasma insulin, 24‐hr ambulant mean glucose, and glycemic variability. However, metformin attenuated the increase in whole‐body insulin sensitivity and VO₂max after AET. In the metformin group, there was no overall change in whole‐body insulin sensitivity after AET due to positive and negative responders. Metformin also abrogated the exercise‐mediated increase in skeletal muscle mitochondrial respiration. The change in whole‐body insulin sensitivity was correlated to the change in mitochondrial respiration. Mitochondrial protein synthesis rates assessed during AET were not different between treatments. The influence of metformin on AET‐induced improvements in physiological function was highly variable and associated with the effect of metformin on the mitochondria. These data suggest that prior to prescribing metformin to slow aging, additional studies are needed to understand the mechanisms that elicit positive and negative responses to metformin with and without exercise.     

Effect of exercise training on passive stiffness in locomotor skeletal muscle: role of extracellular matrix

The purpose ofthis study was to evaluate the effect of endurance exercise training onboth locomotor skeletal muscle collagen characteristics and passivestiffness properties in the young adult and old rat. Young(3-mo-old) and senescent (23-mo-old) male Fischer 344 rats wererandomly assigned to either a control or exercise training group[young control (YC), old control (OC), young trained (YT), oldtrained (OT)]. Exercise training consisted of treadmill runningat ~70% of maximal oxygen consumption (45 min/day, 5 days/wk, for 10 wk). Passive stiffness (stress/strain) of the soleus (Sol) muscle fromall four groups was subsequently measured in vitro at 26°C.Stiffness was significantly greater for Sol muscles in OC rats comparedwith YC rats, but in OT rats exercise training resulted in muscles withstiffness characteristics not different from those in YC rats. Solmuscle collagen concentration and the level of the nonreduciblecollagen cross-link hydroxylysylpyridinoline (HP) significantlyincreased from young adulthood to senescence. Although training had noeffect on Sol muscle collagen concentration in either age group, itresulted in a significant reduction in the level of Sol muscle HP in OTrats. In contrast, exercise had no effect on HP in the YT animals.These findings indicate that 10 wk of endurance exercise significantlyalter the passive viscoelastic properties of Sol muscle in old but notin young adult rats. The coincidental reduction in the principalcollagen cross-link HP also observed in response to training in OTmuscle highlights the potential role of collagen in influencing passivemuscle viscoelastic properties.

     

Early muscular and metabolic adaptations to prolonged exercise training in humans

A short-term training program involving 2 h of daily exercise at 59% of peak O2 uptake (VO2max) repeated for 10-12 consecutive days was employed to determine the significance of adaptations in energy metabolic potential on alterations in energy metabolism and substrate utilization in working muscle. The initial VO2max determined before training on the eight male subjects was 53.0 +/- 2.0 (SE) ml.kg-1.min-1. Analysis of samples obtained by needle biopsy from the vastus lateralis muscle before exercise (0 min) and at 15, 60, and 99 min of exercise indicated that on the average training resulted (P less than 0.05) in a 6.5% higher concentration of creatine phosphate, a 9.9% lower concentration of creatine, and a 39% lower concentration of lactate. Training had no effect on ATP concentration. These adaptations were also accompanied by a reduction in the utilization in glycogen such that by the end of exercise glycogen concentration was 47.1% higher in the trained muscle. Analysis of the maximal activities of representative enzymes of different metabolic pathways and segments indicated no change in potential in the citric acid cycle (succinate dehydrogenase, citrate synthase), beta-oxidation (3-hydroxyacyl CoA dehydrogenase), glucose phosphorylation (hexokinase), or potential for glycogenolysis (phosphorylase) and glycolysis (pyruvate kinase, phosphofructokinase, alpha-glycerophosphate dehydrogenase, lactate dehydrogenase). With the exception of increases in the capillary-to-fiber area ratio in type IIa fibers, no change was found in any fiber type (types I, IIa, and IIb) for area, number of capillaries, capillary-to-fiber area ratio, or oxidative potential with training.(ABSTRACT TRUNCATED AT 250 WORDS)     

Conserved multi-tissue transcriptomic adaptations to exercise training in humans and mice

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Specificity of physiological adaptation to endurance training in distance runners and competitive walkers

The present study was designed to evaluate the specificity of physiological adaptation to extra endurance training in five female competitive walkers and six female distance runners. The mean velocity (v) during training, corresponding to 4 mM blood lactate [onset of blood lactate accumulation (OBLA)] during treadmill incremental exercise (training v was 2.86 m.s-1, SD 0.21 in walkers and 4.02 m.s-1, SD 0.11 in runners) was added to their normal training programme and was performed for 20 min, 6 days a week for 8 weeks, and was called extra training. An additional six female distance runners performed only their normal training programme every day for about 120 min at an exercise intensity equivalent to their lactate threshold (LT) (i.e. a running v of about 3.33 m.s-1). After the extra training, there were statistically significant increases in blood lactate variables (i.e. oxygen uptake (VO2) at LT, v at LT, VO2 at OBLA, v at OBLA; P less than 0.05), and running v for 3,000 m (P less than 0.01) in the running training group. In the walking training group, there were significant increases in blood lactate variables (i.e., v at LT, v at OBLA; P less than 0.05), and walking economy. In contrast, there were no significant changes in lactate variables, running v and economy in the group of runners which carried out only the normal training programme. It is suggested that the changes in blood lactate variables such as LT and OBLA played a role in improving v of both the distance runners and the competitive walkers.(ABSTRACT TRUNCATED AT 250 WORDS)     

Functional adaptations of rat skeletal muscle arterioles to aerobic exercise training.

This study tested the hypothesis that both structural and functional adaptations of arterioles occur within the skeletal muscle of rats aerobically trained for 8-10 wk with treadmill exercise. The training regimen used has been shown to elicit a 37% increase in plantaris citrate synthase activity but did not result in an elevation in citrate synthase activity in the spinotrapezius or gracilis muscles of rats used in this study. In the in vivo resting spinotrapezius muscle, arteriole diameters were similar in sedentary (SED) and trained (TR) rats. However, large- (1A) and intermediate- (2A) sized arterioles dilated proportionately more in TR than in SED rats during 1- to 8-Hz muscle contractions, even though the passive mechanical properties (circumference-passive wall tension relationships) were similar between groups. Vascular casts demonstrated a trend for an increase in the number of small (3A) arterioles and an approximately 20% increase in the passive diameter of 1A and 2A arterioles in the spinotrapezius muscle of TR rats. In contrast, in the gracilis muscle, arteriole diameters and density were identical in SED and TR rats, but the capillary-to-muscle fiber ratio was approximately 15% higher in TR rats. The results suggest that aerobic exercise training can greatly increase functional vasodilation and induce a slight increase in vascular density in skeletal muscle tissues, even if the oxidative capacity of these tissues is not increased by the training regimen.     

Concentric adaptation of the left ventricle in response to controlled upper body exercise training.

Upper body exercise has many applications to the rehabilitation and maintenance of cardiovascular health of individuals who are unable to exercise their lower body. The hemodynamic loads of upper body aerobic exercise are characterized by relatively high blood pressure and relatively low venous return. It is not clear how the left ventricle adapts to the specific hemodynamic loads associated with this form of exercise training. The purpose of this study was to measure left ventricular structure and function in previously sedentary men by using echocardiography before and after 12 wk of aerobic arm-crank exercise training (n = 22) or a time control period (n = 22). Arm-crank peak oxygen consumption (in ml x kg(-1) x min(-1)) increased by 16% (P < 0.05) after training, and significant differences (P < 0.05) were found in wall thickness (from 0.86 to 0.99 cm) but not in left ventricular internal dimension in diastole or systole. This suggested a concentric pattern of left ventricular hypertrophy that persisted after scaling to changes in anthropometric characteristics. No differences (P < 0.05) were found for any measurements of resting left ventricular function. We conclude that upper body aerobic exercise training results in a specific left ventricular adaptation that is characterized by increased left ventricular wall thickness but no change in chamber dimension.     

Modulation of tumor-induced angiogenesis by proteins of extracellular matrix.

The formation of new vessels is a known event in enlarging tumors. Furthermore, the metastatic potential is abrogated or reduced markedly in the absence of neovascularization. Shedding of tumor cells into the circulation is not observed until vascularization has occurred. As a result, the interruption of neovascularization could be a good target for cancer control. This research was an attempt to see if two proteins present in extracellular matrix, collagen and fibronectin (FN), could modify the tumor-induced angiogenesis. The strong angiogenic response induced by S13 tumor cells in the skin of BALB/c mice was blocked by treatment with FN and FN-derived peptides. In contrast, collagen did not modify tumor-induced angiogenesis.