Acute exercise stimulates the renin-angiotensin-aldosterone axis: adaptive changes in runners

The plasma concentrations of aldosterone and its known regulators, plasma renin, potassium and ACTH, were examined during graded intensities of treadmill exercise (50, 70 and 90% of maximal oxygen uptake, VO2max). Sedentary men (n = 7) and two groups of runners of different training status (moderately trained, 15-25 miles/week, n = 7; highly trained, greater than 45 miles/week, n = 7) were studied in an attempt to define whether physical training causes changes in aldosterone homeostasis. Acute exercise was associated with elevations in plasma aldosterone, renin activity, potassium and ACTH in all three groups of subjects at exercise intensities of 70 and 90% VO2max. There were no differences in any of the responses among the three groups except for a blunted response of PRA at 90% VO2max in highly trained athletes. The exercise-induced rise of plasma aldosterone concentration did not correlate with changes in the concentration of its regulatory substances. We conclude that exercise stimulates the renin-angiotensin-aldosterone axis in an intensity-dependent fashion. With increased physical training identical hormonal and metabolic responses result at increased absolute workloads.     

Exercise-induced alterations in skeletal muscle myosin heavy chain phenotype: dose-response relationship.

This study investigated the effects of exercise training duration on the myosin heavy chain (MHC) isoform distribution in rat locomotor muscles. Female Sprague-Dawley rats (120 days old) were assigned to either a sedentary control group or to one of three endurance exercise training groups. Trained animals ran on a treadmill at approximately 75% maximal O2 uptake for 10 wk (4-5 days/wk) at one of three different exercise durations (30, 60, or 90 min/day). Training resulted in increases (P < 0.05) in citrate synthase activity in the soleus and extensor digitorum longus in both the 60 and 90 min/day duration groups and in the plantaris (Pla) in all three exercise groups. All durations of training resulted in a reduction (P < 0.05) in the percentage of MHCIIb and an increase (P < 0.05) in the percentage of MHCIIa in the Pla. The magnitude of change in the percentage of MHCIIb in the Pla increased as a function of the training duration. In the extensor digitorum longus, 90 min of daily exercise promoted a decrease (P < 0.05) in percentage of MHCIIb and increases (P < 0.05) in the percentages of MHCI, MHCIIa, and MHCIId/x. Finally, training durations >/=60 min resulted in an increase (P < 0.05) in the percentage of MHCI and a concomitant decrease (P < 0.05) in the percentage of MHCIIa in the soleus. These results demonstrate that increasing the training duration elevates the magnitude of the fast-to-slow shift in MHC phenotype in rat hindlimb muscles.     

Regional muscle blood flow capacity and exercise hyperemia in high-intensity trained rats

The purpose of this study was to determine the effects of high-intensity treadmill exercise training on 1) the regional distribution of muscle blood flow within and among muscles in rats during high-intensity treadmill exercise (phase I) and 2) on the total and regional hindlimb skeletal muscle blood flow capacities as measured in isolated perfused rat hindquarters during maximal papaverine vasodilation (phase II). Two groups of male Sprague-Dawley rats were trained 5 days/wk for 6 wk with a program consisting of 6 bouts/day of 2.5-min runs at 60 m/min up a 15% grade with 4.5-min rest periods between bouts. After training, blood flows were measured with the radiolabeled microsphere technique (phase I) in pair-weighted sedentary control and exercise-trained rats while they ran at 60 m/min (0% grade). In phase II of the study, regional vascular flow capacities were determined at three perfusion pressures (30, 40, and 50 mmHg) in isolated perfused hindquarters of control and trained rats maximally vasodilated with papaverine. The results indicate that this exercise training program produces increases in the vascular flow capacity of fast-twitch glycolytic muscle tissue of rats. However, these changes were not apparent in the magnitude or distribution of muscle blood flow in conscious rats running at 60 m/min, since blood flows within and among muscles during exercise were the same in trained and control rats.     

Activation of JNK in rat heart by exercise: effect of training

The purpose of the study was to determine whether exercise would activate JNK in the heart and whether chronic exercise training would alter the response. Untrained rats were familiarized with the treadmill and assigned to one of four groups: low intensity (LI), 10 min, 0%, 15 m/min; medium intensity (MI), 10 min, 0%, 33 m/min; high intensity (HI), 10 min, 25%, 33 m/min; long duration (LD), 30 min, 0%, 15 m/min. Another cohort of rats was subjected to a progressive 6 wk high-intensity training protocol that produced a 12% increase in heart mass. In untrained rats, JNK activity was LI: 1.5 (fold nonrun control), MI: 2.0, HI: 2.5, LD: 1.25 immediately after a single bout of exercise. In trained rats, no activation of JNK above baseline was detected after either a 10-min or 1-h bout of exercise. We concluded that treadmill exercise activates JNK in the rat heart in an intensity-dependent manner and that chronic training abrogates the myocardial JNK response to a bout of exercise.     

Attenuation of force deficit after lengthening contractions in soleus muscle from trained rats.

The purposes of this study were 1) to determine the extent to which endurance training reduces the functional deficit induced by lengthening contractions in the soleus (Sol) muscle and 2) to determine whether young and old rats training at a comparable relative exercise intensity would demonstrate a similar protective effect from lengthening-contraction-induced injury. Young (3-mo-old) and old (23-mo-old) male Fischer 344 rats were randomly assigned to either a control or exercise training group [young control (YC), old control (OC), young trained (YT), old trained (OT)]. Exercise training consisted of 10 wk of treadmill running (15% grade, 45 min/day, and 5 days/wk) such that by the end of training the young and old rats were exercising at 27 and 15 m/min, respectively. After training, contractile properties of the Sol muscle were measured in vitro at 26 degrees C. The percent decrease in maximal isometric specific force (P(o)) was determined after a series of 20 lengthening contractions (20% strain from optimal muscle length, 1 contraction every 5 s). After the lengthening-contraction protocol, Sol muscle P(o) was decreased by approximately 26% (19.6 vs. 14.6 N/cm(2)) and 28% (14.8 vs. 9.6 N/cm(2)) in the YC and OC rats, respectively. After exercise training, the reduction in P(o) was significantly (P < 0.05) attenuated to a similar degree ( approximately 13%) in both YT rats (18.7 vs. 16.2 N/cm(2)) and OT rats (15.8 vs. 13.7 N/cm(2)). It is concluded that exercise training attenuates the force deficit after repeated lengthening contractions to a comparable extent in young and old rats training at a similar exercise intensity.     

Cardiovascular responses of 70- to 79-yr-old men and women to exercise training

This study determined the effects of endurance or resistance exercise training on maximal O2 consumption (VO2max) and the cardiovascular responses to exercise of 70- to 79-yr-old men and women. Healthy untrained subjects were randomly assigned to a control group (n = 12) or to an endurance (n = 16) or resistance training group (n = 19). Training consisted of three sessions per week for 26 wk. Resistance training consisted of one set of 8-12 repetitions on 10 Nautilus machines. Endurance training consisted of 40 min at 50-70% VO2max and at 75-85% VO2max for the first and last 13 wk of training, respectively. The endurance training group increased its VO2max by 16% during the first 13 wk of training and by a total of 22% after 26 wk of training; this group also increased its maximal O2 pulse, systolic blood pressure, and ventilation, and decreased its heart rate and perceived exertion during submaximal exercise. The resistance training group did not elicit significant changes in VO2max or in other maximal or submaximal cardiovascular responses despite eliciting 9 and 18% increases in lower and upper body strength, respectively. Thus healthy men and women in their 70s can respond to prolonged endurance exercise training with adaptations similar to those of younger individuals. Resistance training in older individuals has no effect on cardiovascular responses to submaximal or maximal treadmill exercise.     

Isometric handgrip training reduces arterial pressure at rest without changes in sympathetic nerve activity

The purpose of this study was to determine whether isometric handgrip (IHG) training reduces arterial pressure and whether reductions in muscle sympathetic nerve activity (MSNA) mediate this drop in arterial pressure. Normotensive subjects were assigned to training (n = 9), sham training (n = 7), or control (n = 8) groups. The training protocol consisted of four 3-min bouts of IHG exercise at 30% of maximal voluntary contraction (MVC) separated by 5-min rest periods. Training was performed four times per week for 5 wk. Subjects' resting arterial pressure and heart rate were measured three times on 3 consecutive days before and after training, with resting MSNA (peroneal nerve) recorded on the third day. Additionally, subjects performed IHG exercise at 30% of MVC to fatigue followed by muscle ischemia. In the trained group, resting diastolic (67 +/- 1 to 62 +/- 1 mmHg) and mean arterial pressure (86 +/- 1 to 82 +/- 1 mmHg) significantly decreased, whereas systolic arterial pressure (116 +/- 3 to 113 +/- 2 mmHg), heart rate (67 +/- 4 to 66 +/- 4 beats/min), and MSNA (14 +/- 2 to 15 +/- 2 bursts/min) did not significantly change following training. MSNA and cardiovascular responses to exercise and postexercise muscle ischemia were unchanged by training. There were no significant changes in any variables for the sham training and control groups. The results indicate that IHG training is an effective nonpharmacological intervention in lowering arterial pressure.     

Effects of repetitive exercise on neonatal rat skeletal muscle oxidative capacity

Since little is known about the training response to exercise in neonatal animals, this study was undertaken to elucidate the potential of oxidative system adaptations in developing skeletal muscle of rats during 50 days of daily treadmill running. The training regimen involved male and female rats (10 days old) initially running 0.1 mph, 0% grade, for 15 min. The program progressed to 1 mph, 25% grade, for 60 min by 50 days of age. At 25 days of age, pyruvate and palmitate oxidative capacity, and citrate synthase activity in red vastus muscle homogenates were elevated in the trained group (T) compared with age- and sex-matched controls (C). These increases were also observed for each subsequent time point tested and occurred in spite of the fact that the peak oxidative capacity of neonatal red vastus muscle was 46% greater than adult values. Further, trained animals tested at 45 days of age responded with a 12% increase in maximal oxygen consumption (Vo2max) compared with controls (P less than 0.05). Assays of muscle phosphofructokinase and of creatine phosphokinase activity conducted at this time point revealed no difference between T and C groups. Collectively, these data suggest that neonatal rats can be successfully trained and that they respond to an endurance-type program qualitatively similarly to adult rats.     

Training does not protect against exhaustive exercise-induced lactate transport capacity alterations

The effects of endurance training on lactate transport capacity remain controversial. This study examined whether endurance training 1) alters lactate transport capacity, 2) can protect against exhaustive exercise-induced lactate transport alteration, and 3) can modify heart and oxidative muscle monocarboxylate transporter 1 (MCT1) content. Forty male Wistar rats were divided into control (C), trained (T), exhaustively exercised (E), and trained and exercised (TE) groups. Rats in the T and TE groups ran on a treadmill (1 h/day, 5 days/wk at 25 m/min, 10% incline) for 5 wk; C and E were familiarized with the exercise task for 5 min/day. Before being killed, E and TE rats underwent exhaustive exercise (25 m/min, 10% grade), which lasted 80 and 204 min, respectively (P < 0.05). Although lactate transport measurements (zero-trans) did not differ between groups C and T, both E and TE groups presented an apparent loss of protein saturation properties. In the trained groups, MCT1 content increased in soleus (+28% for T and +26% for TE; P < 0.05) and heart muscle (+36% for T and +33% for TE; P < 0.05). Moreover, despite the metabolic adaptations typically observed after endurance training, we also noted increased lipid peroxidation byproducts after exhaustive exercise. We concluded that 1) endurance training does not alter lactate transport capacity, 2) exhaustive exercise-induced lactate transport alteration is not prevented by training despite increased MCT1 content, and 3) exercise-induced oxidative stress may enhance the passive diffusion responsible for the apparent loss of saturation properties, possibly masking lactate transport regulation.     

Microvascular and myocardial contractile responses to ischemia: influence of exercise training.

We hypothesized that exercise training preserves endothelium-dependent relaxation, lessens receptor-mediated constriction of coronary resistance arteries, and reduces myocardial contractile dysfunction in response to ischemia. After 10 wk of treadmill running or cage confinement, regional and global indexes of left ventricular contractile function were not different between trained and sedentary animals in response to three 15-min periods of ischemia (long-term; n = 17), one 5-min bout of ischemia (short-term; n = 18), or no ischemia (sham-operated; n = 24). Subsequently, coronary resistance vessels ( approximately 106 +/- 4 microm ID) were isolated and studied using wire myographs. Maximal ACh-evoked relaxation was approximately 25, 40, and 60% of KCl-induced preconstriction after the long-term, short-term, and sham-operated protocols, respectively, and was similar between groups. Maximal sodium nitroprusside-evoked relaxation also was similar between groups among all protocols, and vasoconstrictor responses to endothelin-1 and U-46619 were not different in trained and sedentary rats after short-term ischemia or sham operation. We did observe that, after long-term ischemia, maximal tension development in response to endothelin-1 and U-46619 was blunted (P < 0.05) in trained animals by approximately 70 and approximately 160%, respectively. These results support our hypothesis that exercise training lessens receptor-mediated vasoconstriction of coronary resistance vessels after ischemia and reperfusion. However, training did not preserve endothelial function of coronary resistance vessels, or myocardial contractile function, after ischemia and reperfusion.     

Endurance training restores peritoneal macrophage function in post-MI congestive heart failure rats.

Congestive heart failure (CHF) induces a state of immune activation, and peritoneal macrophages (M phi s) may play an important role in the development and progression of one such condition. Moderate endurance training modulates peritoneal M phi function. We evaluated the effect of endurance training on different stages of the phagocytic process and in the production of interleukin-6 (IL-6), interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) after LPS stimulation. Either ligation of the left coronary artery or Sham operations were performed in adult Wistar rats. After 4 wk, control (Sham operated) and MI (ligation of the left coronary artery) animals were randomly assigned to either a sedentary (Sham-operated sedentary, n = 7 and MI sedentary, n = 10) or a trained group (Sham-operated trained, n = 8 and MI trained, n = 8). Trained rats ran on a treadmill (0% grade at 13-20 m/min) for 60 min/day, 5 days/wk, for 8-10 wk, whereas sedentary rats had only limited activity. Training increased maximal oxygen uptake normalized for body weight (ml.kg(-1).min(-1)), as well as skeletal muscle citrate synthase maximal activity, when compared with sedentary groups. The resident and total cell number, the chemotaxis index, and the production of TNF-alpha stimulated by LPS were significantly higher in the MI sedentary group when compared with the Sham sedentary group. Moderate endurance training reversed these alterations promoted by post-MI. These results demonstrate that moderate intensity exercise training modulates peritoneal M phi function and induces beneficial metabolic effects in rats with post-MI CHF.     

Effects of different durations of exercise on macrophage functions in mice.

The effects of differing durations of daily exercise on macrophage functions in mice were studied. Male ICR mice aged 4 wk were divided into five groups: a nonexercise group (control) and four exercise groups with differing daily exercise durations of 15--120 min (Exr groups). The exercise applied was 5 days/wk treadmill running at 13 m/min for 12 wk. The potentiation of the phagocytosis function of the reticuloendothelial system and the glucose consumption of peritoneal macrophages in the Exr 30, 60, and 120 groups were significantly higher than those in the control group. Superoxide anion production of peritoneal macrophages in both the absence and the presence of phorbol 12-myristate 13-acetate in the Exr 60 and 120 groups was significantly higher than that in the control group. The acid phosphatase and beta-glucuronidase activities of peritoneal macrophages in the Exr 30, 60, and 120 groups were significantly increased. These results suggest that treadmill running exercise for at least 30 min/day (30--120 min) effectively enhances macrophage functions in mice. These data provide preliminary evidence indicating that chronic exercise-induced increases in phagocytic activity exhibit a dose-dependent relationship with exercise duration.     

Step ergometry: is it task-specific training?

Maximal exercise responses were measured before and after 10 weeks of training in two groups of men, one trained on a treadmill (n = 12) and the other on a step ergometer (n = 9); the groups were pre- and post-tested on both machines to examine the specificity of the training modes. Training for both groups consisted of 3 days week-1, 30 min day-1, progressing to 50 min day-1, at an intensity of 75%-80% heart rate maximum reserve. Pre-training maximal oxygen uptake (VO2max) was significantly higher on the treadmill for both groups (X = 8.5%). VO2max increased 6.9% on the treadmill (P less than 0.05) and 6.9% (P greater than 0.05) on the step ergometer after treadmill training. The small increases may be attributed to the specificity of the testing protocols used to elicit VO2max. Significant (P less than 0.01) increases in VO2max were found for both modalities after step-ergometry training (treadmill = 11.8%; step ergometer = 23.2%). These increases resulted in equal post-test VO2max values (4.05 l min-1; 51 ml kg-1 min-1) on the step ergometer and treadmill. The significant increases in VO2max found for both modalities after step-ergometry training shows that (1) step ergometry is an effective training modality, and (2) its effects can be measured on the treadmill and therefore it is not task-specific training.     

Effect of training on fibre composition and phosphate metabolites in rest measured in vitro in muscles of young pigs.

1. Fibre type composition and phosphate metabolites were studied in m. longissimus thoracis (MLT), m. rectus femoris (MRF) and m. triceps brachii (MTB) in trained (N = 6) and sedentary (N = 6) pigs. 2. Samples were analyzed histochemically and by means of in vitro 31P NMR spectroscopy. 3. Training (duration 11 weeks) consisted of treadmill running at a speed of 1.1 m/sec. The daily exercise time of trained animals gradually increased from 10 min during the very first days to 60 min at the end of the 4th week. 4. During the final 7 weeks exercise time remained unchanged. Sedentary animals were not subjected to training. 5. A higher proportion of type beta R fibres in MRF, MTB and MLT and a lower proportion of type alpha W fibres were found in the trained group of animals compared to the control group. 6. In MLT no significant differences in the proportion of type alpha W were observed between both groups. 7. No significant differences in average fibre diameter of muscle fibres were found between groups. 8. No differences in concentration of phosphate compounds were observed between trained and sedentary groups. 9. Muscles with a higher proportion of type IIb fibres in both groups of pigs contained higher amounts of phosphocreatine (PCr) and were also characterized by a higher ratio of PCr to inorganic phosphate (Pi).     

Hormonal and vascular fluid responses to maximal exercise in trained and untrained males

The trained condition is associated with alterations in fluid regulation. In attempt to elucidate mechanisms responsible for these differences, resting, postexercise (maximal treadmill exercise of 8-13 min duration), and recovery measurements were made in seven trained (mean peak O2 consumption was 60.5 +/- 1.6 ml.kg-1.min-1) and seven untrained (mean peak O2 consumption was 40.7 +/- 1.7 ml.kg-1.min-1) male subjects. Samples were obtained by venipuncture with subjects seated. No significant differences in resting plasma osmolality (Osm), sodium, potassium, antidiuretic hormone (ADH), aldosterone, renin activity, or atrial natriuretic factor were found between groups. Maximal exercise produced significant increases in all of the above variables. Values immediately postexercise were similar between groups except for plasma Osm and sodium, which were significantly higher in the untrained group. Despite a reduction in plasma volume of equal magnitude in both groups, trained subjects demonstrated an increase in vascular proteins and mean corpuscular volume during exercise. This increase in plasma protein may be an important initiating factor responsible for the elevated plasma volume after 1-h recovery from exercise in the trained group. Lastly, similar ADH responses despite lower Osm in trained subjects may indicate that training increases the sensitivity of ADH to osmotic stimulation.     

Effect of training on the rating of perceived exertion at the ventilatory threshold

The purpose of this study was to determine the effect of training on the rating of perceived exertion (RPE) at the ventilatory threshold. College students were assigned to either training (n = 17) or control (n = 10) groups. Trainers completed 18 interval training sessions (five X 5 min cycling at 90-100% VO2max) and 8 continuous training sessions (40 min running or cycling) in 6 weeks. Pre- and post-training, cardiorespiratory, metabolic, and perceptual variables were measured at the ventilatory threshold during graded exercise tests on a cycle ergometer. Ventilatory threshold was that point above which VE X VO2-1 increased abruptly relative to work rate. Post-training means of trained and control subjects were compared using analysis of covariance, with pre-training values as covariates. Following training, the adjusted means for the trained subjects were significantly greater (p less than 0.05) than for controls for VO2max (6%), and for work rate (20%), VO2 (23%), and %VO2max (13%) at the ventilatory threshold. However, adjusted means for RPE at the ventilatory threshold were not significantly different (2%). Both before and after training, exercise at the ventilatory threshold was perceived as 'somewhat hard' to 'hard' (RPE = 13-15) by both groups. The relationship between RPE and %VO2max was altered by training, with trained subjects having a lower RPE at a given %VO2max. It is concluded that RPE at the ventilatory threshold is not affected by training, despite that after training the ventilatory threshold occurs at a higher work rate and is associated with higher absolute and relative metabolic and cardiorespiratory demands.     

Exercise training changes autonomic cardiovascular balance in mice.

Experiments were performed to investigate the influence of exercise training on cardiovascular function in mice. Heart rate, arterial pressure, baroreflex sensitivity, and autonomic control of heart rate were measured in conscious, unrestrained male C57/6J sedentary (n = 8) and trained mice (n = 8). The exercise training protocol used a treadmill (1 h/day; 5 days/wk for 4 wk). Baroreflex sensitivity was evaluated by the tachycardic and bradycardic responses induced by sodium nitroprusside and phenylephrine, respectively. Autonomic control of heart rate and intrinsic heart rate were determined by use of methylatropine and propranolol. Resting bradycardia was observed in trained mice compared with sedentary animals [485 +/- 9 vs. 612 +/- 5 beats/min (bpm)], whereas mean arterial pressure was not different between the groups (106 +/- 2 vs. 108 +/- 3 mmHg). Baroreflex-mediated tachycardia was significantly enhanced in the trained group (6.97 +/- 0.97 vs. 1.6 +/- 0.21 bpm/mmHg, trained vs. sedentary), whereas baroreflex-mediated bradycardia was not altered by training. The tachycardia induced by methylatropine was significantly increased in trained animals (139 +/- 12 vs. 40 +/- 9 bpm, trained vs. sedentary), whereas the propranolol effect was significantly reduced in the trained group (49 +/- 11 vs. 97 +/- 11 bpm, trained vs. sedentary). Intrinsic heart rate was similar between groups. In conclusion, dynamic exercise training in mice induced a resting bradycardia and an improvement in baroreflex-mediated tachycardia. These changes are likely related to an increased vagal and decreased sympathetic tone, similar to the exercise response observed in humans.     

Differential effects of mild therapeutic exercise during a period of inactivity on power generation in soleus type I single fibers with age

The purpose of this study was to investigate the effects of mild therapeutic exercise (treadmill) in preventing the inactivity-induced alterations in contractile properties (e.g., power, force, and velocity) of type I soleus single fibers in three different age groups. Young adult (5- to 12-mo-old), middle-aged (24- to 31-mo-old), and old (32- to 40-mo-old) F344BNF1 rats were randomly assigned to three experimental groups: weight-bearing control (CON), non-weight bearing (NWB), and NWB with exercise (NWBX). NWB rats were hindlimb suspended for 2 wk, representing inactivity. The NWBX rats were hindlimb suspended for 2 wk and received therapeutic exercise on a treadmill four times a day for 15 min each. Peak power and isometric maximal force were reduced following hindlimb suspension (HS) in all three age groups. HS decreased fiber diameter in young adult and old rats (-21 and -12%, respectively). Specific tension (isometric maximal force/cross-sectional area) was significantly reduced in both the middle-aged (-36%) and old (-23%) rats. The effects of the mild therapeutic exercise program on fiber diameter and contractile properties were age specific. Mild treadmill therapeutic exercise attenuated the HS-induced reduction in fiber diameter (+17%, 93% level of CON group) and peak power (μN·fiber length·s(-1)) (+46%, 63% level of CON group) in young adult rats. In the middle-aged animals, this exercise protocol improved peak power (+60%, 100% level of CON group) and normalized power (kN·m(-2)·fiber length·s(-1)) (+45%, 108% level of CON group). Interestingly, treadmill exercise resulted in a further reduction in shortening velocity (-42%, 67% level of CON group) and specific tension (-29%, 55% level of CON group) in the old animals. These results suggest that mild treadmill exercise is beneficial in attenuating and preventing inactivity-induced decline in peak power of type I soleus single fibers in young adult and middle-aged animals, respectively. However, this exercise program does not prevent the HS-induced decline in muscle function in the old animals.     

Conditioned exercise method for use with nonhuman primates

The objective of this study was to demonstrate the feasibility of using appetitive methods to train adult male olive baboons (Papio cynocephalus anubis), who were socially housed and fitted with indwelling catheter/ transducer systems, to exercise on an inclined, motorized, moving treadmill. All subjects were first trained to walk on a motorized treadmill for 30 min at a speed of approximately 1.6 km/hr on a 0 grade. Upon completion of initial exercise training, six animals were assigned to a low exercise group (LOW), six were assigned to a moderate exercise group (MOD), and six were assigned to a sedentary control group (SED). The LOW group exercised 30 min per day on an elevated treadmill, the MOD group exercised 60 min per day on an elevated treadmill and the SED group did not perform any treadmill exercise. The 12 animals comprising the LOW and MOD groups were exercised 4 days per week and their performance was increased over a subsequent 30-week experimental period. We gradually increased speed and grade demands over several weeks and produced an animal model capable of traveling at speeds up to 5.5 km/hr on a 22% grade and distances up to 3,353 m horizontally and 549 m vertically in a 1-hr session. © 1992 Wiley-Liss, Inc.     

Exercise and improved insulin sensitivity in older women: evidence of the enduring benefits of higher intensity training.

Few studies have compared the relative benefits of moderate- vs. higher intensity exercise training on improving insulin sensitivity in older people while holding exercise volume constant. Healthy older (73 +/- 10 yr) women (N = 25) who were inactive, but not obese, were randomized into one of three training programs (9-mo duration): 1) high-intensity [80% peak aerobic capacity (V(O2)peak); T(H)] aerobic training; 2) moderate-intensity (65% V(O2)peak; T(M)) aerobic training; or 3) low-intensity (stretching) placebo control (50% V(O2)peak); C(TB)). Importantly, exercise volume (300 kcal/session) was held constant for subjects in both the T(H) and the T(M) groups. V(O2)peak was determined by using a graded exercise challenge on a treadmill. Total body fat and lean mass were determined with dual-energy X-ray absorptiometry. The rate of insulin-stimulated glucose utilization as well as the suppression of lipolysis were determined approximately 72 h after the final exercise bout by using a two-step euglycemic-hyperinsulinemic clamp. We observed improved glucose utilization at the higher insulin dose with training, but these improvements were statistically significant only in the T(H) (21%; P = 0.02) compared with the T(M) (16%; P = 0.17) and C(TB) (8%; P = 0.37) groups and were observed without changes in either body composition or V(O2)peak. Likewise in the T(H) group, we detected a significant improvement in insulin-stimulated suppression (%) of adipose tissue lipolysis at the low-insulin dose (38-55%, P < 0.05). Our findings suggest that long-term higher intensity exercise training provides more enduring benefits to insulin action compared with moderate- or low-intensity exercise, likely due to greater transient effects.