Training-induced Increase in Bone Mineral Density between Growing Male and Female Rats.

The purpose of this study was to determine the existence of sex differences in the resistance training-induced elevation in bone mineral density (BMD) and bone strength (Fmax) during the growth period in rats. 16 male (M) and 16 female (F) rats (approx. 8 weeks old) were randomly divided into sedentary control (MC=8, FC=8), and resistance-trained (RT) groups (M-RT=8, F-RT=8). The RT groups were conditioned to climb a vertical ladder 4 consecutive times (per exercise session) with weights attached to their tail 3 days per week for a total of 6 weeks. After 6 weeks, there were no interaction effects (sex×exercise). The main effect of sex indicated no difference in tibial BMD (in g/cm(2)) for males (0.226±0.005) compared to females (0.221±0.004). However, Fmax (in Newtons) was significantly greater for males (131.3±5.3) compared to females (89.9±3.0). The main effect of exercise indicated that tibial BMD and Fmax were significantly greater for RT groups (0.234±0.004 g/cm(2) and 120.9±7.4 Newtons) compared to controls (0.212±0.003 g/cm(2) and 100.3±5.1 Newtons). The results indicate that during growth, there were no sex differences in the training-induced elevation in BMD and bone mechanical properties.

Different training volumes yield equivalent increases in BMD.

The purpose of this study was to determine if an exercise threshold existed in stimulating an elevation in bone mineral density (BMD), via resistance training, during the growth period in male rats. 27 male rats were randomly divided into Â-Control (Con, n=9), 3 ladder climb resistance trained group (3LC, n=9), and 6 ladder climb resistance trained group (6LC, n=9). The 3LC and 6LC groups were conditioned to climb a vertical ladder with weights appended to their tail 3 days/wk for a total of 6 wks, but the 6LC group performed significantly more work than the 3LC group. After 6 weeks, left tibial BMD (mean±SD) was significantly greater for 3LC (0.225±0.006 g/cm (2)) and 6LC (0.234±0.008 g/cm (2)) when compared to Con (0.202±0.013 g/cm (2)). Further, bone strength (force to failure in Newtons) was significantly greater for 3LC (132.7±13.7) and 6LC (130.0±22.8) compared to Con (102.0±10.1). There was no significant difference in BMD or bone strength between 3LC and 6LC. The results indicate that both resistance training programs were equally effective in elevating BMD and bone strength in growing rats. These data suggest that during growth, there is a stimulation threshold where more work per exercise session is ineffective in promoting additional bone formation.

Equal BMD after daily or triweekly exercise in growing rats.

The purpose of this study was to examine the efficacy of continuous resistance training (3 days/wk) compared to interrupted resistance training where 20-24 h separated an exercise bout (i. e. 6 days/wk) for enhancing bone mineral density (BMD) in growing male rats. The total volume of work performed per week between the two resistance training programs was equivalent by design. Young male rats were randomly divided into Control (Con, n=9), 3 days/wk resistance trained group (RT3, n=9), and 6 days/wk resistance trained group (RT6, n=9). The RT3 and RT6 groups were conditioned to climb a vertical ladder with weights appended to their tail for a total of 6 wks. After 6 wks, BMD (assessed via DXA) from the left tibia was significantly greater for RT3 (0.242+/-0.004 g/cm (2)) and RT6 (0.244+/-0.004 g/cm (2)) compared to Con (0.226+/-0.003 g/cm (2)). Further, serum osteocalcin (oc, in ng/ml) was significantly greater for RT3 (75.8+/-4.4) and RT6 (73.5+/-3.8) compared to Con (53.4+/-2.4). There was no significant difference in BMD or serum OC between RT3 and RT6 groups. The results indicate that both resistance training programs were equally effective in elevating bone mineral density in young, growing rats.

Interrupted resistance training and BMD in growing rats.

A resistance training program, where the exercise was uninterrupted (UT, i.e. continuous repetitions) was compared against another resistance training program where the exercise was interrupted (IT, i.e. 2 exercise sessions during a training day) for enhancing bone modeling and bone mineral density (BMD) in maturating animals. The total volume of work performed between the two resistance training programs was equivalent by design. Young male rats (approximately 8 weeks old) were randomly divided into Control (Con, n=8), UT (n=8) and IT (n=7) resistance trained groups. The UT and IT groups were conditioned to climb a vertical ladder with weights appended to their tail 3 days/week for 6 weeks. After the 6 week training regimen (Mean+/-SD), tibial BMD (assessed via DXA) was significantly greater for UT (0.237+/-0.008 g/cm(2)) and IT (0.238+/-0.005 g/cm(2)) compared to Con (0.223+/-0.004 g/cm(2)). Further, serum osteocalcin (OC) was significantly greater for UT (45.65+/-2.83 ng/ml) and IT (46.33+/-4.60 ng/ml) compared to Con (37.86+/-4.04 ng/ml). There was no significant difference in BMD or serum OC between UT and IT groups. The results indicate that both resistance training programs were equally effective in elevating BMD in growing animals.

Interrupted vs. uninterrupted training on BMD during growth.

This study compared a resistance training program where the exercise was uninterrupted (UT, i.e., continuous repetitions) against a resistance training program where the exercise was interrupted (IT, i.e., 3 exercise sessions during a training day) for enhancing bone modeling and bone mineral density (BMD) in maturating animals. The total volume of work performed between the two resistance training programs was equivalent by design. 24 young male rats were randomly divided into Control (Con, n = 8), UT (n = 8) and IT (n = 8) resistance trained groups. The UT and IT groups were conditioned to climb a vertical ladder with weights appended to their tail 3 days/wk for 6 wks. After the 6-wk program, serum osteocalcin was not significantly different between groups, whereas the adjusted urinary deoxypyridinoline (DPD) was significantly lower for both UT (81.03 +/- 5.53) and IT (88.30 +/- 7.29) compared to Con (128.13 +/- 9.99). Tibial BMD (assessed via DXA) was significantly greater for UT (0.222 +/- 0.005 g/cm (2)) and IT (0.219 +/- 0.003 g/cm (2)) when compared to Con (0.205 +/- 0.004 g/cm (2)). There was no significant difference in DPD or BMD between UT and IT groups. The results indicate that both interrupted and continuous, uninterrupted resistance training programs were equally effective in stimulating bone modeling.

Resistance training and bone mineral density during growth.

This study examined the efficacy of two different resistance training programs in enhancing bone modeling and bone mineral density (BMD) in maturating rats. One exercise mode involved lifting a lighter weight with more repetitions (LI), while the other regimen involved lifting a heavier weight with fewer repetitions (HI) where the total volume of work between exercise programs was equivalent by design. Twenty-three male rats were randomly divided into control (Con, n = 8), LI (n = 7), and HI (n = 8) groups. The LI and HI groups were conditioned to climb a vertical ladder with weights appended to their tail 4 days/wk for 6 wks. After training, serum osteocalcin (OC) was significantly (p < 0.05) higher in both HI (45.2 +/- 1.7 ng/ml) and LI (39.1 +/- 2.2 ng/ml) when compared to Con (29.9 +/- 0.9 ng/ml). Left tibial BMD was significantly (p < 0.05) greater for HI (0.231 +/- 0.004 g/cm (2)) when compared to both LI (0.213 +/- 0.003 g/cm (2)) and Con (0.206 +/- 0.005 g/cm (2)) with no significant difference between LI and Con. The results indicate that both HI and LI are effective in elevating serum OC, implicating an osteogenic response; however, only HI resulted in a significant elevation in BMD.

Lactate removal is not enhanced in nonstimulated perfused skeletal muscle after endurance training.

The effects of endurance training (running 40 m/min grade for 60 min, 5 days/wk for 8 wk) on skeletal muscle lactate removal was studied in rats by utilizing the isolated hindlimb perfusion technique. Hindlimbs were perfused (single-pass) with Krebs-Henseleit bicarbonate buffer, fresh bovine erythrocytes (hematocrit approximately 30%), 10 mM lactate, and [U-14C]lactate (30,000 dpm/ml). Arterial and venous blood samples were collected every 10 min for the duration of the experiment to assess lactate uptake. During perfusions, no significant differences in skeletal muscle lactate uptake were observed between trained (7.31 +/- 0.20 micromol/min) and control hindlimbs (6.98 +/- 0.43 micromol/min). In support, no significant differences were observed for [14C]lactate uptake in trained (22,776 +/- 370 dpm/min) compared with control hindlimbs (21,924 +/- 1,373 dpm/min). Concomitant with these observations, no significant differences were observed between groups for oxygen consumption (4.93 +/- 0.18 vs. 4.92 +/- 0.13 micromol/min), net skeletal muscle glycogen synthesis (7.1 +/- 0.4 vs. 6.5 +/- 0.3 micromol x 40 min(-1) x g(-1)), or 14CO2 production (2,203 +/- 185 vs. 2,098 +/- 155 dpm/min), trained and control, respectively. These findings indicate that endurance training does not affect lactate uptake or alter the metabolic fate of lactate in quiescent skeletal muscle.

Strength training does not alter the effects of testosterone propionate injections on high-density lipoprotein cholesterol concentrations.

The purpose of the study was to examine the long-term effects of a high-volume strength training program (vertical ladder climbing) and testosterone propionate injections (intraperitoneal) on serum lipid and lipoprotein concentrations in male Sprague-Dawley rats. The animals were randomly divided into a testosterone (T)-treated group (dose per injection, 2.5 mg/kg testosterone propionate solubilized in 1 mL safflower oil) and a control (C) group (injected with an isovolumic amount of safflower oil alone). Animals were further divided into a strength-trained group (E) and a sedentary group (S). The 10-week resistance training program consisted of weights (100% of body mass) appended to the tail as the animal climbed an 85-cm ladder to volitional fatigue. Following 10 weeks of strength training and testosterone injections, body weight was not significantly different between the main effects of strength training exercise (TE + CE v TS + CS) and testosterone injections (TE + TS v CE + CS) or between groups. Testicular mass (mean +/- SE) was measured as a relative indicator of testosterone effects. Both TE and TS had significantly reduced testicular mass (2.56 +/- 0.04 and 2.38 +/- 0.03 g, respectively) compared with CE and CS (3.49 +/- 0.03 and 3.49 +/- 0.04 g, respectively). No significant differences were observed between groups for total serum cholesterol, serum triglycerides, or serum low-density lipoprotein cholesterol (LDL-C). In contrast, significant decreases in high-density lipoprotein cholesterol (HDL-C) were observed for both TE (26.7 +/- 1.6 mg/dL) and TS (27.5 +/- 1.3 mg/dL) compared with CE (48.7 +/- 2.9 mg/dL) and CS (43.5 +/- 2.6 mg/dL). As a result, the total cholesterol to HDL-C ratio was significantly greater for TS + TE (4.7 +/- 0.1) compared with CS + CE (2.9 +/- 0.2). These observations suggest that in animals, a 10-week program of high-volume strength training does not elicit any beneficial effect on the lipid or lipoprotein status, nor does it attenuate the altered lipoprotein profile induced by testosterone propionate injections.

Temporal effects of testosterone propionate injections on serum lipoprotein concentrations in rats.

UNLABELLED: The chronic abuse of androgenic anabolic steroids, a group of synthetic derivatives of testosterone, to improve athletic performance have demonstrated compromised serum lipoprotein concentrations reflecting an elevated risk for cardiovascular disease. While the detrimental alterations in the lipoprotein profile have been reported consistently for orally administered androgenic anabolic steroids, the reports examining the effects of parenteral administration of testosterone upon the lipid profile remain equivocal. PURPOSE: The purpose of this study was to determine whether compromised serum lipoprotein concentrations would be manifest in rats receiving testosterone injections (twice per week) over the time course of 7 wk. METHODS: Male rats were randomly assigned to either an experimental group (dose per injection, 3 mg x kg(-1) testosterone propionate solubilized in 1 mL of safflower oil) or a control group (injected with an isovolumic amount of safflower oil alone). The effects of the steroid regimen on the serum lipoprotein profiles were followed after 1, 3, 5, and 7 wk of injections. To assess the relative effects of testosterone propionate, testicular mass was determined at the time of sacrifice. RESULTS: Testicular mass (mean +/- SE) was significantly lower (P<0.01) in the experimental group, 3.08+/-0.03 g, compared with that in controls, 3.82+/-0.05 g, by week 3 and continued to decline for the remainder of the steroid regimen, reaching a nadir of 2.70+/-0.01 g at week 5. No significant differences were observed between groups for total serum cholesterol, serum triacylglycerols, or serum low density lipoprotein (LDL)-C at any time point. However, at week 7, serum high density lipoprotein (HDL)-C (mean +/- SE) was significantly lower (P<0.02) in the testosterone treated animals, 32+/-2 mg x dL(-1), compared with that in controls, 47+/-2 mg x dL(-1). As a result, the ratio of total cholesterol to HDL-C (mean +/- SE) significantly increased (P<0.02) by the seventh week in the testosterone treated group, 3.5+/-0.2, versus controls, 2.5+/-0.2. CONCLUSIONS: The results suggest that while testosterone propionate injections elicit a reduction in testicular mass within 3 wk, the lipoprotein profile is not altered until week 7. Further, the only compromised parameter under the conditions of this study is the decrease in serum HDL-C.

Training enhanced hepatic gluconeogenesis: the importance for glucose homeostasis during exercise.

Endurance training has long been known to improve the individual's resistance to exercise-induced hypoglycemia. Traditionally attributed to a reduction in glucose uptake subsequent to enhanced fat oxidation, this issue has only recently been directly addressed. This paper briefly reviews the evidence for reduced glucose uptake versus enhanced glucose production in the improved hypoglycemic resistance following training. While whole body glucose removal and production may be reduced following training, this has only been demonstrated under exercising conditions in which glycemia demonstrates little deviation from rest. Under exercise conditions where untrained animals demonstrate substantial reductions in blood glucose, training enhanced hypoglycemic resistance has been shown to result entirely from enhanced glucose production via gluconeogenesis. Using the in situ perfused liver preparation, the authors have provided direct evidence for a training enhanced hepatic gluconeogenic capacity. The site of adaptation within the gluconeogenic pathway has now been constrained to below the level of the triose phosphates. Lack of evidence for suppressed skeletal muscle glucose uptake following training, a uniform observation for humans and rats, is also discussed. It is concluded that the improved hepatic gluconeogenic capacity of endurance trained individuals, at least in rats, is critical to their demonstrated resistance to exercise-induced hypoglycemia.

Enhanced hepatic gluconeogenic capacity for selected precursors after endurance training.

The effects of endurance training (running 90 min/day, 30 m/min, approximately 10% grade) on hepatic gluconeogenesis were studied in 24-h-fasted rats by using the isolated liver perfusion technique. After isolation, livers were perfused (single pass) for 30 min with Krebs-Henseleit bicarbonate buffer and fresh bovine red blood cells (hematocrit 20-24%) with no added substrate. Alanine (10 mM), dihydroxyacetone (20 mM), or glutamine (10 mM) was then added to the reservoir, and perfusions continued for 60 min. No significant differences were observed in perfusate pH, hematocrit, bile production, or serum alanine aminotransferase effluxing from livers from trained or control animals for any perfusion. Livers from trained animals that were perfused with 10 mM alanine demonstrated significantly higher rates of glucose production compared with livers from control animals (0.51 +/- 0.04 vs. 0.40 +/- 0.02 micromol.min-1.g liver-1, respectively). Elevations of a similar magnitude were observed for rates of [14C]alanine incorporation into [14C]glucose in livers from trained vs. control animals (8,797 +/- 728 vs. 6,962 +/- 649 dpm.min-1.g liver-1, respectively). Significant increases were also observed in hepatic alanine uptake (30%), oxygen consumption (23%), urea release (22%), and 14CO2 production (29%) of livers of endurance-trained animals. In contrast, no significant differences between groups were observed for hepatic glucose output after perfusions with either dihydroxyacetone (1.75 +/- 0.06 micromol.min-1.g liver-1) or glutamine (0.62 +/- 0.04 micromol.min-1.g liver-1). Further, during perfusions with dihydroxyacetone and glutamine, training had no significant impact on precursor uptake, oxygen consumption, or urea output. The current findings indicate a training-induced adaptation for hepatic gluconeogenesis located below the level of the triose phosphates.

Training suppresses hepatic lactate dehydrogenase activity without altering the isoenzyme profile.

A decrease in hepatic lactate dehydrogenase (LDH) activity following endurance training has been a consistent observation. In the present study, we sought to determine whether the training-induced decrease in hepatic LDH activity (pyruvate = substrate) was associated with a shift in the isoenzyme profile and/or alteration in other kinetic parameters. Animals (rats) were randomly assigned to either an endurance trained group (running 90 min at 30 m.min-1, 10% grade) or sedentary control group. Eight weeks of endurance training resulted in a significant decrease in maximal hepatic LDH activity for the forward reaction (pyruvate-->lactate), 107.3 +/- 5.5 mumol.min-1.g-1, when compared with control animals, 147.3 +/- 5.6 mumol.min-1.g-1. A similar decrease was observed for maximal LDH activity in the reverse reaction (lactate-->pyruvate), 49.8 +/- 2.1 vs 66.7 +/- 2.9 mumol.min-1.g-1, trained and controls, respectively. Training was also observed to decrease the Km for the reverse reaction, 5.18 +/- 0.78 mM vs 6.94 +/- 0.55 mM, for trained and controls, respectively. Km for the forward reaction was unaffected by training. Gel electrophoresis with densitometric evaluation revealed no shift in the isoenzyme pattern following endurance training. LDH5 accounted for 89% +/- 2%, whereas 6% +/- 0.5% was observed in LDH4, and 4% +/- 0.3% was observed in LDH3 for both groups. The densitometric area was approximately 34% lower from trained liver homogenates, a fractional decrease similar to that observed for maximal LDH activity. The decrease in hepatic LDH activity with endurance training appears attributable to a down regulation of enzyme content, with no significant alteration in isoenzyme distribution.

Endurance training fails to inhibit skeletal muscle glucose uptake during exercise.

The effects of endurance training (running 30 m/min, 10% grade for 90 min, 5 days/wk for 12 wk) on skeletal muscle glucose uptake during steady-state exercise (running 20 m/min) were studied in fed rats. A bolus injection of 2-[1,2-3H]deoxyglucose was administered to assess the glucose metabolic index (R'g), an indicator of glucose uptake, in individual tissues of the animal. After 55 min of rest or moderate exercise, various tissues were analyzed for accumulation of phosphorylated 2-[1,2-3H]-deoxyglucose and/or glycogen content. No differences were observed between groups in the resting glycogen content for any of the muscle samples examined. Resting plasma glucose concentrations were not significantly different between groups. Furthermore, no significant differences were observed in R'g between groups for any of the muscle examined (tibialis anterior, extensor digitorum longus, soleus, white gastrocnemius, red gastrocnemius). During exercise, plasma glucose concentrations were not significantly different between groups. Exercise significantly elevated R'g above resting values in the tibialis anterior (5-fold), soleus (3-fold), and red gastrocnemius (7.5-fold). Despite an elevated R'g for specific muscles during exercise, no significant differences were observed in glucose uptake between groups for any tissue examined. Concomitantly, trained animals exhibited significantly less muscle glycogen depletion during exercise compared with control animals. Liver glycogen levels were also significantly higher post-exercise in trained vs. control animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Enhanced gluconeogenesis from lactate in perfused livers after endurance training.

The effects of endurance training (running 90 min/day at 30 m/min, 10% grade) on hepatic gluconeogenesis were studied in 24-h-fasted rats with use of the isolated liver perfusion technique. After isolation, the liver was perfused (single pass) for 30 min with Krebs-Henseleit bicarbonate buffer and fresh bovine erythrocytes (hematocrit 22-24%) with no added substrate. Subsequent to the "washout" period, the reservoir was elevated with various concentrations of lactate and [U-14C]lactate (10,000 dpm/ml) to assess hepatic glucose production. Relative flow rates were not significantly different between trained (1.94 +/- 0.05 ml/g liver) and control livers (1.91 +/- 0.05 ml/g liver). Furthermore, no significant differences were observed in perfusate pH, hematocrit, bile production, or serum alanine aminotransferase effluxing from trained or control livers. At saturating arterial lactate concentrations (> 2 mM), the maximal rate (Vmax) for hepatic glucose production was significantly higher for trained (0.91 +/- 0.04 mumol.min-1 x g liver-1) than for control livers (0.73 +/- 0.02 mumol.min-1 x g liver-1). That this reflected increased gluconeogenesis is supported by a significant elevation in the Vmax for [14C]glucose production from trained (13,150 +/- 578 dpm.min-1 x g liver-1) compared with control livers (10,712 +/- 505 dpm.min-1 x g liver-1). Significant increases were also observed in the Vmax for lactate uptake (25%), O2 consumption (19%), and 14CO2 production (23%) from endurance-trained livers. The Km for hepatic glucose output, approximately 1.05 mM lactate, was unchanged after endurance training. These findings demonstrate that chronic physical activity results in an elevated capacity for hepatic gluconeogenesis, as assessed in situ at saturating lactate concentrations.

Training improves glucose homeostasis in rats during exercise via glucose production.

The effects of endurance training (running 1 h/day at 35 m/min, 10% grade) on glucose homeostasis during exercise (running 20 m/min) was studied in 30-h fasted rats. Primed-continuous infusion of [6-3H]- and [U-14C]glucose were employed to assess rates of appearance (Ra), disappearance (Rd), and apparent recycling. Training resulted in a 65% increase in skeletal muscle succinate dehydrogenase (SDH) activity but did not significantly influence body weight. Resting blood glucose concentrations were not significantly different between controls, 5.01 +/- 0.19 mM, and trained animals, 4.86 +/- 0.16 mM. Exercise resulted in a more rapid decline in blood glucose levels for control animals, reaching a value of 2.35 +/- 0.39 mM at 60 min, compared with 3.69 +/- 0.47 mM for trained animals. Glucose Ra was not significantly different between groups at rest, and rose for both groups during exercise. However, for controls Ra plateaued between 15 and 60 min of exercise at 11.03 +/- 0.73 mumol.100 g-1.min-1, whereas trained animals demonstrated a continuous rise to 17.13 +/- 1.18 mumol.100 g-1.min-1. Glucose Rd values were not significantly different between groups during the first 30 min of exercise but were significantly higher for trained animals during the final 30 min. As a result of the higher glucose Ra, trained animals demonstrated a smaller mean difference between Ra and Rd during exercise when compared with controls, -0.27 +/- 0.14 vs. -0.96 +/- 0.17 mumol.100 g-1.min-1. Trained animals further demonstrated significantly higher rates of glucose carbon recycling during the final 30 min of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)