Monocyte and T-cell responses to exercise training in elderly subjects

The purpose of this study was to examine the effects of exercise training on age-related impairment of immune parameters related to T-cell activation in elderly individuals. Twenty-four elderly subjects were assigned to an exercise training group (EXC: 3 men, 9 women; age 61-76 years) or a nonexercise control group (CON: 4 men, 8 women; age 62-79 years). Subjects in EXC participated in exercise sessions 2 d·wk(-1) for 12 weeks. The training session included stretching and endurance exercise (10 minutes), resistance training comprised leg extension, leg press, hip abduction, and hip adduction using exercise machine and each subject's body weight. Subjects in CON maintained their normal physical activity levels during the study period. Blood samples were collected before and after the training period. Samples were measured for the numbers of leukocytes, lymphocytes, and monocytes, and for CD3(+), CD4(+), CD8(+), CD28(+)CD4(+), CD28(+)CD8(+), TRL-4(+)CD14(+), and CD80(+)CD14(+) cells. The number of leukocytes, lymphocytes, monocytes, CD3(+), CD4(+), and CD8(+) cells did not change after 12 weeks in either EXC or CON. The number of CD28(+)CD8(+) cells increased significantly after training in EXC (p ≤ 0.05), although CON showed no significant change. In the EXC group, CD80(+)CD14(+) cell counts were significantly higher after training (p ≤ 0.05), but the TLR-4(+)CD14(+) cell counts were unchanged. In the CON group, no significant alteration existed in TLR-4(+)CD14(+) and CD80(+)CD14(+) cell numbers. In conclusion, exercise training in elderly people is associated with increased CD28-expressing Tc cells and CD80-expressing monocytes. Therefore, exercise training might upregulate monocyte and T-cell-mediated immunity in elderly people.     

Effects of resistance training on selected indexes of immune function in elderly women.

Women aged 67-84 yr were randomly assigned to either resistance exercise (RE, n = 15) or control group (C, n = 14). RE group completed 10 wk of resistance training, whereas C group maintained normal activity. Blood samples were obtained from the RE group (at the same time points as for resting C) at rest, immediately after resistance exercise, and 2 h after exercise before (week 0) and after (week 10) training. Mononuclear cell (CD3+, CD3+CD4+, CD3+CD8+, CD19+, and CD3-CD16+CD56+) number, lymphocyte proliferative (LP) response to mitogen, natural cell-mediated cytotoxicity (NCMC), and serum cortisol levels were determined. Strength increased significantly in RE subjects (%change 8-repetition maximum = 148%). No significant group, exercise time, or training effects were found for CD3+, CD3+CD4+, or CD3+CD8+ cells, but there was a significant exercise time effect for CD3-CD16+CD56+ cells. LP response was not different between groups, across exercise time, or after training. NCMC was increased immediately after exercise for RE subjects at week 0 and for RE and C groups at week 10. The week 0 and week 10 NCMC values were above baseline for both RE and C groups 2 h after exercise. In conclusion, acute resistance exercise did not result in postexercise suppression of NCMC or LP, and 10 wk of resistance training did not influence resting immune measures in women aged 67-84 yr.     

Effects of different macronutrient consumption following a resistance-training session on fat and carbohydrate metabolism

The effect of consuming meals of different macronutrient content on substrate oxidation following resistance exercise was examined in 9 resistance-trained men (26.2 +/- 2.4 years). Subjects completed 3 resistance exercise bouts of 8 exercises and 1 warm-up set (50% of 10 repetition maximum [RM]), which were followed by 3 sets of 10 repetitions (72.7 +/- 1.9% 10RM), with 60 seconds of rest between sets. Forty-five minutes after exercise, subjects consumed meals of high fat (HF, 37% carbohydrate, 18% protein, and 45% fat), high carbohydrate (HC, 79% carbohydrate, 20% protein, and 1% fat), or water (CON). Fat and carbohydrate oxidation were determined at 15-minute periods after meal consumption for 165 minutes. Blood was collected at preexercise (pre), premeal (0 minutes), and 15, 30, 45, 60, 90, 120, 150, and 180 minutes postmeal and was analyzed for insulin, glucose, triacylglycerols, and glycerol. There were no significant differences among the meal conditions for fat and carbohydrate oxidation. Insulin and glucose concentrations were significantly higher (p < 0.05) following HC at 15, 30, 45, 60, and 90 minutes compared to HF and CON. Triacylglycerol concentrations were significantly higher (p < 0.05) following HF at 90, 120, 150, and 180 minutes compared to HC and CON. Fat and carbohydrate oxidation were not affected by differences in macronutrient meal consumption after an acute bout of resistance training. Different macronutrient consumption does influence insulin, glucose, and triacylglycerol concentrations after resistance exercise.     

Quantitation of resistance training using the session rating of perceived exertion method

The purpose of this study was to apply the session rating of perceived exertion (RPE) method, which is known to work with aerobic training, to resistance training. Ten men (26.1 +/- 10.2 years) and 10 women (22.2 +/- 1.8 years), habituated to both aerobic and resistance training, performed 3 x 30 minutes aerobic training bouts on the cycle ergometer at intensities of 56%, 71%, and 83% Vo(2) peak and then rated the global intensity using the session RPE technique (e.g., 0-10) 30 minutes after the end of the session. They also performed 3 x 30 minutes resistance exercise bouts with 2 sets of 6 exercises at 50% (15 repetitions), 70% (10 repetitions), and 90% (4 repetitions) of 1 repetition maximum (1RM). After each set the exercisers rated the intensity of that exercise using the RPE scale. Thirty minutes after the end of the bout they rated the intensity of the whole session and of only the lifting components of the session, using the session RPE method. The rated intensity of exercise increased with the %Vo(2) peak and the %1RM. There was a general correspondence between the relative intensity (%Vo(2) peak and % 1RM) and the session RPE. Between different types of resistance exercise at the same relative intensity, the average RPE after each lift varied widely. The resistance training session RPE increased as the intensity increased despite a decrease in the total work performed (p < 0.05). Mean RPE and session RPE-lifting only also grew with increased intensity (p < 0.05). In many cases, the mean RPE, session RPE, and session RPE- lifting only measurements were different at given exercise intensities (p < 0.05). The session RPE appears to be a viable method for quantitating the intensity of resistance training, generally comparable to aerobic training. However, the session RPE may meaningfully underestimate the average intensity rated immediately after each set.     

Endurance training partially reverses dietary-induced leptin resistance in rodent skeletal muscle

Leptin acutely stimulates skeletal muscle fatty acid (FA) metabolism in lean rodents and humans. This stimulatory effect is eliminated following the feeding of high-fat diets in rodents as well as in obese humans. The mechanism(s) responsible for the development of skeletal muscle leptin resistance is unknown; however, a role for increased suppressor of cytokine signaling-3 (SOCS3) inhibition of the leptin receptor has been demonstrated in other rodent tissues. Furthermore, whether exercise intervention is an effective strategy to prevent or attenuate the development of skeletal muscle leptin resistance has not been investigated. Toward this end, 48 Sprague-Dawley rats (175-190 g; approximately 2-3 mo of age) were fed control or high-fat (60% kcal) diets for 4 wk and either remained sedentary or were treadmill trained. In control diet-fed animals that remained sedentary (CS) or were endurance trained (CT), leptin stimulated FA oxidation (CS +32 +/- 15%, CT +30 +/- 17%; P < 0.05), suppressed triacylglycerol (TAG) esterification (CS -17 +/- 7%, CT -24 +/- 8%; P < 0.05), and reduced the esterification-to-oxidation ratio (CS -19 +/- 13%, CT -29 +/- 10%; P < 0.001) in soleus muscle. High-fat feeding induced leptin resistance in the soleus of sedentary rats (FS), whereas endurance exercise training (FT) restored the ability of leptin to suppress TAG esterification (-19 +/- 9%, P = 0.038). Training did not completely restore the ability of leptin to stimulate FA oxidation. High-fat diets stimulated SOCS3 mRNA expression irrespective of training status (FS +451 +/- 120%, P = 0.024; FT +381 +/- 141%, P = 0.023). Thus the development of skeletal muscle leptin resistance appears to involve an increase in SOCS3 mRNA expression. Endurance training was generally effective in preventing the development of leptin resistance, although this did not appear to require a decrease in SOCS3 expression. Future studies should examine changes in the actual protein content of SOCS3 in muscle and establish whether aerobic exercise is also effective in treating leptin resistance in humans.     

Attenuation of T-lymphocyte demargination and adhesion molecule expression in response to moderate exercise in physically fit individuals.

The effects of physical fitness on leukocyte demargination and cellular adhesion molecule (CAM) responses to moderate exercise were examined. We assessed leukocyte subsets and CAM expression before, immediately after, and 10 min after a 20-min treadmill exercise at 65-70% peak oxygen consumption in fit vs. nonfit individuals. Physical fitness was determined by peak oxygen consumption during a treadmill test. Catecholamine levels were determined by radioenzymatic assay, and enumeration of cells and detection of CAM expression were assessed by flow cytometry. As expected, exercise led to significant increases in numbers of leukocyte subsets, regardless of fitness level (P < 0.01). Values returned to near resting levels 10 min after exercise. More importantly, physically fit individuals showed attenuated responses to the moderate-exercise challenge in numbers of CD3(+), CD4(+), CD8(+), memory (CD45RO(+)) CD4, and naive (CD45RA(+)62L(+)) CD4 and CD8 lymphocytes. Postexercise human leukocyte antigen-DR absent memory CD4(+) cell numbers were also lower in fit subjects. Increases in CD62L-expressing CD4(+) and CD8(+) lymphocytes and CD11a- expressing lymphocytes after exercise were also attenuated in fit individuals compared with nonfit individuals (P < 0.05). Catecholamine levels increased to a similar extent (P < 0.01) in both fitness groups. The findings suggest that physical fitness attenuates demargination of selected lymphocyte subsets in response to moderate exercise. Although the differences in plasma catecholamine responses were not significant between the groups, a possible mediating role of the sympathetic system remains to be further investigated. Being physically fit may offset exaggerated immune cell responses to stress.     

Effect of nutritionally enriched coffee consumption on aerobic and anaerobic exercise performance

The purpose of this study was to compare nutritionally enriched JavaFit coffee (JF) to commercially available decaffeinated coffee (P) with regard to impact on endurance and anaerobic power performance in a physically active, college-aged population. Ten subjects (8 men, 2 women) performed two 30-second Wingate anaerobic power tests and 2 cycle ergometer tests (75% VO2 max) to exhaustion. Mean VO2 was measured during each endurance exercise protocol. Excess postexercise oxygen consumption (EPOC) and respiratory exchange ratio (RER) were recorded for 30 minutes following all exercise sessions. Area under the curve analysis was used to compare EPOC between JF and P for all exercise sessions. No differences were seen between JF and P in any of the power performance measures. However, time to exhaustion was significantly (p = 0.05) higher in JF (35.3 +/- 15.2 minutes) compared with P (27.3 +/- 10.7 minutes). No difference between JF and P were seen in EPOC in either the aerobic or anaerobic exercise sessions. A significant (p < 0.05) difference in average 30-minute postanaerobic power exercise RER was seen between JF (0.87 +/- 0.04) and P (0.83 +/- 0.03), but not following endurance exercise. A nutritionally-enriched coffee beverage appears to enhance time to exhaustion during aerobic exercise, but does not provide an ergogenic benefit during anaerobic exercise.     

The effect of acute resistance exercise on serum malondialdehyde in resistance-trained and untrained collegiate men

The purposes of this study were to determine whether acute resistance exercise increases serum malondialdehyde (MDA) levels postexercise, and if so, whether resistance exercise training status influences the magnitude of the exercise-induced lipid peroxidation response. Twelve recreationally resistance-trained (RT) and 12 untrained (UT) men who did not have resistance exercise experience in the past year participated in this study. All subjects completed an 8-exercise circuit resistance exercise protocol consisting of 3 sets of 10 repetitions at 10 repetitions maximum for each exercise. Blood samples were obtained pre-exercise, at 5 minutes postexercise, and at 6, 24, and 48 hours postexercise. At pre-exercise, MDA (nmol.ml(-1)) averaged 3.41 +/- 0.25 (RT) and 3.20 +/- 0.25 (UT) and did not differ (p > 0.05) either between groups or over time. Creatine kinase (IU.L(-1)) was significantly (p < 0.05) elevated 5 minutes postexercise (170.6 +/- 25.8), 6 hours postexercise (290.3 +/- 34.4), 24 hours postexercise (365.5 +/- 49.9), and 48 hours postexercise (247.5 +/- 38.5) as compared with pre-exercise (126.4 +/- 20.2) for both groups. There was no difference (p > 0.05) in CK activity between groups. This study indicated that moderate-intensity whole-body resistance exercise had no effect on serum MDA concentration in RT and UT subjects.     

Strength training reduces arterial blood pressure but not sympathetic neural activity in young normotensive subjects.

The effects of resistance training on arterial blood pressure and muscle sympathetic nerve activity (MSNA) at rest have not been established. Although endurance training is commonly recommended to lower arterial blood pressure, it is not known whether similar adaptations occur with resistance training. Therefore, we tested the hypothesis that whole body resistance training reduces arterial blood pressure at rest, with concomitant reductions in MSNA. Twelve young [21 +/- 0.3 (SE) yr] subjects underwent a program of whole body resistance training 3 days/wk for 8 wk. Resting arterial blood pressure (n = 12; automated sphygmomanometer) and MSNA (n = 8; peroneal nerve microneurography) were measured during a 5-min period of supine rest before and after exercise training. Thirteen additional young (21 +/- 0.8 yr) subjects served as controls. Resistance training significantly increased one-repetition maximum values in all trained muscle groups (P < 0.001), and it significantly decreased systolic (130 +/- 3 to 121 +/- 2 mmHg; P = 0.01), diastolic (69 +/- 3 to 61 +/- 2 mmHg; P = 0.04), and mean (89 +/- 2 to 81 +/- 2 mmHg; P = 0.01) arterial blood pressures at rest. Resistance training did not affect MSNA or heart rate. Arterial blood pressures and MSNA were unchanged, but heart rate increased after 8 wk of relative inactivity for subjects in the control group (61 +/- 2 to 67 +/- 3 beats/min; P = 0.01). These results indicate that whole body resistance exercise training might decrease the risk for development of cardiovascular disease by lowering arterial blood pressure but that reductions of pressure are not coupled to resistance exercise-induced decreases of sympathetic tone.     

The effect of magnesium deficiency on glucose stimulated insulin secretion in rats

Weanling Sherman rats were pair-fed for 8 days on a control or a magnesium deficient diet containing 70.5% sucrose. After a 12-hour fast, the rats were injected intraperitoneally with glucose (250 mg/100 g body weight) and arterial blood was drawn at 0, 15, 30, 60, 90 minutes after injection. Before glucose loading, in magnesium deficient rats, plasma magnesium levels were significantly increased. The plasma triglyceride concentration was significantly higher in magnesium deficient rats compared to controls. After glucose loading, in the control group, the plasma insulin concentrations increased to 67.9 +/- 5.8 microU/ml at 15 minutes and returned to pretreatment levels by 30 minutes; in the magnesium-deficient rats, the plasma insulin levels were significantly lower at 15 minutes 32.9 +/- 5.6 microU/ml (P less than 0.01) and returned more slowly to the pre-challenge level. No significant differences were observed in plasma glucose levels between the two groups of rats.     

Resistance training alters the response of fed state mixed muscle protein synthesis in young men

Ten healthy young men (21.0 +/- 1.5 yr, 1.79 +/- 0.1 m, 82.7 +/- 14.7 kg, means +/- SD) participated in 8 wk of intense unilateral resistance training (knee extension exercise) such that one leg was trained (T) and the other acted as an untrained (UT) control. After the 8 wk of unilateral training, infusions of L-[ring-d(5)]phenylalanine, L-[ring-(13)C(6)]phenylalanine, and d(3)-alpha-ketoisocaproic acid were used to measure mixed muscle protein synthesis in the T and UT legs by the direct incorporation method [fractional synthetic rate (FSR)]. Protein synthesis was determined at rest as well as 4 h and 28 h after an acute bout of resistance exercise performed at the same intensity relative to the gain in single repetition maximum before and after training. Training increased mean muscle fiber cross-sectional area only in the T leg (type I: 16 +/- 10%; type II: 20 +/- 19%, P < 0.05). Acute resistance exercise increased muscle protein FSR in both legs at 4 h (T: 162 +/- 76%; UT: 108 +/- 62%, P < 0.01 vs. rest) with the increase in the T leg being significantly higher than in the UT leg at this time (P < 0.01). At 28 h postexercise, FSR in the T leg had returned to resting levels; however, the rate of protein synthesis in the UT leg remained elevated above resting (70 +/- 49%, P < 0.01). We conclude that resistance training attenuates the protein synthetic response to acute resistance exercise, despite higher initial increases in FSR, by shortening the duration for which protein synthesis is elevated.     

Increased concentrations of interleukin 1-β in whole blood cultures supernatants after 12 weeks of moderate endurance exercise

The aim of the study was to investigate whether a regular moderate endurance exercise programme influenced the in vitro cytokine synthesis by stimulated whole blood cultures. To this end, eight healthy subjects exercised moderately by running for 3-5 h a week over a period of 12 weeks, whilst seven other healthy subjects served as the control group. The intensity of the exercise was determined by lactic acid concentrations in the blood which were maintained between 1.8 and 2.5 mmol x l(-1). Over the period of training the running velocity producing the 4 mmol x l(-1) lactic acid threshold increased from 2.86 (SD 0.83) m x s(-1) to 3.06+/-0.79 m x s(-1) (P < or = 0.008). Blood samples were taken at rest before and after the training programme. The following blood parameters were determined: leucocyte count, differential leucocyte count, lymphocyte subpopulations [CD14 positive (+)/CD45+, CD4+/ CD25+, CD8+, CD16+/CD122+]. Whole blood cultures were stimulated with lipopolysaccarides [interleukin (IL)-1 beta and IL-6] and staphylococcal enterotoxin B [IL-2, soluble interleukin 2 receptor (sIL2-R) and interferon (IFN)-gamma]. Cytokine concentrations in the supernatants were measured using an enzyme-linked immunosorbent assay. The white blood cell count, differential leucocyte count, lymphocyte subset distribution and the expression of the CD25 and CD122 antigen on lymphocytes were unchanged by training. After the training programme the IL-1 beta production changed significantly [1496 (SD 264) pg ml(-1) before, compared to 2127 (SD 672) pg ml(-1) after training, P < or = 0.008]. In the control group these parameters remained unchanged. With respect to changes in the values in both groups the syntheses of IL-1 beta (P < or = 0.023) and IL-6 (P < or = 0.021) were significantly higher after regular training. The syntheses of IL-2, sIL-2 and INF-gamma were not significantly influenced. Regular endurance exercise influenced the in vitro production of monocyte derived cytokines, while the effect of exercise on the cytokines synthesized by T-cells appeared to be of lesser importance.     

Resistance-training-induced adaptations in skeletal muscle protein turnover in the fed state

Resistance training changes the balance of muscle protein turnover, leading to gains in muscle mass. A longitudinal design was employed to assess the effect that resistance training had on muscle protein turnover in the fed state. A secondary goal was investigation of the potential interactive effects of creatine (Cr) monohydrate supplementation on resistance-training-induced adaptations. Young (N = 19, 23.7 +/- 3.2 year), untrained (UT), healthy male subjects completed an 8-week resistance-training program (6 d/week). Supplementation with Cr had no impact on any of the variables studied; hence, all subsequent data were pooled. In the UT and trained (T) state, subjects performed an acute bout of resistance exercise with a single leg (exercised, EX), while their contralateral leg acted as a nonexercised (NE) control. Following exercise, subjects were fed while receiving a primed constant infusion of [d5]- and [15N]-phenylalanine to determine the fractional synthetic and breakdown rates (FSR and FBR), respectively, of skeletal muscle proteins. Acute exercise increased FSR (UT-NE, 0.065 +/- 0.025 %/h; UT-EX, 0.088 +/- 0.032 %/h; P < 0.01) and FBR (UT-NE, 0.047 +/- 0.023 %/h; UT-EX, 0.058 +/- 0.026 %/h; P < 0.05). Net balance (BAL = FSR - FBR) was positive in both legs (P < 0.05) but was significantly greater (+65%) in the EX versus the NE leg (P < 0.05). Muscle protein FSR and FBR were greater at rest following T (FSR for T-NE vs. UT-NE, +46%, P < 0.01; FBR for T-NE vs. UT-NE, +81%, P < 0.05). Resistance training attenuated the acute exercise-induced rise in FSR (T-NE vs. T-EX, +20%, P = 0.65). The present results demonstrate that resistance training resulted in an elevated resting muscle protein turnover but an attenuation of the acute response of muscle protein turnover to a single bout of resistance exercise.     

Effects of endurance exercise training on muscle glycogen accumulation in humans.

The purpose of this investigation was to determine whether endurance exercise training increases the ability of human skeletal muscle to accumulate glycogen after exercise. Subjects (4 women and 2 men, 31 +/- 8 yr old) performed high-intensity stationary cycling 3 days/wk and continuous running 3 days/wk for 10 wk. Muscle glycogen concentration was measured after a glycogen-depleting exercise bout before and after endurance training. Muscle glycogen accumulation rate from 15 min to 6 h after exercise was twofold higher (P < 0.05) in the trained than in the untrained state: 10.5 +/- 0.2 and 4.5 +/- 1.3 mmol. kg wet wt(-1). h(-1), respectively. Muscle glycogen concentration was higher (P < 0.05) in the trained than in the untrained state at 15 min, 6 h, and 48 h after exercise. Muscle GLUT-4 content after exercise was twofold higher (P < 0.05) in the trained than in the untrained state (10.7 +/- 1.2 and 4.7 +/- 0.7 optical density units, respectively) and was correlated with muscle glycogen concentration 6 h after exercise (r = 0.64, P < 0.05). Total glycogen synthase activity and the percentage of glycogen synthase I were not significantly different before and after training at 15 min, 6 h, and 48 h after exercise. We conclude that endurance exercise training enhances the capacity of human skeletal muscle to accumulate glycogen after glycogen-depleting exercise.     

Exercise increases serum Hsp72 in humans

Recent evidence suggests that heat shock proteins (Hsps) may have an important systemic role as a signal to activate the immune system. Since acute exercise is known to induce Hsp72 (the inducible form of the 70-kDa family of Hsp) in a variety of tissues including contracting skeletal muscle, we hypothesized that such exercise would result in the release of Hsp72 from stressed cells into the blood. Six humans (5 males, 1 female) ran on a treadmill for 60 minutes at a workload corresponding to 70% of their peak oxygen consumption. Blood was sampled from a forearm vein at rest (R), 30 minutes during exercise, immediately postexercise (60 minutes), and 2, 8, and 24 hours after exercise. These samples were analyzed for serum Hsp72 protein. In addition, plasma creatine kinase (CK) was measured at these time points as a crude marker of muscle damage. With the exception of the sample collected at 30 minutes, muscle biopsies (n = 5 males) were also obtained from the vastus lateralis at the time of blood sampling and analyzed for Hsp72 gene and protein expression. Serum Hsp72 protein increased from rest, both during and after exercise (0.13 0.10 vs 0.87+/-0.24 and 1.02+/-0.41 ng/mL at rest, 30 and 60 minutes, respectively, P < 0.05, mean SE). In addition, plasma CK was elevated (P < 0.05) 8 hours postexercise. Skeletal muscle Hsp72 mRNA expression increased 6.5-fold (P < 0.05) from rest 2 hours postexercise, and although there was a tendency for Hsp72 protein expression to be elevated 2 and 8 hours following exercise compared with rest, results were not statistically significant. The increase in serum Hsp72 preceded any increase in Hsp72 gene or protein expression in contracting muscle, suggesting that Hsp72 was released from other tissues or organs. This study is the first to demonstrate that acute exercise can increase Hsp72 in the peripheral circulation, suggesting that during stress these proteins may indeed have a systemic role.     

Arterial compliance of rowers: implications for combined aerobic and strength training on arterial elasticity

Regular endurance exercise increases central arterial compliance, whereas resistance training decreases it. It is not known how the vasculature adapts to a combination of endurance and resistance training. Rowing is unique, because its training encompasses endurance- and strength-training components. We used a cross-sectional study design to determine arterial compliance of 15 healthy, habitual rowers [50 +/- 9 (SD) yr, 11 men and 4 women] and 15 sedentary controls (52 +/- 8 yr, 10 men and 5 women). Rowers had been training 5.4 +/- 1.2 days/wk for 5.7 +/- 4.0 yr. The two groups were matched for age, body composition, blood pressure, and metabolic risk factors. Central arterial compliance (simultaneous ultrasound and applanation tonometry on the common carotid artery) was higher (P < 0.001) and carotid beta-stiffness index was lower (P < 0.001) in rowers than in sedentary controls. There were no group differences for measures of peripheral (femoral) arterial stiffness. The higher central arterial compliance in rowers was associated with a greater cardiovagal baroreflex sensitivity, as estimated during a Valsalva maneuver (r = 0.54, P < 0.005). In conclusion, regular rowing exercise in middle-aged and older adults is associated with a favorable effect on the elastic properties of the central arteries. Our results suggest that simultaneously performed endurance training may negate the stiffening effects of strength training.     

Effect of a pre-exercise energy supplement on the acute hormonal response to resistance exercise

The effect of a pre-exercise energy sport drink on the acute hormonal response to resistance exercise was examined in eight experienced resistance trained men. Subjects were randomly provided either a placebo (P: maltodextrin) or the supplement (S: combination of branched chain amino acids, creatine, taurine, caffeine, and glucuronolactone). Subjects performed 6 sets of no more than 10 repetitions of the squat exercise at 75% of their 1 repetition maximum (1RM) with 2 minutes of rest between sets. Blood draws occurred at baseline pre-exercise, immediately post- (IP), 15 minutes post- (15P), and 30-minutes post (30P) exercise for measurement of serum growth hormone, total and free testosterone, cortisol, and insulin concentrations. Although significant differences were seen only at set 5, the total number of repetitions and training volume tended (p = 0.08) to be higher with S compared to P. Serum growth hormone and insulin concentrations were significantly higher at 15P and IP, respectively, in S compared to P. Results suggest that a pre-exercise energy S consumed 10 minutes before resistance exercise can enhance acute exercise performance by increasing the number of repetitions performed and the total volume of exercise. The enhanced exercise performance resulted in a significantly greater increase in both growth hormone and insulin concentrations, indicating an augmented anabolic hormone response to this pre-exercise S.     

Hypertrophy of skeletal muscle in diabetic rats in response to chronic resistance exercise.

This study had the following objectives: 1) to determine whether diabetic rats could increase muscle mass due to a physiological manipulation (chronic resistance exercise), 2) to determine whether exercise training status modifies the effect of the last bout of exercise on elevations in rates of protein synthesis, and 3) to determine whether chronic resistance exercise alters basal glycemia. Groups consisted of diabetic or nondiabetic rats that performed progressive resistance exercise for 8 wk, performed acute resistance exercise, or remained sedentary. Arterial plasma insulin in diabetic groups was reduced by about one-half (P < 0.05) compared with nondiabetic groups. Soleus and gastrocnemius-plantaris complex muscle wet weights were lower because of diabetes, but in response to chronic exercise these muscles hypertrophied in diabetic (0.028 +/- 0.003 vs. 0.032 +/- 0.0015 g/cm for sedentary vs. exercised soleus and 0.42 +/- 0.068 vs. 0.53 +/- 0.041 g/cm for sedentary vs. exercised gastrocnemius-plantaris, both P < 0.05) but not in nondiabetic (0.041 +/- 0.0026 vs. 0.042 +/- 0.003 g/cm for sedentary vs. exercised soleus and 0.72 +/- 0.015 vs. 0.69 +/- 0.013 g/cm for sedentary vs. exercised gastrocnemius-plantaris) rats when muscle weight was expressed relative to tibial length or body weight (data not shown). Another group of diabetic rats that lifted heavier weights showed muscle hypertrophy. Rates of protein synthesis were higher in red gastrocnemius in chronically exercised than in sedentary rats: 155 +/- 11 and 170 +/- 7 nmol phenylalanine incorporated x g muscle(-1) x h(-1) in exercised diabetic and nondiabetic rats vs. 110 +/- 14 and 143 +/- 7 nmol phenylalanine incorporated x g muscle(-1) x h(-1) in sedentary diabetic and nondiabetic rats. These elevations, however, were lower than in acutely exercised (but untrained) rats: 176 +/- 15 and 193 +/- 8 nmol phenylalanine incorporated x g muscle(-1) x h(-1) in diabetic and nondiabetic rats. Finally, chronic exercise training in diabetic rats was associated with reductions in basal glycemia, and such reductions did not occur in sedentary diabetic groups. These data demonstrate that, despite lower circulating insulin concentrations, diabetic rats can increase muscle mass in response to a physiological stimulus.     

Cell numbers and in vitro responses of leucocytes and lymphocyte subpopulations following maximal exercise and interval training sessions of different intensities.

In vitro lymphocyte function and the mobilisation of peripheral blood leucocytes was examined in eight trained subjects who undertook an incremental exercise test to exhaustion and a series of interval training sessions. Venous blood samples were obtained before the incremental test, immediately after, and 30, 60, and 120 min after the test. Interval training sessions were undertaken on separate days and the exercise intensities for each of the different sessions were 30%, 60%, 90% and 120% of their maximal work capacity respectively, as determined from the incremental exercise test. There were 15 exercise periods of 1-min duration separated by recovery intervals of 2 min in each session. Venous blood samples were obtained immediately after each training session. Significant increases in lymphocyte subpopulations (CD3+, CD4+, CD8+, CD20+, and CD56+) occurred following both maximal and supramaximal exercise. This was accompanied by a significant decrease in the response of cultures of peripheral blood lymphocytes to Concanavalin A (ConA), a T-cell mitogen. The state of lymphocyte activation in vivo as measured by CD25+ surface antigen was not, however, affected by acute exercise. The total number of lymphocytes, distribution of lymphocyte subpopulations and in vitro lymphocyte response to ConA had returned to pre-exercise levels within half an hour of termination of exercise but serum cortisol concentrations had not begun to fall at this time. There was a significant decrease in the CD4+:CD8+ cell ratio following exercise; this was more the result of increases in CD3-CD8+ cells (CD8+ natural killer cells) than to CD3+CD8+ cells (CD8+ T-lymphocytes). Decreased responsiveness of T-cells to T-cell mitogens, postexercise, may have been the result of decreases in the percentage of T-cells in postexercise mixed lymphocyte cultures rather than depressed cell function. The cause of this was an increase in the percentage of natural killer cells which did not respond to the T-cell mitogen. The results indicated that while a substantial immediate in vitro "immunomodulation" occurred with acute exercise, this did not reflect an immunosuppression but was rather the result of changes in the proportions of reactive cells in mononuclear cell cultures. We have also demonstrated that the degree of the change in distribution of lymphocyte subpopulation numbers and responsiveness of peripheral blood mononuclear cells in in vitro mitogen reactions increased with increasing exercise intensity. Plasma volume changes may have contributed to some of the changes seen in leucocyte population and subpopulation numbers during and following exercise.     

Distribution and mitogen response of peripheral blood lymphocytes after exertional heat injury.

To determine whether immune disturbances during exertional heat injury (EHI) could be distinguished from those due to exercise (E), peripheral lymphocyte subset distributions and phytohemagglutinin-stimulated CD69 mitogen responses as discriminated by flow cytometry were studied in military recruits [18.7 +/- 0.3 (SE) yr old] training in warm weather. An E group (3 men and 3 women) ran 1.75-2 miles. During similar E, 11 recruits (10 men and 1 woman) presented with suspected EHI. EHI (40.4 +/- 0.3 degrees C) vs. E (38.6 +/- 0.2 degrees C) body temperature was significantly elevated (P < 0.05). Heat illness was largely classified as EHI, not heatstroke, because central nervous system manifestations were generally mild. Blood was collected at E completion or EHI onset (0 h) and 2 and 24 h later. At 0 h (EHI vs. E), suppressor, natural killer, and total lymphocyte counts were significantly elevated, helper and B lymphocyte counts remained similar, and the helper-to-suppressor ratio was significantly depressed. By 2 h, immune cell dynamics between groups were similar. From 0 to 24 h, T lymphocyte subsets revealed significantly reduced phytohemagglutinin responses (percent CD69 and mean CD69 fluorescent intensity) in EHI vs. E. Thus immune cell dynamics with EHI were distinguishable from E. Because heat stress as reported in exercise or heatstroke is associated with similar immune cell disturbances, these findings in EHI contributed to the suggestion that heat stress of varying severity shares a common pathophysiological process influencing the immune system.