Human blood neutrophil responses to prolonged exercise with and without a thermal clamp.

The purpose of this study was to investigate the effects of prolonged exercise with and without a thermal clamp on neutrophil trafficking, bacterial-stimulated neutrophil degranulation, stress hormones, and cytokine responses. Thirteen healthy male volunteers (means +/- SE: age 21 +/- 1 yr; mass 74.9 +/- 2.1 kg; maximal oxygen uptake 58 +/- 1 ml x kg(-1) x min(-1)) completed four randomly assigned, 2-h water-immersion trials separated by 7 days. Trials were exercise-induced heating (EX-H: water temperature 36 degrees C), exercise with a thermal clamp (EX-C: 24 degrees C), passive heating (PA-H: 38.5 degrees C), and control (CON: 35 degrees C). EX-H and EX-C was comprised of 2 h of deep water running at 58% maximal oxygen uptake. Blood samples were collected at pre-, post-, and 1 h postimmersion. Core body temperature was unaltered on CON, clamped on EX-C (-0.02 degrees C), and rose by 2.23 degrees C and 2.31 degrees C on EX-H and PA-H, respectively. Exercising with a thermal clamp did not blunt the neutrophilia postexercise (EX-C postexercise: 9.6 +/- 1.1 and EX-H postexercise: 9.8 +/- 1.0 x 10(9)/liter). Neutrophil degranulation decreased (P < 0.01) similarly immediately after PA-H (-21%), EX-C, and EX-H (-28%). EX-C blunted the circulating norepinephrine, cortisol, granulocyte-colony stimulating factor, and IL-6 response (P < 0.01) but not the plasma epinephrine and serum growth hormone response. These results show a similar neutrophilia and decrease in neutrophil degranulation after prolonged exercise with and without a thermal clamp. As such, the rise in core body temperature does not appear to mediate neutrophil trafficking and degranulation responses to prolonged exercise. In addition, these results suggest a limited role for cortisol, granulocyte-colony stimulating factor, and IL-6 in the observed neutrophil responses to prolonged exercise.     

Supramaximal exercise mobilizes hematopoietic progenitors and reticulocytes in athletes

Marathon runners show increased circulating CD34+ cell counts and postexercise release of interleukin-6 (IL-6), granulocyte-colony stimulating factor (G-CSF) and flt3-ligand (Bonsignore MR, Morici G, Santoro A, Pegano M, Cascio L, Bonnano A, Abate P, Mirabella F, Profita M, Insalaco G, Gioia M, Vignola AM, Majolino I, Testa U, and Hogg JC. J Appl Physiol 93: 1691-1697, 2002). In the present study we hypothesized that supramaximal ("all-out") exercise may acutely affect circulating progenitors and reticulocytes and investigated possible mechanisms involved. Progenitor release was measured by flow cytometry (n = 20) and clonogenic assays (n = 6) in 20 young competitive rowers (13 M, 7 F, age +/- SD: 17.1 +/- 2.1 yr, peak O2 consumption: 56.5 +/- 11.4 ml.min(-1).kg(-1)) at rest and shortly after 1,000 m "all-out." Release of reticulocytes, cortisol, muscle enzymes, neutrophil elastase, and several cytokines/growth factors was measured. Supramaximal exercise doubled circulating CD34+ cells (rest: 7.6 +/- 3.0, all-out: 16.3 +/- 9.1 cells/mul, P < 0.001), and increased immature reticulocyte fractions; AC133+ cells doubled, suggesting release of angiogenetic precursors. Erythrocyte burst forming units and colony forming units for granulocytes-monocytes and all blood series increased postexercise by 3.4-, 5.5-, and 4.8-fold, respectively (P < 0.01 for all). All-out rowing acutely increased plasma cortisol, neutrophil elastase, flt3-ligand, hepatocyte growth factor, VEGF, and transforming growth factor-beta1, and decreased erythropoietin; K-ligand, stromal-derived factor-1, IL-6, and G-CSF were unchanged. Therefore, all-out exercise is a physiological stimulus for progenitor release in athletes. Release of reticulocytes and proangiogenetic cells and mediators suggests tissue hypoxia as possibly involved in progenitor mobilization.     

Diurnal variation, response to eccentric exercise, and association of inflammatory mediators with muscle damage variables.

This investigation determined whether inflammatory mediators 1) have diurnal variations, 2) respond to high-force eccentric exercise, and 3) associate with markers of muscle damage after high-force eccentric exercise. College-aged men and women (n = 51) completed exercise (3 x 15 maximal eccentric elbow flexor actions using 1 arm) and control conditions in random order. Blood was collected preexercise and 4, 8, 12, 24, 48, and 96 h postexercise. Additional measures included maximal isometric force and midbiceps arm circumference (to detect swelling). Serum and plasma were analyzed for soluble tumor necrosis factor receptor-1 (sTNFR1), IL-6, C-reactive protein, cortisol, and creatine kinase (CK) activity. Relative to the 7:00 AM point in the control condition, diurnal decreases were measured at 12:00 PM and 4:00 PM for IL-6 and at 12:00 PM, 4:00 PM, and 8:00 PM for sTNFR1 and cortisol. sTNFR1, IL-6, CK, swelling, and soreness were higher in the exercise compared with the control condition. The largest of the inflammatory mediator responses was measured for IL-6 8 h postexercise in the exercise (3.00 +/- 3.59 pg/ml) relative to the control condition (1.15 +/- 0.99 pg/ml). The IL-6 response (time-matched exercise--control concentration) at 8 h associated (r > 0.282) with muscle soreness at 24 and 96 h, and the cortisol response at 8 h associated (r > 0.285) with swelling at 8, 24, and 96 h. Thus soreness and swelling, but not CK and strength loss, had a low association with the inflammatory response following eccentric exercise.     

Influence of gender, menstrual phase, and oral contraceptive use on immunological changes in response to prolonged cycling.

This study determined the influence of gender, menstrual phase (MP), and oral contraceptive (OC) use on immunological changes in response to endurance exercise. Twelve women and 11 men similar in age, aerobic power, and activity level cycled for 90 min at 65% maximal aerobic power. Women were OC users (n = 6) or nonusers (NOC) and cycled during the follicular (Fol) and the luteal (Lut) phases. Venous blood was collected before and after exercise to determine leukocyte counts, IL-6 concentrations, and cortisol. Higher resting levels of neutrophils (approximately 1.5-fold) and cortisol (approximately 2.5-fold) were found in OC vs. NOC and men. Exercise-induced immune cell count and IL-6 changes were similar between men and NOC, except for an approximately 38% greater lymphocyte response in NOC vs. men (P = 0.07). Neutrophil, monocyte, and lymphocyte responses to exercise during Lut in OC were greater than during Fol and also greater than the responses in men (P < or = 0.003). Changes in immune cell counts were consistently greater during Lut in OC vs. NOC, regardless of MP, but only neutrophil responses reached statistical significance (P = 0.01). The exercise-induced change in IL-6 was approximately 80% greater in NOC vs. OC during Fol (P = 0.06), but it was similar between these groups during Lut. Cortisol changes with exercise were not different between groups or MP. These results highlight the necessity to control for gender, and in particular OC use, when designing studies evaluating exercise and immunology.     

Low-dose estrogen therapy does not change postexercise hypotension, sympathetic nerve activity reduction, and vasodilation in healthy postmenopausal women

The aim of this study was to determine whether estrogen therapy enhances postexercise muscle sympathetic nerve activity (MSNA) decrease and vasodilation, resulting in a greater postexercise hypotension. Eighteen postmenopausal women received oral estrogen therapy (ET; n=9, 1 mg/day) or placebo (n=9) for 6 mo. They then participated in one 45-min exercise session (cycle ergometer at 50% of oxygen uptake peak) and one 45-min control session (seated rest) in random order. Blood pressure (BP, oscillometry), heart rate (HR), MSNA (microneurography), forearm blood flow (FBF, plethysmography), and forearm vascular resistance (FVR) were measured 60 min later. FVR was calculated. Data were analyzed using a two-way ANOVA. Although postexercise physiological responses were unaltered, HR was significantly lower in the ET group than in the placebo group (59+/-2 vs. 71+/-2 beats/min, P<0.01). In both groups, exercise produced significant decreases in systolic BP (145+/-3 vs. 154+/-3 mmHg, P=0.01), diastolic BP (71+/-3 vs. 75+/-2 mmHg, P=0.04), mean BP (89+/-2 vs. 93+/-2 mmHg, P=0.02), MSNA (29+/-2 vs. 35+/-1 bursts/min, P<0.01), and FVR (33+/-4 vs. 55+/-10 units, P=0.01), whereas it increased FBF (2.7+/-0.4 vs. 1.6+/-0.2 ml x min(-1) x 100 ml(-1), P=0.02) and did not change HR (64+/-2 vs. 65+/-2 beats/min, P=0.3). Although ET did not change postexercise BP, HR, MSNA, FBF, or FVR responses, it reduced absolute HR values at baseline and after exercise.     

Estrogen attenuates the exercise pressor reflex in female cats.

In humans, the pressor and muscle sympathetic nerve responses to static exercise are less in women than in men. The difference has been attributed to the effect of estrogen on the exercise pressor reflex. Estrogen receptors are abundant in areas of the dorsal horn receiving input from group III and IV muscle afferents, which comprise the sensory limb of the exercise pressor reflex arc. These findings prompted us to investigate the effect of estrogen on the spinal pathway of the exercise pressor reflex arc. Previously, we found that the threshold concentration of 17beta-estradiol needed to attenuate the exercise pressor reflex in male decerebrate cats was 10 microg/ml (Schmitt PM and Kaufman MP. J Appl Physiol 94: 1431-1436, 2003). The threshold concentration for female cats, however, is not known. Consequently, we applied 17beta-estradiol to a well covering the L6-S1 spinal cord in decerebrate female cats. The exercise pressor reflex was evoked by electrical stimulation of the L7 or S1 ventral root, a maneuver that caused the hindlimb muscles to contract statically. We found that the pressor response to contraction averaged 38 +/- 7 mmHg before the application of 17beta-estradiol (0.01 microg/ml) to the spinal cord, whereas it averaged only 23 +/- 4 mmHg 30 min after application (P < 0.05). Recovery of the pressor response to contraction was not obtained for 2 h after application of 17beta-estradiol. Application of 17beta-estradiol in a dose of 0.001 microg/ml had no effect on the exercise pressor reflex (n = 5). We conclude that the concentration of 17beta-estradiol required to attenuate the exercise pressor reflex is 1,000 times more dilute in female cats than that needed to attenuate this reflex in male cats.     

Reductions in blood pressure after acute exercise by hypertensive rats

Postexercise reductions in blood pressure at rest have been reported for hypertensive subjects. To determine whether post-exercise hypotension would occur in spontaneously hypertensive rats and to test the hypothesis that any reductions would result because of decreases in regional vascular resistances, hypertensive rats (n = 19) were instrumented with indwelling arterial catheters and Doppler probes to measure regional blood flows from the iliac, superior mesenteric, and renal arteries. Data were collected from animals who performed a 20- and a 40-min treadmill test at between 60 and 70% of their maximum O2 uptake. When the animals ran for 20 min, there was a pre- to postexercise drop in mean arterial pressure (MAP) from 158 +/- 3.6 to 150 +/- 3.6 mmHg (P less than 0.05), which was recorded 30 min after the exercise had ceased. The pre- to postexercise reduction in MAP after 40 min of treadmill running was from 154 +/- 3.1 to 138 +/- 3.0 mmHg (P less than 0.05) as recorded 30 min postexercise. Postexercise heart rate was significantly lower after the 40-min exercise bout, from a preexercise mean of 351 +/- 3 beats/min to 324 +/- 5 beats/min 30 min after the treadmill had stopped. Surprisingly, marked pre- to postexercise reductions in regional vascular resistance were not observed in either the iliac, superior mesenteric, or renal vascular beds. These data demonstrated the existence of postexercise hypotension in genetic hypertensive rats and suggested that reductions in cardiac output were the primary hemodynamic mechanism for this finding.     

Plasma adrenocorticotropin and cortisol responses to brief high-intensity exercise in humans

The purpose of this study is to examine plasma cortisol and adrenocorticotropin (ACTH) levels following a brief high-intensity bout of exercise. Each subject (n = 6) performed a 1-min bout of exercise on a cycle ergometer at 120% of his maximum O2 uptake. Blood samples were collected at rest, immediately following the exercise bout, and at 5, 15, and 30 min postexercise. Mean (+/- SE) plasma ACTH levels increased significantly (P less than 0.05) from 2.2 +/- 0.4 pmol/l at rest to 6.2 +/- 1.7 pmol/l immediately following exercise. Mean (+/- SE) plasma cortisol levels increased significantly from 0.40 +/- 0.04 mumol/l at rest to 0.52 +/- 0.04 mumol/l at 15 min postexercise. These data show that brief high-intensity exercise results in significant increases in plasma cortisol and ACTH levels. Furthermore, the temporal sequence between the two hormones suggests that the increase in plasma cortisol levels following brief high-intensity exercise is the result of ACTH-induced steroidogenesis in the adrenal cortex.     

Postexercise alpha-adrenergic receptor hyporesponsiveness in hypertensive rats is due to nitric oxide

We tested the hypothesis that a single bout of dynamic exercise produces a postexercise hypotension (PEH) and alpha(1)-adrenergic receptor hyporesponsiveness in spontaneously hypertensive rats (SHR). The postexercise alpha(1)-adrenergic receptor hyporesponsiveness is due to an enhanced buffering of vasoconstriction by nitric oxide. Male (n = 8) and female (n = 5) SHR were instrumented with a Doppler ultrasonic flow probe around the femoral artery. Distal to the flow probe, a microrenathane catheter was inserted into a branch of the femoral artery for the infusion of the alpha(1)-adrenergic receptor agonist phenylephrine (PE). A microrenathane catheter was inserted into the descending aorta via the left common carotid artery for measurements of arterial pressure (AP) and heart rate. Dose-response curves to PE (3.8 x 10(-3) - 1.98 x 10(-2)microg/kHz) were generated before and after a single bout of dynamic exercise. Postexercise AP was reduced in male (13 +/- 3 mmHg) and female SHR (18 +/- 7 mmHg). Postexercise vasoconstrictor responses to PE were reduced in males due to an enhanced influence of nitric oxide. However, in females, postexercise vasoconstrictor responses to PE were not altered. Results suggest that nitric oxide- mediated alpha(1)-adrenergic receptor hyporesponsiveness contributes to PEH in male but not female SHR.     

Quercetin's influence on exercise-induced changes in plasma cytokines and muscle and leukocyte cytokine mRNA.

Trained male cyclists (n = 40) ingested quercetin (Q; n = 20) (1,000 mg/day) or placebo (P; n = 20) supplements under randomized, double-blinded methods for 3 wk before and during a 3-day period in which subjects cycled for 3 h/day at approximately 57% maximal work rate. Blood samples were collected before and after each exercise session and assayed for plasma IL-6, IL-10, IL-1ra, IL-8, TNF-alpha, and monocyte chemoattractant protein 1, and leukocyte IL-10, IL-8, and IL-1ra mRNA. Muscle biopsies were obtained before and after the first and third exercise sessions and assayed for NF-kappaB and cyclooxygenase-2 (COX-2), IL-6, IL-8, IL-1beta, and TNF-alpha mRNA. Postexercise increases in plasma cytokines did not differ between groups, but the pattern of change over the 3-day exercise period tended to be lower in Q vs. P for IL-8 and TNF-alpha (P = 0.094 for both). mRNA increased significantly postexercise for each cytokine measured in blood leukocyte and muscle samples. Leukocyte IL-8 and IL-10 mRNA were significantly reduced in Q vs. P (interaction effects, P = 0.019 and 0.012, respectively) with no other leukocyte or muscle mRNA group differences. Muscle NF-kappaB did not increase postexercise and did not differ between Q and P. Muscle COX-2 mRNA increased significantly postexercise but did not differ between Q and P. In summary, 1 g/day quercetin supplementation by trained cyclists over a 24-day period diminished postexercise expression of leukocyte IL-8 and IL-10 mRNA, indicating that elevated plasma quercetin levels exerted some effects within the blood compartment. Quercetin did not, however, influence any of the muscle measures, including NF-kappaB content, cytokine mRNA, or COX-2 mRNA expression across a 3-day intensified exercise period.     

Differences in the postexercise threshold for cutaneous active vasodilation between men and women

The purpose of this study was to evaluate the possible differences in the postexercise cutaneous vasodilatory response between men and women. Fourteen subjects (7 men and 7 women) of similar age, body composition, and fitness status remained seated resting for 15 min or cycled for 15 min at 70% of peak oxygen consumption followed by 15 min of seated recovery. Subjects then donned a liquid-conditioned suit. Mean skin temperature was clamped at approximately 34 degrees C for 15 min. Mean skin temperature was then increased at a rate of 4.3 +/- 0.8 degrees C/h while local skin temperature was clamped at 34 degrees C. Skin blood flow was measured continuously at two forearm skin sites, one with (UT) and without (BT) (treated with bretylium tosylate) intact alpha-adrenergic vasoconstrictor activity. The exercise threshold for cutaneous vasodilation in women (37.51 +/- 0.08 degrees C and 37.58 +/- 0.04 degrees C for UT and BT, respectively) was greater than that measured in men (37.33 +/- 0.06 degrees C and 37.35 +/- 0.06 degrees C for UT and BT, respectively) (P < 0.05). Core temperatures were similar to baseline before the start of whole body warming for all conditions. Postexercise heart rate (HR) for the men (77 +/- 4 beats/min) and women (87 +/- 6 beats/min) were elevated above baseline (61 +/- 3 and 68 +/- 4 beats/min for men and women, respectively), whereas mean arterial pressure (MAP) for the men (84 +/- 3 mmHg) and women (79 +/- 3 mmHg) was reduced from baseline (93 +/- 3 and 93 +/- 4 mmHg for men and women, respectively) (P < 0.05). A greater increase in HR and a greater decrease in the MAP postexercise were noted in women (P < 0.05). No differences in core temperature, HR, and MAP were measured in the no-exercise trial. The postexercise threshold for cutaneous vasodilation measured at the UT and BT sites for men (37.15 +/- 0.03 degrees C and 37.16 +/- 0.04 degrees C, respectively) and women (37.36 +/- 0.05 degrees C and 37.42 +/- 0.03 degrees C, respectively) were elevated above no exercise (36.94 +/- 0.07 degrees C and 36.97 +/- 0.05 degrees C for men and 36.99 +/- 0.09 degrees C and 37.03 +/- 0.11 degrees C for women for the UT and BT sites, respectively) (P < 0.05). A difference in the magnitude of the thresholds was measured between women and men (P < 0.05). We conclude that women have a greater postexercise onset threshold for cutaneous vasodilation than do men and that the primary mechanism influencing the difference between men and women in postexercise skin blood flow is likely the result of an altered active vasodilatory response and not an increase in adrenergic vasoconstrictor tone.     

Effects of the menstrual cycle and sex on postexercise hemodynamics

Factors associated with the menstrual cycle, such as the endogenous hormones estrogen and progesterone, have dramatic effects on cardiovascular regulation. It is unknown how this affects postexercise hemodynamics. Therefore, we examined the effects of the menstrual cycle and sex on postexercise hemodynamics. We studied 14 normally menstruating women [24.0 (4.2) yr; SD] and 14 men [22.5 (3.5) yr] before and through 90 min after cycling at 60% .VO2(peak) for 60 min. Women were studied during their early follicular, ovulatory, and mid-luteal phases; men were studied once. In men and women during all phases studied, mean arterial pressure was decreased after exercise throughout 60 min (P < 0.001) postexercise and returned to preexercise values at 90 min (P = 0.089) postexercise. Systemic vascular conductance was increased following exercise in both sexes throughout 60 min (P = 0.005) postexercise and tended to be elevated at 90 min postexercise (P = 0.052), and femoral vascular conductance was increased following exercise throughout 90 min (P < 0.001) postexercise. Menstrual phase and sex had no effect on the percent reduction in arterial pressure (P = 0.360), the percent rise in systemic vascular conductance (P = 0.573), and the percent rise in femoral vascular conductance (P = 0.828) from before to after exercise, nor did the pattern of these responses differ across recovery with phase or sex. This suggests that postexercise hemodynamics are largely unaffected by sex or factors associated with the menstrual cycle.     

Effect of hydration state on resistance exercise-induced endocrine markers of anabolism, catabolism, and metabolism.

Hypohydration (decreased total body water) exacerbates the catabolic hormonal response to endurance exercise with unclear effects on anabolic hormones. Limited research exists that evaluates the effect of hypohydration on endocrine responses to resistance exercise; this work merits attention as the acute postexercise hormonal environment potently modulates resistance training adaptations. The purpose of this study was to examine the effect of hydration state on the endocrine and metabolic responses to resistance exercise. Seven healthy resistance-trained men (age = 23 +/- 4 yr, body mass = 87.8 +/- 6.8 kg, body fat = 11.5 +/- 5.2%) completed three identical resistance exercise bouts in different hydration states: euhydrated (EU), hypohydrated by approximately 2.5% body mass (HY25), and hypohydrated by approximately 5.0% body mass (HY50). Investigators manipulated hydration status via controlled water deprivation and exercise-heat stress. Cortisol, epinephrine, norepinephrine, testosterone, growth hormone, insulin-like growth factor-I, insulin, glucose, lactate, glycerol, and free fatty acids were measured during euhydrated rest, immediately preceding resistance exercise, immediately postexercise, and during 60 min of recovery. Body mass decreased 0.2 +/- 0.4, 2.4 +/- 0.4, and 4.8 +/- 0.4% during EU, HY25, and HY50, respectively, supported by humoral and urinary changes that clearly indicated subjects achieved three distinct hydration states. Hypohydration significantly 1) increased circulating concentrations of cortisol and norepinephrine, 2) attenuated the testosterone response to exercise, and 3) altered carbohydrate and lipid metabolism. These results suggest that hypohydration can modify the hormonal and metabolic response to resistance exercise, influencing the postexercise circulatory milieu.     

Early-phase neuroendocrine responses and strength adaptations following eccentric-enhanced resistance training

The purpose of this study was to evaluate the early-phase muscular performance adaptations to 5 weeks of traditional (TRAD) and eccentric-enhanced (ECC+) progressive resistance training and to compare the acute postexercise total testosterone (TT), bioavailable testosterone (BT), growth hormone (GH), and lactate responses in TRAD- and ECC+-trained individuals. Twenty-two previously untrained men (22.1 +/- 0.8 years) completed 1 familiarization and 2 baseline bouts, 15 exercise bouts (i.e., 3 times per week for 5 weeks), and 2 postintervention testing bouts. Anthropometric and 1 repetition maximum (1RM) measurements (i.e., bench press and squat) were assessed during both baseline and postintervention testing. Following baseline testing, participants were randomized into TRAD (4 sets of 6 repetitions at 52.5% 1RM) or ECC+ (3 sets of 6 repetitions at 40% 1RM concentric and 100% 1RM eccentric) groups and completed the 5-week progressive resistance training protocols. During the final exercise bout, blood samples acquired at rest and following exercise were assessed for serum TT, BT, GH, and blood lactate. Both groups experienced similar increases in bench press (approximately 10%) and squat (approximately 22%) strength during the exercise intervention. At the conclusion of training, postexercise TT and BT concentrations increased (approximately 13% and 21%, respectively, p < 0.05) and GH concentrations increased (approximately 750-1200%, p < 0.05) acutely following exercise in both protocols. Postexercise lactate accumulation was similar between the TRAD (5.4 +/- 0.4) and ECC+ (5.6 +/- 0.4) groups; however, the ECC+ group's lactate concentrations were significantly lower than those of the TRAD group 30 to 60 minutes into recovery. In conclusion, TRAD training and ECC+ training appear to result in similar muscular strength adaptations and neuroendocrine responses, while postexercise lactate clearance is enhanced following ECC+ training.     

Enhanced plasma IL-6 and IL-1ra responses to repeated vs. single bouts of prolonged cycling in elite athletes.

The impact of repeated bouts of exercise on plasma levels of interleukin (IL)-6 and IL-1 receptor antagonist (IL-1ra) was examined. Nine well-trained men participated in four different 24-h trials: Long [two bouts of exercise, at 0800-0915 and afternoon exercise (Ex-A), separated by 6 h]; Short (two bouts, at 1100-1215 and Ex-A, separated by 3 h); One (single bout performed at the same Ex-A as second bout in prior trials); and Rest (no exercise). All exercise bouts were performed on a cycle ergometer at 75% of maximal O(2) uptake and lasted 75 min. Peak IL-6 observed at the end of Ex-A was significantly higher in Short (8.8 +/- 1.3 pg/ml) than One (5.2 +/- 0.7 pg/ml) but not compared with Long (5.9 +/- 1.2 pg/ml). Peak IL-1ra observed 1 h postexercise was significantly higher in Short (1,774 +/- 373 pg/ml) than One (302 +/- 53 pg/ml) but not compared with Long (1,276 +/- 451 pg/ml). We conclude that, when a second bout of endurance exercise is performed after only 3 h of recovery, IL-6 and IL-1ra responses are elevated. This may be linked to muscle glycogen depletion.     

Aged men display blunted biorhythmic variation of muscle performance and physiological responses.

Aging is known to disrupt the "biological clock" that governs physiological variables at rest. This study sought to determine whether aged men demonstrated biorhythmic variation in muscle performance during resistance exercise and physiological responses to that stimulus. Ten aged (75.6 +/- 1.6 yr; mean +/- SE) men completed an isokinetic testing protocol of knee extensors and flexors at 0800, 1200, 1600, and 2000 h. Although time of day variation in peak torque was detectable, significant (P < or = 0.05) oscillation was established only in the knee flexors at 3.14 rad/s. Heart rate, blood pressure, and rectal temperature displayed no significant variation, but trends (P < 0.10) in oscillation of postexercise blood pressure and rectal temperature were noted. Temporal patterns in biorhythmic variation of muscle performance, as well as thermal and cardiovascular measures, emulated those observed in a previous study involving young men where the magnitude of variation was sufficient to achieve statistical significance. Similar to our earlier findings in young men, however, pre- and postexercise testosterone and cortisol concentrations demonstrated significant variation among aged men. These data confirm the blunting of biorhythmic variation in muscle performance and physiological variables, except for circulating hormones, in aged men.     

Physiological changes in hemostasis associated with acute exercise

Acute exercise enhances fibrinolytic (FA), factor VIII coagulant and factor VIII ristocetin cofactor activities, and increases the concentration of factor VIII-related antigen. Little is known concerning the mechanisms of these changes. To investigate possible relationships between exercise-induced changes in blood lactate, 2,3-diphosphoglycerate (DPG), and the hemostatic variables, a branching multistage treadmill protocol was used to exercise male volunteers to a maximum effort. Blood samples were drawn before, immediately post-, and 8 min postexercise. All hemostatic variables were significantly (P less than 0.05) increased postexercise. Highest values for factor VIII coagulant, factor VIII-related antigens and factor VIII ristocetin cofactor were observed at 8 min postexercise. Significant (P less than 0.001) correlations were found postexercise for lactate with factor VIII coagulant (r = 0.64), while no association between pre-, post-, or 8 min postexercise. Postexercise lactate demonstrated a significant correlation (r = +0.81), which was strengthened by including the preexercise high-density lipoprotein (HDL) concentrations (r = +0.87). Consequently, the expected postexercise FA may be calculated from the observed values for postexercise lactate and preexercise HDL. The correlations of lactate with postexercise FA and with postexercise factor VIII coagulant may reflect a common stimulus for these exercise-induced changes.     

Age-related enhancement of fatigue resistance is evident in men during both isometric and dynamic tasks.

It has been suggested that the effects of old age on the ability to resist fatigue may be task dependent. To test one aspect of this hypothesis, we compared the neuromuscular responses of nine young (26 +/- 4 yr, mean +/- SD) and nine older (72 +/- 4 yr) healthy, relatively sedentary men to intermittent isometric (3 min, 5 s contract/5 s rest) and dynamic (90 at 90 degrees /s) maximum voluntary contractions (MVC) of the ankle dorsiflexor muscles. To assess the mechanisms of fatigue (defined as the ratio of postexercise MVC to preexercise MVC), we also measured isometric central activation ratios (CAR), tetanic torque, contractile properties, and compound muscle action potentials before and immediately after exercise. Because dynamic contractions are more neurally complex and metabolically demanding than isometric contractions, we expected an age-related fatigue resistance observed during isometric exercise to be absent during dynamic exercise. In contrast, older men (O) fatigued less than young (Y) during both isometric (O = 0.77 +/- 0.07, Y = 0.66 +/- 0.02, mean +/- SE; P < 0.01) and dynamic (O = 0.45 +/- 0.07, Y = 0.27 +/- 0.02; P = 0.04) contractions (ratio of postexercise to preexercise MVC), with no evidence of peripheral activation failure in either group. We observed no obvious limitations in central activation in either group, as assessed using isometric CAR methods, after both isometric and dynamic contractions. Preexercise half-time of tetanic torque relaxation, which was longer in O compared with Y, was linearly associated with fatigue resistance during both protocols (r = 0.62 and 0.66, P < or = 0.004, n = 18). These results suggest that relative fatigue resistance is enhanced in older adults during both isometric and isokinetic contractions and that age-related changes in fatigue may be due largely to differences within the muscle itself.