Preserved flow-mediated dilation in the inactive legs of spinal cord-injured individuals

The aim of the study was to assess endothelial function, measured by flow-mediated dilation (FMD), in an inactive extremity (leg) and chronically active extremity (arm) within one subject. Eleven male spinal cord-injured (SCI) individuals and eleven male controls (C) were included. Echo Doppler measurements were performed to measure FMD responses after 10 and 5 min of arterial occlusion of the leg (superficial femoral artery, SFA) and the arm (brachial artery, BA), respectively. A nitroglycerine spray was administered to determine the endothelium independent vasodilatation in the SFA. In the SFA, relative changes in FMD were significantly enhanced in SCI compared with C (SCI: 14.1 +/- 1.3%; C: 9.2 +/- 2.3%), whereas no differences were found in the BA (SCI: 12.5 +/- 2.9%; C: 14.2 +/- 3.3%). Because the FMD response is directly proportional to the magnitude of the stimulus, the FMD response was also expressed relative to the shear rate. No differences between the groups were found for the FMD-to-shear rate ratio in the SFA (SCI:0.061 +/- 0.023%/s(-1); C: 0.049 +/- 0.024%/s(-1)), whereas the FMD-to-shear rate ratio was significantly decreased in the BA of SCI individuals (SCI: 0.037 +/- 0.01%/s(-1); C: 0.061 +/- 0.027%/s(-1)). The relative dilatory response to nitroglycerine did not differ between the groups. (SCI: 15.6 +/- 2.0%; C: 13.4 +/- 2.3%). In conclusion, our results indicate that SCI individuals have a preserved endothelial function in the inactive legs and possibly an attenuated endothelial function in the active arms compared with controls.     

Changes in arterial distensibility and flow-mediated dilation after acute resistance vs. aerobic exercise

Previous research has shown significantly lower arterial distensibility (AD) after resistance exercise (RE) yet higher AD after aerobic exercise (AE). These changes may be related to exercise-induced differences in vasodilatory capacity. The purpose of this study was to investigate the vasodilatory and AD responses to acute AE and RE. Forearm blood flow (FBF) during reactive hyperemia (RH) was assessed before and 60 minutes after exercise, whereas aortic and femoral pulse wave velocity was measured as an index of arterial stiffness pre, 40, and 60 minutes after an acute bout of AE (30-minute leg ergometry at 65% of VO2peak) and RE (3 sets, 10 reps; upper and lower body at 65% 1 repetition maximum) in 10 male subjects (24.9 ± 0.86 years). Area under the curve (AUC) was employed to determine differences in flow. After the intervention, we found that central pulse wave velocity decreased 8% after AE and remained depressed at this level through 60 minutes of observation, whereas RE increased central pulse wave velocity 9.8% from pre to 40 and 60 minutes postexercise. Area under the curve for FBF-RH significantly increased 38% after RE, yet there was no significant change after AE. Forearm vasodilatory capacity increased after acute RE but not after acute AE. This suggests that changes in AD may be disassociated from changes in vasodilatory capacity after acute exercise. Further, in a direct comparison of RE vs. AE, we have shown that RE has greater increases in limb blood flow and augments postexercise hypotension greater at 40 minutes postexercise when compared to AE.     

Heterogenous vasodilator pathways underlie flow-mediated dilation in men and women

This study investigated the sex differences in the contribution of nitric oxide (NO) and prostaglandins (PGs) to flow-mediated dilation (FMD). Radial artery (RA) FMD, assessed as the dilatory response to 5-min distal cuff occlusion, was repeated after three separate brachial artery infusions of saline (SAL), N(G)-monomethyl-L-arginine (L-NMMA), and ketorolac (KETO) + L-NMMA in healthy younger men (M; n = 8) and women (W; n = 8). In eight subjects (4 M, 4W) RA FMD was reassessed on a separate day with drug order reversed (SAL, KETO, and L-NMMA + KETO). RA FMD was calculated as the peak dilatory response observed relative to baseline (%FMD) and expressed relative to the corresponding area under the curve shear stress (%FMD/AUC SS). L-NMMA reduced %FMD similarly and modestly (P = 0.68 for sex * trial interaction) in M and W (all subjects: 10.0 ± 3.8 to 7.6 ± 4.7%; P = 0.03) with no further effect of KETO (P = 0.68). However, all sex * trial and trial effects on %FMD/AUC SS for l-NMMA and KETO + l-NMMA were insignificant (all P > 0.20). There was also substantial heterogeneity of the magnitude and direction of dilator responses to blockade. After l-NMMA infusion, subjects exhibited both reduced (n = 14; range: 11 to 78% decrease) and augmented (n = 2; range: 1 to 96% increase) %FMD. Following KETO + l-NMMA, seven subjects exhibited reduced dilation (range: 10 to 115% decrease) and nine subjects exhibited augmented dilation (range: 1 to 212% increase). Reversing drug order did not change the nature of the findings. These findings suggest that RA FMD is not fully or uniformly NO dependent in either men or women, and that there is heterogeneity in the pathways underlying the conduit dilatory response to ischemia.     

Characterization of the cortisol response to incremental exercise in physically active young men

This study examined the cortisol response to incremental exercise; specifically to see if there was an increase in blood cortisol levels at low intensity exercise (i.e., < 60% VO2 intensity threshold) and determine whether a linear relationship existed between the blood cortisol responses and exercise of increasing workloads (i.e., intensity). Healthy, physically active young men (n = 11) completed exercise tests involving progressive workload stages (3 min) to determine peak oxygen uptake responses (VO2). Blood specimens were collected at rest and at the end of each stage and analyzed for cortisol. Results showed cortisol was significantly increased from resting levels at the end of the first exercise stage (80 W; 41.9 +/- 5.4% peak VO2) and remained significantly elevated from rest until the exercise ended. Interestingly, however, the cortisol concentrations observed at 80 W through 200 W did not significantly differ from one another. Thereafter, during the final two stages of exercise the cortisol concentrations increased further (p < 0.01). The subjects exceeded their individual lactate thresholds over these last two stages of exercise. Regression modeling to characterize the cortisol response resulted in significant regression coefficients (r = 0.415 [linear] and r = 0.655 [3rd order polynominal], respectively; p < 0.05). Comparative testing (Hotelling test) between the two regression coefficents revealed the polynominal model (sigmoidal curve) was the significantly stronger of the two (p = 0.05). In conclusion, the present findings refute the concept that low intensity exercise will not provoke a significant change in blood cortisol levels and suggest the response to incremental exercise involving increasing exercise workloads (i.e., intensities) are not entirely linear in nature. Specifically, a sigmoid curve more highly accurately characterizes the cortisol response to such exercise.     

Remote ischemic preconditioning prevents reduction in brachial artery flow-mediated dilation after strenuous exercise

Strenuous exercise is associated with an immediate decrease in endothelial function. Repeated bouts of ischemia followed by reperfusion, known as remote ischemic preconditioning (RIPC), is able to protect the endothelium against ischemia-induced injury beyond the ischemic area. We examined the hypothesis that RIPC prevents the decrease in endothelial function observed after strenuous exercise in healthy men. In a randomized, crossover study, 13 healthy men performed running exercise preceded by RIPC of the lower limbs (4 × 5-min 220-mmHg bilateral occlusion) or a sham intervention (sham; 4 × 5-min 20-mmHg bilateral occlusion). Participants performed a graded maximal treadmill running test, followed by a 5-km time trial (TT). Brachial artery endothelial function was examined before and after RIPC or sham, as well as after the 5-km TT. We measured flow-mediated dilation (FMD), an index of endothelium-dependent function, using high-resolution echo-Doppler. We also calculated the shear rate area-under-the-curve (from cuff deflation to peak dilatation; SR(AUC)). Data are described as mean and 95% confidence intervals. FMD changed by <0.6% immediately after both ischemic preconditioning (IPC) and sham interventions (P > 0.30). In the sham trial, FMD changed from 5.1 (4.4-5.9) to 3.7% (2.6-4.8) following the 5-km TT (P = 0.02). In the RIPC trial, FMD changed negligibly from 5.4 (4.4-6.4) post-IPC and 5.7% (4.6-6.8) post 5-km TT (P = 0.60). Baseline diameter, SR(AUC), and time-to-peak diameter were all increased following the 5-km TT (P < 0.05), but these changes did not influence the IPC-mediated maintenance of FMD. In conclusion, these data indicate that strenuous lower-limb exercise results in an acute decrease in brachial artery FMD of ～1.4% in healthy men. However, we have shown for the first time that prior RIPC of the lower limbs maintains postexercise brachial artery endothelium-dependent function at preexercise levels.     

Effect of acute exercise on some haematological parameters and neutrophil functions in active and inactive subjects

In this work we studied the possible effects of acute exercise on some haematological parameters and on some functions of neutrophils in seven active and six inactive subjects. Physical exercise (10 min on a cycle ergometer at a heart rate of 150 beats · min^–1) induced a significant increase in total leucocyte, lymphocyte and neutrophil concentrations in active subjects; serum iron and ferritin concentrations were lower in active compared to inactive subjects. Cellular adhesion, bactericidal activity and superoxide anion production did not change after exercise, while we also observed some differences between active and inactive subjects before exercise. In particular, the neutrophils from active subjects showed a significantly higher percentage of adhesion, higher bactericidal activity and lower superoxide anion production. In conclusion, the training induced changes in some neutrophil functions, while acute exercise influenced, overall, leucocyte concentrations.     

Lipid oxidation according to intensity and exercise duration in overweight men and women

Objective: Our objective was to compare the effect of different exercise intensities on lipid oxidation in overweight men and women. Research Methods and Procedures: Nine young, healthy, overweight men and women were studied (age, 31.4 ± 2.3 and 26.7 ± 2.1 years; BMI, 27.9 ± 0.4 and 27.2 ± 0.5; for men and women, respectively). On one study day, the subjects first performed 30 minutes of cycling exercise at 30% of their maximal oxygen uptake (Vo _2max; E1 session), followed by 30 minutes of exercise at 50% Vo _2max (E2 session). On a second study day, a similar E1 session was followed by 30 minutes of exercise at 70% Vo _2max (E3 session). From the gas exchange measurements, the respiratory exchange ratio (RER) and the fat oxidation rate (FOR) were calculated. Plasma concentrations of glycerol and non‐esterified fatty acids (NEFAs) were assayed. Results: RER was significantly lower for women during only the E1 session. For both sexes, RER decreased over time during the E2 and E3 sessions. During the E1 session, the FOR per kilogram of lean mass (LM) was higher among women, and it did not change over time despite an increase in plasma NEFAs. FOR per kilogram of LM was higher during the E2 exercise for both sexes. During E2 and E3 sessions, as the exercise time was prolonged, the FOR/kg LM increased simultaneously with the increase in the plasma glycerol. Discussion: Lipid oxidation during exercise is optimized for moderate and lengthy exercise. The enhancement of lipid oxidation occurring over time during moderate‐ and high‐intensity exercises could be, in part, linked to the improvement of lipid mobilization. This fact is discussed to shed light on exercise modalities as a tool for the management of overweight.     

Dose-dependent increases in flow-mediated dilation following acute cocoa ingestion in healthy older adults

An inverse relation exists between intake of flavonoid-rich foods, such as cocoa, and cardiovascular-related mortality. Favorable effects of flavonoids on the endothelium may underlie these associations. We performed a randomized, double-blind, placebo-controlled study to test the hypothesis that acute cocoa ingestion dose dependently increases endothelium-dependent vasodilation, as measured by an increase in brachial artery flow-mediated dilation (FMD), in healthy older adults. Measurements were obtained before (preingestion) and after (1- and 2-h postingestion) ingestion of 0 (placebo), 2, 5, 13, and 26 g of cocoa in 23 adults (63 ± 2 yr old, mean ± SE). Changes in brachial artery FMD 1- and 2-h postingestion compared with preingestion were used to determine the effects of cocoa. FMD was unchanged 1 (Δ-0.3 ± 0.2%)- and 2-h (Δ0.1 ± 0.1%) after placebo (0 g cocoa). In contrast, FMD increased both 1-h postingestion (2 g cocoa Δ0.0 ± 0.2%, 5 g cocoa Δ0.8 ± 0.3%, 13 g cocoa Δ1.0 ± 0.3%, and 26 g cocoa Δ1.6 ± 0.3%: P < 0.05 compared with placebo for 5, 13, and 26 g cocoa) and 2-h postingestion (2 g cocoa Δ0.5 ± 0.3%, 5 g cocoa Δ1.0 ± 0.3%, 13 g cocoa Δ1.4 ± 0.2%, and 26 g cocoa Δ2.5 ± 0.4%: P < 0.05 compared with placebo for 5, 13, and 26 g cocoa) on the other study days. A serum marker of cocoa ingestion (total epicatechin) correlated with increased FMD 1- and 2-h postingestion (r = 0.44-0.48; both P < 0.05). Collectively, these results indicate that acute cocoa ingestion dose dependently increases brachial artery FMD in healthy older humans. These responses may help to explain associations between flavonoid intake and cardiovascular-related mortality in humans.     

Cardiovascular response to exercise in younger and older men

Measurements of cardiac performance for humans at various ages is influenced by the variable examined, the population and techniques employed, and the factors that co-vary with age, including the presence of disease and physical conditioning. Interstudy differences in the extent to which occult coronary disease is present in older subjects and in the level of physical conditioning among subjects may underlie the variable perspectives contained in the literature of how aging affects cardiovascular function. In carefully screened, highly motivated but not athletically trained community-dwelling subjects, resting cardiovascular parameters are not age related except for systolic blood pressure, which increases with age. During vigorous exercise the mechanisms used to achieve a high level of cardiac output shift from a dependence on a catecholamine-mediated increase in heart rate and inotropy to a dependence on the Frank Starling mechanism. One reason for the age difference in cardiovascular response to exercise may be a diminished responsiveness to beta-adrenergic stimulation in these subjects. In other elderly subjects who cannot exercise to high work loads, a decline in stroke volume as well as heart rate at peak exercise has been observed. Whether the inability of these individuals to augment stroke volume is caused by a decrease in the ability of the heart to increase diastolic filling, by a decrease in systolic pump function caused by an increased afterload, by intrinsic myocardial contractile defects, or by a greater diminution of the cardiovascular response to beta-adrenergic stimuli is presently unknown.     

The oxygen delivery response to acute hypoxia during incremental knee extension exercise differs in active and trained males

Background

It is well known that hypoxic exercise in healthy individuals increases limb blood flow, leg oxygen extraction and limb vascular conductance during knee extension exercise. However, the effect of hypoxia on cardiac output, and total vascular conductance is less clear. Furthermore, the oxygen delivery response to hypoxic exercise in well trained individuals is not well known. Therefore our aim was to determine the cardiac output (Doppler echocardiography), vascular conductance, limb blood flow (Doppler echocardiography) and muscle oxygenation response during hypoxic knee extension in normally active and endurance-trained males.

Methods

Ten normally active and nine endurance-trained males (VO_2max = 46.1 and 65.5 mL/kg/min, respectively) performed 2 leg knee extension at 25, 50, 75 and 100% of their maximum intensity in both normoxic and hypoxic conditions (FIO₂ = 15%; randomized order). Results were analyzed with a 2-way mixed model ANOVA (group × intensity).

Results

The main finding was that in normally active individuals hypoxic sub-maximal exercise (25 – 75% of maximum intensity) brought about a 3 fold increase in limb blood flow but decreased stroke volume compared to normoxia. In the trained group there were no significant changes in stroke volume, cardiac output and limb blood flow at sub-maximal intensities (compared to normoxia). During maximal intensity hypoxic exercise limb blood flow increased approximately 300 mL/min compared to maximal intensity normoxic exercise.

Conclusion

Cardiorespiratory fitness likely influences the oxygen delivery response to hypoxic exercise both at a systemic and limb level. The increase in limb blood flow during maximal exercise in hypoxia (both active and trained individuals) suggests a hypoxic stimulus that is not present in normoxic conditions.

     

Leukocytosis occurs in response to resistance exercise in men

The purpose of this study was to determine the effects of a single bout of resistance exercise on immune cell numbers of moderately active men. Subjects were 16 male volunteers (mean +/- standard deviation [SD] age 30 +/- 7 years, height 180.1 +/- 7.0 cm, mass 83.97 +/- 10.33 kg); 8 were randomly assigned to treatment and 8 to control groups. Treatment was a common resistance training routine (3 sets of 8-10 repetitions at 75% of 1 repetition maximum) of 8 large muscle mass exercises using resistance machines. Blood samples were drawn before exercise and at 0 minutes (P0), 15 minutes (P15), and 30 minutes (P30) postexercise. Control subjects sat quietly in the training facility; blood was drawn at the same intervals as treatment. Leukocyte and lymphocyte (LY) subpopulation numbers were determined. Statistical analysis was analysis of variance (ANOVA) (repeated measures, p < or = 0.050) and multiple comparisons (Dunn method) to isolate variability. All leukocyte subpopulations, except basophils (BA) and eosinophils (EO), increased and counts declined by P15 and P30. Only neutrophils (NE) did not return to preexercise levels by P30. The majority of resistance exercise induced leukocytosis was due to an increase in circulating LY (natural killer cells increased most, CD4+/CD8+ ratio unchanged) and monocytes (MO). The transient, inconsequential immune cell population responses to resistance exercise are similar to those during aerobic activity. The lack of large alterations in and rapid recovery from cell number changes suggests that resistance exercise is not immunosuppressive.     

Antioxidant status and oxidative stress at rest and in response to acute exercise in judokas and sedentary men

It is well recognized that acute strenuous exercise is accompanied by an increase in free-radical production and subsequent oxidative stress, in addition to changes in blood antioxidant status. Chronic exercise provides protection against exercise-induced oxidative stress by upregulating endogenous antioxidant defense systems. Little is known regarding the protective effect afforded by judo exercise. Therefore, we determined antioxidant and oxidative stress biomarkers at rest and in response to acute exercise in 10 competitive judokas and 10 sedentary subjects after mixed exercise (anaerobic followed by aerobic). The subjects performed a Wingate test, followed by 30 minutes of aerobic exercise performed at 60% of maximal aerobic power. Blood samples were taken, by an intravenous catheter, at rest (R), immediately after the physical exercise (P0), and at 5 (P5), 10 (P10), and 20 (P20) minutes postexercise. The measured parameters included the activity of the antioxidant enzymes superoxide dismutase, glutathione peroxidase, and glutathione reductase, in addition to α-tocopherol, and total antioxidant status. Malondialdehyde was measured as a representation of lipid peroxidation. At rest, the judokas had higher values for all antioxidant and oxidative stress markers as compared to the sedentary subjects (p < 0.05). Plasma concentrations of all parameters except for α-tocopherol increased significantly above resting values for both the judokas and sedentary subjects (p < 0.05) and remained elevated at 20 minutes postexercise. A significant postexercise decrease was observed for α-tocopherol (p < 0.05) at P20 for judokas and at P5 for sedentary subjects. These data indicate that competitive judo athletes have higher endogenous antioxidant protection compared to sedentary subjects. However, both groups of subjects experience an increase in exercise-induced oxidative stress that is not different.     

Effect of acute sympathetic nervous system activation on flow-mediated dilation of brachial artery

We tested the hypothesis that flow-mediated dilation (FMD) of the brachial artery would be impaired by acute increases in sympathetic nervous system activity (SNA) in models where similar peak shear stress stimulus was achieved by varying the duration of forearm muscle ischemia. Eleven healthy young men were studied under four different conditions, each with its own control: lower body suction (LBS), cold pressor test (CPT), mental arithmetic task (MAT), and activation of muscle chemoreflex (MCR). The duration of ischemia before observation of FMD by ultrasound imaging was 5 min each for control, LBS, and CPT; 3 min for MAT; and 2-min for MCR. Peak shear rate was not different between control and any of the SNA conditions, although total shear in the first minute was reduced in MAT. MCR was the only condition in which brachial artery vasoconstriction was observed before forearm occlusion [4.38 (SD 0.53) vs. control 4.60 (SD 0.53) mm, P < 0.05]; however, diameter increased to the same absolute value as that of the control, so the percent FMD was greater for MCR [9.85 (SD 2.33) vs. control 5.29 (SD 1.50)%]. Blunting of the FMD response occurred only in the CPT model [1.51 (SD 1.20)%]. During SNA, the increase in plasma cortisol from baseline was significant only for MCR; the increase in plasma norepinephrine was significant for MCR, LBS, and CPT; and the increase in epinephrine was significant only for MCR. These results showed that the four models employed to achieve increases in SNA had different effects on baseline brachial artery diameter and that blunted FMD is not a general response to increased SNA.     

Kinetics of cardiorespiratory response to dynamic and rhythmic-static exercise in men

Kinetics of cardiorespiratory response to dynamic (DE) and then to rhythmic-static exercise (RSE) was compared in nine male subjects exercising in an upright position on a cycle ergometer at an intensity of about 50% VO2max and a mean pedalling frequency of 60 rpm over 5 min. Respiratory frequency (fR), tidal volume (VT), minute ventilation (VE), heart rate (fc), stroke volume (SV), and cardiac output (Qt) were measured continuously. The RSE caused a greater increase in fR than DE, whereas VT increased more during DE. The effect of reciprocal changes in fR and VT was that VE and its kinetics, expressed as a time constant (tau), did not differ between experimental situations. The ventilatory equivalent for O2 (VE: VO2) was greater for RSE (31.3) than for DE (23.0, P less than 0.01). Elevation of fc was similar for both types of exercise. The SV increased suddenly at the beginning of DE from 54 ml to 74 ml and then decreased to the end of exercise. At the onset of RSE only a moderate increase in SV was observed, from 56 ml to 62 ml, and then SV remained stable. The DE caused a greater and faster increase in Qt (4.20 l.min-1, for tau equal to 16.1 s) than RSE (3.25 l.min-1, for tau equal to 57.0 s, P less than 0.05 and P less than 0.002, respectively). Total peripheral resistance was almost 40% greater for RSE than for DE. No relationship was found between Qt and VE at the first 15 s of both types of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiorespiratory response to exercise in men repeatedly exposed to extreme altitude

The ventilatory and heart rate responses to exercise were studied in four experienced high-altitude climbers at sea level and during a 6-wk period above 4,500 m to discover whether their responses to hypoxia were similar to those of high-altitude natives. Comparison was made with results from four scientists who lacked their frequent exposure to extreme altitude. The climbers had greater Vo2max at sea level and altitude but similar ventilatory responses to increasing exercise. On acute hypoxia at sea level their ventilatory response was less than that of scientists. Their heart rate response did not differ from that of scientists at sea level, but with acclimatization the reduction in response was significantly greater. Alveolar gas concentrations were similar after acclimatization, but climbers achieved these changes more rapidly. The increase in hematocrit was similar in the two groups. It is concluded that these climbers, unlike high-altitude residents, have cardiorespiratory responses to exercise similar to those of other lowlanders except that their ventilatory response was lower and the reduction in their heart rate response was greater.     

Exercise training enhances flow-mediated dilation in spontaneously hypertensive rats

This study investigated the effect of exercise training on the flow-mediated dilation (FMD) in gastrocnemius muscle arteries from spontaneously hypertensive rats (SHR). SHR and WKY rats were divided into sedentary and exercised groups. After swimming exercise for eight weeks, the isolated arteries were mounted on pressurized myograph and FMD responses examined. The role of nitric oxide (NO), prostaglandins (PGs) and endothelium derived hyperpolarizing factor (EDHF) on FMD were assessed by obtaining dilation responses in the presence and absence of pharmacological antagonists. N(omega)-nitro-L-arginine methyl ester (L-NAME), indomethacin (INDO) and tetraethylamonium (TEA) were used to inhibit nitric oxide synthase, cyclooxygenase and EDHF-mediated responses, respectively. The FMD response was significantly blunted in arteries of SHR compared with WKY rats, and, improved by exercise training in SHR (SHR-ET) group. In SHR arteries, L NAME and TEA did not affect dilation responses to flow, while INDO led to a significant enhancement in this response. Although dilation response was not altered by L-NAME in arteries obtained from trained SHR, TEA caused a significant attenuation and INDO led to significant increases. These results demonstrate that exercise training improves FMD in SHR, and, this enhancement induced by exercise training occurs through EDHF-mediated mechanism(s).     

Water exchange induced by unilateral exercise in active and inactive skeletal muscles.

Water exchange was evaluated in active (E-leg) and inactive skeletal muscles by using (1)H-magnetic resonance imaging. Six healthy subjects performed one-legged plantar flexion exercise at low and high workloads. Magnetic resonance imaging measured calf cross-sectional area (CSA), transverse relaxation time (T2), and apparent diffusion capacity (ADC) at rest and during recovery. After high workload, inactive muscle decreased CSA and T2 by 2.1% (P < 0.05) and 3.1% (P < 0.05), respectively, and left ADC unchanged. E-leg simultaneously increased CSA, T2, and ADC by 4.2% (P < 0.001), 15.5% (P < 0.05), and 12.5% (P < 0.001), respectively. In conclusion, ADC and T2 correlated highly with muscle volume, indicative of extravascular water displacement closely related to muscle activity and perfusion, which was presumably a combined effect of increased intracellular osmoles and hydrostatic forces as driving forces. A distinguishable muscle temperature release was initially detected in the E-leg after high workload, and the ensuing recovery of ADC and T2 indicated delayed interstitial restitution than restitution of the intracellular compartment. Furthermore, absorption of extravascular water was detected in inactive muscles at contralateral high-intensity exercise.     

Changes in venous blood content from active and inactive hindlimb during isotonic exercise

Venous blood samples were obtained from either exercising (n = 9) or nonexercising (n = 8) hindlimb during a progressive isotonic exercise in rabbits anesthetized with urethane and chloralose. Each experimental session consisted of 5-min nonexercise periods alternated with 6-min exercise periods, followed by a 10-min postexercise period. During each exercise period, stimulation of the distal stump of the right sciatic nerve at 1 Hz induced plantar flexions which lifted loads comparable to 2, 5, 8, 30, or 50% of an afterload at which only an isometric tension developed. Free-flowing venous blood samples were obtained before the first exercise period, during the last minute of each exercise period, and 10 min following the last exercise session. Increases in [Na+], [K+] and lactate concentration were obtained in blood from active limbs. Only lactate concentration increased in blood from nonexercising limbs, while [K+] decreased slightly. Inferences concerning the vascular volume response to this protocol would be quite different depending on the blood sampling site. Changes in blood from inactive tissue, further, may indicate only saturation of homeostatic mechanisms which normally compensate for vascular volume alterations initiated in active tissue.