Effects of 12 weeks of aerobic exercise on body composition and vascular compliance in obese boys.

AIM: This study tested the hypothesis that 12 weeks of air board exercise would enhance cardiorespiratory fitness and vascular compliance and reduce % body fat in obese Korean boys. METHODS: Twenty-two obese boys (>30% body fat) were studied. They were divided into 2 groups- an aerobic exercise group (N.=12), which trained 3 days/week, 50 min/day for 12 weeks, and a control group (N.=10). Control subjects only performed activities involved in their physical education classes. Body composition, cardiovascular fitness (20 m multistage endurance test performance) and vascular compliance were assessed before and after the completion of exercise training. RESULTS: The % changes in body fat (-4.6±0.9 vs. -1.5±1.0%), fat mass (-5.4±1.5 vs. -0.1±1.6%) and performance on the cardiovascular fitness test (14.3±2.5 vs. 3.7±1.6%) were greater in the exercise group than in the controls Compared to controls, % increases in vascular compliance were greater in the arms and legs of the exercise group (left arm: 2.8±0.5 vs. 2.0±2.9%; left leg: 2.6±1.2 vs. -0.5±2.0%; right arm: 2.9±0.9 vs. 0.3±2.9%; right leg: 4.8±1.8 vs. 1.5±2.0%). CONCLUSION: Results suggest that exercise training can reduce % body fat and enhance vascular compliance in obese male adolescents; changes that may reduce the risk for later development of cardiovascular disease.

Role of angiotensin II in hemodynamic responses to dynamic exercise in miniswine.

Angiotensin II (ANG II) is a potent vasoconstrictor of splanchnic and renal resistance vessels. Because ANG II increases during exercise and blood flow in the splanchnic and renal circulations decreases, we tested the hypothesis that ANG II plays a role in arterial blood pressure and regional blood flow responses to treadmill running in the miniswine. Consequently, 11 pigs were instrumented with epicardial electrocardiogram leads and left atrial and aortic catheters to assess mean arterial blood pressure (MAP), heart rate (HR), myocardial contractility, cardiac output, and regional blood flow during treadmill running. Each animal exercised for 20 min at 80% of its maximal HR reserve. Exercise was performed in the absence and presence of the ANG II AT1 receptor antagonist losartan (15-20 mg/kg). ANG II AT1 receptor blockade attenuated the MAP and systemic vascular resistance responses to dynamic exercise but had no effect on cardiac output, HR, or myocardial contractility. In addition, blood flow increased and/or regional vascular resistance decreased in the heart, kidneys, stomach, small intestine, and colon, whereas the reverse occurred in the skin and spleen. These data suggest that ANG II contributes to the increase in MAP and redistribution of cardiac output associated with dynamic exercise.

Potentiation of the exercise pressor reflex by muscle ischemia.

The reflex responses to static contraction are augmented by ischemia. The metabolic "error signals" that are responsible for these observed responses are unknown. Therefore this study was designed to test the hypothesis that static contraction-induced pressor responses, which are enhanced during muscle ischemia, are the result of alterations in muscle oxygenation, acid-base balance, and K+. Thus, in 36 cats, the pressor response, active muscle blood flow, and muscle venous pH, PCO2, PO2, lactate, and K+ were compared during light and intense static contractions with and without arterial occlusion. During light contraction (15-16% of maximal), active muscle blood flow increased without and decreased with arterial occlusion (+35 +/- 12 vs. -60 +/- 11%). Arterial occlusion augmented these pressor responses by 132 +/- 25%. Without arterial occlusion, changes (P less than 0.05) were seen in PO2, O2 content, PCO2, and K+. Lactate and pH were unchanged. With arterial occlusion, changes in muscle PCO2 were augmented and significant changes were seen in pH and lactate. During intense static contraction (67-69% of maximal), muscle blood flow decreased without arterial occlusion (-39 +/- 9%) and decreased further during occlusion (-81 +/- 6%). Arterial occlusion augmented the pressor responses by 39 +/- 12%. All metabolic variables increased during contraction without arterial occlusion, but occlusion failed to augment any of these changes. These data suggest that light static ischemic contractions cause increases in muscle PCO2 and lactate and decreases in pH that may signal compensatory reflex-induced changes in arterial blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Endogenous bradykinin in the thoracic spinal cord contributes to the exercise pressor reflex.

This investigation tested the hypothesis that bradykinin causes excitatory effects in the thoracic spinal cord that augment the exercise pressor reflex. Thus we performed 30 s of electrically stimulated static contraction of the hindlimb in the anesthetized cat (alpha-chloralose) to provoke reflex-induced increases in mean arterial pressure, maximal rate of rise of left ventricular pressure (dP/dt), and heart rate (i.e., the exercise pressor reflex). These three responses were compared before and 15 min after intrathecal injection of 2 micrograms (n = 3), 10 micrograms (n = 6), or 50 micrograms (n = 3) of the selective bradykinin B2- receptor antagonist HOE-140 into the thoracic spinal cord or 10 micrograms of this antagonist into the lumbar (n = 3) spinal cord. In three of the six cats in which 10 micrograms of HOE-140 were injected into the thoracic spinal cord, an additional contraction was performed 60-90 min after treatment. The 2-microgram dose of HOE-140 had no effect on the exercise pressor reflex. Injection of 10 micrograms of this antagonist into the thoracic spinal cord reduced the contraction-evoked pressor, maximal dP/dt, and heart rate responses by 49 +/-7, 58 +/- 4, and 64 +/- 13%, respectively (P < 0.05). Fifty micrograms of HOE-140 failed to attenuate these responses further. In the three cats in which an additional contraction was performed 60-90 min after treatment with 10 micrograms of the antagonist, blood pressure and dP/dt responses had returned, in part, toward initial values. Neither intravenous (n = 3) nor intrathecal injection of 10 micrograms of HOE-140 into the lumbar spinal cord had any effect on the contraction-induced cardiovascular responses. Thoracic injection of 50-200 ng of bradykinin provoked a pressor response of 26 +/- 5 mmHg that was abolished by a similar injection of 10 micrograms of HOE-140. These data suggest that endogenous bradykinin contributes to the exercise pressor reflex by an excitatory action in the thoracic spinal cord.

Bradykinin-induced chemoreflexes from skeletal muscle: implications for the exercise reflex.

We examined the cardiovascular response to bradykinin stimulation of skeletal muscle afferents and the effect of prostaglandins on this response. Intra-arterial injection of 1 microgram bradykinin into the gracilis muscle of cats reflexly increased mean arterial pressure by 16 +/- 2 mmHg, left ventricular end-diastolic pressure by 1.6 +/- 0.6 mmHg, maximal dP/dt by 785 +/- 136 mmHg/s, heart rate by 11 +/- 2 beats/min, and mean aortic flow by 22 +/- 3 ml/min. The hemodynamic responses were abolished following denervation of the gracilis muscle. The increases in mean arterial pressure and maximal dP/dt were reduced by 68 and 45%, respectively, following inhibition of prostaglandin synthesis with indomethacin (2-8 mg/kg iv). Treatment with prostaglandin E2 (PGE2, 15-25 micrograms ia) restored the initial increase in mean arterial pressure, but not dP/dt, caused by bradykinin stimulation. Injection of PGE2 (15-30 micrograms ia) into the gracilis, without prior treatment with indomethacin, augmented the bradykinin-induced increases in mean arterial pressure and dP/dt. We conclude that small doses of bradykinin injected into skeletal muscle are capable of reflexly activating the cardiovascular system and that prostaglandins are necessary for the full manifestation of the corresponding hemodynamic response. The pattern of hemodynamic adjustment following bradykinin injection into skeletal muscle is very similar to that induced by static exercise. Therefore, it is possible that intense exercise provides a stimulus for this bradykinin-induced reflex in vivo.

Bradykinin in reflex cardiovascular responses to static muscular contraction.

We examined the contribution of bradykinin to the reflex hemodynamic response evoked by static contraction of the hindlimb of anesthetized cats. During electrical stimulation of ventral roots L7 and S1, we compared the cardiovascular responses to hindlimb contraction before and after the following interventions: inhibition of converting enzyme (kininase II) with captopril (3-4 mg/kg, n = 6); inhibition of kallikrein activity with aprotinin (Trasylol, 20,000-30,000 KIU/kg, n = 8); and injection of carboxypeptidase B (500-750 U/kg, n = 7). Treatment with captopril augmented the rise in mean arterial blood pressure and maximal time derivative of pressure (dP/dt) caused by static contraction from 21 +/- 3 to 39 +/- 7 mmHg and 1,405 +/- 362 to 2,285 +/- 564 mmHg/s, respectively. Aprotinin attenuated the contraction-induced rise in mean arterial blood pressure (28 +/- 4 to 9 +/- 2 mmHg) and maximal dP/dt (1,284 +/- 261 to 469 +/- 158 mmHg/s). Carboxypeptidase B reduced the cardiovascular response to static contraction. Thus the mean arterial blood pressure response was decreased from 36 +/- 12 to 24 +/- 11 mmHg, maximal dP/dt from 1,618 +/- 652 to 957 +/- 392 mmHg/s, and heart rate from 12 +/- 2 to 7 +/- 1 beats/min. These data suggest that stimulation of muscle afferents by bradykinin contributes to a portion of the reflex cardiovascular response to static contraction.

Reactive oxygen species modify reflex cardiovascular responses to static contraction.

Reactive oxygen species can reflexly activate the cardiovascular system through stimulation of abdominal visceral afferents. The mechanism appears to involve hydroxyl radicals. We tested the hypothesis that reactive oxygen species contribute to the reflex cardiovascular response to static muscle contraction (i.e., the exercise pressor reflex). Thus blood pressure and heart rate responses to 5 min of intermittent electrically stimulated static contraction of the triceps surae muscles (15 s on, 15 s off) in anesthetized cats were compared before and after intravenous administration of the free radical scavengers dimethylthiourea (DMTU; 10 mg/kg; n = 8) or deferoxamine (Def; 10 mg/kg; n = 15). The contraction-induced pressor response was augmented from 51 +/- 6 to 61 +/- 7 mmHg after treatment with DMTU (P < 0.05) and from 44 +/- 8 to 58 +/- 8 mmHg after administration of Def (P < 0.05). Corresponding heart rate responses were not affected by either drug. Because this DMTU- or Def-induced augmentation of the exercise pressor reflex may have been due to a reduction in free radical-evoked vasodilation in the contracting skeletal muscle, popliteal artery blood velocity was measured with a Doppler flow transducer before and during contraction in the absence and presence of Def (n = 8). Blood velocity during contraction was not altered by Def (16 +/- 5 vs. 24 +/- 6 cm/s). These data suggest that reactive oxygen species exert an inhibitory effect on the exercise pressor reflex that is not associated with their local vasodilator properties. This response is opposite to that observed during stimulation of visceral afferents by reactive oxygen species.

Spinal vasopressin modulates the reflex cardiovascular response to static contraction.

Recent evidence has demonstrated that arginine vasopressin (AVP) may modulate primary afferent activity of nociceptors in the dorsal horn of the spinal cord. Because nociceptors are group III and IV afferents, spinal AVP also may modulate the activity of group III and IV afferents that cause reflex cardiovascular responses to muscle contraction. Thus, we compared the pressor (mean arterial pressure), myocardial contractile (dP/dt), and heart rate (HR) responses to electrically induced static contraction of the cat hindlimb before and after lumbar intrathecal (IT) injection (L1-L7) of AVP (n = 9), the V1 receptor antagonist d(CH2)5Tyr(Me)AVP (n = 6), the V2 receptor antagonist d(CH2)5[D-Ile2,Ile4,Ala-NH2(9)]AVP (n = 6), and the V2 agonist [Val4,D]AVP (n = 8). After IT injection of AVP (0.1 or 1 nmol) the pressor and contractile responses to static contraction were attenuated by 55 and 44%, respectively. HR was unchanged. Forty-five to 60 min after AVP injection, the contraction-induced pressor and contractile responses were restored to control levels. V1 receptor blockade augmented contraction-induced increases in mean arterial pressure (36%) and dP/dt (49%) but not HR. V2 receptor blockade had no effect on the cardiovascular response to contraction, whereas selective V2 stimulation attenuated the dP/dt (-20%) and HR (-33%) responses but not the pressor response. These results suggest that AVP attenuates the reflex cardiovascular response to contraction by modulating sensory nerve transmission from contracting muscle primarily via a V1 receptor mechanism in the lumbar spinal cord.

Bradykinin contributes to the exercise pressor reflex: mechanism of action.

This study determined the receptors responsible for mediating bradykinin's effect on skeletal muscle afferents that cause the pressor reflex in anesthetized cats. In eight cats, 1 microgram of bradykinin was injected intra-arterially into the gracilis muscle before and after intravenous injection of a kinin B2-receptor antagonist (NPC 17731, 20 micrograms/kg). Initial injection of bradykinin reflexly increased mean arterial pressure by 23 +/- 7 mmHg, maximal change in pressure over time by 439 +/- 272 mmHg/s, and heart rate by 11 +/- 4 beats/min. The hemodynamic response to bradykinin was abolished by kinin B2-receptor blockade. Similar injection of the kinin B1-receptor agonist des-Arg9-bradykinin caused no cardiovascular responses (n = 6). In eight different animals, mean arterial pressure, maximal change in left ventricular pressure over time, and heart rate responses to 30 s of electrically stimulated hindlimb contraction were attenuated by 50 +/- 6, 55 +/- 7, and 41 +/- 8%, respectively, after kinin B2-receptor blockade. In eight other animals, mean arterial pressure, maximal change in left ventricular pressure over time, and heart rate responses were reduced by 58 +/- 8, 66 +/- 6, and 40 +/- 12%, respectively, after inhibition of prostaglandin synthesis with indomethacin (2.5-3 mg/kg iv) and were then abolished by subsequent B2-receptor blockade. These data suggest that bradykinin contributes to the exercise pressor reflex through its action on kinin B2 receptors located on the nerve endings of the muscle afferents.(ABSTRACT TRUNCATED AT 250 WORDS)

Reflex effect of skeletal muscle mechanoreceptor stimulation on the cardiovascular system.

To determine the potential for mechanical stimulation of skeletal muscle to contribute to the reflex cardiovascular response to static contraction (exercise reflex), we examined the cardiovascular effects caused by either passive stretch or external pressure applied to the triceps surae muscles. First, the triceps surae were stretched to an average developed tension of 4.8 +/- 0.3 kg. This resulted in increases in mean arterial pressure (MAP) of 28 +/- 7 mmHg, dP/dt of 1,060 +/- 676 mmHg/s, and heart rate (HR) of 6 +/- 2 beats/min (P less than 0.05). Additionally, increments of 0.3, 0.5, 1.0, 2.0, 4.0, and 8.0 kg of tension produced by passive stretch elicited pressor responses of -6 +/- 1, 7 +/- 1, 16 +/- 3, 21 +/- 8, 28 +/- 6, and 54 +/- 9 mmHg, respectively. External pressure, applied with a cuff to the triceps surae to produce intramuscular pressures (125-300 mmHg) that were similar to those seen during static contraction, also elicited small increases in MAP (4 +/- 1 to 10 +/- 1 mmHg) but did not alter HR. Transection of dorsal roots L5-L7 and S1 abolished the responses to passive stretch and external pressure. Moreover, when the triceps surae were stretched passively to produce a pattern and amount of tension similar to that seen during static hindlimb contraction, a significant reflex cardiovascular response occurred. During this maneuver, the pressor response averaged 51% of that seen during contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Interactions between angiotensin II and nitric oxide during exercise in normal and heart failure rats.

We hypothesized that nitric oxide (NO) opposes ANG II-induced increases in arterial pressure and reductions in renal, splanchnic, and skeletal muscle vascular conductance during dynamic exercise in normal and heart failure rats. Regional blood flow and vascular conductance were measured during treadmill running before (unblocked exercise) and after 1) ANG II AT(1)-receptor blockade (losartan, 20 mg/kg ia), 2) NO synthase (NOS) inhibition [N(G)-nitro-L-arginine methyl ester (L-NAME); 10 mg/kg ia], or 3) ANG II AT(1)-receptor blockade + NOS inhibition (combined blockade). Renal conductance during unblocked exercise (4.79 +/- 0.31 ml x 100 g(-1) x min(-1) x mmHg(-1)) was increased after ANG II AT(1)-receptor blockade (6.53 +/- 0.51 ml x 100 g(-1) x min(-1) x mmHg(-1)) and decreased by NOS inhibition (2.12 +/- 0.20 ml x 100 g(-1) x min(-1) x mmHg(-1)) and combined inhibition (3.96 +/- 0.57 ml x 100 g(-1) x min(-1) x mmHg(-1); all P < 0.05 vs. unblocked). In heart failure rats, renal conductance during unblocked exercise (5.50 +/- 0.66 ml x 100 g(-1) x min(-1) x mmHg(-1)) was increased by ANG II AT(1)-receptor blockade (8.48 +/- 0.83 ml x 100 g(-1) x min(-1) x mmHg(-1)) and decreased by NOS inhibition (2.68 +/- 0.22 ml x 100 g(-1) x min(-1) x mmHg(-1); both P < 0.05 vs. unblocked), but it was unaltered during combined inhibition (4.65 +/- 0.51 ml x 100 g(-1) x min(-1) x mmHg(-1)). Because our findings during combined blockade could be predicted from the independent actions of NO and ANG II, no interaction was apparent between these two substances in control or heart failure animals. In skeletal muscle, L-NAME-induced reductions in conductance, compared with unblocked exercise (P < 0.05), were abolished during combined inhibition in heart failure but not in control rats. These observations suggest that ANG II causes vasoconstriction in skeletal muscle that is masked by NO-evoked dilation in animals with heart failure. Because reductions in vascular conductance between unblocked exercise and combined inhibition were less than would be predicted from the independent actions of NO and ANG II, an interaction exists between these two substances in heart failure rats. L-NAME-induced increases in arterial pressure during treadmill running were attenuated (P < 0.05) similarly in both groups by combined inhibition. These findings indicate that NO opposes ANG II-induced increases in arterial pressure and in renal and skeletal muscle resistance during dynamic exercise.

Bradykinin release from contracting skeletal muscle of the cat.

Results of previous studies from our laboratory suggest that bradykinin has a role in the exercise pressor reflex elicited by static muscle contraction. The purpose of this study was to quantify the release of bradykinin from contracting skeletal muscle. In 18 cats, blood samples were withdrawn directly from the venous effluent of the triceps surae muscles immediately before and after 30 s of static contraction producing peak muscle tensions of 33, 50, and 100% of maximum electrically stimulated contraction. Contractions producing muscle tensions of 50 and 100% of maximum increased muscle venous bradykinin levels by 27 +/- 9 and 19 +/- 10 pg/ml, respectively. Conversely, 33% maximum contraction did not alter muscle venous bradykinin concentrations. However, when captopril was administered to slow the degradation of bradykinin, muscle venous bradykinin increased from 68 +/- 15 pg/ml at rest to 106 +/- 18 after contractions of 33% of maximum. When muscle ischemia was induced by 2 min of arterial occlusion before and during 30 s of 33% of maximum contraction, muscle venous bradykinin increased by 15 +/- 5 pg/ml. In addition, contraction-induced changes in muscle venous pH and lactate strongly correlated with bradykinin concentrations (r = 0.80 and 0.83, respectively). These data demonstrate that static contraction of relatively high intensity evokes the release of bradykinin from skeletal muscle and that ischemia, decreased pH, and increased lactate are strongly correlated with this release.

Reflex cardiovascular and ventilatory responses to increasing H+ activity in cat hindlimb muscle.

Static exercise increases arterial pressure, heart rate, and ventilation, effects which are believed in part to arise reflexly from a metabolic stimulus in the working muscle. In anesthetized cats, we tested the hypothesis that intra-arterial injections of lactic and hydrochloric acid, which created levels of these substances in muscle similar to those seen during contraction, reflexly increased cardiovascular and ventilatory function. Hydrochloric acid (32 and 57 mM; 1 ml) injected into the arterial supply of the triceps surae decreased intramuscular pH from 7.26 +/- 0.05 to 7.17 +/- 0.05 (P less than 0.01) and reflexly increased arterial pressure (23 +/- 7 mmHg; P less than 0.01), heart rate (11 +/- 2 beats/min; P less than 0.001), and ventilation (187 +/- 72 ml/min; P less than 0.05). Static contraction of the triceps surae decreased intramuscular pH from 7.28 +/- 0.06 to 7.13 +/- 0.06 (P less than 0.01). Lactic acid was more potent in causing reflexes than was equimolar HCl. For example, lactic acid containing 4 mM lactate and 0.87 mM H+ reflexly increased arterial pressure, heart rate, and ventilation, whereas 0.87 mM HCl did not. Intra-arterial sodium lactate (13 and 33 mM) at a neutral pH had no effect on these variables. We conclude that contraction-induced accumulation of H+, especially that arising from lactic acid, might provide a metabolic stimulus to evoke reflex autonomic effects.

Effects of chronic exercise during aging on muscle and end-plate morphology in rats.

Terminal sprouting, myofiber atrophy, and fiber type changes were studied in soleus and distal gastrocnemius muscles of 21- and 26-mo-old rats and in rats who performed treadmill running from 21 to 26 mo. End-plate structure and muscle fiber types were demonstrated by staining for acetylcholinesterase and myosin ATPase activity. Terminal sprouting was expressed as the percentage of end plates with growth configurations. Fiber atrophy was assessed as percentage of small-diameter fibers. In all three groups, the percentage of small-diameter fibers was significantly smaller and the percentage of growth configurations significantly larger in the soleus than in the gastrocnemius. The exercised-soleus group had a significantly higher percentage of growth configurations than the 26-mo controls, which had a higher percentage than the 21-mo controls. Percentages among gastrocnemius groups were not different. Fiber type was similar among gastrocnemius groups. However, the exercised-soleus had significantly more slow-twitch fibers than the controls. These data suggest that the soleus responds differently to chronic exercise during aging than does the gastrocnemius.

Intramuscular accumulation of prostaglandins during static contraction of the cat triceps surae.

We previously demonstrated that muscle afferent endings are sensitized by exogenous prostaglandins during static contraction of skeletal muscle. The purpose of this study was to determine whether 30 s of static hindlimb contraction, induced by electrical stimulation of the cat sciatic nerve, increases the concentration of immunoreactive prostaglandin E2 (iPGE2) and 6-ketoprostaglandin F1 alpha (i6-keto-PGF1 alpha, the stable metabolite of prostaglandin I2) in muscle tissue. In addition, the role of ischemia in augmenting prostanoid production was examined. Gastrocnemius muscle was obtained by freeze-clamping tissue, and prostaglandins were extracted from muscle homogenates and measured by radioimmunoassay. Compared with precontraction values, high-intensity (68% of maximal tension) static contraction elevated gastrocnemius iPGE2 and i6-keto-PGF1 alpha by 45 and 53%, respectively (P less than 0.01). Likewise, when blood flow to the gastrocnemius was attenuated by arterial occlusion during and 2 min before low-intensity contraction (29% maximal tension), the intramuscular iPGE2 concentration was increased by 71% (P less than 0.01). Conversely, low-intensity contraction (30% of maximal tension) and arterial occlusion without contraction did not alter the concentration of either prostanoid. Our findings demonstrate that prostaglandins accumulate in muscle during static contraction. We believe that local muscle ischemia may provide a stimulus for this phenomenon. These prostaglandins therefore are available to sensitize afferent endings responsible for reflex adjustments during static muscle contraction.

Production of hydroxyl radicals in contracting skeletal muscle of cats.

Reactive oxygen species increase during exhaustive contraction of skeletal muscle, but characterization of the specific species involved and their rates of production during nonexhaustive muscle contraction have not been investigated. We hypothesized that the production rate of hydroxyl radical (.OH) increases in contracting muscle and that this rate is attenuated by pretreatment with deferoxamine (Def) or dimethylthiourea (DMTU). We measured the rate of production of .OH before, during, and after 5 min of intermittent static contraction of the triceps surae muscles in cats (n = 6) using the formation of p-, m-, and o-tyrosines by hydroxylation of phenylalanine. L-Phenylalanine (30 mg/kg i.v.) was administered to each animal 3 min before contraction. Blood samples were collected from the popliteal vein 1 min before contraction; 1, 3, and 4.5 min during contraction; and 1 min after contraction. During and after contraction, the cumulative production rates of p-, m-, and o-tyrosines were elevated by 42.84 +/- 5.41, 0.25 +/- 0.04, and 0.21 +/- 0.03 nmol.min-1.g-1, respectively, compared with noncontracting triceps surae muscles. Pretreatment with Def (10 mg/kg i.v.; n = 5) or DMTU (10 mg/kg i.v.; n = 4) decreased the cumulative rates of production of p-, m-, and o-tyrosines during and after contraction. Additionally, the rate of tyrosine production increased in proportion to the percentage of maximal tension developed by the triceps surae muscles. These results directly demonstrate that .OH is produced in vivo in the skeletal muscle of cats during intermittent static contraction and that production can occur before the onset of fatigue.

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

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

Effects of caffeine on blood pressure, heart rate, and forearm blood flow during dynamic leg exercise.

This study examined the acute effects of caffeine on the cardiovascular system during dynamic leg exercise. Ten trained, caffeine-naive cyclists (7 women and 3 men) were studied at rest and during bicycle ergometry before and after the ingestion of 6 mg/kg caffeine or 6 mg/kg fructose (placebo) with 250 ml of water. After consumption of caffeine or placebo, subjects either rested for 100 min (rest protocol) or rested for 45 min followed by 55 min of cycle ergometry at 65% of maximal oxygen consumption (exercise protocol). Measurement of mean arterial pressure (MAP), forearm blood flow (FBF), heart rate, skin temperature, and rectal temperature and calculation of forearm vascular conductance (FVC) were made at baseline and at 20-min intervals. Plasma ANG II was measured at baseline and at 60 min postingestion in the two exercise protocols. Before exercise, caffeine increased both systolic blood pressure (17%) and MAP (11%) without affecting FBF or FVC. During dynamic exercise, caffeine attenuated the increase in FBF (53%) and FVC (50%) and accentuated exercise-induced increases in ANG II (44%). Systolic blood pressure and MAP were also higher during exercise plus caffeine; however, these increases were secondary to the effects of caffeine on resting blood pressure. No significant differences were observed in heart rate, skin temperature, or rectal temperature. These findings indicate that caffeine can alter the cardiovascular response to dynamic exercise in a manner that may modify regional blood flow and conductance.

Static contraction causes a reflex-induced release of arginine vasopressin in anesthetized cats.

We tested the hypothesis that brief static contraction of the triceps surae muscle causes reflex-induced increases in plasma arginine vasopressin (AVP) in anesthetized cats. Arterial blood samples, for measurement of plasma AVP, were taken before and after 30 s of electrically stimulated static contraction performed at a low intensity (<20% of maximal; n = 5), a high intensity (>70% of maximal; n = 7), and a high intensity after denervation of the triceps surae (n = 5). The low intensity contraction protocol was repeated during alpha-adrenergic blockade (n = 7) to minimize potential baroreflex-induced inhibition of AVP release. Passive stretch of the triceps surae was conducted (n = 5) to determine effects of muscle mechanoreceptor stimulation on the release of AVP. Low intensity contraction had no effect on plasma AVP. During alpha-adrenergic blockade, this same contraction intensity caused this peptide to increase from 12.8 +/- 2.1 to 17.7 +/- 2.6 pg/ml. High intensity contraction caused an increase in AVP (13.2 +/- 3.5 to 26.1 +/- 6.6 pg/ml) that was abolished by denervation (14.4 +/- 3. 7 vs. 17.1 +/- 6.6 pg/ml). Passive stretch had no effect on plasma AVP. These findings suggest that brief static contraction causes increases in plasma AVP that are reflex in nature, intensity dependent, opposed by the arterial baroreflex, and probably unrelated to muscle mechanoreceptor activation.

The isometric athlete.

A number of normal daily and athletic activities require isometric or static exercise. Such sports as weight lifting and other high-resistance activities are used by athletes to gain strength and skeletal muscle bulk. However, static exercise also causes significant increases in blood pressure, heart rate, myocardial contractility, and cardiac output. These changes occur in response to central neural irradiation, called central command, as well as a reflex originating from statically contracting muscle. Studies have demonstrated that blood pressure appears to be the regulated variable, presumably because the increased pressure provides blood flow into muscles that have compressed their arterial inflow as a result of increases in intramuscular pressure created by contraction. Thus, static exercise is characterized by a pressure load to the heart and can be differentiated from dynamic (isotonic) exercise, which involves a volume load to the heart. Physical training with static exercise leads to concentric cardiac, particularly left ventricular, hypertrophy, whereas training with dynamic exercise leads to eccentric hypertrophy. Furthermore, the magnitude of cardiac hypertrophy is much less in athletes training with static than dynamic exercise. Neither systolic nor diastolic function is altered by the hypertrophic process associated with static exercise training. Many of the energy requirements for static exercise, particularly during more severe levels of exercise, are met by anaerobic glycolysis because the contracting muscle becomes deprived of blood flow. Training with repetitive static exercise therefore causes little increase in oxygen transport capacity, so that maximal oxygen consumption is either not or only minimally increased. Peripheral cardiovascular adaptations also can occur in response to static exercise training. Although controversial, these adaptations include modest decreases in resting blood pressure, smaller increases in blood pressure during a given workload, increases in muscle capillary-to-fiber ratio, improved lipid and lipoprotein profiles, and increases in glucose and insulin responsiveness. Some of these adaptations also have been found in cardiac patients and hypertensive patients and without any concomitant cardiovascular complications. However, in both healthy individuals and those with cardiovascular disease, the manner in which resistance training is performed may dictate the extent to which these adjustments take place. Specifically, training that involves frequent repetitions of moderate weight (and hence contains dynamic components) seems to produce the most beneficial results.