Forearm blood flow follows work rate during submaximal dynamic forearm exercise independent of sex.

To test the hypothesis that sex influences forearm blood flow (FBF) during exercise, 15 women and 16 men of similar age [women 24.3 +/- 4.0 (SD) vs. men 24.9 +/- 4.5 yr] but different forearm muscle strength (women 290.7 +/- 44.4 vs. men 509.6 +/- 97.8 N; P < 0.05) performed dynamic handgrip exercise as the same absolute workload was increased in a ramp function (0.25 W/min). Task failure was defined as the inability to maintain contraction rate. Blood pressure and FBF were measured on separate arms during exercise by auscultation and Doppler ultrasound, respectively. Muscle strength was positively correlated with endurance time (r = 0.72, P < 0.01) such that women had a shorter time to task failure than men (450.5 +/- 113.0 vs. 831.3 +/- 272.9 s; P < 0.05). However, the percentage of maximal handgrip strength achieved at task failure was similar between sexes (14% maximum voluntary contraction). FBF was similar between women and men throughout exercise and at task failure (women 13.6 +/- 5.3 vs. men 14.5 +/- 4.9 ml.min(-1).100 ml(-1)). Mean arterial pressure was lower in women at rest and during exercise; thus calculated forearm vascular conductance (FVC) was higher in women during exercise but similar between sexes at task failure (women 0.13 +/- 0.05 vs. men 0.11 +/- 0.04 ml.min(-1).100 ml(-1).mmHg(-1)). In conclusion, the similar FBF during exercise was achieved by a higher FVC in the presence of a lower MAP in women than men. Still, FBF remained coupled to work rate (and presumably metabolic demand) during exercise irrespective of sex.     

Reduced leg blood flow during dynamic exercise in older endurance-trained men

It is currentlyunclear whether aging alters the perfusion of active muscles duringlarge-muscle dynamic exercise in humans. To study this issue, directmeasurements of leg blood flow (femoral vein thermodilution) andsystemic arterial pressure during submaximal cycle ergometry (70, 140, and 210 W) were compared between six younger (Y; 22-30 yr) and sixolder (O; 55-68 yr) chronically endurance-trainedmen. Whole body O₂uptake, ventilation, and arterial and femoral venous samples forblood-gas, catecholamine, and lactate determinations were alsoobtained. Training duration (min/day), estimated leg muscle mass(dual-energy X-ray absorptiometry; Y, 21.5 ± 1.2 vs. O, 19.9 ± 0.9 kg), and blood hemoglobin concentration (Y, 14.9 ± 0.4 vs. O, 14.7 ± 0.2 g/dl) did not significantly differ (P > 0.05) between groups. Leg bloodflow, leg vascular conductance, and femoral venousO₂ saturation were ~20-30%lower in the older men at each work rate (allP < 0.05), despite similarlevels of whole body O₂ uptake. At210 W, leg norepinephrine spillover rates and femoral venous lactateconcentrations were more than twofold higher in the older men.Pulmonary ventilation was also higher in the older men at 140 (+24%)and 210 (+39%) W. These results indicate that leg blood flow andvascular conductance during cycle ergometer exercise are significantlylower in older endurance-trained men in comparison to their youngercounterparts. The mechanisms responsible for this phenomenon and theextent to which they operate in other groups of older subjects deservefurther attention.

     

Sweat rate vs. forearm blood flow during lower body negative pressure

Skin blood flow is inhibited when hyperthermia and added hypovolemic stresses are superimposed. We tested the hypothesis that part of this inhibition is a reduced drive for cutaneous active vasodilatation (AVD) with sweat rate (SR) taken as an indirect measure of the efferent drive for cutaneous AVD. We also inquired whether SR itself changes with redistribution of blood volume. Six healthy supine men were subjected to lower body negative pressure (LBNP) after heating in water-perfused suits increased esophageal temperatures (Tes) to a mean of 37.2 degrees C and at least doubled SR and forearm vascular conductance (FVC). Heating continued throughout LBNP and recovery. Sweat rate did not decrease with LBNP onset, although SR-Tes slopes during LBNP were reduced 28% from control. In four subjects the SR-Tes slope did not recover when LBNP was discontinued. These observations suggest that SR is not an effector of the low-pressure baroreflex. In contrast to SR, FVC abruptly fell 22% at the onset of LBNP. Thereafter, FVC-Tes slopes near zero or less occurred. The major effector for FVC inhibition with LBNP appears to be the neural vasoconstrictor system. A minor component due to reduced drive for cutaneous AVD probably occurs as well.     

Regional distribution of blood flow during mild dynamic leg exercise in the baboon

Five chair-restrained baboons were trained with operant techniques and a food reward to perform dynamic leg exercise. Cardiac output and blood flows to most tissues were determined by radioactive microsphere distribution. After 2 min of exercise mean arterial blood pressure had increased by 11 +/- 3% (SE), heart rate by 34 +/- 7%, cardiac output by 50 +/- 12%, and O2 consumption by 157 +/- 17%. The blood flow to exercising leg muscle increased by 585 +/- 338% and to the myocardium by 35 +/- 19%. Blood flow to torso and limb skin fell by 38 +/- 4 and 38 +/- 6%, respectively, and similar reductions occurred in adipose tissue blood flow. Nonworking skeletal muscle blood flow decreased by 30 +/- 10%. Renal blood flow was lowered by 16 +/-2%. The lower visceral organs had more variable responses, but when grouped together total splanchnic blood flow fell by 21 +/- 9%. Blood flow to the brain was unchanged with exercise, whereas spinal cord perfusion increased 23 +/- 3%. Thus during short dynamic exercise baboons redistributed blood flow away from skin, fat, nonworking muscles, and visceral organs to supply the needs of exercising muscles. Our data suggest the baboon is a useful animal model for investigating vascular responses of tissues, such as torso skin, adipose, individual visceral organs, and the spinal cord, that cannot be examined in humans.     

Perceived exertion related to heart rate and blood lactate during arm and leg exercise

To compare some psychophysiological responses to arm exercise with those to leg exercise, an experiment was carried out on electronically braked bicycle ergometers, one being adapted for arm exercise. Eight healthy males took part in the experiment with stepwise increases in exercise intensity every 4 min: 40-70-100-150-200 W in cycling and 20-35-50-70-100 W in arm cranking. Towards the end of each 4 min period, ratings of perceived exertion were obtained on the RPE scale and on a new category ratio (CR) scale:heart rate (HR) and blood lactate accumulation (BL) were also measured. The responses obtained were about twice as high or more for arm cranking than for cycling. The biggest difference was found for BL and the smallest for HR and RPE. The incremental functions were similar in both activities, with approximately linear increases in HR and RPE and positively accelerating functions for CR (exponents about 1.9) and BL (exponents 2.5 and 3.3 respectively). When perceived exertion (according to the CR scale) was set as the dependent variable and a simple combination of HR and BL was used as the independent variable, a linear relationship was obtained for both kinds of exercise, as has previously been found in cycling, running, and walking. The results thus give support for the following generalization: For exercise of a steady state type with increasing loads the incremental curve for perceived exertion can be predicted from a simple combination of HR and BL.     

Carotid baroreflex control of heart rate and blood pressure during ES leg cycling in paraplegics.

This study investigated control of heart rate (HR) and mean arterial pressure (MAP) at rest and during electrical stimulation (ES) leg cycling exercise (LCE) in paraplegics (Para). Seven men with complete spinal lesions (T(5)-T(11)) and six able-bodied (AB) men participated in this study. Beat-to-beat changes in HR and MAP were recorded during carotid sinus perturbation. Carotid baroreflex function curves were derived at rest and during ES-LCE for Para and during voluntary cycling (Vol) for AB. From rest to ES-LCE, oxygen uptake (VO(2)) increased (by 0.43 l/min) and HR rose (by 11 beats/min), yet MAP remained unchanged. In AB, Vol increased VO(2) (by 0.53 l/min), HR (by 22 beats/min), and MAP (by 8 mmHg). ES-LCE did not alter the carotid sinus pressure (CSP)-MAP relationship, but it displaced the CSP-HR relationship upward relative to rest. No rightward shift was observed during ES-LCE. Vol by AB produced an upward and rightward displacement of the CSP-MAP and CSP-HR relationships relative to rest. These findings suggested that the carotid sinus baroreflex was not reset during ES-LCE in Para.     

Respiratory muscle work compromises leg blood flow during maximal exercise

Harms, Craig A., Mark A. Babcock, Steven R. McClaran, DavidF. Pegelow, Glenn A. Nickele, William B. Nelson, and Jerome A. Dempsey.Respiratory muscle work compromises leg blood flow during maximalexercise. J. Appl. Physiol.82(5): 1573-1583, 1997.We hypothesized that duringexercise at maximal O₂ consumption (O_{2 max}),high demand for respiratory muscle blood flow() would elicit locomotor muscle vasoconstrictionand compromise limb . Seven male cyclists(O_{2 max} 64 ± 6 ml · kg¹ · min¹)each completed 14 exercise bouts of 2.5-min duration atO_{2 max} on a cycleergometer during two testing sessions. Inspiratory muscle work waseither 1) reduced via aproportional-assist ventilator, 2)increased via graded resistive loads, or3) was not manipulated (control).Arterial (brachial) and venous (femoral) blood samples, arterial bloodpressure, leg (legs;thermodilution), esophageal pressure, andO₂ consumption(O₂) weremeasured. Within each subject and across all subjects, at constantmaximal work rate, significant correlations existed(r = 0.74-0.90;P < 0.05) between work of breathing(Wb) and legs (inverse), leg vascular resistance (LVR), and leg O₂(O_{2 legs};inverse), and between LVR and norepinephrine spillover. Mean arterialpressure did not change with changes in Wb nor did tidal volume orminute ventilation. For a ±50% change from control in Wb,legs changed 2 l/min or 11% of control, LVRchanged 13% of control, and O₂extraction did not change; thusO_{2 legs}changed 0.4 l/min or 10% of control. TotalO_{2 max} was unchangedwith loading but fell 9.3% with unloading; thusO_{2 legs}as a percentage of totalO_{2 max} was 81% incontrol, increased to 89% with respiratory muscle unloading, anddecreased to 71% with respiratory muscle loading. We conclude that Wbnormally incurred during maximal exercise causes vasoconstriction inlocomotor muscles and compromises locomotor muscle perfusion andO₂.

     

Failure of prostaglandins to modulate the time course of blood flow during dynamic forearm exercise in humans

Shoemaker, J. K., H. L. Naylor, Z. I. Pozeg, and R. L. Hughson. Failure of prostaglandins to modulate the time course ofblood flow during dynamic forearm exercise in humans.J. Appl. Physiol. 81(4):1516-1521, 1996.The time course and magnitude of increases inbrachial artery mean blood velocity (MBV; pulsed Doppler), diameter(D; echo Doppler), mean perfusionpressure (MPP; Finapres), shear rate ( = 8 ^· MBV/D), andforearm blood flow (FBF = MBV ^· r²)were assessed to investigate the effect that prostaglandins (PGs) haveon the hyperemic response on going from rest to rhythmic exercise inhumans. While supine, eight healthy men performed 5 min of dynamichandgrip exercise by alternately raising and lowering a 4.4-kg weight(~10% maximal voluntary contraction) with a work-to-rest cycle of1:1 (s/s). When the exercise was performed with the arm positionedbelow the heart, the rate of increase in MBV and wasfaster compared with the same exercise performed above the heart.Ibuprofen (Ibu; 1,200 mg/day, to reduce PG-induced vasodilation) andplacebo were administered orally for 2 days before two separate testingsessions in a double-blind manner. Resting heart rate was reduced inIbu (52 ± 3 beats/min) compared with placebo (57 ± 3 beats/min)(P < 0.05) without change to MPP.With placebo, D increased in both armpositions from ~4.3 mm at rest to ~4.5 mm at 5 min of exercise(P < 0.05). This response was notaltered with Ibu (P > 0.05). Ibudid not alter the time course of MBV or forearm blood flow(P > 0.05) in either arm position. The was significantly greater in Ibu vs. placebo at 30 and 40 s of above the heart exercise and for all time points after 25 sof below the heart exercise (P < 0.05). Because PG inhibition altered the time course of at the brachial artery, but not FBF, it was concludedthat PGs are not essential in regulating the blood flow responses todynamic exercise in humans.

     

Hypohydration affects forearm vascular conductance independent of heart rate during exercise.

Elevated body core temperature stimulates cutaneous vasodilation, which can be modified by nonthermal factors. To test whether hypohydration affects forearm vascular conductance discretely from relative alterations in heart rate (HR), eight trained cyclists exercised progressively for 20 min each at 60, 120, and 180 W [approximately 22, 37, and 55% of maximal cycling O2 consumption (VO2peak), respectively] in a warm humid environment (dry bulb temperature 30 degrees C; wet bulb temperature 24 degrees C). Esophageal temperature and forearm blood flow were measured every 30 s, and mean arterial pressure and HR were measured at rest and during each exercise intensity (minutes 15, 35, and 55). In the hypovolemic (HP) compared with the euvolemic (EU) state, blood volume was contracted by 24-h fluid restriction an average of 510 ml, and this difference was sustained throughout exercise. The esophageal temperature and HR responses were similar between EU and HP states at 60 and 120 W but were significantly (P < 0.05) higher in HP by the end of 180 W. In contrast, the forearm blood flow response was significantly (P < 0.05) depressed during exercise at 120 and 180 W in HP, whereas mean arterial pressure remained similar between conditions. When body core temperature is elevated in a hypohydrated state, forearm vascular conductance is reduced at exercise intensities of approximately 37% VO2peak, which is independent of relative changes in HR. These findings are consistent with the notion that during exercise an attenuated cutaneous vasodilation is elicited by alterations in regionalized sympathetic outflow, which is unaccompanied by activation of cardiac pacemaker cells.     

Effects of emphysema on diaphragm blood flow during exercise

Chronichyperinflation of the lung in emphysema displaces the diaphragmcaudally, thereby placing it in a mechanically disadvantageous positionand contributing to the increased work of breathing. We tested thehypothesis that total and regional diaphragm blood flows are increasedin emphysema, presumably reflecting an increased diaphragm energeticdemand. Male Syrian Golden hamsters were randomly divided intoemphysema (E; intratracheal elastase 25 units/100 g body wt) andcontrol (C; saline) groups, and experiments were performed 16-20wk later. The regional distribution of blood flow withinthe diaphragm was determined by using radiolabeled microspheres inhamsters at rest and during treadmill exercise (walking at 20 feet/min,20% grade). Consistent with pronounced emphysema, lung volume per unitbody weight was greater in E hamsters (C, 59.3 ± 1.8; E, 84.5 ± 5.0 ml/kg; P < 0.001) and arterialPO₂ was lower both at rest (C, 74 ± 3; E, 59 ± 2 Torr; P < 0.001) and during exercise (C, 93 ± 3; E, 69 ± 4 Torr; P < 0.001). At rest, total diaphragm blood flow was not different between C and Ehamsters (C, 47 ± 4; E, 38 ± 4 ml · min¹ · 100 g¹;P = 0.18). In both C and E hamsters,blood flow at rest was lower in the ventral costal region of thediaphragm than in the dorsal and medial costal regions and the cruraldiaphragm. During exercise in both C and E hamsters, blood flowsincreased more in the dorsal and medial costal regions and in thecrural diaphragm than in the ventral costal region. Total diaphragmblood flow was greater in E hamsters during exercise (C, 58 ± 7; E,90 ± 14 ml · min¹ · 100 g¹;P = 0.03), as a consequence ofsignificantly higher blood flows in the medial and ventral costalregions and crural diaphragm. In addition, exercise-induced increasesin intercostal (P < 0.005) andabdominal (P < 0.05) muscle bloodflows were greater in E hamsters. The finding that diaphragm blood flowwas greater in E hamsters during exercise supports the contention thatemphysema increases the energetic requirements of the diaphragm.