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Biomedical subjects

G W Mack

Publications and source records attributed to G W Mack.

At least 55 records · Page 3Linked to original sources

Effects of varied air velocity on sweating and evaporative rates during exercise.

This study was designed to determine the extent to which changes in the evaporative power of the environment (Emax) affect sweating and evaporative rates. Six male subjects undertook four 60-min bouts of cycle ergometer exercise at 56% maximal O2 uptake (VO2max).Emax was varied by differences in ambient temperature and airflow; two exercise bouts took place at 24 degrees C and two at 35 degrees C, with air velocity at < 0.2 and 3.0 m/s in both. Total sweat production was estimated from body weight loss, whereas whole body evaporative rate was measured continuously from a Potter beam balance. Body core temperature was measured continuously from a thermocouple in the esophagus (T(es)), with mean skin temperature (Tsk) computed each minute from thermocouples at eight sites. Total body sweat loss was significantly greater (P < 0.05) in the 0.2- than in the 3.0-m/s condition at both 24 and 35 degrees C. Tsk was higher (P < 0.05) in the still-air conditions at both temperatures, but final T(es) was significantly higher (P < 0.05) in still air only in the 35 degrees C environment. Thus the reduced Emax in still air caused a greater heat storage, thereby stimulating a greater total sweat loss. However, in part because of reduced skin wettedness, the slope of the sweat rate-to-T(es) relation at 35 degrees C in the 3.0-m/s condition was 118% that at 0.2 m/s (P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Comparison of the forearm and calf blood flow response to thermal stress during dynamic exercise.

To examine the hypothesis that the skin blood flow response to body heating is not uniform over the entire body surface, we compared forearm (FBF) and calf (CBF) blood flow responses to an increase in core temperature (esophageal temperature, Tes) during dynamic exercise. We studied 13 physically active men during semi-recumbent one leg exercise and/or intermittent supine cycle exercise at 35 degrees C. During 30 min of one leg exercise, Tes, FBF, and CBF in the nonactive leg increased from 36.94 +/- 0.09 degrees C, 5.7 +/- 1.2, and 5.6 +/- 0.6 ml.(min.100 ml)-1 at rest to 37.97 +/- 0.10 degrees C, 27.0 +/- 2.4, and 11.1 +/- 0.8 ml.(min.100 ml)-1, respectively. The increase in blood flow per unit increase in Tes was much less in the calf than in the forearm. The ratio of the peak to resting blood flow averaged 6.5 in the forearm and 2.5 in the calf. During 60 min of intermittent supine two leg exercise, Tes, FBF, and CBF increased from 36.96 +/- 0.06 degrees C, 7.9 +/- 1.5, and 5.6 +/- 0.7 ml.(min.100 ml)-1 at rest to 37.91 +/- 0.07 degrees C, 23.6 +/- 3.0, and 11.4 +/- 1.9 ml.(min.100 ml)-1, respectively. Skin blood flow (SkBF) in the forearm and calf was estimated by using a simple cylindrical model, assuming skin thickness and resting muscle blood flow to be 0.2 cm and 2 ml.(min.100 ml)-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Elevated central venous pressure: a consequence of exercise training-induced hypervolemia?

Resting blood volumes and arterial and central venous pressures (CVP) were measured in 14 men before and after exercise training to determine whether training-induced hypervolemia is accompanied by a change in total vascular capacitance. In addition, resting levels of plasma arginine vasopressin (AVP), atrial natriuretic peptide (ANP), aldosterone (Ald), and norepinephrine (NE) were measured. The same measurements were conducted in seven subjects who did not undergo exercise and acted as controls. Exercise training consisted of 10 wk of controlled cycle exercise for 30 min/day, 4 days/wk at 75-80% of maximal O2 uptake (VO2max). A training effect was verified by a 20% increase in VO2max, a resting bradycardia, and a 9% increase in blood volume. Mean arterial blood pressure was unaltered by exercise training, but resting CVP increased by 16% (P less than 0.05). The percent change in blood volume from before to after training was linearly related to the percent change in CVP (r = 0.903, P less than 0.05). As a consequence of elevations in both blood volume and CVP, the volume-to-pressure ratio was unchanged after exercise training. Plasma AVP, ANP, Ald, and NE were unaltered. Our results indicate that elevated CVP is a consequence of training-induced hypervolemia without alteration in total effective venous capacitance.

Adult↗

Water and electrolyte balance in the vascular space during graded exercise in humans.

We analyzed the changes in water content and electrolyte concentrations in the vascular space during graded exercise of short duration. Six male volunteers exercised on a cycle ergometer at 20 degrees C (relative humidity = 30%) as exercise intensity was increased stepwise until voluntary exhaustion. Blood samples were collected at exercise intensities of 29, 56, 70, and 95% of maximum aerobic power (VO2max). A curvilinear relationship between exercise intensity and Na+ concentration in plasma ([Na+]p) was observed. [Na+]p significantly increased at 70% VO2max and at 95% VO2max was approximately 8 meq/kgH2O higher than control. The change in lactate concentration in plasma ([Lac-]p) was closely correlated with the change in [Na+]p (delta[Na+]p = 0.687 delta[Lac-]p + 1.79, r = 0.99). The change in [Lac-]p was also inversely correlated with the change in HCO3- concentration in plasma (delta[HCO3-]p = -0.761 delta[Lac-]p + 0.22, r = -1.00). At an exercise intensity of 95% VO2max, 60% of the increase in plasma osmolality (Posmol) was accounted for by an increase in [Na+]p. These results suggest that lactic acid released into the vascular space from active skeletal muscles reacts with [HCO3-]p to produce CO2 gas and Lac-. The data raise the intriguing notion that increase in [Na+]p during exercise may be caused by elevated Lac-.

Adult↗

Effect of hypovolemia on forearm vascular resistance control during exercise in the heat.

To determine the influence of hypovolemia on the control of forearm vascular resistance (FVR) during dynamic exercise, we studied five physically active men during 60 min of supine cycle ergometer exercise bouts at 35 degrees C in control (normovolemic) and hypovolemic conditions. Hypovolemia was achieved by 3 days of diuretic administration and resulted in an average decrease in plasma volume of 15.9%. Relative to normovolemia, hypovolemia caused an attenuation of the progressive rise in forearm blood flow (P less than 0.05) and an increase in heart rate (P less than 0.05) during exercise. Because mean arterial blood pressure during hypovolemic exercise was well maintained, the attenuation of forearm blood flow was due entirely to a relative increase in FVR. At the onset of dynamic exercise, FVR was increased significantly in control and hypovolemic conditions by 13.2 and 27.1 units, respectively. The increase in FVR was significantly different between control and hypovolemic conditions as well. We attributed the increased vasoconstrictor bias during hypovolemia to cardiopulmonary baroreceptor unloading and/or an increased sensitivity to cardiopulmonary baroreceptor unloading. We concluded that reduced blood flow to the periphery during exercise in the hypovolemic condition was caused entirely by an increase in vascular resistance, thereby preserving arterial blood pressure and adequate perfusion to the organs requiring increased flow.

Adult↗

Plasma volume expansion in humans after a single intense exercise protocol.

We used intense intermittent exercise to produce a 10% expansion of plasma volume (PV) within 24 h and tested the hypothesis that PV expansion is associated with an increase in plasma albumin content. The protocol consisted of eight 4-min bouts of exercise at 85% maximal O2 uptake with 5-min recovery periods between bouts. PV, plasma concentrations of albumin and total protein (TP), and plasma osmolality were measured before and during exercise and at 1, 2, and 24 h of recovery from exercise. During exercise, PV decreased by 15%, while plasma TP and albumin content remained at control levels. At 1 h of recovery, plasma albumin content was elevated by 0.17 +/- 0.04 g/kg body wt, accounting for the entire increase in plasma TP content. PV returned to control level at 1 h of recovery without fluid intake by the subjects, despite a 820 +/- 120-g reduction in body weight. At 2 h of recovery, plasma TP content remained significantly elevated, and plasma TP and albumin concentration were significantly elevated. At 24 h of recovery, PV was expanded by 4.5 +/- 0.7 ml/kg body wt (10 +/- 1%), estimated from hematocrit and hemoglobin changes, and by 3.8 +/- 1.3 ml/kg body wt (8 +/- 3%), measured by Evans blue dye dilution. Plasma albumin content was increased by 0.19 +/- 0.05 g/kg body wt at 24 h of recovery. If 1 g of albumin holds 18 ml of water, this increase in plasma albumin content can account for a 3.4-ml/kg body wt expansion of the PV. No significant changes in plasma osmolality occurred during recovery, but total plasma osmotic content increased in proportion to PV.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Cardiopulmonary baroreflex control of forearm vascular resistance after acute blood volume expansion.

We report the stimulus-response characteristics of cardiopulmonary (CP) baroreflex control of forearm vascular resistance (FVR) in young adult male volunteers before and after: 1) blood volume expansion (8 ml/kg infusion of 5% human serum albumin solution, n = 5) and 2) a redistribution of blood volume toward the heart (6 degrees head-down tilt (HDT), n = 6). We assessed the relationship between reflex stimulus (i.e., changes in central venous pressure (CVP] and response (i.e., FVR) during unloading of CP mechanoreceptors with lower body negative pressure (0 to -20 mm Hg). Changes in CVP were estimated from changes in venous pressure of a large peripheral vein of the dependent arm with the subject in the right lateral decubitus position. In all conditions, reflex forearm vasoconstriction occurred in response to a reduction in estimated CVP. The absolute change in FVR per unit of CVP was reduced from -4.24 +/- 1.68 to -2.15 +/- 1.16 units/mm Hg (p less than 0.05) following blood volume expansion but was similar before (-3.34 +/- 0.89 units/mm Hg) and during 6 degrees HDT (-3.30 +/- 0.92 units/mm Hg). The reduced sensitivity of the CP baroreflex following volume expansion was manifested primarily as a smaller FVR response to LBNP (p less than 0.05). Blood volume expansion and 6 degrees HDT increased resting estimated CVP by 1.5 and 0.9 mm Hg, respectively (p less than 0.05) and resting levels of FVR decreased slightly.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Diminished baroreflex control of forearm vascular resistance following training.

The stimulus-response characteristics of cardiopulmonary baroreflex control of forearm vascular resistance (FVR units in mm Hg.min.100 ml.ml-1) were studied in 14 volunteers before and after 10 wk of endurance training. We assessed the relationship between reflex stimulus (changes in central venous pressure, CVP) and response (FVR) during unloading of cardiopulmonary baroreceptors with lower body negative pressure (LBNP, 0 to -20 mm Hg). Changes in CVP during LBNP were estimated from pressure changes in a large peripheral vein in the dependent arm of the subject in the right lateral decubitus position. Maximal oxygen uptake (VO2max) and total blood volume increased with endurance training from 37.8 +/- 1.4 ml.min-1.kg-1 and 63.6 +/- 2.1 ml.kg-1 to 45.3 +/- 1.4 ml.min-1.kg-1 and 69.3 +/- 2.8 ml.kg-1, respectively (P less than 0.05). Reflex forearm vasoconstriction occurred in response to a reduction in estimated CVP, and the absolute change in FVR per unit of CVP was reduced from -5.96 +/- 0.79 to -4.06 +/- 0.52 units.mm Hg-1 (P less than 0.05) following exercise training but was unchanged from -6.10 to 0.57 to -6.22 +/- 0.94 units.mm Hg-1 for the time control group (N = 7). Resting values for FVR were similar before and after exercise training; however, resting estimated CVP was elevated from 9.5 +/- 0.5 mm Hg before training to 11.3 +/- 0.6 mm Hg after training.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effect of saline infusion during exercise on thermal and circulatory regulations.

To quantify the effect of an acute increase in plasma volume (PV) on forearm blood flow (FBF), heart rate (HR), and esophageal temperature (Tes) during exercise, we studied six male volunteers who exercised on a cycle ergometer at 60% of maximal aerobic power for 50 min in a warm [(W), 30 degrees C, less than 30% relative humidity (rh)] or cool environment [(C), 22 degrees C, less than 30% rh] with isotonic saline infusion [Inf(+)] or without infusion [Inf(-)]. The infusion was performed at a constant rate of 0.29 ml.kg body wt-1.min-1 for 20-50 min of exercise to mimic fluid intake during exercise. PV decreased by approximately 5 ml/kg body wt within the first 10 min of exercise in all protocols. Therefore, PV in Inf(-) was maintained at the same reduced level by 50 min of exercise in both ambient temperatures, whereas PV in Inf(+) increased toward the preexercise level and recovered approximately 4.5 ml/kg body wt by 50 min in both temperatures. The restoration of PV during exercise suppressed the HR increase by 6 beats/min at 50 min of exercise in W; however, infusion had no effect on HR in C. In W, FBF in Inf(+) continued to increase linearly as Tes rose to 38.1 degrees C by the end of exercise, whereas FBF in Inf(-) plateaued when Tes reached approximately 37.7 degrees C. The infusion in C had only a minor effect on FBF.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Control of total peripheral resistance during hyperthermia in rats.

To elucidate the effect of blood volume on the circulatory adjustment to heat stress, we studied alpha-chloralose-anesthetized rats at three levels of blood volume: normovolemia (NBV), hypervolemia (HBV; +32% plasma volume by isotonic albumin solution infusion), and hypovolemia (LBV; -16% plasma volume by furosemide administration). Body surface heating was performed with an infrared lamp to raise arterial blood temperature (Tb) at the rate of approximately 0.1 degree C/min. Before heating, central venous pressure (CVP) was significantly higher in HBV (0.41 +/- 0.25 mmHg) and lower in LBV (-1.44 +/- 0.22 mmHg) than in NBV (-0.41 +/- 0.10 mmHg). The Tb at which CVP started to decrease was approximately 40 degrees C in HBV, approximately 41 degrees C in NBV, and approximately 42 degrees C in LBV, and it decreased by 1.53 +/- 0.14, 1.92 +/- 0.24, and 0.62 +/- 0.14 mmHg from 37 to 43 degrees C of Tb in HBV, NBV, and LBV, respectively. Stroke volume was closely correlated with CVP, and this relationship was not affected by Tb. Heart rate responses to the raised Tb were similar among the three groups. Mean arterial pressure (MAP) was not affected by blood volume modification or CVP and was maintained at preheating (Tb 37 degrees C) level until Tb rose to 40 degrees C. Above this Tb, MAP increased until Tb reached 43 degrees C (+30-40 mmHg) for all three groups. Total peripheral resistance (TPR) was inversely correlated with CVP, and the slope of the linear relationship between TPR and CVP in LBV was three- to fourfold steeper than in NBV or HBV.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Cutaneous vascular reflexes during exercise in the heat.

Eight relatively fit men performed cycle ergometer exercise (50% VO2max) for 30 min at 35 degrees C, less than 40% rh. To determine the importance of changes in cardiac filling pressure on the cutaneous vascular responses during exercise, we compared data from eight control (normovolemic) and four hypovolemic (19.5% decrease in plasma volume (PV) induced by diuretics) experiments. Cardiac output was maintained at 13.9 +/- 0.8 l.min-1 during steady state exercise in the two conditions. However, heart rate was higher (P less than 0.05) and stroke volume (SV) was slightly, although not statistically lower during hypovolemic exercise. Forearm venous compliance (FVC) was significantly lower during hypovolemic exercise than during control exercise (P less than 0.05). The increases in forearm blood flow and arterial blood pressure during exercise were not affected significantly by hypovolemia. FVC and SV in both conditions were linearly related to changes in central venous pressure during exercise (r2 = 0.88 and 0.78, respectively). Since changes in arterial pressure during exercise were not correlated with the observed arteriomotor and venomotor responses, we concluded that low pressure baroreceptors may have induced peripheral vascular reflexes, which act to maintain cardiac output during exercise in the heat.

Adult↗

Thermoregulation in mildly hypertensive men during beta-adrenergic blockade.

Nonselective beta 1,beta 2-adrenergic blockade (nBB) reduces the cutaneous blood flow and sweating responses to exercise in normotensive men and results in a relative increase in heat storage. To determine whether hypertensives incur similar problems in thermoregulation, we studied six mildly hypertensive men during 30 min of cycle ergometer exercise at 60% maximum O2 uptake at 22 degrees C. Each subject ingested either propranolol (Pr, 80 mg; nBB), metoprolol (Me, 50 mg; cardioselective, sBB), pindolol (Pi, 5 mg; nBB), or placebo (Pl) capsules 2 h before exercise in a double-blind crossover design. Steady-state exercise heart rate, systolic blood pressure (SBP), and cardiac output (Q) were reduced from means (+/- SD) of 134 +/- 7 beats.min-1, 181 +/- 5 mm Hg, and 14.5 +/- 0.9 l.min-1, respectively, with Pl to 107 +/- 3 beats.min-1, 159 +/- 7 mm Hg, and 12.7 +/- 1.1 l.min-1, respectively, with beta-blockade (BB, average of Pr, Me, and Pi) (P less than 0.05). During nBB, we found 1) a decrease in peak forearm blood flow (FBF) and 2) a reduction in the slopes of the FBF-esophageal temperature (Tes) and local chest sweat rate-Tes (Pr only) relationships. These resulted in a trend toward higher Tes at 30 min of exercise. Forearm vascular resistance was increased with nBB but not sBB, demonstrating a relative cutaneous vasoconstriction during nBB. Since nBB and sBB produced similar effects on the central circulatory variables (SBP and Q) but had different effects on FBF and FVR, our data do not support a role for baroreflexes in the altered control of FBF during BB.

Analysis of Variance↗

Shift in body fluid compartments after dehydration in humans.

To investigate the influence of [Na+] in sweat on the distribution of body water during dehydration, we studied 10 volunteer subjects who exercised (40% of maximal aerobic power) in the heat [36 degrees C, less than 30% relative humidity (rh)] for 90-110 min to produce a dehydration of 2.3% body wt (delta TW). After dehydration, the subjects rested for 1 h in a thermoneutral environment (28 degrees C, less than 30% rh), after which time the changes in the body fluid compartments were assessed. We measured plasma volume, plasma osmolality, and [Na+], [K+], and [Cl-] in plasma, together with sweat and urine volumes and their ionic concentrations before and after dehydration. The change in the extracellular fluid space (delta ECF) was estimated from chloride distribution and the change in the intracellular fluid space (delta ICF) was calculated by subtracting delta ECF from delta TW. The decrease in the ICF space was correlated with the increase in plasma osmolality (r = -0.74, P less than 0.02). The increase in plasma osmolality was a function of the loss of free water (delta FW), estimated from the equation delta FW = delta TW - (loss of osmotically active substance in sweat and urine)/(control plasma osmolality) (r = -0.79, P less than 0.01). Free water loss, which is analogous to "free water clearance" in renal function, showed a strongly inverse correlation with [Na+] in sweat (r = -0.97, P less than 0.001). Fluid movement out of the ICF space attenuated the decrease in the ECF space.(ABSTRACT TRUNCATED AT 250 WORDS)

Algorithms↗

Role of osmolality and plasma volume during rehydration in humans.

To determine how the sodium content of ingested fluids affects drinking and the restoration of the body fluid compartments after dehydration, we studied six subjects during 4 h of recovery from 90-110 min of a heat [36 degrees C, less than 30% relative humidity (rh)] and exercise (40% maximal aerobic power) exposure, which caused body weight to decrease by 2.3%. During the 1st h, subjects rested seated without any fluids in a thermoneutral environment (28 degrees C, less than 30% rh) to allow the body fluid compartments to stabilize. Over the next 3 h, subjects rehydrated ad libitum using tap water and capsules containing either placebo (H2O-R) or 0.45 g NaCl (Na-R) per 100 ml water. During the 3-h rehydration period, subjects restored 68% of the lost water during H2O-R, whereas they restored 82% during Na-R (P less than 0.05). Urine volume was greater in H2O-R than in Na-R; thus only 51% of the lost water was retained during H2O-R, whereas 71% was retained during Na-R (P less than 0.05). Plasma osmolality was elevated throughout the rehydration period in Na-R, whereas it returned to the control level by 30 min in H2O-R (P less than 0.05). Changes in free water clearance followed changes in plasma osmolality. The restoration of plasma volume during Na-R was 174% of that lost. During H2O-R it was 78%, which seemed to be sufficient to diminish volume-dependent dipsogenic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Involvement of sodium retention hormones during rehydration in humans.

We investigated the relation between involuntary dehydration and the mechanisms affecting Na+ retention in the body, focusing on the renin-angiotensin-aldosterone system. Six adult males were dehydrated to 2.3% of their body weight by an exercise-heat regimen, followed by rehydration (180 min) with tap water (H2O-R) or 0.45% NaCl solution (Na-R). We measured plasma renin activity (PRA) and aldosterone levels (PA) before dehydration (control), after dehydration, and at 60, 120, and 180 min of rehydration. During the 3-h rehydration period, subjects, restored 51% of the water lost during H2O-R and 71% during Na-R (P less than 0.05). Plasma volume was reduced by an average of 4.5% after dehydration. After 180 min of rehydration, plasma volume restoration during Na-R was to 174% of that lost, and during H2O-R it was to 78% of that lost. We found significant correlations between the change in plasma volume and PRA (r = -0.70, P less than 0.001) and between PRA and PA (r = 0.71, P less than 0.001). In both recovery conditions, PRA increased significantly after dehydration (P less than 0.05) and decreased almost to the control level by 180 min of rehydration, at which time the plasma volume deficit was restored. The change in PA paralleled that in PRA. The rate of sodium excretion was correlated with PA levels in both groups (r = -0.58, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effect of beta-adrenergic blockade on thermoregulation during exercise.

To resolve conflicting reports concerning the effects of beta-blockade (BB) on thermoregulatory reflexes during exercise, we studied six fit men during 40 min of cycle ergometer exercise at 60% maximum O2 consumption at ambient temperatures of 22 and 32 degrees C. Two hours before exercise, each subject ingested a capsule containing either 80 mg of propranolol or placebo in single-blind fashion. Heart rate at 40 min of exercise was reduced (P less than 0.01) from 125 to 103 beats min at 22 degrees C and 137 to 104 beats min at 32 degrees C, demonstrating effective BB. After 40 min of exercise, esophageal temperature (Tes) was elevated with BB (P less than 0.05) from 37.66 +/- 0.04 to 38.14 +/- 0.03 and 38.13 +/- 0.04 to 38.41 +/- 0.04 degrees C at 22 and 32 degrees C, respectively. The elevated Tes resulted from a reduced core-to-skin heat flux at both temperatures, indicated by a reduction in the slope of the forearm blood flow (FBF)-Tes relationship, and a decrease in maximal FBF. Systolic blood pressure was decreased 20 mmHg with BB (P less than 0.01), whereas diastolic blood pressure was unchanged, reducing arterial pulse pressure (PP). Because PP was decreased and cardiac filling pressure was presumably not reduced (since cardiac stroke volume was elevated), we suggest that at least a part of the relative increase in peripheral vasomotor tone during BB was the consequence of reduced sinoaortic baroreceptor stimulation.

Administration, Oral↗

Diminished baroreflex control of forearm vascular resistance in physically fit humans.

The stimulus-response characteristics of cardiopulmonary baroreflex control of forearm vascular resistance (FVR) were studied in five unfit [UF, maximal O2 consumption (VO2 max) = 38.5 ml X min-1 X kg-1] and six fit (F, VO2 max = 57.0 ml X min-1 X kg-1) subjects. We assessed the relationship between reflex stimulus, i.e., changes in central venous pressure (CVP) and response, i.e., FVR, during selective unloading of the cardiopulmonary mechanoreceptors with lower body negative pressure (0 to -20 mmHg). The linear relationship between FVR and CVP, the gain of this baroreflex, was significantly diminished in the F subjects, -2.42 +/- 0.57 U/mmHg, compared with the UF, -5.15 +/- 0.58 U/mmHg. Both groups, F and UF, had similar resting values for CVP and FVR; thus the diminished gain in F subjects was not simply an artifact resulting from a shift of the set point along the baroreflex stimulus-response curve. We also found a linear relationship between baroreflex gain and total blood volume (r = 0.59, P less than 0.05). We conclude that the gain of this vascular reflex is attenuated in trained individuals and is related to cardiovascular adaptations, such as an increased blood volume, associated with exercise training.

Blood Pressure↗